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  1. Pineal parenchymal tumor of intermediate differentiation: Case series and literature review: Is it time for a consensus?

    Fri, 18 Apr 2025 20:34:01 -0000

    Pineal parenchymal tumor of intermediate differentiation: Case series and literature review: Is it time for a consensus? Category: Article Type: Siddharth Srinivasan1, Ajay Hegde2, Rajesh Nair3, Ravi Teja Jampani3, Mohammad Ashraf4, Dhanwanth Chigurupati4, Bharat Kumar Raju3, Susanth Subramanian3, Udgam Baxi3, Yasaswi Kanneganti3, Sarah Johnson5, Bhavna Nayal6, Geeta Vasudevan6, Deepak Nayak6, Girish Menon3Department of Neurosurgery, Institute … Continue reading Pineal parenchymal tumor of intermediate differentiation: Case series and literature review: Is it time for a consensus?
    <div><!DOCTYPE html PUBLIC "-//W3C//DTD HTML 4.0 Transitional//EN" "http://www.w3.org/TR/REC-html40/loose.dtd"> <html><head><meta http-equiv="content-type" content="text/html; charset=utf-8"></head><body><div class="row"><div class="col-lg-9 col-sm-8 col-xs-12"><div class="media-body details-body"> <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13511"><h2 class="media-heading"><h2 class="media-heading">Pineal parenchymal tumor of intermediate differentiation: Case series and literature review: Is it time for a consensus?</h2></h2></a> </div><div class="disp_categories"> <p><label>Category: </label><span></span></p> <p><label>Article Type: </label><span></span></p> </div><a href="mailto:siddharth.srinivasan93@gmail.com" target="_top">Siddharth Srinivasan</a><sup>1</sup>, <a href="mailto:dr.ajayhegde@gmail.com" target="_top">Ajay Hegde</a><sup>2</sup>, <a href="mailto:rajesh.nair@manipal.edu" target="_top">Rajesh Nair</a><sup>3</sup>, <a href="mailto:jcravitejachowdary@gmail.com" target="_top">Ravi Teja Jampani</a><sup>3</sup>, <a href="mailto:mohammad.ashraf6@nhs.scot" target="_top">Mohammad Ashraf</a><sup>4</sup>, <a href="mailto:dhanwanth.chigurupati@nhs.scot" target="_top">Dhanwanth Chigurupati</a><sup>4</sup>, <a href="mailto:bharatkmr@gmail.com" target="_top">Bharat Kumar Raju</a><sup>3</sup>, <a href="mailto:susanth.s@manipal.edu" target="_top">Susanth Subramanian</a><sup>3</sup>, <a href="mailto:udgambaxi@gmail.com" target="_top">Udgam Baxi</a><sup>3</sup>, <a href="mailto:yasaswi2u@gmail.com" target="_top">Yasaswi Kanneganti</a><sup>3</sup>, <a href="mailto:johnson.sarah27@mayo.edu" target="_top">Sarah Johnson</a><sup>5</sup>, <a href="mailto:bhavna.nayal@manipal.edu" target="_top">Bhavna Nayal</a><sup>6</sup>, <a href="mailto:geeta.v@manipal.edu" target="_top">Geeta Vasudevan</a><sup>6</sup>, <a href="mailto:deepak.nayak@manipal.edu" target="_top">Deepak Nayak</a><sup>6</sup>, <a href="mailto:girish.menon@manipal.edu" target="_top">Girish Menon</a><sup>3</sup><ol class="smalllist"><li>Department of Neurosurgery, Institute of Neurosciences, Glasgow, United Kingdom</li><li>Department of Neurosurgery, Manipal Hospital, Bengaluru, Karnataka, India</li><li>Department of Neurosurgery, Kasturba Medical College and Hospital, Manipal, Karnataka, India</li><li>Department of Neurosurgery, Institute of Neurological Sciences, Glasgow, United Kingdom</li><li>Department of Neurosurgery, Mayo Clinic, Rochester, Minnesota, United States</li><li>Department of Pathology, Kasturba Medical College and Hospital, Manipal, Karnataka, India</li></ol><p><strong>Correspondence Address:</strong><br>Girish Menon, Department of Neurosurgery, Kasturba Medical College and Hospital, Manipal, Karnataka, India.<br></p><p><strong>DOI:</strong>10.25259/SNI_1068_2024</p>Copyright: © 2025 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.<div class="parablock"><p><strong>How to cite this article: </strong>Siddharth Srinivasan1, Ajay Hegde2, Rajesh Nair3, Ravi Teja Jampani3, Mohammad Ashraf4, Dhanwanth Chigurupati4, Bharat Kumar Raju3, Susanth Subramanian3, Udgam Baxi3, Yasaswi Kanneganti3, Sarah Johnson5, Bhavna Nayal6, Geeta Vasudevan6, Deepak Nayak6, Girish Menon3. Pineal parenchymal tumor of intermediate differentiation: Case series and literature review: Is it time for a consensus?. 18-Apr-2025;16:138</p></div><div class="parablock"><p><strong>How to cite this URL: </strong>Siddharth Srinivasan1, Ajay Hegde2, Rajesh Nair3, Ravi Teja Jampani3, Mohammad Ashraf4, Dhanwanth Chigurupati4, Bharat Kumar Raju3, Susanth Subramanian3, Udgam Baxi3, Yasaswi Kanneganti3, Sarah Johnson5, Bhavna Nayal6, Geeta Vasudevan6, Deepak Nayak6, Girish Menon3. Pineal parenchymal tumor of intermediate differentiation: Case series and literature review: Is it time for a consensus?. 18-Apr-2025;16:138. Available from: <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13511">https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13511</a></p></div> </div> <div class="col-lg-3 col-sm-4 col-xs-12"><div class="article-detail-sidebar"><div class="icon sidebar-icon clearfix add-readinglist-icon"><button id="bookmark-article" class="add-reading-list-article">Add to Reading List</button><button id="bookmark-remove-article" class="remove-reading-list-article">Remove from Reading List</button></div><div class="icon sidebar-icon clearfix"><a class="btn btn-link" target="_blank" type="button" id="OpenPdf" href="https://surgicalneurologyint.com/wp-content/uploads/2025/04/13511/SNI-16-138.pdf"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/pdf-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a target="_blank" href="javascript:void(0);" onclick="return PrintArticle();"><img decoding="async" src="https://i0.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/file-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a class="btn btn-link" type="button" id="EmaiLPDF"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/mail-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a></div><div class="date"> <p>Date of Submission<br><span class="darkgray">11-Dec-2024</span></p> <p>Date of Acceptance<br><span class="darkgray">12-Feb-2025</span></p> <p>Date of Web Publication<br><span class="darkgray">18-Apr-2025</span></p> </div> </div></div> </div> <!--.row --><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a href="javascript:void(0);" name="Abstract">Abstract</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><strong>Background</strong>Pineal parenchymal tumor of intermediate differentiation (PPTID) is a rare tumor. This study aims to evaluate patient outcomes and propose a treatment algorithm based on existing literature and our case series.</p><p><strong>Methods</strong>This prospective observational study includes seven patients diagnosed with PPTID through histopathology. We analyzed their clinical presentation, magnetic resonance imaging findings, surgical approaches, histopathological and immunohistochemical analysis, adjuvant treatments, and outcomes. We conducted univariate and multivariate statistical analyses.</p><p><strong>Results</strong>The mean patient age was 40 years, with a male predominance. All patients presented with hydrocephalus, four of which required cerebrospinal fluid diversion procedures. The average tumor size was 3.13cm, with 85.7% showing brain invasion. Surgical outcomes included one gross total resection, two near total resections, and four subtotal resections. The supracerebellar infratentorial (Krause) approach was used in 71.4% of cases. About 85.7% were diagnosed with grade 3 PPTID. Five patients received adjuvant radiotherapy. The analysis showed each additional mitosis unit decreased survival by 0.17 units, equating to roughly 2 months (<i>P</i> </p><p><strong>Conclusion</strong>We propose a treatment algorithm for PPTID and highlight the importance of further research to understand its biological characteristics. Safe maximal resection appears beneficial for higher-grade PPTID, but the role of adjuvant treatment after complete resection of lower-grade tumors remains uncertain.</p><p><strong>Keywords: </strong>Hydrocephalus, Pineal gland, Pineal parenchymal tumor of intermediate differentiation, Pineal parenchymal tumor, Radiotherapy, Safe maximal resection</p><p></p></div> </div></body></html> </div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"><p></p><p><inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="SNI-16-138-inline001.tif"/></p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="INTRODUCTION">INTRODUCTION</a></h3><div class="clearfix"></div><div class="hline"></div><p>The pineal gland, traditionally addressed as Descartes’ seat of the soul, is a pine-cone-shaped structure located in the superior aspect of the posterior third ventricular recess.[<xref ref-type="bibr" rid="ref47"> <a href='#ref47'>47</a> </xref>] The gland has been theorized to be a center of “rational thought.” It secretes an indoleamine, “melatonin,” which is responsible not only for orchestrating the circadian rhythm in vertebrates but also for recently discovered antineoplastic properties.[<xref ref-type="bibr" rid="ref16"> <a href='#ref16'>16</a> </xref>] About 95% of the pineal gland comprises pinealocytes with dendritic projections and 5% glial cells.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>] Unfortunately, both of the above cell lines are harbingers of neoplasia.[<xref ref-type="bibr" rid="ref7"> <a href='#ref7'>7</a> </xref>,<xref ref-type="bibr" rid="ref44"> <a href='#ref44'>44</a> </xref>,<xref ref-type="bibr" rid="ref68"> <a href='#ref68'>68</a> </xref>] The most common pineal region tumors are germ cell tumors, and they account for 50% of intracranial germ cell tumors.[<xref ref-type="bibr" rid="ref49"> <a href='#ref49'>49</a> </xref>] On the contrary, parenchymal tumors are relatively rare compared to germ cell tumors and comprise <1% of CNS tumors.[<xref ref-type="bibr" rid="ref12"> <a href='#ref12'>12</a> </xref>,<xref ref-type="bibr" rid="ref67"> <a href='#ref67'>67</a> </xref>] In 2021, the World Health Organization (WHO) classified pineal parenchymal tumors as pineocytoma, pineoblastoma, papillary pineal tumors, pineal parenchymal tumors of intermediate differentiation (PPTID), and desmoplastic myxoid tumor of the pineal region – SMARCB1-mutant.[<xref ref-type="bibr" rid="ref38"> <a href='#ref38'>38</a> </xref>] Pineal parenchymal tumors are neoplasms arising from pineocytes. Pineocytomas are benign tumors and have an indolent course. The other end of the spectrum comprises pineoblastomas, which are aggressive tumors with a 5-year survival rate of <60%.[<xref ref-type="bibr" rid="ref35"> <a href='#ref35'>35</a> </xref>,<xref ref-type="bibr" rid="ref36"> <a href='#ref36'>36</a> </xref>]</p><p>PPTIDs represent an even rarer subset within the pineal parenchymal tumors (10–50%).[<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>,<xref ref-type="bibr" rid="ref40"> <a href='#ref40'>40</a> </xref>] PPTID was first described by Schild <i>et al</i>. in 1993 and was included as a part of the WHO classification in 2000.[<xref ref-type="bibr" rid="ref57"> <a href='#ref57'>57</a> </xref>] Verily, these entities are regarded as neoplasms with histology blending with both pineocytoma and pineoblastoma.[<xref ref-type="bibr" rid="ref40"> <a href='#ref40'>40</a> </xref>] The optimal treatment strategy for this type of tumor has not been devised due to its rarity. The question of whether such tumors can be effectively treated with surgery, a combination of adjuvant chemotherapy and radiation, or radiotherapy alone remains a topic of ongoing debate.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>]</p><p>Therefore, we bring to light a series of seven cases of PPTID from a tertiary care neurosurgical unit in South Asia, which can add to understanding the progress and outcome of this ailment.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="MATERIALS AND METHODS">MATERIALS AND METHODS</a></h3><div class="clearfix"></div><div class="hline"></div><p>The Institutional Ethics Board review clearance was obtained (IRB:48/2023). Informed consent was obtained from all patients and their next of kin.</p><h3 class = "title3">Patients</h3><p>Seven patients with histologically proven PPTID treated in the Department of Neurosurgery, Kasturba Medical College and Hospital, Manipal, Karnataka, India, between January 2014 and January 2024 were a part of this cohort. This study analyzed the clinical records, clinical presentation, preoperative neurological deficits, radiological features, surgical strategy executed, histopathological features, immuno-histochemistry markers, postoperative complications/neurological deficits, adjuvant treatment, recurrence of tumor, 5-year outcomes based on modified Rankin scale (mRS) dichotomized into good as 0–3 and poor as 4–6, and overall survival. The data of the above seven patients are shown in <xref ref-type="table" rid="T1"> <a href='#T1'> Table 1 </a> </xref>. Moreover, we conducted an exhaustive search on PUBMED and MEDLINE, employing MeSH terms and specific keywords such as “pineal parenchymal tumors” and “pineal parenchymal tumors of intermediate differentiation.” Since 2008, we have gathered and reviewed all accessible articles on PPTID. When the available data were deemed sufficient to infer the extent of resection, adjuvant treatment, and outcomes, we compiled this information into <xref ref-type="table" rid="T2"> <a href='#T2'> Table 2 </a> </xref>. The purpose of this literature review was to understand how, over time and with increased awareness among clinicians, the trends in diagnosis, treatment, and outcomes have evolved.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T1'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13511/SNI-16-138-t001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 1:</h3><p>Summary of the seven patients in our case series.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T2'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13511/SNI-16-138-t002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 2:</h3><p>Summary of articles from 2008 on PPTID.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3">Caveats in managing PPTID</h3><p>Broadly, the following issues were factored into consideration for optimizing and executing a holistic treatment strategy individualized to each of our patients:</p><p><list list-type="order"> <list-item><p>Treatment for acute hydrocephalus – Endoscopic Third Ventriculostomy (ETV), Ventriculoperitoneal Shunt (VP shunt), or External Ventricular Drain (EVD).</p></list-item> <list-item><p>Tissue diagnosis – Endoscopic third ventriculostomy/ stereotactic biopsy versus open surgical biopsy?</p></list-item> <list-item><p>Pre-operative imaging – Plane of tumor on magnetic resonance imaging (MRI) with adjacent vital structures, that is, brainstem, thalamus, and deep venous system.</p></list-item> <list-item><p>Approach to be undertaken for the definitive surgery – Supracerebellar infratentorial (Krause), Infraoccipital transtentorial (Poppen), or Interhemispheric transcallosal?[<xref ref-type="bibr" rid="ref48"> <a href='#ref48'> 48 </a> </xref>]</p></list-item> <list-item><p>The extent of resection – based on the plane of tumor preoperatively and intraoperatively.</p></list-item> <list-item><p>Adjuvant radiation is based on histopathological examination, the extent of resection, and recurrence.</p></list-item> </list></p><h3 class = "title3">We defined the extent of resection as</h3><h3 class = "title3" style="color:green;">Gross-total resection</h3><p><list list-type="bullet"> <list-item><p>Complete microscopic resection and no evidence of residual tumor on postoperative imaging</p></list-item> </list></p><h3 class = "title3" style="color:green;">Near-total resection</h3><p><list list-type="bullet"> <list-item><p>Complete microscopic resection with some radiological evidence of residual tumor on postoperative imaging.</p></list-item> </list></p><h3 class = "title3" style="color:green;">Sub-total resection</h3><p><list list-type="bullet"> <list-item><p>50–70% tumor decompression performed. A significant amount of the tumor was not removed due to adhesion/ loss of plane with adjacent vital structures.</p></list-item> </list></p><h3 class = "title3">Statistical analysis</h3><p>Due to the non-parametric nature of our data set and the small sample size due to disease rarity, we applied the Spearman correlation coefficient and Fischer’s exact test to identify any possible association. Univariate and multivariate statistical analyses, including log-rank test and Cox regression analysis for assessing all variables against survival outcomes, were conducted using IBM Statistical Package for the Social Sciences software for Mac OS.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="RESULTS">RESULTS</a></h3><div class="clearfix"></div><div class="hline"></div><h3 class = "title3">Demographics and clinical symptomatology</h3><p>All our patients were adults with a mean age of 40.43 ± 10.03 (years). Five (71.4%) of the group were male, and 2 (28.6%) were female. All seven patients had either clinical symptoms or radiological evidence of hydrocephalus. Apart from hydrocephalus, the clinical presentation was predominantly that of headache (71.4%), papilledema (71.4%), projectile vomiting (57.1%), diplopia (42.9%), and others, which are shown in <xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1 </a> </xref>. None of the tumors were detected incidentally.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F1'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13511/SNI-16-138-g001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 1:</h3><p>Graph depicting the clinical symptomatology in our patient cohort.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3">Imaging characteristics</h3><p>On MRI of the brain with intravenous Gadolinium contrast, most patients had a bulky, solid tumor with heterogeneous contrast enhancement (85.7 %). The mean tumor size was 3.13 ± 1.34 cm. Four patients had calcifications (57.1%). In 85.7 % of cases, there was adjacent brain invasion in the form of loss of plane superiorly between the thalamus, tectal plate, 4<sup>th</sup> ventricular floor, or complete brainstem involvement inferiorly. Preoperative complete neuraxial screening was not performed. All patients had negative tumor markers such as alpha-fetoprotein, human chorionic gonadotropin, and carcinoembryonic antigen.</p><h3 class = "title3">Cerebrospinal fluid (CSF) diversion</h3><p>Four out of seven patients required CSF diversion (57.1%). Two patients underwent ETV (28.57%). In patients where ETV was undertaken to treat the hydrocephalus, tumor biopsy was precluded by the inter-thalamic adhesions obstructing the path.</p><h3 class = "title3">Definitive surgery</h3><p>Our strategy for the surgical corridor was planned based on the displacement of the internal cerebral veins, the vein of Galen, and the lateral/anterior extent of the tumor. If the veins were displaced cranially, Krause’s approach (71.4%) was favored over Poppen’s (14.3 %). In one patient, due to the anterior projection of the tumor into the 3<sup>rd</sup> ventricle and vein of Galen draping the tumor posteriorly, an interhemispheric trans-callosal, trans-choroidal approach was utilized.</p><h3 class = "title3">Grade of resection and complications</h3><p>The extent of tumor resection and the need for adjuvant treatment was tailored to individual patients based on preoperative MRI and intraoperative tumor plane with an adjacent normal eloquent brain. In only 1 patient (14.3 %), gross total resection was undertaken. The other six patients underwent either a subtotal (57.1%) or a near-total resection (28.6%) due to poorly defined arachnoid planes. Two patients developed immediate postoperative complications. One patient developed a tectal infarct and became vegetative, following which his mRS did not improve. The other patient developed an operative site hematoma, which was managed conservatively with anti-edema measures, after which the patient improved. We postulate that the complications were due to a lack of clear arachnoid planes, distorted anatomy, and significant vascularity of the tumor, which is a challenge in itself to secure hemostasis in a deep, narrow surgical corridor besieged by vital structures.</p><h3 class = "title3">Histopathological examination and immunohistochemistry</h3><p>Six out of seven patients in our study group had grade 3 PPTID (85.71%). The presence of high mitoses diagnosed a higher grade of the tumor [<xref ref-type="fig" rid="F2"> <a href='#F2'> Figure 2a </a> </xref>] and the Ki-67 index [<xref ref-type="fig" rid="F2"> <a href='#F2'> Figure 2b </a> </xref>]. The mean (standard deviation [SD]) of Mitoses was 10.43 (8.12). The median (interquartile range [IQR]) of Mitoses was 6.00 (5–13). The Mitoses ranged from 5 to 26. The mean (SD) of Ki-67 was 19.14 (19.97). The median (IQR) of Ki-67 was 12.00 (7-26). The Ki-67 ranged from 1 to 55. Six patients (85.7%) were positive for synaptophysin [<xref ref-type="fig" rid="F2"> <a href='#F2'> Figure 2c </a> </xref>].</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F2'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13511/SNI-16-138-g002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 2:</h3><p>(a) Tumor composed of sheets of neoplastic tumor cells showing pleomorphism and increased mitosis suggestive of pineal parenchymal tumor of intermediate differentiation (H&E, ×40). (b) Tumor cells showing high Ki67 index (×10). (c) Tumor cells showing immunoreactivity to Synaptophysin (×40). (d) Photomicrograph showing uniform cells with round nuclei, moderate amount of eosinophilic cytoplasm, and absence of mitosis (H&E, ×40). H & E: Hematoxylin and Eosin Stain</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3">Tumor grade change</h3><p>One patient demonstrated a grade change from pineocytoma [<xref ref-type="fig" rid="F2"> <a href='#F2'> Figure 2d </a> </xref>] to PPTID after a 5-year disease-free interval.</p><p>Following the second surgery, she developed hydrocephalus, for which she underwent a VP shunt. During the second surgery, only a subtotal decompression of the tumor was plausible due to adhesions with adjacent structures.</p><h3 class = "title3">Mitoses of tumor and survival</h3><p>Non-parametric tests (Spearman Correlation) were used to explore the correlation between the two variables, as at least one of the variables was not normally distributed. Mitoses and survival (Years) had a strong negative correlation, which was statistically significant (rho = −0.85, <i>P</i> = 0.016). For every 1 unit increase in mitoses, the survival (Years) decreases by 0.17 units, that is, around 2 months [<xref ref-type="fig" rid="F3"> <a href='#F3'> Figure 3 </a> </xref>].</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F3'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13511/SNI-16-138-g003.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 3:</h3><p>Co-relation between mitoses and survival based on Spearman’s Co-relation coefficient.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3">Adjuvant treatment</h3><p>All patients with Karnofsky Performance Status (KPS) of more than 70 were subjected to adjuvant whole-brain radiation therapy (RT) with a boost to the pineal region. The typical radiation dosage administered was 55 Gy delivered in 25–30 fractions. In two patients (28.5%), the residual tumor was stable and showed a good response to RT. In one patient, the tumor demonstrated a remarkable response, and there was complete radiological remission of the disease on follow-up. Two patients (28.5%) developed a recurrence of the tumor despite RT. One patient (14.2%) did not receive RT since the biopsy was suggestive of pineocytoma, and she had undergone a gross total resection. After 60 months, she developed a recurrence. After the second surgery, she is receiving RT and is on follow-up. Two patients (28.5%) did not receive RT due to aggressive disease progression and poor KPS.</p><h3 class = "title3">Recurrence and leptomeningeal spread</h3><p>Three patients (42.8%) developed recurrence after 6 months, 18 months, and 60 months, respectively, after the first surgery. One patient succumbed to the aggressive recurrent disease, while the other two patients are on follow-up treatment. Two patients (28.5%) developed leptomeningeal seeding of the tumor on follow-up imaging.</p><h3 class = "title3">Outcome and survival</h3><p>Four out of 7 patients (57.1%) are on follow-up with good outcomes (mRS <3). One patient had an aggressive tumor occupying the whole of the four<sup>th</sup> ventricle and was adherent to the floor at the time of diagnosis. One patient developed an extensive recurrence with leptomeningeal spread, following which the patient and family opted for palliative care. The mean survival rate in our patient data set was 35 months ± 2 months (51.7%) over a follow-up of 120 months. All patients were on regular, compliant follow-up. The 5-year progression-free rate was 71.43 % in this cohort of patients. However, due to the small sample size, we could not demonstrate a statistically significant association between the tumor grade and progression-free survival/overall survival.</p><h3 class = "title3">Illustrative cases</h3><h3 class = "title3" style="color:green;">Case 2</h3><p>A 50-year-old male presented with a homogenous T1 isointense non-contrast-enhancing tumor on MRI [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4a </a> </xref>]. Planning the approach to a posterior third ventricular tumor is essential in attaining good tumor decompression without causing undue complications. On a more detailed analysis of the MRI, we noticed that he had a very steep tentorial angle with the vein of the Galen complex draping the tumor posteriorly. Hence, a transcallosal, subchoroidal approach was advocated for this case. Near-total tumor resection was achieved in this case [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4b </a> </xref>].</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F4'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13511/SNI-16-138-g004.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 4:</h3><p>(a) Case 2: magnetic resonance imaging (MRI) – brain, mid-sagittal section T1 contrast sequence: Non-enhancing pineal region tumor, with vein of Galen Complex draping the tumor posteriorly. (b) Case 2: Postoperative computed tomography (CT) brain: Craniotomy defect centered around the coronal suture, Interhemispheric trans callosal sub-choroidal approach was advocated. Near-total resection (NTR) was achieved. (c) Case 3: Before radiotherapy (RT) – MRI brain axial T1 contrast sequence demonstrating the extensive nature of the lesion extending rostrally to involve the thalamus (d) Case 3: After RT–MRI brain axial T1 contrast, depicting good response to RT. (e) Case 4: Preoperative CT brain showing homogenous hyperdensity suggesting that pineal parenchymal tumor of intermediate differentiation can not only have speckled or peripheral calcifications. (f) Case 4: Postoperative MRI demonstrating NTR. (g) Case 3: Before RT–MRI brain T1 contrast mid-sagittal section showing a diffuse heterogeneous contrast-enhancing tumor involving the thalamus and callosum. (h) Case 3: After RT– MRI brain T1 post contrast sequence mid- sagittal section. Complete radiological remission of the lesion is noted. The neurovascular structures, including the vein of Galen complex, can be well delineated. (i) Case 7: Homogenous contrast-enhancing lesion on T1 MRI, with visibly well-defined planes. HPE was suggestive of pineocytoma. (j) Case 7: Postoperative CT brain. Gross-total resection of the tumor was achieved. (k) Case 7: MRI brain after 5 years of disease-free interval depicting an aggressive recurrence with poor planes and supra-tentorial extension. (l) Case 6: Neuraxis screening for this patient revealed diffuse leptomeningeal contrast-enhancing lesions suggestive of drop metastasis.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3" style="color:green;">Case 4</h3><p>A 48-year-old male presented with a homogenously calcified lesion in the pineal recess [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4c </a> </xref>]. He underwent a near-total resection. The tumor was dissected from the midbrain. Part of the tumor adherent to the vein of the Galen complex was not removed [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4d </a> </xref>].</p><h3 class = "title3" style="color:green;">Case 5</h3><p>A 25-year-old female presented with signs and symptoms suggestive of raised intracranial pressure (ICP). MRI brain with contrast revealed a large tumor in the pineal recess extending rostrally to involve the thalamus [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4e </a> </xref> and <xref ref-type="fig" rid="F4"> <a href='#F4'> f </a> </xref>]. She underwent tumor decompression and biopsy. Post-surgery, she was subjected to radiotherapy. She received 55Gy over 30 fractions with a pineal region boost. This patient was diagnosed with high-grade PPTID and underwent a subtotal decompression. However, she demonstrated an excellent response to radiotherapy, and there was complete radiological remission on follow-up imaging [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4g </a> </xref> and <xref ref-type="fig" rid="F4"> <a href='#F4'> h </a> </xref>].</p><h3 class = "title3" style="color:green;">Case 7</h3><p>A 48-year-old lady presented with symptoms suggestive of raised ICP. MRI brain evaluation revealed homogenous enhancing posterior third ventricular tumor [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4i </a> </xref>]. She underwent gross total resection as demonstrated on the postoperative computed tomography brain [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4j </a> </xref>]. The biopsy was suggestive of pineocytoma. Five years later, she presented with similar complaints, and the MRI showed an aggressive recurrence of the tumor with a significant component extending above the tentorium [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4k </a> </xref>]. This time, due to the adherence of the tumor to the deep venous system, only a subtotal decompression was achieved. Biopsy revealed grade 3 PPTID.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="DISCUSSION">DISCUSSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Since the incorporation of PPTID into the WHO classification system in 2000, more discoveries and advancements have been made in diagnosing and treating these tumors.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>,<xref ref-type="bibr" rid="ref61"> <a href='#ref61'>61</a> </xref>,<xref ref-type="bibr" rid="ref68"> <a href='#ref68'>68</a> </xref>,<xref ref-type="bibr" rid="ref75"> <a href='#ref75'>75</a> </xref>] Nevertheless, to this day, there remains a lack of consensus on the optimal approach and guidelines for directing treatment options for this tumor. What exacerbates the situation is that the incorrect grouping of these tumors may underestimate the likelihood of CSF seeding (as illustrated in <xref ref-type="fig" rid="F4"> <a href='#F4'>Figure 4l</a> </xref>, which depicts a patient from our cohort exhibiting leptomeningeal dissemination) and prognosis.[<xref ref-type="bibr" rid="ref57"> <a href='#ref57'>57</a> </xref>]</p><p>PPTID can manifest across all age demographics, predominantly in adults.[<xref ref-type="bibr" rid="ref25"> <a href='#ref25'>25</a> </xref>,<xref ref-type="bibr" rid="ref45"> <a href='#ref45'>45</a> </xref>,<xref ref-type="bibr" rid="ref57"> <a href='#ref57'>57</a> </xref>] All our patients were adults with a mean age of 40 years. Contrary to the available literature, most of our patients were male (71.4%).[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>,<xref ref-type="bibr" rid="ref39"> <a href='#ref39'>39</a> </xref>,<xref ref-type="bibr" rid="ref42"> <a href='#ref42'>42</a> </xref>] Some series highlight equal sex distribution.[<xref ref-type="bibr" rid="ref11"> <a href='#ref11'>11</a> </xref>] Our patients exhibited symptoms consistent with hydrocephalus, aligning with findings from most series. In addition, we observed that Parinaud syndrome is a rare presentation, even when radiological evidence indicates the involvement of the midbrain tectum.</p><p>Many authors emphasize that gross total resection of tumors translates into better overall survival. It is crucial for the skilled neurosurgeon to carefully weigh the pros and cons of pursuing an aggressive gross total resection, considering the potential neurological morbidity involved. We opt for a safe maximal resection followed by adjuvant radiation akin to that utilized for pineoblastoma or a high-grade glioma to mitigate the risk of neurological deficits.[<xref ref-type="bibr" rid="ref5"> <a href='#ref5'>5</a> </xref>,<xref ref-type="bibr" rid="ref41"> <a href='#ref41'>41</a> </xref>,<xref ref-type="bibr" rid="ref60"> <a href='#ref60'>60</a> </xref>,<xref ref-type="bibr" rid="ref63"> <a href='#ref63'>63</a> </xref>] It is imperative to remain cognizant that injury to critical structures such as the vein of the Galen complex, posterior thalamus, or midbrain tectum can result in significant morbidity. When the tumor exhibits well-defined arachnoid planes, advocating for a gross total resection is feasible. In our series, most patients (85.7%) underwent either a near-total or subtotal resection followed by adjuvant radiation. Our outcomes align with those reported in other series. Endoscopic surgery or endoscope-assisted microsurgery has gained popularity over the past few years, and studies have demonstrated better gross total resection and reduced rates of hydrocephalus.[<xref ref-type="bibr" rid="ref72"> <a href='#ref72'>72</a> </xref>]</p><p>The histopathological diagnosis is the most crucial yet perplexing aspect of PPTID. These tumors exhibit significant histological heterogeneity, and their behavior often defies prediction.[<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>] While some authors propose an aggressive treatment approach regardless of the tumor grade, others advocate for tumor decompression followed by adjuvant radiation therapy.[<xref ref-type="bibr" rid="ref11"> <a href='#ref11'>11</a> </xref>,<xref ref-type="bibr" rid="ref13"> <a href='#ref13'>13</a> </xref>] Many have utilized adjuvant temozolomide chemotherapy, whereas others have used procarbazine, vincristine, lomustine, nimustine, carboplatin, and interferon B in different combinations.[<xref ref-type="bibr" rid="ref69"> <a href='#ref69'>69</a> </xref>,<xref ref-type="bibr" rid="ref74"> <a href='#ref74'>74</a> </xref>] It was traditionally considered that chemotherapeutic agents have poor blood-brain barrier penetration.[<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>] However, post-irradiation, there is a possibility that due to capillary bed disruption, the blood-brain barrier is more permissible to chemotherapeutic agents, which could be the rationale.[<xref ref-type="bibr" rid="ref6"> <a href='#ref6'>6</a> </xref>] Nonetheless, some authors even propose that we might be overtreating PPTID, suggesting that it can be managed effectively with radiation therapy alone.[<xref ref-type="bibr" rid="ref13"> <a href='#ref13'>13</a> </xref>] We opted not to administer chemotherapy to any of our patients. Among the cohort, three out of seven patients exhibited stable disease and are alive, while one patient demonstrated an excellent response to radiotherapy. This suggests a potential radiosensitivity of the tumor. However, Chalif <i>et al</i>., in a recent study, concluded that radiotherapy does not affect the outcomes of grade 2 PPTID.[<xref ref-type="bibr" rid="ref8"> <a href='#ref8'>8</a> </xref>]</p><p>In general, PPTIDs demonstrate moderately high cellularity, mild-to-moderate nuclear atypia, and moderate mitotic activity, displaying diffuse or lobulated growth patterns.[<xref ref-type="bibr" rid="ref37"> <a href='#ref37'>37</a> </xref>] Further prognostic stratification is facilitated by assessing the extent of necrosis, the mitotic index, and the presence of neurofilament protein.[<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>,<xref ref-type="bibr" rid="ref14"> <a href='#ref14'>14</a> </xref>,<xref ref-type="bibr" rid="ref25"> <a href='#ref25'>25</a> </xref>] The 2007 WHO Classification of Central Nervous System Tumors considers 2 variables – proliferative activity and immunoreactivity for neurofilament protein – as outcome predictors.[<xref ref-type="bibr" rid="ref11"> <a href='#ref11'>11</a> </xref>,<xref ref-type="bibr" rid="ref56"> <a href='#ref56'>56</a> </xref>] These tumors can generally present a positive expression for neurofilament, synaptophysin, renal S antigen, and chromogranin A.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>] Neurofilament protein expression has a very debatable role in predicting outcomes. Jouvet <i>et al</i>. suggested that neurofilament is expressed only in low-grade PPTID (grade 2) and correlates with better outcomes.[<xref ref-type="bibr" rid="ref25"> <a href='#ref25'>25</a> </xref>] However, various studies over the last decade have questioned its utility.[<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>,<xref ref-type="bibr" rid="ref75"> <a href='#ref75'>75</a> </xref>] Due to the variability of neurofilament expression, other immunohistochemistry markers, such as the MIB-1 labeling index (MIB-LI) and Ki-67, have been considered more reliable for diagnostic purposes.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>,<xref ref-type="bibr" rid="ref27"> <a href='#ref27'>27</a> </xref>,<xref ref-type="bibr" rid="ref53"> <a href='#ref53'>53</a> </xref>] MIB-LI and mitoses have a significant implication in the prognostication of the disease and in determining recurrence.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>,<xref ref-type="bibr" rid="ref19"> <a href='#ref19'>19</a> </xref>,<xref ref-type="bibr" rid="ref21"> <a href='#ref21'>21</a> </xref>,<xref ref-type="bibr" rid="ref27"> <a href='#ref27'>27</a> </xref>,<xref ref-type="bibr" rid="ref64"> <a href='#ref64'>64</a> </xref>] More recently, it has been discovered that an in-frame mutation in the KBTBD4 gene is positive in approximately 80% of cases and is specific to PPTID. Consequently, this discovery can aid in clearly distinguishing PPTID from pineocytoma, allowing for a more definitive diagnosis beyond solely relying on pineocytomatous pseudo-rosettes.[<xref ref-type="bibr" rid="ref65"> <a href='#ref65'>65</a> </xref>]</p><p>Numerous authors have made efforts to classify the tumor based on histopathological characteristics. Yu <i>et al</i>. classified tumors into high-risk and low-risk groups. The high-risk group comprised a mitotic count ≥3/10 high-power field (HPF) or Ki67 LI ≥5, whereas the low-risk group was defined as mitotic count <3/10 HPF and Ki67 LI <5.[<xref ref-type="bibr" rid="ref75"> <a href='#ref75'>75</a> </xref>] The former category is associated with dismal outcomes. Chatterjee <i>et al</i>. have proposed a classification for PPTIDs with mitosis <4/10 HPF and Ki-67 <5% as grade II and cases with mitosis >4/10 HPF and/or Ki-67 >5% as grade III PPTID.[<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>] While these classification systems can assist in forecasting outcomes and planning adjuvant treatment for the high-risk category, they do not assist in devising holistic tumor management strategies. In our series, all patients had mitoses > 5/10 HPF, and 6 out of 7 patients (85.7%) had Ki-67 >5%. Only an increase in mitotic count demonstrated a correlation with survival and achieved statistical significance. We did not find a significant statistical association between Ki-67 and outcomes. In one patient, the tumor exhibited a grade change, initially presenting with absent mitoses, which subsequently increased to 15–20/10 HPFs and Ki-67 of 3 % upon diagnosis as PPTID grade 3. Apart from our patient, various other reports have documented grade changes in pineal tumors.[<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>,<xref ref-type="bibr" rid="ref28"> <a href='#ref28'>28</a> </xref>,<xref ref-type="bibr" rid="ref31"> <a href='#ref31'>31</a> </xref>,<xref ref-type="bibr" rid="ref52"> <a href='#ref52'>52</a> </xref>] From these instances, one may deduce that PPTID is an intermediary pathological condition capable of originating or transitioning from a pineocytoma, displaying the propensity to advance into or imitate the characteristics of a pineoblastoma. This may suggest that it is unlikely that PPTID arises <i>de novo</i>.</p><p>In 2011, the guidelines set forth by the British Neurooncology Society for rare tumors offer a delineated algorithm elucidating the procedural steps to be undertaken in managing a tumor located within the pineal region. The British Neuro-oncology Society recommends surgical resection as the primary intervention for PPTID while indicating that the efficacy of radiotherapy remains uncertain.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>,<xref ref-type="bibr" rid="ref58"> <a href='#ref58'>58</a> </xref>] Indeed, the current landscape reveals a notable absence of consensus regarding diagnostic methodologies and therapeutic strategies. However, similar to the above guidelines and review by Mallick <i>et al</i>., we have devised a simple pragmatic algorithm that can help clinicians tailor their treatment for PPTID [<xref ref-type="fig" rid="F5"> <a href='#F5'>Figure 5</a> </xref>].[<xref ref-type="bibr" rid="ref42"> <a href='#ref42'>42</a> </xref>] Due to a lack of strong evidence, we have not incorporated adjuvant chemotherapy into the algorithm. However, the algorithm serves as a foundational framework for managing patients and a stepping stone for future research.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F5'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13511/SNI-16-138-g005.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 5:</h3><p>A practical management algorithm for pineal parenchymal tumor of intermediate differentiation. PPTID: Pineal parenchymal tumor of intermediate differentiation, ETV: Endoscopic third ventriculostomy, GTR: Gross total resection, STR: Sub total resection, NTR: Near total resection, MRI: Magnetic resonance imaging, RT: Radiotherapy, CSF: Cerebrospinal fluid</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3">Limitations</h3><p>Due to the rarity of the disease, data can only be derived from a small sample size case series. This indicates the need for systematic reviews. We humbly acknowledge the criticism for not incorporating neuraxial screening at the presentation. We strongly emphasize that MRI screening of the neuraxis is essential in PPTID. However, we remain uncertain about the necessity of routine CSF sampling. Given the diversity in the existing literature and our small sample size, conducting a quantitative meta-analysis was not feasible. This is primarily due to the limited availability of literature, which consists mainly of case reports and a few small case series.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CONCLUSION">CONCLUSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Drawing on insights and observations from various eminent authors over the past two decades, a tentative consensus may be reached suggesting that low-grade PPTID could potentially undergo gross total resection safely, given the preservation of the tumor-arachnoid interface. Conversely, in cases of high-grade PPTID, surgical precision is paramount to avoid grave neurological deficits/morbidity. Following near-total or subtotal resection, adjuvant chemo/radiotherapy becomes imperative for comprehensive management and better overall survival.</p><p>Definitive lacunae revolve around these pivotal questions: -</p><p><list list-type="order"> <list-item><p>In the scenario where a high-grade lesion has undergone gross total resection, is adjuvant therapy mandatory, or is there an acceptable level of risk in opting for vigilant follow-up with regular imaging?</p></list-item> <list-item><p>Should patients with low-grade PPTID, despite gross total resection, require rigorous follow-up imaging or adjuvant therapy, considering its potential for progression to a higher-grade recurrence?</p></list-item> </list></p><p>The above questions are still devoid of answers and will require larger multicenter observational studies to address.</p><p></p><p></p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Ethical Approval">Ethical Approval</a></h3><div class="clearfix"></div><div class="hline"></div><p>The research/study approved by the Institutional Review Board at Manipal Academy of Higher Education, approval number: IRB/48/2023 dated June 05 2023</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Declaration of patient consent">Declaration of patient consent</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors certify that they have obtained all appropriate patient consent.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Financial Support and Sponsorship">Financial Support and Sponsorship</a></h3><div class="clearfix"></div><div class="hline"></div><p>Nil.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Conflicts of Interest">Conflicts of Interest</a></h3><div class="clearfix"></div><div class="hline"></div><p>There are no conflicts of interest.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Use of artificial intelligence (AI)-assisted technology for manuscript preparation">Use of artificial intelligence (AI)-assisted technology for manuscript preparation</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript, and no images were manipulated using AI.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Disclaimer">Disclaimer</a></h3><div class="clearfix"></div><div class="hline"></div><p>The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.</p></div> </div></div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"><h3 class="blogheading pull-left Main-Title col-lg-9 col-sm-8 col-xs-12"><a href="javascript:void(0);" name="Acknowledgement">Acknowledgement</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors would like to thank Ms. Shubavati, Chief Secretary, Department of Neurosurgery, for her constant assistance and support in executing this study.</p></div> </div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a name="References" href="javascript:void(0);">References</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><a href='javascript:void(0);' name='ref1' style='text-decoration: none;'>1.</a> Amato-Watkins AC, Lammie A, Hayhurst C, Leach P. Pineal parenchymal tumours of intermediate differentiation-An evidence-based review of a new pathological entity. Br J Neurosurg. 2016. 30: 11-5</p><p><a href='javascript:void(0);' name='ref2' style='text-decoration: none;'>2.</a> Arivazhagan A, Anandh B, Santosh V, Chandramouli BA. Pineal parenchymal tumors--utility of immunohistochemical markers in prognostication. Clin Neuropathol. 2008. 27: 325-33</p><p><a href='javascript:void(0);' name='ref3' style='text-decoration: none;'>3.</a> Bando T, Ueno Y, Shinoda N, Imai Y, Ichikawa K, Kuramoto Y. Therapeutic strategy for pineal parenchymal tumor of intermediate differentiation (PPTID): Case report of PPTID with malignant transformation to pineocytoma with leptomeningeal dissemination 6 years after surgery. J Neurosurg. 2018. 130: 2009-15</p><p><a href='javascript:void(0);' name='ref4' style='text-decoration: none;'>4.</a> Bielle F, Navarro S, Bertrand A, Cornu P, Mazeron JJ, Jouvet A. Late dural relapse of a resected and irradiated pineal parenchymal tumor of intermediate differentiation. Clin Neuropathol. 2014. 33: 424-7</p><p><a href='javascript:void(0);' name='ref5' style='text-decoration: none;'>5.</a> Bonosi L, Marrone S, Benigno UE, Buscemi F, Musso S, Porzio M. Maximal safe resection in glioblastoma surgery: A systematic review of advanced intraoperative image-guided techniques. Brain Sci. 2023. 13: 216</p><p><a href='javascript:void(0);' name='ref6' style='text-decoration: none;'>6.</a> Brown WR, Blair RM, Moody DM, Thore CR, Ahmed S, Robbins ME. Capillary loss precedes the cognitive impairment induced by fractionated whole-brain irradiation: A potential rat model of vascular dementia. J Neurol Sci. 2007. 257: 67-71</p><p><a href='javascript:void(0);' name='ref7' style='text-decoration: none;'>7.</a> Carr C, O’Neill BE, Hochhalter CB, Strong MJ, Ware ML. Biomarkers of pineal region tumors: A review. Ochsner J. 2019. 19: 26-31</p><p><a href='javascript:void(0);' name='ref8' style='text-decoration: none;'>8.</a> Chalif EJ, Murray RD, Mozaffari K, Chillakuru YR, Shim T, Monfared A. Malignant pineal parenchymal tumors in adults: A national cancer database analysis. Neurosurgery. 2022. 90: 807</p><p><a href='javascript:void(0);' name='ref9' style='text-decoration: none;'>9.</a> Chatterjee D, Lath K, Singla N, Kumar N, Radotra BD. Pathologic prognostic factors of pineal parenchymal tumor of intermediate differentiation. Appl Immunohistochem Mol Morphol. 2019. 27: 210-5</p><p><a href='javascript:void(0);' name='ref10' style='text-decoration: none;'>10.</a> Chen YL, Tai LH, Lieu AS. Recurrent pineal parenchymal tumor of intermediate differentiation with intratumoral hemorrhage: A case report and review of the literature. Rare Tumors. 2023. 15: 20363613231177537</p><p><a href='javascript:void(0);' name='ref11' style='text-decoration: none;'>11.</a> Choque-Velasquez J, Resendiz-Nieves JC, Jahromi BR, Colasanti R, Raj R, Tynninen O. Pineal parenchymal tumors of intermediate differentiation: A long-term follow-up study in Helsinki neurosurgery. World Neurosurg. 2019. 122: e729-39</p><p><a href='javascript:void(0);' name='ref12' style='text-decoration: none;'>12.</a> Cuccia F, Mortellaro G, Cespuglio D, Valenti V, DE Gregorio G, Quartuccio E. A Case report of adult pineoblastoma occurring in a pregnant woman. Anticancer Res. 2019. 39: 2627-31</p><p><a href='javascript:void(0);' name='ref13' style='text-decoration: none;'>13.</a> Das P, Mckinstry S, Devadass A, Herron B, Conkey DS. Are we over treating Pineal Parenchymal tumour with intermediate differentiation? Assessing the role of localised radiation therapy and literature review. SpringerPlus. 2016. 5: 26</p><p><a href='javascript:void(0);' name='ref14' style='text-decoration: none;'>14.</a> Fauchon F, Jouvet A, Paquis P, Saint-Pierre G, Mottolese C, Ben Hassel M. Parenchymal pineal tumors: A clinicopathological study of 76 cases. Int J Radiat Oncol Biol Phys. 2000. 46: 959-68</p><p><a href='javascript:void(0);' name='ref15' style='text-decoration: none;'>15.</a> Favero G, Bonomini F, Rezzani R. Pineal gland tumors: A review. Cancers. 2021. 13: 1547</p><p><a href='javascript:void(0);' name='ref16' style='text-decoration: none;'>16.</a> Favero G, Moretti E, Bonomini F, Reiter RJ, Rodella LF, Rezzani R. Promising antineoplastic actions of melatonin. Front Pharmacol. 2018. 9: 1086</p><p><a href='javascript:void(0);' name='ref17' style='text-decoration: none;'>17.</a> Fèvre-Montange M, Vasiljevic A, Frappaz D, Champier J, Szathmari A, Aubriot Lorton MH. Utility of Ki67 immunostaining in the grading of pineal parenchymal tumours: A multicentre study. Neuropathol Appl Neurobiol. 2012. 38: 87-94</p><p><a href='javascript:void(0);' name='ref18' style='text-decoration: none;'>18.</a> Fomchenko EI, Erson-Omay EZ, Kundishora AJ, Hong CS, Daniel AA, Allocco A. Genomic alterations underlying spinal metastases in pediatric H3K27M-mutant pineal parenchymal tumor of intermediate differentiation: Case report. J Neurosurg Pediatr. 2019. 25: 121-30</p><p><a href='javascript:void(0);' name='ref19' style='text-decoration: none;'>19.</a> Fukuoka K, Sasaki A, Yanagisawa T, Suzuki T, Wakiya K, Adachi J. Pineal parenchymal tumor of intermediate differentiation with marked elevation of MIB-1 labeling index. Brain Tumor Pathol. 2012. 29: 229-34</p><p><a href='javascript:void(0);' name='ref20' style='text-decoration: none;'>20.</a> Han SJ, Clark AJ, Ivan ME, Parsa AT, Perry A. Pathology of pineal parenchymal tumors. Neurosurg Clin N Am. 2011. 22: 335-40</p><p><a href='javascript:void(0);' name='ref21' style='text-decoration: none;'>21.</a> Heim S, Beschorner R, Mittelbronn M, Keyvani K, Riemenschneider MJ, Vajtai I. Increased mitotic and proliferative activity are associated with worse prognosis in papillary tumors of the pineal region. Am J Surg Pathol. 2014. 38: 106-10</p><p><a href='javascript:void(0);' name='ref22' style='text-decoration: none;'>22.</a> Ito K, Aihara Y, Chiba K, Oda Y, Kawamata T. A case of a pineal parenchymal tumor of intermediate differentiation with bifocal lesions differentiated by negative placental alkaline phosphatase in the spinal fluid. Childs Nerv Syst. 2024. 40: 2935-9</p><p><a href='javascript:void(0);' name='ref23' style='text-decoration: none;'>23.</a> Ito T, Kanno H, Sato K, Oikawa M, Ozaki Y, Nakamura H. Clinicopathologic study of pineal parenchymal tumors of intermediate differentiation. World Neurosurg. 2014. 81: 783-9</p><p><a href='javascript:void(0);' name='ref24' style='text-decoration: none;'>24.</a> Jacus MO, Daryani VM, Harstead KE, Patel YT, Throm SL, Stewart CF. Pharmacokinetic properties of anticancer agents for the treatment of CNS tumors: Update of the literature. Clin Pharmacokinet. 2016. 55: 297-311</p><p><a href='javascript:void(0);' name='ref25' style='text-decoration: none;'>25.</a> Jouvet A, Saint-Pierre G, Fauchon F, Privat K, Bouffet E, Ruchoux MM. Pineal parenchymal tumors: A correlation of histological features with prognosis in 66 cases. Brain Pathol Zurich Switz. 2000. 10: 49-60</p><p><a href='javascript:void(0);' name='ref26' style='text-decoration: none;'>26.</a> Kang YJ, Bi WL, Dubuc AM, Martineau L, Ligon AH, Berkowitz AL. Integrated genomic characterization of a pineal parenchymal tumor of intermediate differentiation. World Neurosurg. 2016. 85: 96-105</p><p><a href='javascript:void(0);' name='ref27' style='text-decoration: none;'>27.</a> Kanno H, Nishihara H, Oikawa M, Ozaki Y, Murata J, Sawamura Y. Expression of O6-methylguanine DNA methyltransferase (MGMT) and immunohistochemical analysis of 12 pineal parenchymal tumors. Neuropathology. 2012. 32: 647-53</p><p><a href='javascript:void(0);' name='ref28' style='text-decoration: none;'>28.</a> Kato H, Tanei T, Nishimura Y, Nagashima Y, Ishii M, Nishii T. Pineal parenchymal tumor of intermediate differentiation with late spinal dissemination 13 years after initial surgery: Illustrative case. J Neurosurg Case Lessons. 2023. 5: CASE22475</p><p><a href='javascript:void(0);' name='ref29' style='text-decoration: none;'>29.</a> Kerezoudis P, Yolcu YU, Laack NN, Ruff MW, Khatua S, Daniels DJ. Survival and associated predictors for patients with pineoblastoma or pineal parenchymal tumors of intermediate differentiation older than 3 years: Insights from the National Cancer Database. Neurooncol Adv. 2022. 4: vdac057</p><p><a href='javascript:void(0);' name='ref30' style='text-decoration: none;'>30.</a> Khodayari B, Lien WW. Clinical outcomes for primary parenchymal tumor of intermediate differentiation. Int J Radiat Oncol Biol Phys. 2018. 102: e265</p><p><a href='javascript:void(0);' name='ref31' style='text-decoration: none;'>31.</a> Kim BS, Kim DK, Park SH. Pineal parenchymal tumor of intermediate differentiation showing malignant progression at relapse. Neuropathology. 2009. 29: 602-8</p><p><a href='javascript:void(0);' name='ref32' style='text-decoration: none;'>32.</a> Komakula S, Warmuth-Metz M, Hildenbrand P, Loevner L, Hewlett R, Salzman K. Pineal parenchymal tumor of intermediate differentiation: Imaging spectrum of an unusual tumor in 11 cases. Neuroradiology. 2011. 53: 577-84</p><p><a href='javascript:void(0);' name='ref33' style='text-decoration: none;'>33.</a> Kumar R, Dayal S, Krishna M. Pineal parenchymal tumor with intermediate differentiation-a case report and review of literature from rural India. Indian J Neurosurg. 2020. 9: 55-7</p><p><a href='javascript:void(0);' name='ref34' style='text-decoration: none;'>34.</a> Kunigelis KE, Kleinschmidt-DeMasters BK, Youssef AS, Lillehei KO, Ormond DR. Clinical features of pineal parenchymal tumors of intermediate differentiation (PPTID): A single-institution series. World Neurosurg. 2021. 155: e229-35</p><p><a href='javascript:void(0);' name='ref35' style='text-decoration: none;'>35.</a> Liu AP, Gudenas B, Lin T, Orr BA, Klimo P, Kumar R. Risk-adapted therapy and biological heterogeneity in pineoblastoma: Integrated clinico-pathological analysis from the prospective, multi-center SJMB03 and SJYC07 trials. Acta Neuropathol (Berl). 2020. 139: 259-71</p><p><a href='javascript:void(0);' name='ref36' style='text-decoration: none;'>36.</a> Liu AP, Priesterbach-Ackley LP, Orr BA, Li BK, Gudenas B, Reddingius RE. WNT-activated embryonal tumors of the pineal region: Ectopic medulloblastomas or a novel pineoblastoma subgroup?. Acta Neuropathol (Berl). 2020. 140: 595-7</p><p><a href='javascript:void(0);' name='ref37' style='text-decoration: none;'>37.</a> Louis DN, Perry A, Reifenberger G, von Deimling A, FigarellaBranger D, Cavenee WK. The 2016 World Health Organization classification of tumors of the central nervous system: A summary. Acta Neuropathol (Berl). 2016. 131: 803-20</p><p><a href='javascript:void(0);' name='ref38' style='text-decoration: none;'>38.</a> Louis DN, Perry A, Wesseling P, Brat DJ, Cree IA, FigarellaBranger D. The 2021 WHO Classification of tumors of the central nervous system: A summary. Neurooncology. 2021. 23: 1231-51</p><p><a href='javascript:void(0);' name='ref39' style='text-decoration: none;'>39.</a> Low JT, Kirkpatrick JP, Peters KB. Pineal parenchymal tumors of intermediate differentiation treated with ventricular radiation and temozolomide. Adv Radiat Oncol. 2021. 7: 100814</p><p><a href='javascript:void(0);' name='ref40' style='text-decoration: none;'>40.</a> Lu VM, Luther EM, Eichberg DG, Morell AA, Shah AH, Komotar RJ. Prognosticating survival of pineal parenchymal tumors of intermediate differentiation (PPTID) by grade. J Neurooncol. 2021. 155: 165-72</p><p><a href='javascript:void(0);' name='ref41' style='text-decoration: none;'>41.</a> Lutterbach J, Fauchon F, Schild SE, Chang SM, Pagenstecher A, Volk B. Malignant pineal parenchymal tumors in adult patients: Patterns of care and prognostic factors. Neurosurgery. 2002. 51: 44-55 discussion 55-6</p><p><a href='javascript:void(0);' name='ref42' style='text-decoration: none;'>42.</a> Mallick S, Benson R, Rath GK. Patterns of care and survival outcomes in patients with pineal parenchymal tumor of intermediate differentiation: An individual patient data analysis. Radiother Oncol J Eur Soc Ther Radiol Oncol. 2016. 121: 204-8</p><p><a href='javascript:void(0);' name='ref43' style='text-decoration: none;'>43.</a> Martínez H, Nagurney M, Wang ZX, Eberhart CG, Heaphy CM, Curtis MT. ATRX Mutations in pineal parenchymal tumors of intermediate differentiation. J Neuropathol Exp Neurol. 2019. 78: 703-8</p><p><a href='javascript:void(0);' name='ref44' style='text-decoration: none;'>44.</a> Mayol Del Valle M, De Jesus O, editors. Pineal gland cancer. StatPearls. Treasure Island, FL: StatPearls Publishing; 2024. p. Available from: http://www.ncbi.nlm.nih.gov/books/NBK560567 [Last accessed on 2024 Mar 21]</p><p><a href='javascript:void(0);' name='ref45' style='text-decoration: none;'>45.</a> Mena H, Rushing EJ, Ribas JL, Delahunt B, McCarthy WF. Tumors of pineal parenchymal cells: A correlation of histological features, including nucleolar organizer regions, with survival in 35 cases. Hum Pathol. 1995. 26: 20-30</p><p><a href='javascript:void(0);' name='ref46' style='text-decoration: none;'>46.</a> Miyazaki A, Makino K, Shinojima N, Yamashita S, Mikami Y, Mukasa A. Spinal dissemination of pineal parenchymal tumors of intermediate differentiation over 10 years after initial treatment: A case report. Cureus. 2024. 16: e57147</p><p><a href='javascript:void(0);' name='ref47' style='text-decoration: none;'>47.</a> Montaser AS, Cho EY, Catalino MP, Hanna J, Smith TR, Laws ER. A Surgical perspective on the association between cystic lesions of the pineal gland (descartes’ seat of the soul) and the pituitary (the master gland). J Neurol Surg Part B Skull Base. 2022. 83: e598-602</p><p><a href='javascript:void(0);' name='ref48' style='text-decoration: none;'>48.</a> Nagao S, Kuyama H, Murota T, Suga M, Tanimoto T, Kawauchi M. Surgical approaches to pineal tumors: Complications and outcome. Neurol Med Chir (Tokyo). 1988. 28: 779-85</p><p><a href='javascript:void(0);' name='ref49' style='text-decoration: none;'>49.</a> Nagasawa DT, Lagman C, Sun M, Yew A, Chung LK, Lee SJ. Pineal germ cell tumors: Two cases with review of histopathologies and biomarkers. J Clin Neurosci. 2017. 38: 23-31</p><p><a href='javascript:void(0);' name='ref50' style='text-decoration: none;'>50.</a> Nam JY, Gilbert A, Cachia D, Mandel J, Fuller GN, Penas-Prado M. Pineal parenchymal tumor of intermediate differentiation: A single-institution experience. Neurooncol Pract. 2020. 7: 613-9</p><p><a href='javascript:void(0);' name='ref51' style='text-decoration: none;'>51.</a> Park JH, Kim JH, Kwon DH, Kim CJ, Khang SK, Cho YH. Upfront stereotactic radiosurgery for pineal parenchymal tumors in adults. J Korean Neurosurg Soc. 2015. 58: 334-40</p><p><a href='javascript:void(0);' name='ref52' style='text-decoration: none;'>52.</a> Park TH, Kim SK, Phi JH, Park CK, Kim YH, Paek SH. Survival and malignant transformation of pineal parenchymal tumors: A 30-year retrospective analysis in a single-institution. Brain Tumor Res Treat. 2023. 11: 254-65</p><p><a href='javascript:void(0);' name='ref53' style='text-decoration: none;'>53.</a> Pusztaszeri M, Pica A, Janzer R. Pineal parenchymal tumors of intermediate differentiation in adults: Case report and literature review. Neuropathology. 2006. 26: 153-7</p><p><a href='javascript:void(0);' name='ref54' style='text-decoration: none;'>54.</a> Rahmanzade R, Pfaff E, Banan R, Sievers P, Suwala AK, Hinz F. Genetical and epigenetical profiling identifies two subgroups of pineal parenchymal tumors of intermediate differentiation (PPTID) with distinct molecular, histological and clinical characteristics. Acta Neuropathol (Berl). 2023. 146: 853-6</p><p><a href='javascript:void(0);' name='ref55' style='text-decoration: none;'>55.</a> Samkari AM, Alshehri FD, AlMehdar AS, Matar MY. Pineal parenchymal tumors of intermediate differentiation: A case report and literature review. Cureus. 2023. 15: e50139</p><p><a href='javascript:void(0);' name='ref56' style='text-decoration: none;'>56.</a> Scheithauer BW, Fuller GN, VandenBerg SR. The 2007 WHO Classification of tumors of the nervous system: Controversies in surgical neuropathology. Brain Pathol. 2008. 18: 307-16</p><p><a href='javascript:void(0);' name='ref57' style='text-decoration: none;'>57.</a> Schild SE, Scheithauer BW, Schomberg PJ, Hook CC, Kelly PJ, Frick L. Pineal parenchymal tumors: Clinical, pathologic, and therapeutic aspects. Cancer. 1993. 72: 870-80</p><p><a href='javascript:void(0);' name='ref58' style='text-decoration: none;'>58.</a> Senft C, Raabe A, Hattingen E, Sommerlad D, Seifert V, Franz K. Pineal parenchymal tumor of intermediate differentiation: Diagnostic pitfalls and discussion of treatment options of a rare tumor entity. Neurosurg Rev. 2008. 31: 231-6</p><p><a href='javascript:void(0);' name='ref59' style='text-decoration: none;'>59.</a> Shrateh ON, Jobran AW, Owienah H, Sweileh T, Abulihya M, Shahin N. Large pineal parenchymal tumor of intermediate differentiation causing compression with resultant obstructive hydrocephalus: A case report. Ann Med Surg. 2023. 85: 480</p><p><a href='javascript:void(0);' name='ref60' style='text-decoration: none;'>60.</a> Stoiber EM, Schaible B, Herfarth K, Schulz-Ertner D, Huber PE, Debus J. Long term outcome of adolescent and adult patients with pineal parenchymal tumors treated with fractionated radiotherapy between 1982 and 2003--a single institution’s experience. Radiat Oncol Lond Engl. 2010. 5: 122</p><p><a href='javascript:void(0);' name='ref61' style='text-decoration: none;'>61.</a> Takase H, Tanoshima R, Singla N, Nakamura Y, Yamamoto T. Pineal parenchymal tumor of intermediate differentiation: A systematic review and contemporary management of 389 cases reported during the last two decades. Neurosurg Rev. 2022. 45: 1135-55</p><p><a href='javascript:void(0);' name='ref62' style='text-decoration: none;'>62.</a> Tandean S, Siahaan AM, Loe ML, Indharty RS, Julijamnasi , Sitorus MS. Case report: Implantation metastasis following stereotactic biopsy of pineal parenchymal tumor of intermediate differentiation in an adult patient: An exceptionally rare complication. Front Neurol. 2022. 13: 1019955</p><p><a href='javascript:void(0);' name='ref63' style='text-decoration: none;'>63.</a> Tate MC, Rutkowski MJ, Parsa AT. Contemporary management of pineoblastoma. Neurosurg Clin N Am. 2011. 22: 409-12</p><p><a href='javascript:void(0);' name='ref64' style='text-decoration: none;'>64.</a> Tsumanuma I, Tanaka R, Washiyama K. Clinicopathological study of pineal parenchymal tumors: Correlation between histopathological features, proliferative potential, and prognosis. Brain Tumor Pathol. 1999. 16: 61-8</p><p><a href='javascript:void(0);' name='ref65' style='text-decoration: none;'>65.</a> Vasiljevic A. Pineal parenchymal tumors of intermediate differentiation: in need of a stringent definition to avoid confusion. Scientific commentary on ‘Genetical and epigenetical profiling identifies two subgroups of pineal parenchymal tumors of intermediate differentiation (PPTID) with distinct molecular, histological and clinical characteristics.’. Acta Neuropathol (Berl). 2024. 147: 34</p><p><a href='javascript:void(0);' name='ref66' style='text-decoration: none;'>66.</a> Verma A, Epari S, Bakiratharajan D, Sahay A, Goel N, Chinnaswamy G. Primary pineal tumors-Unraveling histological challenges and certain clinical myths. Neurol India. 2019. 67: 491</p><p><a href='javascript:void(0);' name='ref67' style='text-decoration: none;'>67.</a> Villano JL, Propp JM, Porter KR, Stewart AK, Valyi-Nagy T, Li X. Malignant pineal germ-cell tumors: An analysis of cases from three tumor registries. Neuro-Oncology. 2008. 10: 121-30</p><p><a href='javascript:void(0);' name='ref68' style='text-decoration: none;'>68.</a> Wang KY, Chen MM, Malayil Lincoln CM. Adult primary brain neoplasm, including 2016 World Health Organization classification. Radiol Clin North Am. 2019. 57: 1147-62</p><p><a href='javascript:void(0);' name='ref69' style='text-decoration: none;'>69.</a> Watanabe T, Mizowaki T, Arakawa Y, Iizuka Y, Ogura K, Sakanaka K. Pineal parenchymal tumor of intermediate differentiation: Treatment outcomes of five cases. Mol Clin Oncol. 2014. 2: 197-202</p><p><a href='javascript:void(0);' name='ref70' style='text-decoration: none;'>70.</a> Webb M, Johnson DR, Mahajan A, Brown P, Neth B, Kizilbash SH. Clinical experience and outcomes in patients with pineal parenchymal tumor of intermediate differentiation (PPTID): A single-institution analysis. J Neurooncol. 2022. 160: 527-34</p><p><a href='javascript:void(0);' name='ref71' style='text-decoration: none;'>71.</a> Wu X, Wang W, Lai X, Zhou Y, Zhou X, Li J. CD24 and PRAME are novel grading and prognostic indicators for pineal parenchymal tumors of intermediate differentiation. Am J Surg Pathol. 2020. 44: 11</p><p><a href='javascript:void(0);' name='ref72' style='text-decoration: none;'>72.</a> Xin C, Xiong Z, Yan X, Zolfaghari S, Cai Y, Ma Z. Endoscopic-assisted surgery versus microsurgery for pineal region tumors: A single-center retrospective study. Neurosurg Rev. 2021. 44: 1017-22</p><p><a href='javascript:void(0);' name='ref73' style='text-decoration: none;'>73.</a> Yamashita S, Takeshima H, Hata N, Uchida H, Shinojima N, Yokogami K. Clinicopathologic analysis of pineal parenchymal tumors of intermediate differentiation: A multi-institutional cohort study by the Kyushu Neuro-Oncology Study Group. J Neurooncol. 2023. 162: 425-33</p><p><a href='javascript:void(0);' name='ref74' style='text-decoration: none;'>74.</a> Yi J, Kim H, Choi Y, Seol Y, Kahng D, Choi Y. Successful treatment by chemotherapy of pineal parenchymal tumor with intermediate differentiation: A case report. Cancer Res Treat. 2013. 45: 244-9</p><p><a href='javascript:void(0);' name='ref75' style='text-decoration: none;'>75.</a> Yu T, Sun X, Wang J, Ren X, Lin N, Lin S. Twenty-seven cases of pineal parenchymal tumours of intermediate differentiation: mitotic count, Ki-67 labelling index and extent of resection predict prognosis. J Neurol Neurosurg Psychiatry. 2016. 87: 386-95</p></div> </div></div>
  2. Poor diagnostic value of isocitrate dehydrogenase 1 R132H immunohistochemistry for determination of isocitrate dehydrogenase 1 status in patients with glioblastoma

    Fri, 18 Apr 2025 20:26:15 -0000

    Poor diagnostic value of isocitrate dehydrogenase 1 R132H immunohistochemistry for determination of isocitrate dehydrogenase 1 status in patients with glioblastoma Category: Article Type: Ahmad Faried1, Edward Jaya Hadi2, Hasrayati Agustina2Department of Neurosurgery, Faculty of Medicine, Universitas Padjadjaran, Bandung, IndonesiaDepartment of Anatomical Pathology, Faculty of Medicine, Universitas Padjadjaran, Bandung, IndonesiaCorrespondence Address:Ahmad Faried, Department of Neurosurgery, Faculty … Continue reading Poor diagnostic value of isocitrate dehydrogenase 1 R132H immunohistochemistry for determination of isocitrate dehydrogenase 1 status in patients with glioblastoma
    <div><!DOCTYPE html PUBLIC "-//W3C//DTD HTML 4.0 Transitional//EN" "http://www.w3.org/TR/REC-html40/loose.dtd"> <html><head><meta http-equiv="content-type" content="text/html; charset=utf-8"></head><body><div class="row"><div class="col-lg-9 col-sm-8 col-xs-12"><div class="media-body details-body"> <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13509"><h2 class="media-heading"><h2 class="media-heading">Poor diagnostic value of isocitrate dehydrogenase 1 R132H immunohistochemistry for determination of isocitrate dehydrogenase 1 status in patients with glioblastoma</h2></h2></a> </div><div class="disp_categories"> <p><label>Category: </label><span></span></p> <p><label>Article Type: </label><span></span></p> </div><a href="mailto:ahmad.faried@unpad.ac.id" target="_top">Ahmad Faried</a><sup>1</sup>, <a href="mailto:edwardjayahadi@gmail.com" target="_top">Edward Jaya Hadi</a><sup>2</sup>, <a href="mailto:hasrayati@gmail.com" target="_top">Hasrayati Agustina</a><sup>2</sup><ol class="smalllist"><li>Department of Neurosurgery, Faculty of Medicine, Universitas Padjadjaran, Bandung, Indonesia</li><li>Department of Anatomical Pathology, Faculty of Medicine, Universitas Padjadjaran, Bandung, Indonesia</li></ol><p><strong>Correspondence Address:</strong><br>Ahmad Faried, Department of Neurosurgery, Faculty of Medicine, Universitas Padjadjaran, Bandung, Indonesia.<br></p><p><strong>DOI:</strong>10.25259/SNI_881_2024</p>Copyright: © 2025 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.<div class="parablock"><p><strong>How to cite this article: </strong>Ahmad Faried1, Edward Jaya Hadi2, Hasrayati Agustina2. Poor diagnostic value of isocitrate dehydrogenase 1 R132H immunohistochemistry for determination of isocitrate dehydrogenase 1 status in patients with glioblastoma. 18-Apr-2025;16:140</p></div><div class="parablock"><p><strong>How to cite this URL: </strong>Ahmad Faried1, Edward Jaya Hadi2, Hasrayati Agustina2. Poor diagnostic value of isocitrate dehydrogenase 1 R132H immunohistochemistry for determination of isocitrate dehydrogenase 1 status in patients with glioblastoma. 18-Apr-2025;16:140. Available from: <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13509">https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13509</a></p></div> </div> <div class="col-lg-3 col-sm-4 col-xs-12"><div class="article-detail-sidebar"><div class="icon sidebar-icon clearfix add-readinglist-icon"><button id="bookmark-article" class="add-reading-list-article">Add to Reading List</button><button id="bookmark-remove-article" class="remove-reading-list-article">Remove from Reading List</button></div><div class="icon sidebar-icon clearfix"><a class="btn btn-link" target="_blank" type="button" id="OpenPdf" href="https://surgicalneurologyint.com/wp-content/uploads/2025/04/13509/SNI-16-140.pdf"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/pdf-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a target="_blank" href="javascript:void(0);" onclick="return PrintArticle();"><img decoding="async" src="https://i0.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/file-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a class="btn btn-link" type="button" id="EmaiLPDF"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/mail-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a></div><div class="date"> <p>Date of Submission<br><span class="darkgray">20-Oct-2024</span></p> <p>Date of Acceptance<br><span class="darkgray">15-Mar-2025</span></p> <p>Date of Web Publication<br><span class="darkgray">18-Apr-2025</span></p> </div> </div></div> </div> <!--.row --><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a href="javascript:void(0);" name="Abstract">Abstract</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><strong>Background</strong>The World Health Organization (WHO) classification of central nervous system (CNS) tumors is a major advance toward improving the diagnosis of adult brain tumors. Despite the promise of isocitrate dehydrogenase (IDH) mutations as an important biomarker for glioblastoma, not all institutions have ready access to mutation detection polymerase chain reaction (PCR) methods, and deoxyribonucleic acid (DNA) sequencing may be problematic in very small biopsies. However, a simultaneous evaluation of IDH1 status by DNA sequencing and immunohistochemistry (IHC) to determine the sensitivity and specificity of both methods, along with their predictive value, was unavailable.</p><p><strong>Methods</strong>This retrospective study included 33 patients who underwent surgical resection or biopsy, January 2016–December 2019. The diagnosis of glioblastoma was established. Surgically resected tumor tissues were fixated in 10%-formaldehyde preserved in paraffin-embedded blocks. Glioblastoma was classified according to the 2021 WHO classification of CNS tumors. The enrolled patients were followed up to obtain the overall survival rate (median follow-up time, 30 months).</p><p><strong>Results</strong>Thirty-three patients (14 male; 19 female), mean age of 44.74 ± 15.49 years. Eight had WHO Grade II, 2 with WHO Grade III, and 23 with WHO Grade IV. The sensitivity and specificity of IDH1 IHC were 81.82% (<i>P</i> = 0.0007), a positive predictive value of 90.00% (69.90-98.22%), and a negative predictive value of 69.23% (42.37-87.32%). The survival rate was significantly higher in IDH1 mutant than wild-type IDH1, whether based on IHC or PCR (<i>P</i> = 0.0014).</p><p><strong>Conclusion</strong>IDH1 status evaluation is crucial to predicting the survival rate and important for guiding the treatment decision for patients with glioblastoma. Despite the lesser sensitivity and specificity of IHC in comparison to DNA sequencing in this study, larger prospective studies are needed to validate our preliminary finding.</p><p><strong>Keywords: </strong>Central nervous system tumor, Glioblastoma, Immunohistochemistry, Isocitrate dehydrogenase 1 IDH1 R132H, Polymerase chain reaction</p><p></p></div> </div></body></html> </div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"><p></p><p><inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="SNI-16-140-inline001.tif"/></p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="INTRODUCTION">INTRODUCTION</a></h3><div class="clearfix"></div><div class="hline"></div><p>The new version of the World Health Organization (WHO) classification of central nervous system (CNS) tumors is a significant progress in improving the identification of adult brain tumors.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>] Previously, glioblastoma was identified based on histologic observations of microvascular proliferation and/or necrosis and contained both isocitrate dehydrogenase (IDH)-mutated (10%) and IDH wild-type (90%) tumors with substantially different biological features and prognoses. In the most recent modification, glioblastoma will include solely IDH wild-type tumors.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>,<xref ref-type="bibr" rid="ref23"> <a href='#ref23'>23</a> </xref>] This scheme encourages molecular testing for patients with glioblastoma. Despite the promise of IDH mutations as an important glioblastoma biomarker, not all sites have ready access to mutation detection methods, and deoxyribonucleic acid (DNA) extraction followed by sequencing may be problematic in very small biopsies.[<xref ref-type="bibr" rid="ref16"> <a href='#ref16'>16</a> </xref>]</p><p>Wild-type IDH1 is an important metabolic enzymes that catalyze the oxidative decarboxylation of isocitrate to generate α-ketoglutarate (αKG) and carbon dioxide that play a role in malignancy. The common function of IDH1 active-site mutation is a neomorphic enzyme activity catalyzes the conversion of αKG to D-2-hydroxyglutarate (D2HG). Under physiological conditions, cellular D2HG accumulation is limited due to the actions of the endogenous D2HG dehydrogenase, which catalyzes the conversion of D2HG to αKG. However, the neomorphic activity of mutant IDH causes D2HG to accumulate to supraphysiological levels within cells. Elevated D2HG concentrations can be detected in the serum of patients with IDH-mutant gliomas in patients.[<xref ref-type="bibr" rid="ref5"> <a href='#ref5'>5</a> </xref>]</p><p>IDH1 immunohistochemistry (IHC) can detect cancer cells with mutations by utilizing an antibody specific to the prevalent R132H mutant variant of IDH1.[<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>,<xref ref-type="bibr" rid="ref6"> <a href='#ref6'>6</a> </xref>.<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>,<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>] The IHC method is a viable and less labor-intensive method for detecting IDH1 mutations; nevertheless, its sensitivity and specificity have not been tested by simultaneous sequencing and validation on clinically annotated samples. A recent study found that IDH1 mutation status in glioblastoma patients could be useful diagnostic and prognostic tools, as well as predict the response of glioblastoma management.[<xref ref-type="bibr" rid="ref17"> <a href='#ref17'>17</a> </xref>] Here, we performed a simultaneous evaluation of IDH1 status in glioblastoma using both polymerase chain reaction (PCR) and IHC to determine the sensitivity and specificity of both methods. We chose IHC alongside PCR since, as a gold standard, somehow PCR is not always available in resource-limited settings such as IHC.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="MATERIALS AND METHODS">MATERIALS AND METHODS</a></h3><div class="clearfix"></div><div class="hline"></div><h3 class = "title3">Subjects</h3><p>The Committee of Ethics of the Faculty of Medicine of Padjadjaran University provided ethical approval. This retrospective study comprised 33 patients who had surgical resection or biopsy from January 2016 to December 2019, and the diagnosis of primary glioblastoma was confirmed. Tissues from surgically excised tumors were fixed in 10% formaldehyde and implanted in paraffin blocks. Glioblastoma was classified and graded based on the 2021 WHO classification of CNS cancers.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'> 2 </a> </xref>] All individuals were treated for gliomas using standard procedures. The recruited patients were followed up to determine their overall survival (OS) rate (median follow-up time: 30 months).</p><h3 class = "title3">IDH1 IHC</h3><p>Slides of tumor tissue with a thickness of four microns were deparaffinized and rehydrated. Antigen retrieval was carried out using a decloaking chamber (DC2008INTL; Biocare Medical, Pacheco, CA, USA) at 100°C for 20 min using an antigen retrieval solution (Tris ethylenediaminetetraacetic acid 10 mmol/L, pH 9.0). After cooling at room temperature, sections were washed 2× with phosphate-buffered saline (PBS) for 5 min each. Endogenous peroxidase activity was stopped by dipping sections in 3% hydrogen peroxide blocker (Boster Biological Technology, Pleasanton, CA, USA) for 10 min and rinsed in three changes of PBS. Following the initial processing step, sections were incubated at room temperature with primary antibodies anti-human IDH1 R132H mutant specific AB (GTX57185 Genetex, IHC 132, mouse monoclonal AB, at 1:200 dilution), followed by 30 min of incubation with the poly horseradish peroxidase (HRP) non-biotin detection system. Finally, the sections were counterstained with hematoxylin and eosin, then dehydrated and mounted. Positive results revealed strong cytoplasmic exclusively in tumor cells, while negative controls were produced concurrently for all 33 samples by replacing the primary AB with distilled water.<xref ref-type="bibr" rid="ref6"> <a href='#ref6'> 6 </a> </xref>,<xref ref-type="bibr" rid="ref12"> <a href='#ref12'> 12 </a> </xref> IDH1 status was determined by a pathologist independent of the PCR result.</p><h3 class = "title3">Statistical analysis</h3><p>We used GraphPad Prism v8.0 for the statistical analysis. <i>P</i> < 0.05 was considered as statistically significant.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="RESULTS">RESULTS</a></h3><div class="clearfix"></div><div class="hline"></div><h3 class = "title3">Subjects characteristic</h3><p>This study included 33 patients (14 male and 19 female), with a mean age of 44.74 ± 15.49 years old. According to the 2021 WHO categorization with PCR examination, the participants included eight patients with Grade II, two patients with Grade III, and 23 patients with Grade IV. <xref ref-type="table" rid="T1"> <a href='#T1'> Table 1 </a> </xref> shows a summary of the subjects’ characteristics.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T1'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13509/SNI-16-140-t001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 1:</h3><p>Subject’s Characteristics.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3">The reliability of IHC</h3><p>Direct DNA sequencing validated 23 IDH-wild type and 10 IDH1 gene mutant samples [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1 </a> </xref>]. Nine samples had mutations in the IDH1 R132H site and one in the IDH1 R132G location. While in the IHC analysis, there were 13 samples of IDH1 R132H mutant and 20 samples of IDH-wild type [<xref ref-type="fig" rid="F2"> <a href='#F2'> Figure 2 </a> </xref>]. Six samples of IHC results do not match those from DNA sequencing. Therefore, we discovered that the sensitivity and specificity of IDH1 IHC were 81.82% (<i>P</i> = 0.0007), with a positive predictive value of 90.00% (69.90–98.22%) and a negative predictive value of 69.23% (42.37–87.32%), as shown in <xref ref-type="table" rid="T2"> <a href='#T2'> Table 2 </a> </xref>.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F1'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13509/SNI-16-140-g001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 1:</h3><p>Sequencing results of IDH1 mutations and wild-type samples; (left) wild-type and (right) IDH1 R132H. IDH1: Isocitrate dehydrogenase 1. (Right, in blue arrow): IDH1 mutation at R132H</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F2'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13509/SNI-16-140-g002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 2:</h3><p>IHC results of IDH R132H mutation; (left) positive and (right) negative. IHC: Immunohistochemistry, IDH1: Isocitrate dehydrogenase 1. Magnification: 100x</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T2'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13509/SNI-16-140-t002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 2:</h3><p>Result of IDH1 mutation by IHC analysis and direct sequencing method (<i>n</i>=33).</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3">Survival rate</h3><p>In this study, we discovered that patients with IDH1 mutants had a greater survival rate than patients with wild-type IDH1, whether using IHC or PCR [<xref ref-type="fig" rid="F3"> <a href='#F3'> Figure 3 </a> </xref>], (<i>P</i> = 0.0014). There was no statistical difference in the survival rate between IHC and PCR-confirmed IDH1 mutant [<xref ref-type="table" rid="T3"> <a href='#T3'> Table 3 </a> </xref>], (<i>P ></i> 0.05).</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F3'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13509/SNI-16-140-g003.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 3:</h3><p>The survival rate of patients with IDH1 status. Patients with IDH1 mutant have a higher survival rate than patients with gliomas with wild-type IDH1 status, whether based on the immunohistochemistry or PCR (Log rank mantle cox, <i>P</i> = 0.0014). IDH1: Isocitrate dehydrogenase 1, PCR: Polymerase chain reaction. WT: Wild type, WT-IHC :Wild type-immunohistochemistry.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T3'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13509/SNI-16-140-t003.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 3:</h3><p>Comparison of survival rate at 24 months between immunohistochemistry and PCR-confirmed IDH1 mutant.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="DISCUSSION">DISCUSSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Malignant gliomas are fundamentally a genetic disease that shares characteristics with nearly all human cancers.[<xref ref-type="bibr" rid="ref13"> <a href='#ref13'>13</a> </xref>,<xref ref-type="bibr" rid="ref14"> <a href='#ref14'>14</a> </xref>] They are derived from astrocyte-like neural stem cells that contain oncogenic alterations in the subventricular zone.[<xref ref-type="bibr" rid="ref12"> <a href='#ref12'>12</a> </xref>] The genetic changes that cause gliomagenesis have been the topic of much research.[<xref ref-type="bibr" rid="ref19"> <a href='#ref19'>19</a> </xref>] Notably, homozygous deletion or mutation of tumor suppressor genes cyclin-dependent kinase inhibitor (CDKN2A/B); phosphatase and tensin homolog (PTEN), loss of heterozygosity of chromosome 10q, and oncogenic amplification of epidermal growth factor receptor (EGFR) are identified in primary <i>de novo</i> glioblastoma, while mutations in the TP53 gene are typically detected in secondary glioblastoma.[<xref ref-type="bibr" rid="ref7"> <a href='#ref7'>7</a> </xref>,<xref ref-type="bibr" rid="ref11"> <a href='#ref11'>11</a> </xref>] However, the IDH1 gene is the most investigated in gliomas, as it is more prevalent in low-grade gliomas and is associated with a better prognosis. Thus, molecular detection of IDH1 has been added as a diagnostic criteria for glioblastoma in the most recent WHO CNS tumor classification.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>,<xref ref-type="bibr" rid="ref21"> <a href='#ref21'>21</a> </xref>]</p><p>The assessment of IDH1 status is critical for diagnosis and developing an effective treatment strategy. This can be performed either through DNA sequencing or IHC.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>,<xref ref-type="bibr" rid="ref21"> <a href='#ref21'>21</a> </xref>,<xref ref-type="bibr" rid="ref22"> <a href='#ref22'>22</a> </xref>] IDH1 mutations were identified using PCR and direct sequencing of amplified complementary DNA isolated from fresh frozen or formalin-fixed paraffin-embedded tissue. IHC is commonly conducted as part of the histological investigation.[<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>] The use of a particular antibody that binds the mutant IDH1-R132H proteins enables the identification of mutant tumor cells by IHC in most situations, and this technology has a sensitivity that may exceed normal sequencing.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>]</p><p>In a study comparing IHC to genetic testing, Sporikova <i>et al</i>., discovered that IHC was 100% sensitive and specific for detecting IDH1-R132H mutations, demonstrating that anti-IDH1-R132H immunostaining is a trustworthy technique for assessing the status of IDH1 gene mutations.[<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>] Furthermore, one study found that the concordance rate between IHC and sequencing ranged from 88% to 99%. In five of eight trials, the number of mutations discovered by IHC exceeded that detected by sequencing. This can be explained by the fact that IHC can identify the mutation even if there is just a limited number of IDH1-R132H mutation-positive tumor cells in the sample.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>] However, in our cohort, IHC identification of the IDH1-R132H mutation failed in 6 out of 33 samples (18.2%), with a sensitivity and specificity of 81.82% (<i>P</i> = 0.0007). This failure could be caused by laboratory errors or poor tissue processing. As a result, the molecular-histological definition of gliomas necessitates the practical application of IDH1 genomic sequencing.</p><p>Either based on IHC or PCR, we discovered that the survival rate was significantly higher (<i>P</i> = 0.0014) in patients with IDH1 mutant than in patients with IDH1 wild-type [<xref ref-type="fig" rid="F3"> <a href='#F3'>Figure 3</a> </xref>]. Furthermore, these findings are consistent with those of Howard <i>et al</i>., who reported that the presence of IDH1 R132H mutation in tumor tissue serves as a positive prognostic factor for glioblastoma patients in terms of progression-free survival (PFS) and OS.[<xref ref-type="bibr" rid="ref8"> <a href='#ref8'>8</a> </xref>] Similarly, Tabei <i>et al</i>., and Tateishi and Yamamoto showed that IDH1 mutant glioblastoma patients had a threefold longer survival rate than those with IDH1 wild type.[<xref ref-type="bibr" rid="ref25"> <a href='#ref25'>25</a> </xref>,<xref ref-type="bibr" rid="ref27"> <a href='#ref27'>27</a> </xref>] Iurlaro <i>et al</i>., and Wen and Packer observed an increased median OS in IDH mutant patients. Those with IDH-mutated disease had a median OS of 65 months, whereas patients with IDH wild-type disease had a median OS of 20 months.[<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>,<xref ref-type="bibr" rid="ref28"> <a href='#ref28'>28</a> </xref>] In addition, Iurlaro <i>et al</i>., and Chen <i>et al</i>., reported that the PFS of patients with IDH mutant glioblastoma was improved.[<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>,<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>] In contrast, Zou <i>et al</i>., found no statistically significant difference in OS based on IDH1 mutation status.[<xref ref-type="bibr" rid="ref29"> <a href='#ref29'>29</a> </xref>]</p><p>In our cohort, we found no difference in survival rates between the IHC and sequencing-detected IDH1 mutants; this impact could be related to the small number of samples. Despite its reduced sensitivity and specificity compared to DNA sequencing, IHC is beneficial for detecting the IDH1 R132H mutation, is less expensive, and is more easily available in countries with limited resources. However, the correct identification of mutation status in diffuse gliomas is crucial for identifying appropriate tailored therapies and adhering to the latest 2021 WHO system, which is based on the presence of validated biomarkers, including IDH mutations.</p><p>IHC is an affordable and simple procedure that can be performed with few resources, a powerful technique to study localization and presence/absence of a target at the tissue and cellular level, paraffin embedded and frozen tissue samples can be stored and accessed when required, and stained tissue sections can be stored and referred to whenever required. However, the specificity of antibodies can be variable and needs to be thoroughly checked using appropriate controls. The method is semi-quantitative, and the absolute abundance of the target cannot be reliably determined; the tissue is highly processed and may lead to a loss of information about the natural state. IHC is a multi-step procedure, and variability can be introduced at any stage, leading to poor reproducibility of results.[<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>] Somehow, in countries with limited resources, allocating the available resources to patient care is a crucial component of healthcare policy. Correct diagnosis tools could improve the quality of life of a patient and increase cost-effectiveness.[<xref ref-type="bibr" rid="ref18"> <a href='#ref18'>18</a> </xref>]</p><h3 class = "title3">Study limitation</h3><p>Limitations of this study should be considered, such as the small sample size and lack of control for confounders, may be issued to the retrospective design study.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CONCLUSION">CONCLUSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Assessing IDH1 status is critical for predicting survival rates and directing treatment decisions for patients with gliomas. Despite the lesser sensitivity and specificity of IHC in comparison to DNA sequencing in this study, larger prospective studies are needed to validate our preliminary finding.</p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Ethical approval">Ethical approval</a></h3><div class="clearfix"></div><div class="hline"></div><p>The research/study was approved by the Institutional Review Board at the Faculty of Medicine, Universitas Padjadjaran, Bandung, number 34/UN6.KEP/EC/2022, dated November 20, 2022.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Declaration of patient consent">Declaration of patient consent</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors certify that they have obtained all appropriate patient consent.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Financial support and sponsorship">Financial support and sponsorship</a></h3><div class="clearfix"></div><div class="hline"></div><p>This study supported by the Grants-in-Aid from Indonesian Ministry of Education, Culture, Research and Technology, Grant No. 074/E5/PG.02.00.PL/2024 for Fundamental Research Grant.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Conflicts of interest">Conflicts of interest</a></h3><div class="clearfix"></div><div class="hline"></div><p>There are no conflicts of interest.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Use of artificial intelligence (AI)-assisted technology for manuscript preparation">Use of artificial intelligence (AI)-assisted technology for manuscript preparation</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Disclaimer">Disclaimer</a></h3><div class="clearfix"></div><div class="hline"></div><p>The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.</p></div> </div></div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"></div> </div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a name="References" href="javascript:void(0);">References</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><a href='javascript:void(0);' name='ref1' style='text-decoration: none;'>1.</a> Agnihotri S, Aldape KD, Zadeh G. Isocitrate dehydrogenase status and molecular subclasses of glioma and glioblastoma. Neurosurg Focus. 2014. 37: E13</p><p><a href='javascript:void(0);' name='ref2' style='text-decoration: none;'>2.</a> Bolly HM, Faried A, Hermanto Y, Lubis BP, Tjahjono FP, Hernowo BS. Analysis of mutant isocitrate dehydrogenase 1 immunoexpression, Ki-67 and programmed death ligand 1 in diffuse astrocytic tumours: Study of single center in Bandung, Indonesia. J Korean Neurosurg Soc. 2021. 64: 100-9</p><p><a href='javascript:void(0);' name='ref3' style='text-decoration: none;'>3.</a> Capper D, Zentgraf H, Balss J, Hartmann C, von Deimling A. Monoclonal antibody specific for IDH1 R132H mutation. Acta Neuropathol. 2009. 118: 599-601</p><p><a href='javascript:void(0);' name='ref4' style='text-decoration: none;'>4.</a> Chen N, Yu T, Gong J, Nie L, Chen X, Zhang M. IDH1/2 gene hotspot mutations in central nervous system tumours: Analysis of 922 Chinese patients. Pathology. 2016. 48: 675-83</p><p><a href='javascript:void(0);' name='ref5' style='text-decoration: none;'>5.</a> Elkhaled A, Jalbert LE, Phillips JJ, Yoshihara HA, Parvataneni R, Srinivasan R. Magnetic resonance of 2-hydroxyglutarate in IDH1-mutated low-grade gliomas. Sci Transl Med. 2012. 4: 116ra5</p><p><a href='javascript:void(0);' name='ref6' style='text-decoration: none;'>6.</a> Faried A, Bolly HM, Hermanto Y, Achmad A, Halim D, Tjahjono FP. Prognostic significance of L-type amino acid transported-1 (LAT-1) expression in human astrocytic gliomas. Interdiscip Neurosurg. 2021. 23: 100939</p><p><a href='javascript:void(0);' name='ref7' style='text-decoration: none;'>7.</a> Hata N, Suzuki SO, Murata H, Hatae R, Akagi Y, Sangatsuda Y. Genetic analysis of a case of glioblastoma with oligodendroglial component arising during the progression of diffuse astrocytoma. Pathol Oncol Res. 2015. 21: 839-43</p><p><a href='javascript:void(0);' name='ref8' style='text-decoration: none;'>8.</a> Howard TP, Vazquez F, Tsherniak A, Hong AL, Rinne M, Aguirre AJ. Functional genomic characterization of cancer genomes. Cold Spring Harb Symp Quant Biol. 2016. 81: 237-46</p><p><a href='javascript:void(0);' name='ref9' style='text-decoration: none;'>9.</a> Huang LE. Friend or foe-IDH1 mutations in glioma 10 years on. Carcinogenesis. 2019. 40: 1299-307</p><p><a href='javascript:void(0);' name='ref10' style='text-decoration: none;'>10.</a> Iurlaro R, León-Annicchiarico CL, Muñoz-Pinedo C. Regulation of cancer metabolism by oncogenes and tumor suppressors. Methods Enzymol. 2014. 542: 59-80</p><p><a href='javascript:void(0);' name='ref11' style='text-decoration: none;'>11.</a> Kalkan R, Atli Eİ Özdemir M, Çiftçi E, Aydin HE, Artan S. IDH1 mutations is prognostic marker for primary glioblastoma multiforme but MGMT hypermethylation is not prognostic for primary glioblastoma multiforme. Gene. 2015. 554: 81-6</p><p><a href='javascript:void(0);' name='ref12' style='text-decoration: none;'>12.</a> Lee JH, Lee JE, Kahng JY, Kim SH, Park JS, Yoon SJ. Human glioblastoma arises from subventricular zone cells with low-level driver mutations. Nature. 2018. 560: 243-7</p><p><a href='javascript:void(0);' name='ref13' style='text-decoration: none;'>13.</a> Liu Y, Lang F, Chou FJ, Zaghloul KA, Yang C. Isocitrate dehydrogenase mutations in glioma: Genetics, biochemistry, and clinical indications. Biomedicines. 2020. 8: 294</p><p><a href='javascript:void(0);' name='ref14' style='text-decoration: none;'>14.</a> Louis DN, Perry A, Wesseling P, Brat DJ, Cree IA, FigarellaBranger D. The 2021 WHO Classification of tumors of the central nervous system: A summary. Neuro Oncol. 2021. 23: 1231-51</p><p><a href='javascript:void(0);' name='ref15' style='text-decoration: none;'>15.</a> Louis DN, Wesseling P, Aldape K, Brat DJ, Capper D, Cree IA. cIMPACT-NOW update 6: new entity and diagnostic principle recommendations of the cIMPACT-Utrecht meeting on future CNS tumor classification and grading. Brain Pathol. 2020. 30: 844-56</p><p><a href='javascript:void(0);' name='ref16' style='text-decoration: none;'>16.</a> Macaulay RJ. Impending impact of molecular pathology on classifying adult diffuse gliomas. Cancer Control. 2015. 22: 200-5</p><p><a href='javascript:void(0);' name='ref17' style='text-decoration: none;'>17.</a> Mahmoud MS, Khalifa MK, Nageeb AM, Ezz El-Arab LR, El-Mahdy M, Ramadan A. Clinical impact of IDH1 mutations and MGMT methylation in adult glioblastoma. Egypt J Med Hum Genet. 2024. 25: 42</p><p><a href='javascript:void(0);' name='ref18' style='text-decoration: none;'>18.</a> Mebratie DY, Dagnaw GG. Review of immunohistochemistry techniques: Applications, current status, and future perspectives. Semin Diagn Pathol. 2024. 41: 154-60</p><p><a href='javascript:void(0);' name='ref19' style='text-decoration: none;'>19.</a> Ohgaki H, Kleihues P. The definition of primary and secondary glioblastoma. Clin Cancer Res. 2013. 19: 764-72</p><p><a href='javascript:void(0);' name='ref20' style='text-decoration: none;'>20.</a> O’Hurley G, Sjöstedt E, Rahman A, Li B, Kampf C, Pontén F. Garbage in, garbage out: A critical evaluation of strategies used for validation of IHC biomarkers. Mol Oncol. 2014. 8: 783-98</p><p><a href='javascript:void(0);' name='ref21' style='text-decoration: none;'>21.</a> Picca A, Berzero G, Di Stefano AL, Sanson M. The clinical use of IDH1 and IDH2 mutations in gliomas. Expert Rev Mol Diagn. 2018. 18: 1041-51</p><p><a href='javascript:void(0);' name='ref22' style='text-decoration: none;'>22.</a> Polívka J, Pešta M, Pitule P, Hes O, Holubec L, Polívka J. IDH1 mutation is associated with lower expression of VEGF but not microvessel formation in glioblastoma multiforme. Oncotarget. 2018. 9: 16462-76</p><p><a href='javascript:void(0);' name='ref23' style='text-decoration: none;'>23.</a> Reuss DE, Sahm F, Schrimpf D, Wiestler B, Capper D, Koelsche C. ATRX and IDH1-R132H immunohistochemistry with subsequent copy number analysis and IDH sequencing as a basis for an “integrated” diagnostic approach for adult astrocytoma, oligodendroglioma and glioblastoma. Acta Neuropathol. 2015. 129: 133-46</p><p><a href='javascript:void(0);' name='ref24' style='text-decoration: none;'>24.</a> Sporikova Z, Slavkovsky R, Tuckova L, Kalita O, Megova HM, Jiri E. IDH1/2 mutations in patients with diffuse gliomas: A single center retrospective massively parallel sequencing analysis. Appl Immunohistochem Mol Morphol. 2022. 30: 178-83</p><p><a href='javascript:void(0);' name='ref25' style='text-decoration: none;'>25.</a> Tabei Y, Kobayashi K, Saito K. Survival in patients with glioblastoma at a first progression does not correlate with isocitrate dehydrogenase (IDH)1 gene mutation status. Jpn J Clin Oncol. 2021. 51: 45-53</p><p><a href='javascript:void(0);' name='ref26' style='text-decoration: none;'>26.</a> Takahashi Y, Nakamura H, Makino K, Hide T, Muta D, Kamada H. Prognostic value of isocitrate dehydrogenase 1, O6-methylguanine-DNA methyltransferase promoter methylation, and 1p19q co-deletion in Japanese malignant glioma patients. World J Surg Oncol. 2013. 11: 284</p><p><a href='javascript:void(0);' name='ref27' style='text-decoration: none;'>27.</a> Tateishi K, Yamamoto T, editors. IDH-mutant gliomas. London: Intech Open; 2019. p. 84543</p><p><a href='javascript:void(0);' name='ref28' style='text-decoration: none;'>28.</a> Wen PY, Packer RJ. The 2021 WHO Classification of tumors of the central nervous system: Clinical implications. Neurooncology. 2021. 23: 1215-7</p><p><a href='javascript:void(0);' name='ref29' style='text-decoration: none;'>29.</a> Zou Y, Bai HX, Wang Z, Yang L. Comparison of immunohistochemistry and DNA sequencing for the detection of IDH1 mutations in gliomas. Neuro Oncol. 2015. 17: 477-8</p></div> </div></div>
  3. Mechanical thrombectomy for cerebral embolism due to cardiac papillary fibroelastoma: A case report

    Fri, 18 Apr 2025 20:21:50 -0000

    Mechanical thrombectomy for cerebral embolism due to cardiac papillary fibroelastoma: A case report Category: Article Type: Kentaro Izumi1,2, Youhei Takeuchi1,2, Naoya Iwabuchi1,2, Masahiro Yoshida1,2, Kuniyasu Niizuma3,4,5, Hidenori Endo3Department of Neurosurgery, Osaki Citizen Hospital, Osaki, JapanPreemptive Medicine in the Community of the North Miyagi, Tohoku University Graduate School of Medicine, Sendai, Miyagi, JapanDepartment of Neurosurgery, Tohoku … Continue reading Mechanical thrombectomy for cerebral embolism due to cardiac papillary fibroelastoma: A case report
    <div><!DOCTYPE html PUBLIC "-//W3C//DTD HTML 4.0 Transitional//EN" "http://www.w3.org/TR/REC-html40/loose.dtd"> <html><head><meta http-equiv="content-type" content="text/html; charset=utf-8"></head><body><div class="row"><div class="col-lg-9 col-sm-8 col-xs-12"><div class="media-body details-body"> <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13508"><h2 class="media-heading"><h2 class="media-heading">Mechanical thrombectomy for cerebral embolism due to cardiac papillary fibroelastoma: A case report</h2></h2></a> </div><div class="disp_categories"> <p><label>Category: </label><span></span></p> <p><label>Article Type: </label><span></span></p> </div><a href="mailto:kentaro.izumi.t8@gmail.com" target="_top">Kentaro Izumi</a><sup>1,2</sup>, <a href="mailto:you.takeuchi@olive.plala.or.jp" target="_top">Youhei Takeuchi</a><sup>1,2</sup>, <a href="mailto:d06sm013@yahoo.co.jp" target="_top">Naoya Iwabuchi</a><sup>1,2</sup>, <a href="mailto:myoship1964@gmail.com" target="_top">Masahiro Yoshida</a><sup>1,2</sup>, <a href="mailto:kniizuma@tohoku.ac.jp" target="_top">Kuniyasu Niizuma</a><sup>3,4,5</sup>, <a href="mailto:h-endo@tohoku.ac.jp" target="_top">Hidenori Endo</a><sup>3</sup><ol class="smalllist"><li>Department of Neurosurgery, Osaki Citizen Hospital, Osaki, Japan</li><li>Preemptive Medicine in the Community of the North Miyagi, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan</li><li>Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan</li><li>Department of Translational Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan</li><li>Department of Neurosurgical Engineering, Graduate School of Biomedical Engineering, Tohoku University, Sendai, Miyagi, Japan</li></ol><p><strong>Correspondence Address:</strong><br>Masahiro Yoshida, Department of Neurosurgery, Osaki Citizen Hospital, Osaki, Japan.<br></p><p><strong>DOI:</strong>10.25259/SNI_68_2025</p>Copyright: © 2025 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.<div class="parablock"><p><strong>How to cite this article: </strong>Kentaro Izumi1,2, Youhei Takeuchi1,2, Naoya Iwabuchi1,2, Masahiro Yoshida1,2, Kuniyasu Niizuma3,4,5, Hidenori Endo3. Mechanical thrombectomy for cerebral embolism due to cardiac papillary fibroelastoma: A case report. 18-Apr-2025;16:141</p></div><div class="parablock"><p><strong>How to cite this URL: </strong>Kentaro Izumi1,2, Youhei Takeuchi1,2, Naoya Iwabuchi1,2, Masahiro Yoshida1,2, Kuniyasu Niizuma3,4,5, Hidenori Endo3. Mechanical thrombectomy for cerebral embolism due to cardiac papillary fibroelastoma: A case report. 18-Apr-2025;16:141. Available from: <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13508">https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13508</a></p></div> </div> <div class="col-lg-3 col-sm-4 col-xs-12"><div class="article-detail-sidebar"><div class="icon sidebar-icon clearfix add-readinglist-icon"><button id="bookmark-article" class="add-reading-list-article">Add to Reading List</button><button id="bookmark-remove-article" class="remove-reading-list-article">Remove from Reading List</button></div><div class="icon sidebar-icon clearfix"><a class="btn btn-link" target="_blank" type="button" id="OpenPdf" href="https://surgicalneurologyint.com/wp-content/uploads/2025/04/13508/SNI-16-141.pdf"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/pdf-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a target="_blank" href="javascript:void(0);" onclick="return PrintArticle();"><img decoding="async" src="https://i0.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/file-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a class="btn btn-link" type="button" id="EmaiLPDF"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/mail-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a></div><div class="date"> <p>Date of Submission<br><span class="darkgray">21-Jan-2025</span></p> <p>Date of Acceptance<br><span class="darkgray">19-Mar-2025</span></p> <p>Date of Web Publication<br><span class="darkgray">18-Apr-2025</span></p> </div> </div></div> </div> <!--.row --><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a href="javascript:void(0);" name="Abstract">Abstract</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><strong>Background</strong>Papillary fibroelastoma (PFE) and myxoma are relatively common types of benign cardiac tumors. PFE and myxoma can be associated with fatal embolic events. However, PFE is not widely recognized within the field of cerebrovascular diseases.</p><p><strong>Case Description</strong>A 54-year-old male presented with a sudden onset of left hemiparesis. Three-dimensional computed tomography (CT) angiography revealed incomplete occlusion of the right middle cerebral artery. Thrombolytic therapy with recombinant tissue-type plasminogen activator was performed, followed by mechanical thrombectomy. Reperfusion was achieved within 199 minutes, resulting in thrombolysis in cerebral infarction grade 2b. The retrieved emboli appeared as a white gelatinous substance, which was diagnosed as PFE by histopathological examination. Transesophageal echocardiography and cardiac CT identified a 6-mm mobile mass in the left atrium. PFE in the left atrium was considered to be the source of the embolism and tumor resection was performed on day 18. Histopathological findings of the resected tumor were identical to those of the emboli. The patient was transferred to a rehabilitation facility on day 36, with a modified Rankin Scale score of 2.</p><p><strong>Conclusion</strong>PFE and myxoma share many clinical features, but PFE tends to be smaller, so detection is more challenging and has likely resulted in under-recognition. PFE and myxoma can be associated with fatal embolic events. Resection is recommended for left-sided, mobile, symptomatic tumors larger than 10 mm. The differential diagnosis of embolus retrieved through mechanical thrombectomy should consider both myxoma and PFE and persistent efforts should be made to detect the embolic origin.</p><p><strong>Keywords: </strong>Cardiac myxoma, Cardiac papillary fibroelastoma, Cerebral tumor embolism, Mechanical thrombectomy</p><p></p></div> </div></body></html> </div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"><p></p><p><inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="SNI-16-141-inline001.tif"/></p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="INTRODUCTION">INTRODUCTION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Papillary fibroelastoma (PFE) and myxoma are relatively common types of benign cardiac tumors.[<xref ref-type="bibr" rid="ref12"> <a href='#ref12'>12</a> </xref>,<xref ref-type="bibr" rid="ref13"> <a href='#ref13'>13</a> </xref>,<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>] Both PFE and myxoma can cause severe left-sided embolic events, including ischemic stroke and sudden death. However, PFE is more challenging to detect as the tumor is smaller than myxoma.[<xref ref-type="bibr" rid="ref23"> <a href='#ref23'>23</a> </xref>,<xref ref-type="bibr" rid="ref34"> <a href='#ref34'>34</a> </xref>] In addition, PFE has not been widely recognized within the field of cerebrovascular diseases because cardiac tumors are rare[<xref ref-type="bibr" rid="ref12"> <a href='#ref12'>12</a> </xref>] and infrequently encountered, so they may have been previously overlooked. We present a case of PFE that manifested as cerebral embolism and was treated with mechanical thrombectomy.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CASE REPORT">CASE REPORT</a></h3><div class="clearfix"></div><div class="hline"></div><h3 class = "title3">Patient information</h3><p>A 54-year-old male delivery worker employed by a transportation company experienced a sudden onset of left hemiparesis while at work. He presented to our emergency department 101 min after symptom onset.</p><h3 class = "title3">Clinical findings</h3><p>On arrival, he exhibited severe left hemiparesis, dysarthria, and left hemispatial neglect, with a National Institutes of Health Stroke Scale score of 11. He had no prior medical history. Noncontrast computed tomography (CT) revealed early ischemic changes in the right frontal operculum, temporal operculum, and insular cortex, with an Alberta Stroke Program Early CT Score of 7 [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1a </a> </xref>]. The hyperdense vessel sign was absent in the major cerebral arteries. Three-dimensional CT angiography demonstrated poor visualization of the right middle cerebral artery (MCA) without evidence of cervical carotid stenosis [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1b </a> </xref>]. Concurrent contrast-enhanced CT of the chest revealed no clearly visualized intracardiac thrombi or cardiac tumors [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1c </a> </xref>], and electrocardiography (ECG) showed sinus rhythm.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F1'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13508/SNI-16-141-g001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 1:</h3><p>(a-d) Prethrombectomy images. Noncontrast computed tomography (CT) reveals early ischemic changes in the right frontal operculum, temporal operculum, and insular cortex (a). Three-dimensional CT angiography shows contrast defects at two sites: the right distal M1 segment and the distal M2 segment of the lower trunk, indicated by arrows in (b). Contrast-enhanced CT of the chest reveals no clearly visualized intracardiac thrombi or cardiac tumors (c). Cerebral angiography (left: anteroposterior view; right: lateral view) shows poor contrast at several sites: The distal M1 and the distal M2 segments of the lower trunk of the right middle cerebral artery (MCA), and the right anterior temporal artery, indicated by arrows in (d). (e) Two emboli were retrieved with a stent retriever, corresponding to the contrast defects of MCA. One of them has broken away from the tip of the stent retriever. They appear white and gelatinous. (f and g) Postthrombectomy images. Cerebral angiography (left: anteroposterior view; right: lateral view) shows distal embolization in the frontopolar artery, the posterior parietal artery, and angular artery (indicated by arrows), with reperfusion achieving thrombolysis in cerebral infarction grade 2b (f). Diffusion-weighted magnetic resonance imaging shows high-signal intensity areas in the right frontal operculum, temporal operculum, insular cortex, medial frontal gyrus, cingulate gyrus, putamen, and corona radiata (g).</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3">Diagnosis assessment</h3><p>The etiology of the embolism could not be determined, but embolic occlusion of the right MCA was suspected.</p><h3 class = "title3">Therapeutic intervention</h3><p>Recombinant tissue-type plasminogen activator was administered intravenously at a dose of 0.6 mg/kg, followed by mechanical thrombectomy. Cerebral angiography identified two sites with contrast-filling defects in the distal M1 and the distal M2 segments of the lower trunk of the right MCA. The right anterior temporal artery originating from the M1 segment was also poorly visualized [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1d </a> </xref>]. Antegrade flow in the lower trunk was preserved, but delayed perfusion indicated partial occlusion. A combined thrombectomy was performed using a stent retriever and aspiration catheter. A Traxcess 14 microguidewire (Terumo, Tokyo, Japan) was used coaxially with a Trevo Trak 21 microcatheter (Stryker, Kalamazoo, MI, USA) to access the distal M2 segment of the lower trunk. A Trevo NXT ProVue 4 × 41 mm stent retriever (Stryker) was deployed from the distal M2 segment of the lower trunk to the distal M1 segment. An AXS Catalyst 6 aspiration catheter (Stryker) was advanced to the stent to compress the emboli between the devices. The stent retriever and aspiration catheter were retrieved following the standard procedure. With the guiding catheter’s balloon inflated to occlude the internal carotid artery, both devices were slowly withdrawn together into the guiding catheter. Consequently, two emboli corresponding to the MCA filling defects were removed by the stent retriever [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1e </a> </xref>]. During the procedure, distal embolization occurred in the frontopolar artery, which is a cortical branch of the right anterior cerebral artery, as well as in the posterior parietal artery and the angular artery, both of which are branches of the right MCA. The distribution of these distal emboli suggested that the embolus fragmented during retrieval and migrated to distal vessels, including previously unaffected territory. These distal emboli were unrecoverable, so the procedure was concluded. Recanalization was achieved with thrombolysis in cerebral infarction grade 2b, 199 min after symptom onset [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1f </a> </xref>]. Postprocedure CT revealed no hemorrhagic complications. Diffusion-weighted magnetic resonance imaging on the following day showed high signal intensity in the right frontal operculum, temporal operculum, insular cortex, medial frontal gyrus, cingulate gyrus, putamen, and corona radiata [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1g </a> </xref>]. After treatment, the patient’s symptoms gradually improved; however, mild hemiparesis in the left upper limb remained. This residual neurological deficit was suspected to be attributable to an infarction in the putamen or corona radiata, likely caused by distal embolization.</p><p>Follow-up: Posttreatment evaluation of the embolic source was conducted together with rehabilitation. The retrieved emboli appeared as a white gelatinous substance atypical of conventional thrombi [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1e </a> </xref>]. The gross findings initially suggested the possibility of a cardiac myxoma; however, the actual diagnosis differed from this initial assumption. Histopathological examination of the emboli revealed papillary structures [<xref ref-type="fig" rid="F2"> <a href='#F2'> Figure 2a </a> </xref>]. Each papilla contains a poorly vascularized, eosinophilic myxomatous stroma, which contains collagen fibers. A single layer of endothelial cells lines the surface of the papilla. The presence of myxoma cells characteristic of myxomas was not observed [<xref ref-type="fig" rid="F2"> <a href='#F2'> Figure 2a </a> </xref> and <xref ref-type="fig" rid="F2"> <a href='#F2'> b </a> </xref>]. In conclusion, the emboli were diagnosed as PFE, although the elastic fiber characteristics were not evident. Transthoracic echocardiography did not reveal intracardiac lesions. In contrast to the prethrombectomy chest CT, which did not clearly visualize the cardiac lesion, ECG-synchronized CT identified a 6-mm mass in the left atrium [<xref ref-type="fig" rid="F3"> <a href='#F3'> Figure 3a </a> </xref>], and transesophageal echocardiography confirmed it as a mobile lesion [<xref ref-type="fig" rid="F3"> <a href='#F3'> Figure 3b </a> </xref>]. Based on these findings, the left atrial PFE was considered to be the embolic source. On hospital day 18, the patient underwent open thoracotomy for tumor resection. A gelatinous mass was identified on the superior wall of the left atrium [<xref ref-type="fig" rid="F3"> <a href='#F3'> Figure 3c </a> </xref>] and excised together with the surrounding tissue. Histopathological examination of the resected mass revealed findings identical to those of the emboli [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4a </a> </xref> and <xref ref-type="fig" rid="F4"> <a href='#F4'> b </a> </xref>]. The postoperative course was uneventful. The patient exhibited residual neurological deficits, including fine motor coordination impairments and sensory impairments in the left upper limb, but was ambulatory and regained independence in daily activities within the hospital. On hospital day 36, the patient was transferred to a rehabilitation facility with a modified Rankin Scale score of 2.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F2'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13508/SNI-16-141-g002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 2:</h3><p>Histopathological examination of the emboli (a: Hematoxylin and Eosin staining, 2x, b: Elastica and Masson staining, 4x). (a) The lesion has a papillary structure. Each papilla contains a poorly vascularized, eosinophilic myxomatous stroma. A single layer of endothelial cells lines the surface. Myxoma cells were not observed. (b) Collagen fibers are observed. The elastic fibers are not evident.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F3'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13508/SNI-16-141-g003.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 3:</h3><p>(a) Electrocardiography-synchronized computed tomography shows a 6-mm mass within the left atrium (indicated by an arrow). (b) Transesophageal echocardiography shows mobility of the mass in the left atrium (indicated by an arrow). (c) Intraoperative findings during open thoracotomy for tumor resection show a gelatinous mass in the superior wall of the left atrium (indicated by an arrow).</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F4'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13508/SNI-16-141-g004.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 4:</h3><p>Histopathological examination of the resected tumor (a: Hematoxylin and Eosin staining, 2x, b: Elastica and Masson staining 4x). The lesion was excised along with the myocardium (indicated by arrows) and the endocardium (indicated by arrowheads). The histological features of the tumor are consistent with those of the emboli.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="DISCUSSION">DISCUSSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Cardiogenic or atherosclerotic thrombi cause most cases of cerebral embolism.[<xref ref-type="bibr" rid="ref11"> <a href='#ref11'>11</a> </xref>,<xref ref-type="bibr" rid="ref21"> <a href='#ref21'>21</a> </xref>] However, the underlying cause is rarely nonthrombotic emboli. Nonthrombotic emboli may consist of fat, air, calcified fragments, bacterial clumps, and tumor tissue.[<xref ref-type="bibr" rid="ref11"> <a href='#ref11'>11</a> </xref>,<xref ref-type="bibr" rid="ref21"> <a href='#ref21'>21</a> </xref>] Cerebral tumor embolism is a rare pathological condition, accounting for approximately 0.5% of all ischemic strokes, in which the tumor tissue acts as an embolus, leading to obstruction of the cerebral arteries.[<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>] The most common cause of cerebral tumor embolism is cardiac tumors, such as myxoma, which are responsible for about 50% of cases of cerebral tumor embolism.[<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>,<xref ref-type="bibr" rid="ref33"> <a href='#ref33'>33</a> </xref>] The second most common source is pulmonary tumors, which can lead to cerebral embolism through invasion of the pulmonary veins or the left heart system.[<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>,<xref ref-type="bibr" rid="ref33"> <a href='#ref33'>33</a> </xref>] These epidemiological findings have been confirmed since the increased use of thrombectomy procedures. Historically, the diagnosis of cerebral tumor embolism, excluding autopsy cases, lacked histopathological confirmation of the identity between the embolus and its source. The clinical diagnosis of tumor embolism was made by screening for potential embolic sources and considering the tumor as the most likely cause. Recently, the widespread adoption of thrombectomy has enabled the retrieval of embolus, thus allowing for histopathological confirmation. A more definitive diagnosis is now possible by demonstrating the histopathological identity between the retrieved embolus and the suspected tumor tissue. Consequently, the number of cases of cerebral tumor embolism caused by various tumors has increased.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>-<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>,<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>,<xref ref-type="bibr" rid="ref17"> <a href='#ref17'>17</a> </xref>,<xref ref-type="bibr" rid="ref22"> <a href='#ref22'>22</a> </xref>,<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>,<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>,<xref ref-type="bibr" rid="ref32"> <a href='#ref32'>32</a> </xref>] This development emphasizes the dual role of thrombectomy as both a therapeutic intervention and a diagnostic tool for identifying rare etiologies of ischemic stroke.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>-<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>,<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>,<xref ref-type="bibr" rid="ref17"> <a href='#ref17'>17</a> </xref>,<xref ref-type="bibr" rid="ref22"> <a href='#ref22'>22</a> </xref>,<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>,<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>,<xref ref-type="bibr" rid="ref32"> <a href='#ref32'>32</a> </xref>]</p><p>PFE is a benign cardiac tumor first described by Cheitlin <i>et al</i>. in 1975.[<xref ref-type="bibr" rid="ref5"> <a href='#ref5'>5</a> </xref>] PFE and cardiac myxoma are commonly associated with cerebral tumor embolism.[<xref ref-type="bibr" rid="ref14"> <a href='#ref14'>14</a> </xref>] PFE is a rare cardiac tumor but is the third most common after myxoma and lipoma, with a reported incidence of approximately 0.002% in autopsy studies.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>] However, the detection rate of PFE has risen with advances in echocardiographic imaging, increased utilization of cardiac ultrasonography, and growing awareness of the condition. PFE has possibly surpassed myxoma as the most common benign cardiac tumor.[<xref ref-type="bibr" rid="ref31"> <a href='#ref31'>31</a> </xref>] PFE is generally considered benign, but its true neoplastic nature remains uncertain. The etiology of PFE is not well understood, and its macroscopic, microscopic, and molecular heterogeneity has led to hypotheses that these lesions may represent tumors, hamartomas, organized thrombi, or abnormal endocardial responses to trauma.[<xref ref-type="bibr" rid="ref18"> <a href='#ref18'>18</a> </xref>] Histopathologically, PFE has a characteristic papillary structure. Each papilla consists of a poorly vascularized, eosinophilic myxomatous stroma with dense cores of elastic and collagen fibers. The surface of each papilla is lined by a single layer of endothelial cells that transition into the endocardium at the lesion base. Macroscopically, PFE typically appears as gelatinous, sea anemone-like structures with a lobulated morphology and is frequently pedunculated, usually with a short stalk forming the attachment to the endocardial surface.[<xref ref-type="bibr" rid="ref8"> <a href='#ref8'>8</a> </xref>,<xref ref-type="bibr" rid="ref18"> <a href='#ref18'>18</a> </xref>,<xref ref-type="bibr" rid="ref35"> <a href='#ref35'>35</a> </xref>]</p><p>Cardiac tumors, exemplified by myxomas, are widely recognized as causes of cerebral embolism. However, the increasing detection rates of cardiac tumors indicate that PFE is also a significant cause of cerebral tumor embolism. A study reviewing 37 cases of cerebral tumor embolism treated with thrombectomy reported that 17 cases (45%) were of cardiac origin, including 11 myxomas (29.7%) and 6 PFEs (16.2%).[<xref ref-type="bibr" rid="ref33"> <a href='#ref33'>33</a> </xref>] The similarities and differences between PFE and myxoma are summarized in <xref ref-type="table" rid="T1"> <a href='#T1'>Table 1</a> </xref>. Approximately 80% of PFEs originate from the valvular apparatus or annulus, predominantly in the heart valves of the left side. Among these, 44% arise from the aortic valve, followed by 35% from the mitral valve. In contrast, myxoma typically originates from within the cavities, with 75% occurring in the left atrium and 15–20% in the right atrium. PFE tends to be smaller than myxoma,[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>] with an average size of 9 mm[<xref ref-type="bibr" rid="ref30"> <a href='#ref30'>30</a> </xref>] compared to 50–60 mm for myxoma.[<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>] Consequently, PFE is asymptomatic in about 60% of cases.[<xref ref-type="bibr" rid="ref23"> <a href='#ref23'>23</a> </xref>] Both PFE and myxoma are classified as benign tumors but are associated with severe embolic complications, including ischemic stroke and coronary ischemia.[<xref ref-type="bibr" rid="ref23"> <a href='#ref23'>23</a> </xref>] Embolic events are often caused by fragmentation of the tumor itself or by fibrin thrombi forming on the tumor surface.[<xref ref-type="bibr" rid="ref23"> <a href='#ref23'>23</a> </xref>] Myxoma carries the risk of fatal embolic events, including sudden death, thus requiring urgent surgical excision as the standard treatment.[<xref ref-type="bibr" rid="ref25"> <a href='#ref25'>25</a> </xref>] PFE carries similar embolic risks, but their management is less clear due to the frequent detection of asymptomatic cases.[<xref ref-type="bibr" rid="ref16"> <a href='#ref16'>16</a> </xref>] Surgical intervention is generally recommended for symptomatic, mobile, left-sided, or ≥10 mm lesions.[<xref ref-type="bibr" rid="ref16"> <a href='#ref16'>16</a> </xref>] Careful observation may be considered for asymptomatic cases or if cardiac surgery is high risk.[<xref ref-type="bibr" rid="ref16"> <a href='#ref16'>16</a> </xref>] Anticoagulation therapy has been advocated to prevent embolism from microthrombi, but the evidence supporting this approach remains limited.[<xref ref-type="bibr" rid="ref16"> <a href='#ref16'>16</a> </xref>] Myxoma carries the risk of recurrence, so the standard surgical approach is wide excision, including the surrounding tissues.[<xref ref-type="bibr" rid="ref6"> <a href='#ref6'>6</a> </xref>,<xref ref-type="bibr" rid="ref25"> <a href='#ref25'>25</a> </xref>] In contrast, the postoperative recurrence rate of PFE is reported to be 0–1.6%, so the indications for extended resection remain unclear.[<xref ref-type="bibr" rid="ref19"> <a href='#ref19'>19</a> </xref>,<xref ref-type="bibr" rid="ref30"> <a href='#ref30'>30</a> </xref>,<xref ref-type="bibr" rid="ref31"> <a href='#ref31'>31</a> </xref>]</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T1'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13508/SNI-16-141-t001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 1:</h3><p>Comparison of the characteristics of PFE and myxoma.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>An important point to note in this case is distal embolization. Although distal embolization is common as a technical complication of thrombectomy, the distal embolization in this case may be attributed to the nature of the embolus. Distal embolization typically occurs due to thrombus fragmentation and embolic migration during retrieval.[<xref ref-type="bibr" rid="ref28"> <a href='#ref28'>28</a> </xref>] This was also observed in our case. Thrombectomy was performed using a combined technique with a stent retriever and an aspiration catheter, which resulted in distal embolization. This may be related to the embolus being composed of tumor tissue. Tumor emboli are soft and fragile.[<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>,<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>,<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>] Therefore, retrieving with a stent retriever is more likely to fragment the soft embolus, increasing the risk of distal embolization.[<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>,<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>] In contrast, retrieving with an aspiration catheter is less likely to fragment the embolus and may also shorten the procedure time, potentially making it more suitable for retrieving tumor emboli.[<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>,<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>] In our case, preprocedural evaluation indicated a low likelihood of tumor embolism. However, if tumor embolism had been considered highly likely based on the preprocedural assessment, a more careful selection of the thrombectomy technique would have been warranted.</p><p>In the present case, the macroscopic findings of the retrieved emboli raised the suspicion of a cardiac tumor. Subsequent imaging identified a cardiac lesion, which was surgically resected as the embolic source. Pathological examination confirmed the histopathological identity between the retrieved emboli and the resected tumor tissue, establishing the diagnosis of cerebral tumor embolism caused by cardiac PFE. Only one previous similar case of PFE manifesting as cerebral tumor embolism identified the embolic source by imaging, and surgical resection was performed.[<xref ref-type="bibr" rid="ref14"> <a href='#ref14'>14</a> </xref>] In contrast, scattered reports have suggested PFE as the embolic source based on pathological findings, but the embolic source could not be identified by imaging, so clinical observation was continued without intervention.[<xref ref-type="bibr" rid="ref27"> <a href='#ref27'>27</a> </xref>,<xref ref-type="bibr" rid="ref29"> <a href='#ref29'>29</a> </xref>,<xref ref-type="bibr" rid="ref32"> <a href='#ref32'>32</a> </xref>] PFE may have been underdiagnosed in the past because of its small size and limited recognition within the field of cerebrovascular diseases. In the present case, the lesion was not detected by both contrast-enhanced CT of the chest and transthoracic echocardiography; however, it was successfully identified using ECG-synchronized CT and transesophageal echocardiography. PFE, like myxoma, has the potential to cause fatal embolic events despite their small size. Therefore, persistent efforts to detect these lesions are essential.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CONCLUSION">CONCLUSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>The present case of PFE manifesting as cerebral embolism was treated with mechanical thrombectomy. The differential diagnosis based on the retrieved embolus should consider not only myxoma but also PFE. PFE is smaller and more challenging to detect compared to myxoma but carries a similar risk of fatal embolic events. Therefore, persistent efforts to detect PFE are essential.</p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Ethical approval">Ethical approval</a></h3><div class="clearfix"></div><div class="hline"></div><p>Institutional Review Board approval is not required.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Declaration of patient consent">Declaration of patient consent</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors certify that they have obtained all appropriate patient consent.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Financial support and sponsorship">Financial support and sponsorship</a></h3><div class="clearfix"></div><div class="hline"></div><p>Nil.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Conflicts of interest">Conflicts of interest</a></h3><div class="clearfix"></div><div class="hline"></div><p>There are no conflicts of interest.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Use of artificial intelligence (AI)-assisted technology for manuscript preparation">Use of artificial intelligence (AI)-assisted technology for manuscript preparation</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Disclaimer">Disclaimer</a></h3><div class="clearfix"></div><div class="hline"></div><p>The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.</p></div> </div></div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"></div> </div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a name="References" href="javascript:void(0);">References</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><a href='javascript:void(0);' name='ref1' style='text-decoration: none;'>1.</a> Arai S, Tanaka D, Sakuma M, Tamamura T, Ishihara R, Sato Y. Papillary fibroelastoma of the left ventricular outflow tract; report of a case. Kyobu Geka. 2018. 71: 697-700</p><p><a href='javascript:void(0);' name='ref2' style='text-decoration: none;'>2.</a> Araki S, Maekawa K, Kobayashi K, Sano T, Yabana T, Shibata M. Tumor embolism through right-to-left shunt due to venous invasion of esophageal carcinoma. J Stroke Cerebrovasc Dis. 2020. 29: 105352</p><p><a href='javascript:void(0);' name='ref3' style='text-decoration: none;'>3.</a> Baek SH, Park S, Lee NJ, Kang Y, Cho KH. Effective mechanical thrombectomy in a patient with hyperacute ischemic stroke associated with cardiac myxoma. J Stroke Cerebrovasc Dis. 2014. 23: e417-9</p><p><a href='javascript:void(0);' name='ref4' style='text-decoration: none;'>4.</a> Bhatia S, Ku A, Pu C, Wright DG, Tayal AH. Endovascular mechanical retrieval of a terminal internal carotid artery breast tumor embolus. J Neurosurg. 2010. 112: 572-4</p><p><a href='javascript:void(0);' name='ref5' style='text-decoration: none;'>5.</a> Cheitlin MD, McAllister HA, De Castro CM. Myocardial infarction without atherosclerosis. JAMA. 1975. 231: 951-9</p><p><a href='javascript:void(0);' name='ref6' style='text-decoration: none;'>6.</a> Děrgel M, Gofus J, Smolák P, Stejskal V, Hanke I, Matějka J. Surgical treatment of primary cardiac tumors: 20-year single center experience. Kardiochir Torakochir Pol. 2022. 19: 36-40</p><p><a href='javascript:void(0);' name='ref7' style='text-decoration: none;'>7.</a> Di Vito A, Mignogna C, Donato G. The mysterious pathways of cardiac myxomas: A review of histogenesis, pathogenesis and pathology. Histopathology. 2015. 66: 321-32</p><p><a href='javascript:void(0);' name='ref8' style='text-decoration: none;'>8.</a> Fishbein MC, Ferrans VJ, Roberts WC. Endocardial papillary elastofibromas. Histologic, histochemical, and electron microscopical findings. Arch Pathol. 1975. 99: 335-41</p><p><a href='javascript:void(0);' name='ref9' style='text-decoration: none;'>9.</a> Fujiwara S, Fukumoto S, Watanabe M, Kusakabe K, Aso K, Shinohara T. A case of left middle cerebral artery occlusion diagnosed as malignant lung tumor embolus by mechanical thrombectomy. Jpn J Stroke. 2022. 44: 59-64</p><p><a href='javascript:void(0);' name='ref10' style='text-decoration: none;'>10.</a> Fujiwara Y, Hayashi K, Shibata Y, Furuta T, Yamasaki T, Yamamoto K. Cerebral tumor embolism from thyroid cancer treated by mechanical thrombectomy: Illustrative case. J Neurosurg Case Lessons. 2023. 5: CASE22293</p><p><a href='javascript:void(0);' name='ref11' style='text-decoration: none;'>11.</a> Gomyo M, Tsuchiya K. Cerebral infarctions due to a special embolus. Clin Imagiol. 2022. 38: 321-9</p><p><a href='javascript:void(0);' name='ref12' style='text-decoration: none;'>12.</a> Gowda RM, Khan IA, Nair CK, Mehta NJ, Vasavada BC, Sacchi TJ. Cardiac papillary fibroelastoma: A comprehensive analysis of 725 cases. Am Heart J. 2003. 146: 404-10</p><p><a href='javascript:void(0);' name='ref13' style='text-decoration: none;'>13.</a> Hoffmeier A, Sindermann JR, Scheld HH, Martens S. Cardiac tumors--diagnosis and surgical treatment. Dtsch Arztebl Int. 2014. 111: 205-11</p><p><a href='javascript:void(0);' name='ref14' style='text-decoration: none;'>14.</a> Itrat A, George P, Khawaja Z, Min D, Donohue M, Wisco D. Pathological evidence of cardiac papillary fibroelastoma in a retrieved intracranial embolus. Can J Neurol Sci. 2015. 42: 66-8</p><p><a href='javascript:void(0);' name='ref15' style='text-decoration: none;'>15.</a> Iwata Y, Nozawa Y, Sato S, Sakasai T, Katayama H, Sato M. A case of papillary fibroelastoma originating on interventricular septum. Jpn J Med Ultrasound Technol. 2016. 41: 174-81</p><p><a href='javascript:void(0);' name='ref16' style='text-decoration: none;'>16.</a> Kamamura M, Tanaka H, Suzuki H, Suzuki Y, Shiojiri T. A case of recurrent multiple cardioembolic stroke due to papillary fibroelastoma. Jpn J Stroke. 2021. 43: 524-8</p><p><a href='javascript:void(0);' name='ref17' style='text-decoration: none;'>17.</a> Kim CS, Jung HR, Cho KH, Chang HW, Sohn SI, Choi TH. Forced-suction thrombectomy of an arterial tumor embolism due to metastatic melanoma. Arch Neurol. 2012. 69: 272-3</p><p><a href='javascript:void(0);' name='ref18' style='text-decoration: none;'>18.</a> Kurup AN, Tazelaar HD, Edwards WD, Burke AP, Virmani R, Klarich KW. Iatrogenic cardiac papillary fibroelastoma: A study of 12 cases (1990 to 2000). Hum Pathol. 2002. 33: 1165-9</p><p><a href='javascript:void(0);' name='ref19' style='text-decoration: none;'>19.</a> Maeda T, Sakurada T, Muraki S, Nakashima S, Uchiyama H, Sasaki J. Papillary fibroelastoma arising from the left atrial wall: Report of a case. Kyobu Geka. 2021. 74: 449-52</p><p><a href='javascript:void(0);' name='ref20' style='text-decoration: none;'>20.</a> McAllister HA, Hall RJ, Cooley DA. Tumors of the heart and pericardium. Curr Probl Cardiol. 1999. 24: 57-116</p><p><a href='javascript:void(0);' name='ref21' style='text-decoration: none;'>21.</a> Nakajo M, Hasegawa T, Nakano T, Kamimura K, Yoshiura T. Rare arterial embolisms. Jpn J Imaging Diagn. 2023. 43: 1365-70</p><p><a href='javascript:void(0);' name='ref22' style='text-decoration: none;'>22.</a> Nukata R, Ikeda H, Akaike N, Fujiwara T, Yamashita H, Uezato M. White embolus-induced basilar artery occlusion due to pulmonary vein invasion of a metastasis of a malignant melanoma. Intern Med. 2023. 62: 2889-93</p><p><a href='javascript:void(0);' name='ref23' style='text-decoration: none;'>23.</a> Ohya Y, Fujimoto S, Kanazawa M, Tagawa N, Osaki M, Kitazono T. A case of cardioembolic stroke due to intracardiac papillary fibroelastoma evaluated by using transesophageal echocardiography. Rinsho Shinkeigaku. 2017. 57: 9-13</p><p><a href='javascript:void(0);' name='ref24' style='text-decoration: none;'>24.</a> Oyama T, Asai T, Miyazawa T, Yokoyama K, Kogure Y, Torii A. A case of cerebral tumor embolism from extracardiac lung cancer treated by mechanical thrombectomy. NMC Case Rep J. 2020. 7: 101-5</p><p><a href='javascript:void(0);' name='ref25' style='text-decoration: none;'>25.</a> Pinede L, Duhaut P, Loire R. Clinical presentation of left atrial cardiac myxoma. A series of 112 consecutive cases. Medicine (Baltimore). 2001. 80: 159-72</p><p><a href='javascript:void(0);' name='ref26' style='text-decoration: none;'>26.</a> Pop R, Mihoc D, Manisor M, Richter JS, Lindner V, Janssen-Langenstein R. Republished: Mechanical thrombectomy for repeated cerebral tumor embolism from a thoracic sarcomatoid carcinoma. J Neurointerv Surg. 2018. 10: e26</p><p><a href='javascript:void(0);' name='ref27' style='text-decoration: none;'>27.</a> Salam KA, Rafeeque M, Hashim H, Mampilly N, Noone ML. Histology of thrombectomy specimen reveals cardiac tumor embolus in cryptogenic young stroke. J Stroke Cerebrovasc Dis. 2018. 27: e70-2</p><p><a href='javascript:void(0);' name='ref28' style='text-decoration: none;'>28.</a> Saver JL, Chapot R, Agid R, Hassan A, Jadhav AP, Liebeskind DS. Thrombectomy for distal, medium vessel occlusions: A consensus statement on present knowledge and promising directions. Stroke. 2020. 51: 2872-84</p><p><a href='javascript:void(0);' name='ref29' style='text-decoration: none;'>29.</a> Semerano A, Saliou G, Sanvito F, Genchi A, Gullotta GS, Michel P. Fishing an anemone in the brain: Embolized cardiac fibroelastoma revealed after stroke thrombectomy. Eur Heart J. 2021. 42: 4094-95</p><p><a href='javascript:void(0);' name='ref30' style='text-decoration: none;'>30.</a> Sun JP, Asher CR, Yang XS, Cheng GG, Scalia GM, Massed AG. Clinical and echocardiographic characteristics of papillary fibroelastomas: A retrospective and prospective study in 162 patients. Circulation. 2001. 103: 2687-93</p><p><a href='javascript:void(0);' name='ref31' style='text-decoration: none;'>31.</a> Tamin SS, Maleszewski JJ, Scott CG, Khan SK, Edwards WD, Bruce CJ. Prognostic and bioepidemiologic implications of papillary fibroelastomas. J Am Coll Cardiol. 2015. 65: 2420-9</p><p><a href='javascript:void(0);' name='ref32' style='text-decoration: none;'>32.</a> Tejada J, Galiana A, Balboa O, Clavera B, Redondo-Robles L, Alonso N. Mechanical endovascular procedure for the treatment of acute ischemic stroke caused by total detachment of a papillary fibroelastoma. J Neurointerv Surg. 2014. 6: e37</p><p><a href='javascript:void(0);' name='ref33' style='text-decoration: none;'>33.</a> Toruno M, Al-Janabi O, Karaman I, Ghozy S, Senol YC, Kobeissi H. Mechanical thrombectomy for the treatment of large vessel occlusion due to cancer-related cerebral embolism: A systematic review. Interv Neuroradiol. 2024. p. 15910199241230356</p><p><a href='javascript:void(0);' name='ref34' style='text-decoration: none;'>34.</a> Watanabe T, Maeda T, Inoue S. Papillary fibroelastoma on the tricuspid valve: Report of a case. Kyobu Geka. 2016. 69: 131-3</p><p><a href='javascript:void(0);' name='ref35' style='text-decoration: none;'>35.</a> Zoltowska DM, Sadic E, Becoats K, Ghetiya S, Ali AA, Sattiraju S. Cardiac papillary fibroelastoma. J Geriatr Cardiol. 2021. 18: 346-51</p></div> </div></div>
  4. Adult tentorial medulloblastoma mimicking meningioma: A case report and systematic review

    Fri, 18 Apr 2025 20:13:51 -0000

    Adult tentorial medulloblastoma mimicking meningioma: A case report and systematic review Category: Article Type: Sadeen Sameer Eid1, Arshad Ali2,3,4, Noman Shah5, Amal I. Alawadat6, Muna AbuHejleh7, Issam Al-bozom7, Ghanem Al-sulaiti2Faculty of Medicine, Jordan University of Science and Technology, Irbid, JordanDepartment of Neurosurgery, Neuroscience Institute, Hamad Medical Corporation, Doha, QatarDepartment of Clinical Academic Sciences, College of … Continue reading Adult tentorial medulloblastoma mimicking meningioma: A case report and systematic review
    <div><!DOCTYPE html PUBLIC "-//W3C//DTD HTML 4.0 Transitional//EN" "http://www.w3.org/TR/REC-html40/loose.dtd"> <html><head><meta http-equiv="content-type" content="text/html; charset=utf-8"></head><body><div class="row"><div class="col-lg-9 col-sm-8 col-xs-12"><div class="media-body details-body"> <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13506"><h2 class="media-heading"><h2 class="media-heading">Adult tentorial medulloblastoma mimicking meningioma: A case report and systematic review</h2></h2></a> </div><div class="disp_categories"> <p><label>Category: </label><span></span></p> <p><label>Article Type: </label><span></span></p> </div><a href="mailto:sseid19@med.just.edu.jo" target="_top">Sadeen Sameer Eid</a><sup>1</sup>, <a href="mailto:drarshadali@gmail.com" target="_top">Arshad Ali</a><sup>2,3,4</sup>, <a href="mailto:dr.nomanshah619@gmail.com" target="_top">Noman Shah</a><sup>5</sup>, <a href="mailto:aml0195393@ju.edu.jo" target="_top">Amal I. Alawadat</a><sup>6</sup>, <a href="mailto:mabuhejleh@hamad.qa" target="_top">Muna AbuHejleh</a><sup>7</sup>, <a href="mailto:ialbozom@hamad.qa" target="_top">Issam Al-bozom</a><sup>7</sup>, <a href="mailto:galsulaiti@hamad.qa" target="_top">Ghanem Al-sulaiti</a><sup>2</sup><ol class="smalllist"><li>Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan</li><li>Department of Neurosurgery, Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar</li><li>Department of Clinical Academic Sciences, College of Medicine, Qatar University, Doha, Qatar</li><li>Department of Neurological Sciences, Weill Cornell Medicine, Doha, Qatar</li><li>Department of Neurosurgery, Hamad Medical Corporation, Doha, Qatar</li><li>Faculty of Medicine, University of Jordan, Amman, Jordan</li><li>Department of Histopathology, Hamad Medical Corporation, Doha, Qatar</li></ol><p><strong>Correspondence Address:</strong><br>Arshad Ali, Department of Neurosurgery, Neuroscience Institute, Hamad Medical Corporation, Doha, Qatar.<br></p><p><strong>DOI:</strong>10.25259/SNI_10_2025</p>Copyright: © 2025 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.<div class="parablock"><p><strong>How to cite this article: </strong>Sadeen Sameer Eid1, Arshad Ali2,3,4, Noman Shah5, Amal I. Alawadat6, Muna AbuHejleh7, Issam Al-bozom7, Ghanem Al-sulaiti2. Adult tentorial medulloblastoma mimicking meningioma: A case report and systematic review. 18-Apr-2025;16:143</p></div><div class="parablock"><p><strong>How to cite this URL: </strong>Sadeen Sameer Eid1, Arshad Ali2,3,4, Noman Shah5, Amal I. Alawadat6, Muna AbuHejleh7, Issam Al-bozom7, Ghanem Al-sulaiti2. Adult tentorial medulloblastoma mimicking meningioma: A case report and systematic review. 18-Apr-2025;16:143. Available from: <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13506">https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13506</a></p></div> </div> <div class="col-lg-3 col-sm-4 col-xs-12"><div class="article-detail-sidebar"><div class="icon sidebar-icon clearfix add-readinglist-icon"><button id="bookmark-article" class="add-reading-list-article">Add to Reading List</button><button id="bookmark-remove-article" class="remove-reading-list-article">Remove from Reading List</button></div><div class="icon sidebar-icon clearfix"><a class="btn btn-link" target="_blank" type="button" id="OpenPdf" href="https://surgicalneurologyint.com/wp-content/uploads/2025/04/13506/SNI-16-143.pdf"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/pdf-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a target="_blank" href="javascript:void(0);" onclick="return PrintArticle();"><img decoding="async" src="https://i0.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/file-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a class="btn btn-link" type="button" id="EmaiLPDF"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/mail-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a></div><div class="date"> <p>Date of Submission<br><span class="darkgray">05-Jan-2025</span></p> <p>Date of Acceptance<br><span class="darkgray">23-Mar-2025</span></p> <p>Date of Web Publication<br><span class="darkgray">18-Apr-2025</span></p> </div> </div></div> </div> <!--.row --><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a href="javascript:void(0);" name="Abstract">Abstract</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><strong>Background</strong>Tentorial medulloblastomas in adults are exceedingly rare and may clinically and radiologically mimic meningiomas. This case report, with a systematic review, aims to outline the clinical, radiological, pathological, and management strategies for adult tentorial medulloblastoma.</p><p><strong>Case Description</strong>A 37-year-old male patient presented with headaches, vertigo, and vomiting. Imaging investigations revealed a tentorial extra-axial mass, initially considered a meningioma. The patient subsequently underwent surgical resection followed by chemoradiation. Histopathological examination ultimately identified the mass as an eccentrically located adult medulloblastoma. We conducted a systematic review of the literature, analyzing four studies that reported similar cases. This analysis included clinical and demographic information, diagnosis through imaging and histopathology, treatment methods, and outcomes for seven cases, including our own.</p><p><strong>Conclusion</strong>Adult tentorial medulloblastomas are extremely rare tumors that may mimic meningiomas, posing significant clinical challenges. Accurate diagnosis necessitates advanced imaging techniques and histopathological confirmation. The primary treatment strategy involves maximal surgical resection, supplemented by chemoradiotherapy.</p><p><strong>Keywords: </strong>Adult, Histopathology, Medulloblastoma, Meningioma, Posterior fossa, Tentorial</p><p></p></div> </div></body></html> </div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"><p></p><p><inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="SNI-16-143-inline001.tif"/></p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="INTRODUCTION">INTRODUCTION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Medulloblastomas are classified as the World Health Organization (WHO) grade IV tumors, recognized as highly aggressive embryonal neoplasms with a strong preference for the cerebellum.[<xref ref-type="bibr" rid="ref6"> <a href='#ref6'>6</a> </xref>,<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>] These tumors are primarily diagnosed in pediatric patients, making up approximately 15% of all central nervous system (CNS) tumors in children and over 40% of tumors found in the posterior fossa.[<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>] While medulloblastomas have traditionally been viewed as malignancies primarily affecting children, cases in adults, though rare, do occur, representing <1% of all CNS neoplasms.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>,<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>] In pediatric cases, medulloblastomas typically develop in the midline, involving the cerebellar vermis, and are often linked with symptoms of increased intracranial pressure, such as headaches, vomiting, and ataxia. In contrast, in adults, medulloblastomas are more likely to occur in the lateral cerebellar hemispheres and often manifest with more insidious or atypical symptoms.[<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>] The observed differences in anatomical localization and clinical presentation correspond with specific molecular and genetic variations that affect tumor phenotype, prognosis, and treatment responses.[<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>,<xref ref-type="bibr" rid="ref17"> <a href='#ref17'>17</a> </xref>]</p><p>Understanding adult medulloblastomas is complicated by rare variants, especially in extra-axial locations such as the tentorium cerebelli, which are primarily associated with meningiomas. Tentorial medulloblastomas are extremely rare, and their radiological features may closely resemble those of meningiomas, making accurate diagnosis more challenging.[<xref ref-type="bibr" rid="ref14"> <a href='#ref14'>14</a> </xref>]</p><p>This report outlines an unusual case of tentorial medulloblastoma in an adult patient, thus contributing to the limited literature on this atypical manifestation. Through a systematic review of previous cases, our objective is to clarify the clinical, radiological, and pathological features associated with this case in detail, ultimately addressing the challenges and complexities related to the diagnosis and treatment of such rare neoplasms. In addition, this case emphasizes the necessity of employing advanced imaging modalities and histopathological assessments alongside molecular diagnostic methods in adult medulloblastomas, especially in atypical presentations.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CASE DESCRIPTION">CASE DESCRIPTION</a></h3><div class="clearfix"></div><div class="hline"></div><p>A 37-year-old male presented to the neurology outpatient clinic 3 months ago, complaining of a persistent holocranial headache, imbalance, and fear of falling for 3 weeks. Upon clinical examination, the patient was alert and showed some imbalance while walking. Fundoscopy revealed bilateral hyperemia with blurred margins of the right optic disc.</p><p>The patient was referred to the hospital’s emergency department (ED) due to complaints of a progressively worsening headache, persistent vertigo, and episodes of vomiting. Upon arrival at the ED, a neurological examination indicated no motor deficits except a broad-based gait. A head computed tomography scan revealed a large, tentorial, extra-axial hyperdense mass lesion, which exhibited signs of fourth ventricular compression, leading to supratentorial hydrocephalus [<xref ref-type="fig" rid="F1"> <a href='#F1'>Figure 1</a> </xref>]. Magnetic resonance imaging (MRI) findings demonstrated a right tentorial, bi-lobulated extra-axial lesion extending both infratentorially and supratentorially, characterized by diffusion restriction and substantial contrast enhancement [<xref ref-type="fig" rid="F2"> <a href='#F2'>Figures 2</a> </xref> and <xref ref-type="fig" rid="F3"> <a href='#F3'>3</a> </xref>]. The MR spectroscopic perfusion study revealed a notable increase in choline levels and a high choline-to-N-acetylaspartate (NAA) ratio. The lesion was well-circumscribed but was associated with perilesional parenchymal cerebellar edema involving the midline structures, with left-sided extension, resulting in considerable mass effect and partial effacement of the fourth ventricle. In addition, cerebellar tonsillar herniation was noted, measuring 14 mm, along with signs of hydrocephalus. These MR findings were consistent with a diagnosis of tentorial lesion meningioma.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F1'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13506/SNI-16-143-g001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 1:</h3><p>An unenhanced computed tomography (CT) scan of the brain shows (a) axial, (b) sagittal, and (c) coronal sections revealing a hyperdense mass lesion situated in the right posterior fossa adjacent to the tentorium, accompanied by significant perifocal edema that causes effacement of the fourth ventricle.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F2'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13506/SNI-16-143-g002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 2:</h3><p>(a) Axial sections from magnetic resonance (MR) imaging using T1 weighted, (b) T2 weighted, and (c) perfusion cerebral blood flow scans of the brain illustrate a hypointense mass lesion on both T1 and T2-weighted imaging, along with perifocal edema, while the perfusion scan indicates no significant vascularity, while (d) shows the MR spectroscopic study revealed a notable increase in choline levels and a high choline-to-N-acetylaspartate ratio.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F3'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13506/SNI-16-143-g003.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 3:</h3><p>Gadolinium-enhanced magnetic resonance images depict (a) axial, (b) sagittal, and (c) coronal sections indicating a prominently enhancing mass lesion attached to the right tentorial cerebelli, with slight extension above the tentorium. The perifocal edema exerts a mass effect, causing displacement and effacement of the fourth ventricle.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>The patient underwent a right-sided suboccipital craniotomy for the resection of a tentorial-based lesion. During the operation, there was a well-defined interface between the tumor and the cortex. It appeared grayish-white in color and had a firm consistency. A per-operative frozen section revealed the lesion as a blue round cell tumor, raising suspicion for neuroblastoma while making a diagnosis of meningioma unlikely. Complete resection was achieved, including the supratentorial portion that was resected from the infratentorial surgical exposure.</p><p>The microscopic examination reveals a hypercellular tumor composed of small, round blue cells with uniform, round nuclei. These cells are arranged in a trabecular pattern, separated by fibrous bands, and show numerous mitotic figures [<xref ref-type="fig" rid="F4"> <a href='#F4'>Figure 4a</a> </xref>]. Immunohistochemical studies indicate that the tumor cells are diffusely positive for synaptophysin [<xref ref-type="fig" rid="F4"> <a href='#F4'>Figure 4b</a> </xref>] and Somatostatin receptor 2a (SSTR2A). In addition, the tumor exhibits focal positivity for glial fibrillary acidic protein. Notably, the expression of INI-1 and BRG1 is retained. The tumor is negative for keratin (CK AE1/AE3) [<xref ref-type="fig" rid="F4"> <a href='#F4'>Figure 4c</a> </xref>], chromogranin, NKX2.2, SS18-SSX, smooth muscle markers, and vascular markers. Molecular studies further confirm the diagnosis, revealing mutations in the telomerase reverse transcriptase promoter, smoothened (SMO), and isocitrate dehydrogenase 1 (IDH1) (p.R132C). These mutations are characteristic of Sonic Hedgehog (SHH)--activated medulloblastomas, driven by aberrations in the SHH signaling pathway. The presence of triploidy and a gain of chromosome 3q, identified by chromosomal microarray, further support this molecular subtype. This classification places the tumor in the CNS WHO grade 4 category, highlighting its malignant and aggressive nature.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F4'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13506/SNI-16-143-g004.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 4:</h3><p>(a) A histological image demonstrates a hypercellular malignant tumor composed of small round cells arranged in trabecular formations and separated by fibrous bands (hematoxylin and eosin ×200); (b) Immunohistochemical staining of the tumor cells indicates perinuclear positivity for synaptophysin (×200); (c) Immunohistochemical staining reveals negativity for keratin (CK AE1/AE3) in the tumor cells (×200).</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>In light of the final diagnosis of eccentric medulloblastoma, the screening MRI of the spine and cerebrospinal fluid showed no spinal metastatic spread. The patient was discussed in our weekly neuro-oncology multidisciplinary meeting, and the consensus was to administer chemotherapy (vincristine and cisplatin), followed by radiotherapy of the craniospinal axis and tumor bed in the posterior fossa. At the 6-month follow-up, the patient showed a complete recovery without any neurological deficits.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="MATERIALS AND METHODS">MATERIALS AND METHODS</a></h3><div class="clearfix"></div><div class="hline"></div><h3 class = "title3">Literature search</h3><p>This systematic review was conducted according to the Joanna Briggs Institute (JBI) methodology for systematic reviews of observational studies. The research protocol adhered to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines to ensure comprehensive reporting.</p><h3 class = "title3">Search strategy</h3><p>An extensive search strategy was developed to identify relevant studies addressing rare adult tentorial medulloblastoma cases. The databases searched included Medline, Embase, Scopus, Web of Science, ScienceDirect, Cochrane, Clinical Key, and Access Medicine. The key terms included tentorial medulloblastoma, posterior fossa tumor, adult medulloblastoma, atypical medulloblastoma presentation, mimicking meningioma, radiological meningioma look-alikes, and meningioma differential diagnosis. The search strategy utilized a combination of Medical Subject Headings (MeSH) terms: ((tentorial medulloblastoma) OR (posterior fossa tumor) OR (adult medulloblastoma) OR (atypical medulloblastoma presentation)) AND ((mimicking meningioma) OR (meningioma misdiagnosis) OR (radiological meningioma look-alikes) OR (meningioma differential diagnosis)).</p><h3 class = "title3">Selection and screening process</h3><p>After the initial search, duplicate entries were removed using web-based reference management software (Rayyan). The remaining records were screened based on their titles and abstracts, with two independent reviewers assessing eligibility according to predefined inclusion and exclusion criteria. Studies were considered suitable for inclusion if they reported on adult patients diagnosed with medulloblastoma located in the tentorium, provided sufficient clinical and radiological data, and were published in English.</p><p>Exclusion criteria included studies that focused on pediatric populations, cases involving alternative tumor locations, such as the cerebellopontine angle, nonprimary research (e.g., reviews), and publications in languages other than English. Full-text articles of potentially eligible studies were obtained and assessed for inclusion. Any disagreements with the reviewer were resolved through consensus or consulting a third reviewer. <xref ref-type="fig" rid="F5"> <a href='#F5'> Figure 5 </a> </xref>, the PRISMA flowchart, illustrates the systematic process used for study identification.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F5'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13506/SNI-16-143-g005.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 5:</h3><p>A flowchart based on Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines illustrates the flow of information through various phases of a systematic review.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3">Data extraction</h3><p>Data extraction was performed using a standardized JBI data extraction method in Excel sheets, which systematically captured information regarding study characteristics, patient demographics, clinical presentations, radiological findings, and outcomes of treatment modalities [<xref ref-type="table" rid="T1"> <a href='#T1'> Table 1 </a> </xref>].</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T1'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13506/SNI-16-143-t001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 1:</h3><p>Summary of studies included for full-text analysis.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class = "title3">Quality assessment</h3><p>The quality appraisal of the studies included in this review was conducted using the JBI Critical Appraisal Checklist for Case Reports. This method ensured a comprehensive evaluation of methodological quality while minimizing potential biases identified in the reviewed literature. Due to the limited number of eligible studies and the heterogeneity in the reported outcomes, the extracted data were synthesized narratively. The findings were summarized to provide insights into the rare clinical entity of adult tentorial medulloblastoma, emphasizing diagnostic challenges, treatment strategies, and outcomes [<xref ref-type="table" rid="T2"> <a href='#T2'> Table 2 </a> </xref>].</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T2'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13506/SNI-16-143-t002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 2:</h3><p>JBI critical appraisal checklist for case studies.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="RESULTS">RESULTS</a></h3><div class="clearfix"></div><div class="hline"></div><p>This review included six cases of medulloblastoma that mimicked tentorial meningioma from four previously published articles, which were analyzed in full and summarized alongside our cases [<xref ref-type="table" rid="T1"> <a href='#T1'>Table 1</a> </xref>]. The patients’ ages ranged from 18 to 37 years (mean 28.6, standard deviation ±7.03), with a slight male predominance (4:3). Clinical presentations varied but frequently included headaches in four out of the seven cases, as well as other symptoms associated with increased intracranial pressure, such as vomiting and vertigo – two cases presented with cerebellar signs, which included gait imbalance and truncal instability ataxia. MRI findings consistently demonstrated heterogeneous contrast enhancement, with varying intensity noted among the cases. Diffusion restriction was observed in two cases, including ours. Obstructive hydrocephalus was recorded in three cases at presentation, as seen in our patient. Tonsillar herniation was observed in two cases, including ours, indicating a significant mass effect. Histopathological analysis confirmed the presence of medulloblastoma in all cases. Classification of three cases identified SHH-activated subtypes, including those found in our case. Management strategies primarily involved surgical intervention, with two patients receiving additional adjuvant chemoradiation. Our patient successfully underwent tumor resection, followed by chemoradiation and adjuvant chemotherapy.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="DISCUSSION">DISCUSSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Medulloblastomas account for 15% of CNS tumors in pediatric populations, 40% of all tumors found in the posterior fossa, and 90% of all embryonal tumors, making them one of the most prevalent forms of embryonal tumors originating from the posterior fossa.[<xref ref-type="bibr" rid="ref11"> <a href='#ref11'>11</a> </xref>,<xref ref-type="bibr" rid="ref14"> <a href='#ref14'>14</a> </xref>] The peak incidence of medulloblastomas typically occurs in children aged 5–7 years, with a significantly higher prevalence in males, indicated by a male-to-female ratio of 1.7:1.[<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>] These tumors primarily appear in the midline; however, a few rare, documented cases of extra-axial medulloblastomas have been reported, mainly located in the cerebellopontine angle and the lateral cerebellar hemisphere.[<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>,<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>,<xref ref-type="bibr" rid="ref30"> <a href='#ref30'>30</a> </xref>] In adults, medulloblastomas are relatively rare, comprising only 0.4–1% of all CNS tumors in this demographic, with an annual incidence rate of about 0.6–1 case per million individuals.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>,<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>,<xref ref-type="bibr" rid="ref13"> <a href='#ref13'>13</a> </xref>,<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>,<xref ref-type="bibr" rid="ref25"> <a href='#ref25'>25</a> </xref>] Unlike pediatric cases, adult medulloblastomas are more frequently found eccentrically. To the best of our knowledge, this report represents the fifth documented study and the seventh case of tentorial medulloblastoma in the adult population.</p><p>The commonly reported symptoms include morning headaches, nausea, vomiting, lethargy, and ataxia, primarily attributed to increased intracranial pressure – either due to the tumor mass itself or associated obstructive hydrocephalus – and cerebellar dysfunction.[<xref ref-type="bibr" rid="ref22"> <a href='#ref22'>22</a> </xref>] Previous studies have documented similar clinical presentations. In the case described by Doan <i>et al</i>.,[<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>] there was a 2-week history of headaches accompanied by a syncopal episode. The report by Singh <i>et al</i>.[<xref ref-type="bibr" rid="ref23"> <a href='#ref23'>23</a> </xref>] indicated that the patient experienced a 3-month history of chronic dull, aching headaches on the left side, along with 2.5 months of gait instability. In addition, the study by Meshkini <i>et al</i>.[<xref ref-type="bibr" rid="ref13"> <a href='#ref13'>13</a> </xref>] reported a patient with headache, vomiting, and mild truncal ataxia. Our case also illustrates this classic presentation of a posterior fossa lesion linked to elevated intracranial pressure and mild cerebellar dysfunction, resulting in gait ataxia.</p><p>In the current case, the MRI characteristics of the lesion showed significant enhancement and diffusion restrictions on the MR Spectroscopy, indicating increased neoplastic activity. This finding is further supported by an elevated choline level and a high choline/NAA ratio. Notably, these imaging features can sometimes mimic those typically associated with meningiomas. Becker <i>et al</i>.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>] observed three patients, each presenting different degrees of contrast enhancement categorized as mild, moderate, and slightly moderate, with heterogeneous features, respectively. In addition, Singh <i>et al</i>.[<xref ref-type="bibr" rid="ref23"> <a href='#ref23'>23</a> </xref>] reported mild and heterogeneous enhancement of the tumor, an increased signal for choline and creatine, and the absence of ascending NAA or lipid-lactate signals significantly complicating the differentiation between these two entities. Furthermore, Doan <i>et al</i>.[<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>] emphasized the presence of a tentorial dural-tail sign, similar to what is observed in meningiomas; however, this sign can also appear in medulloblastomas as a manifestation of neoplastic infiltration within the dura mater, extending beyond the primary tumor mass.[<xref ref-type="bibr" rid="ref6"> <a href='#ref6'>6</a> </xref>] These observations underscore that eccentric medulloblastomas, particularly in adults, may pose a diagnostic challenge due to their neuroradiological resemblance to meningiomas.</p><p>According to the 2021 classification by the WHO regarding CNS tumors, medulloblastomas are molecularly classified into four distinct subgroups: wingless integration(WNT)-activated, sonic hedgehog (SHH)-activated, tumor protein 53 (TP53) wild type, SHH-activated TP53 mutant, and nonWNT non-SHH.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>,<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>,<xref ref-type="bibr" rid="ref12"> <a href='#ref12'>12</a> </xref>] In our case, the patient is classified as group 2, identified as SHH-activated and TP53 wild type, as reported by Singh <i>et al</i>.[<xref ref-type="bibr" rid="ref23"> <a href='#ref23'>23</a> </xref>,<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>] However, Doan <i>et al</i>.[<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>] classified their patient solely within the SHH group. It is noteworthy that the SHH subgroup of medulloblastoma is particularly associated with tumors occurring in the cerebellar hemispheres, unlike the other subgroups.[<xref ref-type="bibr" rid="ref14"> <a href='#ref14'>14</a> </xref>,<xref ref-type="bibr" rid="ref16"> <a href='#ref16'>16</a> </xref>] Nevertheless, our case represents a unique instance of SHH-activated medulloblastoma located outside the cerebellar hemispheres in an extra-axial location.</p><p>The SHH-activated subtype of medulloblastoma, as identified in our case, has significant therapeutic implications. Unlike other subtypes, SHH-driven tumors show potential responsiveness to targeted therapies, particularly SMO inhibitors such as vismodegib and sonidegib, which have shown promise in clinical trials.[<xref ref-type="bibr" rid="ref7"> <a href='#ref7'>7</a> </xref>,<xref ref-type="bibr" rid="ref21"> <a href='#ref21'>21</a> </xref>] This subtype also demonstrates distinct patterns of spread and prognosis, with TP53-wild-type cases generally exhibiting better outcomes compared to TP53-mutant variants.[<xref ref-type="bibr" rid="ref19"> <a href='#ref19'>19</a> </xref>,<xref ref-type="bibr" rid="ref29"> <a href='#ref29'>29</a> </xref>] These findings highlight the necessity of molecular profiling in medulloblastoma cases, as it can guide treatment decisions, potentially reducing the need for extensive craniospinal irradiation (CSI) in selected patients.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>]</p><p>The evolving landscape of precision medicine in neurooncology suggests that future strategies may involve tailored therapeutic approaches based on molecular and genetic markers, improving survival while minimizing long-term treatment-related morbidity.[<xref ref-type="bibr" rid="ref18"> <a href='#ref18'>18</a> </xref>-<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>]</p><p>Current treatment regimens are based on pediatric protocols, as specific guidelines for adult medulloblastoma are lacking due to its relative rarity.[<xref ref-type="bibr" rid="ref8"> <a href='#ref8'>8</a> </xref>,<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>] The standard of care currently involves maximal safe resection, adjuvant chemotherapy, and CSI.[<xref ref-type="bibr" rid="ref25"> <a href='#ref25'>25</a> </xref>] Historically, craniospinal radiation was administered postoperatively at a dose of 36 Gy, with an additional boost of 54–55.8 Gy to the posterior fossa tumor bed, owing to the high radiosensitivity of medulloblastomas. Since the 1990s, numerous researchers have demonstrated that incorporating adjuvant chemotherapy significantly enhances the absolute survival rate.[<xref ref-type="bibr" rid="ref5"> <a href='#ref5'>5</a> </xref>,<xref ref-type="bibr" rid="ref28"> <a href='#ref28'>28</a> </xref>] In the documented case by Singh <i>et al</i>.,[<xref ref-type="bibr" rid="ref23"> <a href='#ref23'>23</a> </xref>] the patient underwent surgical intervention followed by chemoradiation, which included etoposide, cisplatin, and CSI. Similarly, Doan <i>et al</i>.[<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>] described a strategy combining surgery, radiotherapy, and adjuvant chemotherapy with vincristine, cisplatin, and cyclophosphamide. These cases illustrate that chemotherapy protocols may vary. In our case, the same standard management approach was utilized: maximal safe resection combined with chemoradiation, followed by radiotherapy.</p><p>The prognosis and clinical outcomes of medulloblastomas vary significantly depending on the molecular subtype and the age of the patient. As in our case, patients with SHH-activated medulloblastomas typically have an intermediate prognosis, falling between the excellent outcomes seen in WNT-activated tumors and the poorer prognosis associated with non-WNT/non-SHH-activated (group 3) medulloblastomas. However, prognosis can be highly variable based on specific clinicopathological features.[<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>,<xref ref-type="bibr" rid="ref27"> <a href='#ref27'>27</a> </xref>] In infants with SHH-activated wild-type medulloblastomas, the outcomes are generally favorable. For young children and adolescents, survival rates exceed 80% unless high-risk factors such as metastatic disease or MYCN amplification are present, which are linked to a worse prognosis.[<xref ref-type="bibr" rid="ref21"> <a href='#ref21'>21</a> </xref>] In adults, SHH-activated medulloblastomas tend to have relatively favorable outcomes, although studies on this age group are limited.[<xref ref-type="bibr" rid="ref29"> <a href='#ref29'>29</a> </xref>]</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CONCLUSION">CONCLUSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Reports regarding tentorial medulloblastomas, especially among the adult population, are notably scarce. These tumors pose considerable diagnostic challenges due to their morphological similarities to meningiomas. Precise identification requires the use of advanced imaging techniques along with detailed histopathological evaluation, which also includes molecular and genetic analyses. The main treatment options involve surgical intervention followed by chemotherapy and/or radiation therapy, highlighting the need for comprehensive evaluation and personalized management strategies for these rare cases.</p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Ethical approval">Ethical approval</a></h3><div class="clearfix"></div><div class="hline"></div><p>Institutional Review Board approval is not required.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Declaration of patient consent">Declaration of patient consent</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors certify that they have obtained all appropriate patient consent.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Financial support and sponsorship">Financial support and sponsorship</a></h3><div class="clearfix"></div><div class="hline"></div><p>Nil.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Conflicts of interest">Conflicts of interest</a></h3><div class="clearfix"></div><div class="hline"></div><p>There are no conflicts of interest.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Use of artificial intelligence (AI)-assisted technology for manuscript preparation">Use of artificial intelligence (AI)-assisted technology for manuscript preparation</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Disclaimer">Disclaimer</a></h3><div class="clearfix"></div><div class="hline"></div><p>The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.</p></div> </div></div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"></div> </div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a name="References" href="javascript:void(0);">References</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><a href='javascript:void(0);' name='ref1' style='text-decoration: none;'>1.</a> Becker RL, Becker AD, Sobel DF. Adult medulloblastoma: Review of 13 cases with emphasis on MRI. Neuroradiology. 1995. 37: 104-8</p><p><a href='javascript:void(0);' name='ref2' style='text-decoration: none;'>2.</a> Choi JY. Medulloblastoma: Current perspectives and recent advances. Brain Tumor Res Treat. 2023. 11: 28-38</p><p><a href='javascript:void(0);' name='ref3' style='text-decoration: none;'>3.</a> Chung EJ, Jeun SS. Extra-axial medulloblastoma in the cerebellar hemisphere. J Korean Neurosurg Soc. 2014. 55: 362-4</p><p><a href='javascript:void(0);' name='ref4' style='text-decoration: none;'>4.</a> Doan N, Patel M, Nguyen H, Janich K, Montoure A, Shabani S. A rare extra-axial midline tentorial adult medulloblastoma with dural-tail sign mimicking a meningioma. Asian J Neurosurg. 2018. 13: 475-7</p><p><a href='javascript:void(0);' name='ref5' style='text-decoration: none;'>5.</a> Evans AE, Jenkin RD, Sposto R, Ortega JA, Wilson CB, Wara W. The treatment of medulloblastoma. Results of a prospective randomized trial of radiation therapy with and without CCNU, vincristine, and prednisone. J Neurosurg. 1990. 72: 572-82</p><p><a href='javascript:void(0);' name='ref6' style='text-decoration: none;'>6.</a> Furtado SV, Venkatesh PK, Dadlani R, Reddy K, Hegde AS. Adult medulloblastoma and the “Dural-tail” sign: A rare mimic of a posterior petrous meningioma. Clin Neurol Neurosurg. 2009. 111: 540-3</p><p><a href='javascript:void(0);' name='ref7' style='text-decoration: none;'>7.</a> Gajjar A, Stewart CF, Ellison DW, Kaste S, Kun LE, Packer RJ. Phase I study of vismodegib in children with recurrent or refractory medulloblastoma: A pediatric brain tumor consortium study. Clin Cancer Res. 2013. 19: 6305-12</p><p><a href='javascript:void(0);' name='ref8' style='text-decoration: none;'>8.</a> Jakacki RI, Burger PC, Zhou T, Holmes EJ, Kocak M, Onar A. Outcome of children with metastatic medulloblastoma treated with carboplatin during craniospinal radiotherapy: A children’s oncology group phase I/II study. J Clin Oncol. 2012. 30: 2648-53</p><p><a href='javascript:void(0);' name='ref9' style='text-decoration: none;'>9.</a> Komori T, editors. The 2021 WHO classification of tumors, 5th edition central nervous system tumors. The 10 basic principles. Brain Tumor Pathol. 2022. 39: 47-50</p><p><a href='javascript:void(0);' name='ref10' style='text-decoration: none;'>10.</a> Kumar R, Achari G, Banerjee D, Chhabra DK. Uncommon presentation of medulloblastoma. Child’s Nerv Syst. 2001. 17: 538-42</p><p><a href='javascript:void(0);' name='ref11' style='text-decoration: none;'>11.</a> Louis DN, Perry A, Reifenberger G, Von Deimling A, Figarella-Branger D, Cavenee WK. The 2016 world health organization classification of tumors of the central nervous system: A summary. Acta Neuropathol. 2016. 131: 803-20</p><p><a href='javascript:void(0);' name='ref12' style='text-decoration: none;'>12.</a> Louis DN, Perry A, Wesseling P, Brat DJ, Cree IA, FigarellaBranger D. The 2021 WHO classification of tumors of the central nervous system: A summary. Neuro Oncol. 2021. 23: 1231-51</p><p><a href='javascript:void(0);' name='ref13' style='text-decoration: none;'>13.</a> Meshkini A, Vahedi A, Meshkini M, Alikhah H, NaghaviBehzad M. Atypical medulloblastoma: A case series. Asian J Neurosurg. 2014. 9: 45-7</p><p><a href='javascript:void(0);' name='ref14' style='text-decoration: none;'>14.</a> Millard NE, De Braganca KC. Medulloblastoma. J Child Neurol. 2015. 31: 1341-53</p><p><a href='javascript:void(0);' name='ref15' style='text-decoration: none;'>15.</a> Northcott PA, Lee C, Zichner T, Stütz AM, Erkek S, Kawauchi D. Enhancer hijacking activates GFI1 family oncogenes in medulloblastoma. Nature. 2014. 511: 428-34</p><p><a href='javascript:void(0);' name='ref16' style='text-decoration: none;'>16.</a> Ostrom QT, Cioffi G, Waite K, Kruchko C, Barnholtz-Sloan JS. CBTRUS statistical report: Primary brain and other central nervous system tumors diagnosed in the United States in 2014-2018. Neuro Oncol. 2021. 23: iii1-105</p><p><a href='javascript:void(0);' name='ref17' style='text-decoration: none;'>17.</a> Perreault S, Ramaswamy V, Achrol AS, Chao K, Liu TT, Shih D. MRI surrogates for molecular subgroups of medulloblastoma. AJNR Am J Neuroradiol. 2014. 35: 1263-9</p><p><a href='javascript:void(0);' name='ref18' style='text-decoration: none;'>18.</a> Ramaswamy V, Hielscher T, Mack SC, Lassaletta A, Lin T, Pajtler KW. Therapeutic impact of cytoreductive surgery and irradiation of posterior fossa ependymoma in the molecular era: A retrospective multicohort analysis. J Clin Oncol. 2016. 34: 2468-77</p><p><a href='javascript:void(0);' name='ref19' style='text-decoration: none;'>19.</a> Ramaswamy V, Remke M, Shih D, Wang X, Northcott PA, Faria CC. Duration of the pre-diagnostic interval in medulloblastoma is subgroup dependent. Pediatr Blood Cancer. 2014. 61: 1190-4</p><p><a href='javascript:void(0);' name='ref20' style='text-decoration: none;'>20.</a> Ramaswamy V, Taylor MD. Medulloblastoma: From myth to molecular. J Clin Oncol. 2017. 35: 2355-63</p><p><a href='javascript:void(0);' name='ref21' style='text-decoration: none;'>21.</a> Robinson GW, Orr BA, Wu G, Gururangan S, Lin T, Qaddoumi I. Vismodegib exerts targeted efficacy against recurrent sonic hedgehog-subgroup medulloblastoma: Results from phase II pediatric brain tumor consortium studies PBTC-025B and PBTC-032. J Clin Oncol. 2015. 33: 2646-54</p><p><a href='javascript:void(0);' name='ref22' style='text-decoration: none;'>22.</a> Sainte-Rose C, Cinalli G, Roux FE, Maixner W, Chumas PD, Mansour M. Management of hydrocephalus in pediatric patients with posterior fossa tumors: The role of endoscopic third ventriculostomy. J Neurosurg. 2001. 95: 791-7</p><p><a href='javascript:void(0);' name='ref23' style='text-decoration: none;'>23.</a> Singh S, Israrahmed A, Verma V, Singh V. Extra-axial tentorial medulloblastoma: A rare presentation of a common posterior fossa tumour. BMJ Case Rep. 2021. 14: e242865</p><p><a href='javascript:void(0);' name='ref24' style='text-decoration: none;'>24.</a> Smoll NR. Relative survival of childhood and adult medulloblastomas and primitive neuroectodermal tumors (PNETs). Cancer. 2012. 118: 1313-22</p><p><a href='javascript:void(0);' name='ref25' style='text-decoration: none;'>25.</a> Sun T, Plutynski A, Ward S, Rubin JB. An integrative view on sex differences in brain tumors. Cell Mol Life Sci. 2015. 72: 3323-42</p><p><a href='javascript:void(0);' name='ref26' style='text-decoration: none;'>26.</a> Taylor MD, Northcott PA, Korshunov A, Remke M, Cho YJ, Clifford SC. Molecular subgroups of medulloblastoma: The current consensus. Acta Neuropathol. 2012. 123: 465-72</p><p><a href='javascript:void(0);' name='ref27' style='text-decoration: none;'>27.</a> Taylor RE, Bailey CC, Robinson K, Weston CL, Ellison D, Ironside J. Results of a randomized study of preradiation chemotherapy versus radiotherapy alone for nonmetastatic medulloblastoma: The international society of paediatric oncology/United Kingdom children’s cancer study group PNET-3 study. J Clin Oncol. 2003. 21: 1581-91</p><p><a href='javascript:void(0);' name='ref28' style='text-decoration: none;'>28.</a> Thompson EM, Hielscher T, Bouffet E, Remke M, Luu B, Gururangan S. Prognostic value of medulloblastoma extent of resection after accounting for molecular subgroup: A retrospective integrated clinical and molecular analysis. Lancet Oncol. 2016. 17: 484-95</p><p><a href='javascript:void(0);' name='ref29' style='text-decoration: none;'>29.</a> Waszak SM, Northcott PA, Buchhalter I, Robinson GW, Sutter C, Groebner S. Spectrum and prevalence of genetic predisposition in medulloblastoma: A retrospective genetic study and prospective validation in a clinical trial cohort. Lancet Oncol. 2018. 19: 785-98</p><p><a href='javascript:void(0);' name='ref30' style='text-decoration: none;'>30.</a> Xia H, Zhong D, Wu X, Li J, Yang Y, Sun X. Medulloblastomas in cerebellopontine angle: Epidemiology, clinical manifestations, imaging features, molecular analysis and surgical outcome. J Clin Neurosci. 2019. 67: 93-8</p></div> </div></div>
  5. Erroneous intramedullary placement of spinal cord stimulator: A case report and review of the literature

    Fri, 18 Apr 2025 19:57:24 -0000

    Erroneous intramedullary placement of spinal cord stimulator: A case report and review of the literature Category: Article Type: Stephen Jaffee, Trent Kite, Dallas E. Kramer, Nestor TomyczDepartment of Neurosurgery, Allegheny Health Network, Pittsburgh, United StatesCorrespondence Address:Trent Kite, Department of Neurosurgery, Allegheny Health Network, Pittsburgh, United States.DOI:10.25259/SNI_1035_2024Copyright: © 2025 Surgical Neurology International This is an open-access … Continue reading Erroneous intramedullary placement of spinal cord stimulator: A case report and review of the literature
    <div><!DOCTYPE html PUBLIC "-//W3C//DTD HTML 4.0 Transitional//EN" "http://www.w3.org/TR/REC-html40/loose.dtd"> <html><head><meta http-equiv="content-type" content="text/html; charset=utf-8"></head><body><div class="row"><div class="col-lg-9 col-sm-8 col-xs-12"><div class="media-body details-body"> <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13505"><h2 class="media-heading"><h2 class="media-heading">Erroneous intramedullary placement of spinal cord stimulator: A case report and review of the literature</h2></h2></a> </div><div class="disp_categories"> <p><label>Category: </label><span></span></p> <p><label>Article Type: </label><span></span></p> </div><a href="mailto:stephen.jaffee@ahn.org" target="_top">Stephen Jaffee</a>, <a href="mailto:tkite@vt.vcom.edu" target="_top">Trent Kite</a>, <a href="mailto:dallas.kramer@ahn.org" target="_top">Dallas E. Kramer</a>, <a href="mailto:nestor.tomycz@ahn.org" target="_top">Nestor Tomycz</a><ol class="smalllist"><li>Department of Neurosurgery, Allegheny Health Network, Pittsburgh, United States</li></ol><p><strong>Correspondence Address:</strong><br>Trent Kite, Department of Neurosurgery, Allegheny Health Network, Pittsburgh, United States.<br></p><p><strong>DOI:</strong>10.25259/SNI_1035_2024</p>Copyright: © 2025 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.<div class="parablock"><p><strong>How to cite this article: </strong>Stephen Jaffee, Trent Kite, Dallas E. Kramer, Nestor Tomycz. Erroneous intramedullary placement of spinal cord stimulator: A case report and review of the literature. 18-Apr-2025;16:144</p></div><div class="parablock"><p><strong>How to cite this URL: </strong>Stephen Jaffee, Trent Kite, Dallas E. Kramer, Nestor Tomycz. Erroneous intramedullary placement of spinal cord stimulator: A case report and review of the literature. 18-Apr-2025;16:144. Available from: <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13505">https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13505</a></p></div> </div> <div class="col-lg-3 col-sm-4 col-xs-12"><div class="article-detail-sidebar"><div class="icon sidebar-icon clearfix add-readinglist-icon"><button id="bookmark-article" class="add-reading-list-article">Add to Reading List</button><button id="bookmark-remove-article" class="remove-reading-list-article">Remove from Reading List</button></div><div class="icon sidebar-icon clearfix"><a class="btn btn-link" target="_blank" type="button" id="OpenPdf" href="https://surgicalneurologyint.com/wp-content/uploads/2025/04/13505/SNI-16-144.pdf"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/pdf-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a target="_blank" href="javascript:void(0);" onclick="return PrintArticle();"><img decoding="async" src="https://i0.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/file-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a class="btn btn-link" type="button" id="EmaiLPDF"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/mail-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a></div><div class="date"> <p>Date of Submission<br><span class="darkgray">04-Dec-2024</span></p> <p>Date of Acceptance<br><span class="darkgray">07-Mar-2025</span></p> <p>Date of Web Publication<br><span class="darkgray">18-Apr-2025</span></p> </div> </div></div> </div> <!--.row --><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a href="javascript:void(0);" name="Abstract">Abstract</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><strong>Background</strong>Spinal cord stimulation is a common treatment for patients with medically refractory chronic neuropathic pain. Before permanent implantation of spinal cord stimulation, patients will undergo a percutaneous trial to ensure the efficacy of the treatment modality and determine the optimal location of placement. While complications from this procedure are rare, there are reports in the literature of infection, epidural hematoma, and even paralysis. There are few reports of percutaneous leads tracking through the spinal cord itself, and subsequently, few reports of management should such a complication take place. Herein, we provide an example of such a phenomenon with no significant postoperative complications, morbidity, or mortality.</p><p><strong>Case Description</strong>A retrospective chart review was completed utilizing the electronic medical record. Data gathered included patient demographics, oncological history, medications, imaging, and operative reports. This is a 64–year-old male with a history of with a history of a traumatic brachial plexus avulsion and right upper extremity amputation at the shoulder after a motorcycle accident approximately 20 years prior presented to our institution with left upper extremity paresthesias, gain imbalance, and urinary incontinence after a permanent percutaneous spinal cord stimulation lead was placed from an outside institution. The patient was found to have the lead tracking through the intramedullary space of his spinal cord. The patient was taken to the operating room for removal of the lead and had no significant complications during his postoperative course.</p><p><strong>Conclusion</strong>There is a paucity of literature regarding the removal of an intramedullary percutaneous spinal cord stimulator lead; herein, we present such a case.</p><p><strong>Keywords: </strong>Case report, Intramedullary, Pain, Stimulation</p><p></p></div> </div></body></html> </div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"><p></p><p><inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="SNI-16-144-inline001.tif"/></p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="INTRODUCTION">INTRODUCTION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Spinal cord stimulation (SCS) is a common treatment for patients with medically refractory chronic neuropathic pain, complex regional pain syndrome, and brachial plexus injuries.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>,<xref ref-type="bibr" rid="ref14"> <a href='#ref14'>14</a> </xref>] Permanent implantation techniques include percutaneous and open laminotomy/laminectomy. While complications are rare, there are reports in the literature of infection, epidural hematoma, and even paralysis. There are few reports of percutaneous leads tracking through the spinal cord itself, and subsequently, few reports of management should such a complication take place.[<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>,<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>,<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>] Muir documented a case report in which a female had a percutaneous SCS lead placed, which traversed through the dura and into the intramedullary space.[<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>] The patient subsequently displayed immediate symptoms such as lower extremity pain and paresthesias and had the lead removed on postoperative day 2.[<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>] Olmsted <i>et al</i>., also published two-cases in which the lead migrated through the dura on implantation; one of the patients developed immediate thoracic allodynia postoperatively upon initial programming, which was the indication for further evaluation of the lead.[<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>] We report our experience with the management of a misplaced cervical percutaneous cervical spinal cord stimulator, which was positioned intramedullary.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CASE DESCRIPTION">CASE DESCRIPTION</a></h3><div class="clearfix"></div><div class="hline"></div><p>A retrospective chart review was completed utilizing the electronic medical record. Data gathered included patient demographics, oncological history, medications, imaging, and operative reports.</p><p>This is a 64-year-old male with a history of a traumatic brachial plexus avulsion and right upper extremity amputation at the shoulder after a motorcycle accident approximately 20 years before presentation presenting with paresthesia in his left upper extremity, balance and gait dysfunction, urinary incontinence and neck pain after placement of a percutaneous spinal cord stimulation lead and pulse generator 1 week ago at an outside institution by the patient’s pain specialist. The patient endorsed the new symptoms began on postoperative day one of his recent implantation. He was sent to the hospital for computed tomography (CT) and myelography studies, and the CT myelogram did show evidence of a malposition of cervical spinal cord stimulation lead, which appeared to be within the intramedullary space of the spinal cord parenchyma [<xref ref-type="fig" rid="F1"> <a href='#F1'>Figures 1</a> </xref> and <xref ref-type="fig" rid="F2"> <a href='#F2'>2</a> </xref>].</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F1'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13505/SNI-16-144-g001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 1:</h3><p>(a) Axial and (b and c) sagittal reconstruction computed tomography myelogram showing all 8 contacts of 8-contact percutaneous spinal cord stimulation lead inside the spinal cord parenchyma.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F2'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13505/SNI-16-144-g002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 2:</h3><p>Myelogram scout radiograph showing 8-contact implanted Spinal cord stimulation (SCS) percutaneous lead and sub-clavicular pulse generator. SCS implanted for neuropathic pain related to traumatic brachial plexus avulsion and arm amputation.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>The patient was admitted to the neurological intensive care unit for close monitoring, started on 4 mg of dexamethasone every 6 h, and was offered an open removal of the cervical percutaneous lead and axillary pulse generator with intraoperative monitoring including continuous/real-time monitoring of the cervical spinal cord was provided using left median, left ulnar, and bilateral tibial nerve somatosensory evoked potentials (SSEP) as well as bilateral trapezius, left upper extremity, and bilateral lower extremity transcranial motor evoked potentials (MEP). C-arm fluoroscopy was used to image the spinal cord stimulation lead within the cervical region as well as the anchor site. The upper thoracic incision was opened with a scalpel, and Metzenbaum scissors were used to open subcutaneous tissues down to the anchor. The spinal cord stimulation lead was carefully removed with gentle traction. A silk purse string stitch was placed around the entrance site of the lead to help reduce the risk of cerebrospinal fluid leaking. There were no changes in SSEPs or MEP with the removal of the spinal cord stimulation lead. Next, the left pulse generator site was opened with a scalpel and Metzenbaum scissors, and the pulse generator was removed from its pocket along with the associated wiring. At this point, the entire spinal cord stimulation system had been removed, and C-arm fluoroscopy confirmed a complete explant of the system [<xref ref-type="fig" rid="F3"> <a href='#F3'>Figure 3</a> </xref>]. No changes were appreciated with intraoperative neuromonitoring. The patient had an uncomplicated postoperative course and suffered no morbidity or mortality from the procedure. Preoperative symptoms such as reported pain, urinary incontinence, gait, and balance dysfunction resolved after lead removal. The patient was discharged to a skilled nursing facility on postoperative day 8.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F3'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13505/SNI-16-144-g003.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 3:</h3><p>Intraoperative fluoroscopy (a) before and (b) after explantation of lead and pulse generator.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="DISCUSSION">DISCUSSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>While spinal cord stimulation has become a crucial operative technique for the treatment of medically refractory neuropathic pain, it is unfortunately common for the implant to be explanted for various reasons, including infection, lack of efficacy, or migration.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>,<xref ref-type="bibr" rid="ref12"> <a href='#ref12'>12</a> </xref>,<xref ref-type="bibr" rid="ref13"> <a href='#ref13'>13</a> </xref>] Stimulator removal has been shown to be a safe endeavor with minimal complications, which can include a similar complication profile to implantation like infection, cerebrospinal fluid leakage, damage to the spinal cord leading to weakness or paresthesia, retained hardware, or epidural hematoma.[<xref ref-type="bibr" rid="ref8"> <a href='#ref8'>8</a> </xref>] A review of the previous literature is appended in <xref ref-type="table" rid="T1"> <a href='#T1'>Table 1</a> </xref>. Topp <i>et al.</i>, identified a cohort of 35 patients who underwent SCS removal and documented minimal complications, with two patients having superficial infections, which resolved with a course of oral antibiotics.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>] The technique for removal depended on the extent of scar tissue formation around the implant and would sometimes necessitate extended laminectomy for removal.[<xref ref-type="bibr" rid="ref6"> <a href='#ref6'>6</a> </xref>,<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>]</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T1'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13505/SNI-16-144-t001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 1:</h3><p>Summary of previously reported cases of percutaneous spinal cord stimulation leads tracking into the spinal cord.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>One of the most common complications of percutaneous procedure is lead migration; however, in this illustrative case, the lead was mispositioned.[<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>,<xref ref-type="bibr" rid="ref7"> <a href='#ref7'>7</a> </xref>] Notably, Eldabe <i>et al</i>., discuss the benefit of an experienced surgeon for lead implantation as the rate of migration appears to be less.[<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>] We utilize a series of retention loops and anchors at our institution to prevent postoperative lead migration of the paddle electrode. Calculation of intraoperative impedances and initial programing is essential to determining if the electrode is intradural or not. A common location for epidural mispositioning is in the ventral epidural space, which can be visualized on intraoperative fluoroscopy. Should this occur, removal and replacement of the lead is paramount to achieving the intended purpose of the surgery and proper stimulation of the dorsal columns and medial lemniscus pathway.</p><p>Safe implantation and explantation of spinal cord stimulators are often done in conjunction with neuromonitoring of MEP and SSEP to ensure that no harm is being done to the spinal cord due to extrinsic compression by the implant or even an intraoperative hematoma. Owen <i>et al</i>. highlight the utilization of neuromonitoring and advocate for the use of a combination of MEP and SSEP in these cases.[<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>] SSEPs are routinely utilized at our institution to determine the appropriate positioning of the paddle electrode. We perform initial programming intra-operatively to assess any skew of laterality of the implant coverage and determine the optimal initial amplitude of stimulation for pain relief. It is unknown if the percutaneous stimulator was placed with the addition of neuromonitoring. During this illustrative case of a mispositioned intramedullary lead, we managed the explantation as a true intramedullary case with extensive neuromonitoring to ensure the safety of removal.[<xref ref-type="bibr" rid="ref5"> <a href='#ref5'>5</a> </xref>]</p><p>While magnetic resonance imaging of our patient did show notable myelomalacia along the prior implant track, the patient had minimal residual symptoms after explantation [<xref ref-type="fig" rid="F4"> <a href='#F4'>Figure 4</a> </xref>]. A postulated theory as to how the implant ended up in the intramedullary space involves the implantation using the Tuohy needle, which may have pierced the dura, and the lead slowly migrated through the intramedullary plane through blunt dissection through the fibers of the spinal cord.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F4'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13505/SNI-16-144-g004.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 4:</h3><p>(a) postoperative magnetic resonance imaging of cervical spine axial view (b) postoperative magnetic resonance imaging of cervical spine sagittal view shows abnormal cord signal in the right aspect of the cord extended from C2 to C7.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CONCLUSION">CONCLUSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>There are few reports about complications involving migration of spinal cord stimulation leads within the intramedullary space of the spinal cord. Herein, we present an illustrative case documenting safe removal with no significant complications.</p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Authors contribution’s">Authors contribution’s</a></h3><div class="clearfix"></div><div class="hline"></div><p>S.J was responsible for the conceptualization and primary manuscript preparation. T.K and D.K assisted with clinical data acquisition and manuscript revisions. N.T acted as a senior author providing supervision.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Ethical approval">Ethical approval</a></h3><div class="clearfix"></div><div class="hline"></div><p>Institutional Review Board approval is not required.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Declaration of patient consent">Declaration of patient consent</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors certify that they have obtained all appropriate patient consent.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Financial support and sponsorship">Financial support and sponsorship</a></h3><div class="clearfix"></div><div class="hline"></div><p>Nil.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Conflicts of interest">Conflicts of interest</a></h3><div class="clearfix"></div><div class="hline"></div><p>There are no conflicts of interest.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Use of artificial intelligence (AI)-assisted technology for manuscript preparation">Use of artificial intelligence (AI)-assisted technology for manuscript preparation</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Disclaimer">Disclaimer</a></h3><div class="clearfix"></div><div class="hline"></div><p>The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.</p></div> </div></div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"></div> </div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a name="References" href="javascript:void(0);">References</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><a href='javascript:void(0);' name='ref1' style='text-decoration: none;'>1.</a> American Association of Neurological Surgeons. Spinal cord stimulation. Available from: https://www.aans.org/patients/conditions-treatments/spinal-cord-stimulation [Last accessed on 2024 Sep 17].</p><p><a href='javascript:void(0);' name='ref2' style='text-decoration: none;'>2.</a> Dupré DA, Tomycz N, Whiting D, Oh M. Spinal cord stimulator explantation: Motives for removal of surgically placed paddle systems. Pain Pract. 2018. 18: 500-4</p><p><a href='javascript:void(0);' name='ref3' style='text-decoration: none;'>3.</a> Eldabe S, Buchser E, Duarte RV. Complications of spinal cord stimulation and peripheral nerve stimulation techniques: A review of the literature. Pain Med. 2016. 17: 325-36</p><p><a href='javascript:void(0);' name='ref4' style='text-decoration: none;'>4.</a> Ghatol D, Widrich J, editors. Intraoperative neurophysiological monitoring. StatPearls. Treasure Island, FL: StatPearls Publishing; 2024. p. Available from: https://www.ncbi.nlm.nih.gov/books/nbk563203 [Last accessed on 2023 Jul 24]</p><p><a href='javascript:void(0);' name='ref5' style='text-decoration: none;'>5.</a> Harland TA, Topp G, Shao K, Pilitsis JG. Revision and replacement of spinal cord stimulator paddle leads. Neuromodulation. 2022. 25: 753-7</p><p><a href='javascript:void(0);' name='ref6' style='text-decoration: none;'>6.</a> Koushik SS, Raghavan J, Saranathan S, Slinchenkova K, Viswanath O, Shaparin N. Complications of spinal cord stimulators-a comprehensive review article. Curr Pain Headache Rep. 2024. 28: 1-9</p><p><a href='javascript:void(0);' name='ref7' style='text-decoration: none;'>7.</a> Maldonado-Naranjo AL, Frizon LA, Sabharwal NC, Xiao R, Hogue O, Lobel DA. Rate of complications following spinal cord stimulation paddle electrode removal. Neuromodulation. 2018. 21: 513-9</p><p><a href='javascript:void(0);' name='ref8' style='text-decoration: none;'>8.</a> Muir L. Intramedullary spinal cord stimulator: Case report. University Lynchburg DMSc doctoral project assignment repository. 2020. 2: </p><p><a href='javascript:void(0);' name='ref9' style='text-decoration: none;'>9.</a> Olmsted ZT, Wu PB, Katouzian A, Dorsi MJ. Intrathecal placement of percutaneous spinal cord stimulation leads: Illustrative cases. J Neurosurg Case Lessons. 2024. 8: CASE24275</p><p><a href='javascript:void(0);' name='ref10' style='text-decoration: none;'>10.</a> Owen JH. Intraoperative stimulation of the spinal cord for prevention of spinal cord injury. Adv Neurol. 1993. 63: 271-88</p><p><a href='javascript:void(0);' name='ref11' style='text-decoration: none;'>11.</a> Patel A, Kafka B, Al Tamimi M. Pseudomeningocele and percutaneous intrathecal lead placement complication for spinal cord stimulator. J Clin Neurosci. 2019. 59: 347-9</p><p><a href='javascript:void(0);' name='ref12' style='text-decoration: none;'>12.</a> Patel SK, Gozal YM, Saleh MS, Gibson JL, Karsy M, Mandybur GT. Spinal cord stimulation failure: Evaluation of factors underlying hardware explantation. J Neurosurg Spine. 2019. 32: 133-8</p><p><a href='javascript:void(0);' name='ref13' style='text-decoration: none;'>13.</a> Pope JE, Stanton-Hicks M. Accidental subdural spinal cord stimulator lead placement and stimulation. Neuromodulation. 2011. 14: 30-2 discussion 33</p><p><a href='javascript:void(0);' name='ref14' style='text-decoration: none;'>14.</a> Sdrulla AD, Guan Y, Raja SN. Spinal cord stimulation: Clinical efficacy and potential mechanisms. Pain Pract. 2018. 18: 1048-67</p><p><a href='javascript:void(0);' name='ref15' style='text-decoration: none;'>15.</a> Topp G, Harland T, Spurgas M, Rock A, Pilitsis JG. Techniques for safe removal of spinal cord stimulation paddle leads. Oper Neurosurg (Hagerstown). 2022. 23: e348-52</p></div> </div></div>
  6. Triple Woven EndoBridge device strategy for recurrent basilar tip aneurysm: A case report

    Fri, 11 Apr 2025 20:14:18 -0000

    Triple Woven EndoBridge device strategy for recurrent basilar tip aneurysm: A case report Category: Article Type: James Russell Withers1, Adam A. Dmytriw2, Omer Doron2, Christopher J. Stapleton2, Aman B. Patel2, Robert W. Regenhardt3Department of Medicine, University of New England College of Osteopathic Medicine, Biddeford, United StatesDepartment of Neurosurgery and Interventional Neuroradiology, Massachusetts General Hospital, Harvard … Continue reading Triple Woven EndoBridge device strategy for recurrent basilar tip aneurysm: A case report
    <div><!DOCTYPE html PUBLIC "-//W3C//DTD HTML 4.0 Transitional//EN" "http://www.w3.org/TR/REC-html40/loose.dtd"> <html><head><meta http-equiv="content-type" content="text/html; charset=utf-8"></head><body><div class="row"><div class="col-lg-9 col-sm-8 col-xs-12"><div class="media-body details-body"> <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13499"><h2 class="media-heading"><h2 class="media-heading">Triple Woven EndoBridge device strategy for recurrent basilar tip aneurysm: A case report</h2></h2></a> </div><div class="disp_categories"> <p><label>Category: </label><span></span></p> <p><label>Article Type: </label><span></span></p> </div><a href="mailto:jwithers1@une.edu" target="_top">James Russell Withers</a><sup>1</sup>, <a href="mailto:adam.dmytriw@gmail.com" target="_top">Adam A. Dmytriw</a><sup>2</sup>, <a href="mailto:odoron@mgh.harvard.edu" target="_top">Omer Doron</a><sup>2</sup>, <a href="mailto:cstapleton@mgh.harvard.edu" target="_top">Christopher J. Stapleton</a><sup>2</sup>, <a href="mailto:abpatel@mgh.harvard.edu" target="_top">Aman B. Patel</a><sup>2</sup>, <a href="mailto:robert.regenhardt@mgh.harvard.edu" target="_top">Robert W. Regenhardt</a><sup>3</sup><ol class="smalllist"><li>Department of Medicine, University of New England College of Osteopathic Medicine, Biddeford, United States</li><li>Department of Neurosurgery and Interventional Neuroradiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States</li><li>Department of Neurosurgery and Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States</li></ol><p><strong>Correspondence Address:</strong><br>James Russell Withers, Department of Medicine, University of New England College of Osteopathic Medicine, Biddeford, United States.<br></p><p><strong>DOI:</strong>10.25259/SNI_445_2024</p>Copyright: © 2025 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.<div class="parablock"><p><strong>How to cite this article: </strong>James Russell Withers1, Adam A. Dmytriw2, Omer Doron2, Christopher J. Stapleton2, Aman B. Patel2, Robert W. Regenhardt3. Triple Woven EndoBridge device strategy for recurrent basilar tip aneurysm: A case report. 11-Apr-2025;16:128</p></div><div class="parablock"><p><strong>How to cite this URL: </strong>James Russell Withers1, Adam A. Dmytriw2, Omer Doron2, Christopher J. Stapleton2, Aman B. Patel2, Robert W. Regenhardt3. Triple Woven EndoBridge device strategy for recurrent basilar tip aneurysm: A case report. 11-Apr-2025;16:128. Available from: <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13499">https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13499</a></p></div> </div> <div class="col-lg-3 col-sm-4 col-xs-12"><div class="article-detail-sidebar"><div class="icon sidebar-icon clearfix add-readinglist-icon"><button id="bookmark-article" class="add-reading-list-article">Add to Reading List</button><button id="bookmark-remove-article" class="remove-reading-list-article">Remove from Reading List</button></div><div class="icon sidebar-icon clearfix"><a class="btn btn-link" target="_blank" type="button" id="OpenPdf" href="https://surgicalneurologyint.com/wp-content/uploads/2025/04/13499/SNI-16-128.pdf"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/pdf-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a target="_blank" href="javascript:void(0);" onclick="return PrintArticle();"><img decoding="async" src="https://i0.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/file-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a class="btn btn-link" type="button" id="EmaiLPDF"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/mail-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a></div><div class="date"> <p>Date of Submission<br><span class="darkgray">09-Jun-2024</span></p> <p>Date of Acceptance<br><span class="darkgray">09-Jan-2025</span></p> <p>Date of Web Publication<br><span class="darkgray">11-Apr-2025</span></p> </div> </div></div> </div> <!--.row --><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a href="javascript:void(0);" name="Abstract">Abstract</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><strong>Background</strong>Coil embolization and surgical clipping are among the treatment options for acutely ruptured cerebral aneurysms. However, wide-neck aneurysms may necessitate stent placement, introducing dual antiplatelet therapy risks during subarachnoid hemorrhage (SAH). The Woven EndoBridge (WEB) intrasaccular device provides a unique solution for wide-neck aneurysms that does not require dual antiplatelet therapy.</p><p><strong>Case Description</strong>This case report details a 56-year-old male with a recurrent basilar tip aneurysm, treated with three WEB devices. He presented with Hunt Hess grade 4 SAH and underwent initial embolization with a WEB 9 × 7.6 mm. He made a significant recovery, but recurrence of the aneurysm base was observed after 6 months. He underwent embolization with a second WEB 7 × 5.6 mm. A year later, follow-up angiography revealed a recurrence of the aneurysm base yet again, and he underwent embolization with a third WEB 5 × 3 mm.</p><p><strong>Conclusion</strong>This case demonstrates the application of the WEB for a ruptured aneurysm, obviating the need for dual antiplatelet therapy and minimizing the risks of re-rupture and extraventricular drain complications. It also demonstrates the technical feasibility of deploying three WEB devices in the same aneurysm, providing a strategy for challenging aneurysm recurrence. The WEB offers a safe approach for intrasaccular flow disruption with satisfactory occlusion rates for recurrent aneurysms.</p><p><strong>Keywords: </strong>Embolization, Ruptured aneurysm, Subarachnoid hemorrhage, Wide aneurysm, Woven EndoBridge</p><p></p></div> </div></body></html> </div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"><p></p><p><inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="SNI-16-128-inline001.tif"/></p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="INTRODUCTION">INTRODUCTION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Coil embolization is among the treatment options for many acutely ruptured cerebral aneurysms.[<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>] It is important to note that surgical clipping can also be utilized for this indication and has certain advantages, particularly for accessible sites, such as the middle cerebral artery, and when decompression is warranted.[<xref ref-type="bibr" rid="ref19"> <a href='#ref19'>19</a> </xref>] Other advantages of surgery include a slightly reduced re-bleed rate and robust securement which can allow the confident use of pressors for vasospasm.[<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>] However, other situations may lend themselves to endovascular approaches, particularly for aneurysms in the posterior circulation and patients with poor neurological status[<xref ref-type="bibr" rid="ref6"> <a href='#ref6'>6</a> </xref>]. One study demonstrated enhanced functional outcomes and improved survival rates after coil embolization compared to clip ligation.[<xref ref-type="bibr" rid="ref6"> <a href='#ref6'>6</a> </xref>] However, coil embolization can be challenging for wide-neck aneurysms, often requiring the placement of a stent in the parent artery. This poses some additional risk during the management of subarachnoid hemorrhage (SAH) given the need for dual antiplatelet therapy. The Woven EndoBridge (WEB) intrasaccular device offers unique advantages for the treatment of wide-neck ruptured aneurysms.[<xref ref-type="bibr" rid="ref11"> <a href='#ref11'>11</a> </xref>,<xref ref-type="bibr" rid="ref16"> <a href='#ref16'>16</a> </xref>]</p><p>The WEB is a nitinol-based electrothermal detachable device that functions as an intra-saccular flow diverter.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'>1</a> </xref>,<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>,<xref ref-type="bibr" rid="ref8"> <a href='#ref8'>8</a> </xref>,<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>,<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>] Food and Drug Administration (FDA)-approved for wide-neck bifurcation intracranial aneurysms, the WEB disrupts blood flow at the aneurysm neck, promoting intrasaccular thrombosis without requiring intravascular implantation or prolonged dual antiplatelet therapy.[<xref ref-type="bibr" rid="ref8"> <a href='#ref8'>8</a> </xref>,<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>] The WEB device can safely secure aneurysms of various sizes in both anterior and posterior circulation during acute SAH.[<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>,<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>] The endovascular treatment of wide-neck aneurysms with the WEB system has proven to be a dependable strategy for inducing flow disruption with satisfactory aneurysm occlusion rates.[<xref ref-type="bibr" rid="ref8"> <a href='#ref8'>8</a> </xref>,<xref ref-type="bibr" rid="ref17"> <a href='#ref17'>17</a> </xref>,<xref ref-type="bibr" rid="ref23"> <a href='#ref23'>23</a> </xref>]</p><p>The WEB device has previously been utilized as a 1<sup>st</sup>-time treatment approach and for aneurysm recurrence following prior treatment. In prior studies, exploring the WEB device as a retreatment option after unsuccessful surgical clipping, WEB was demonstrated to be feasible without significant complications.[<xref ref-type="bibr" rid="ref5"> <a href='#ref5'>5</a> </xref>,<xref ref-type="bibr" rid="ref9"> <a href='#ref9'>9</a> </xref>,<xref ref-type="bibr" rid="ref16"> <a href='#ref16'>16</a> </xref>,<xref ref-type="bibr" rid="ref22"> <a href='#ref22'>22</a> </xref>] Indications for WEB embolization of recurrent aneurysms include recurrence after clipping, coil compaction, recurrence after coiling, and anatomical considerations conducive to WEB placement.[<xref ref-type="bibr" rid="ref14"> <a href='#ref14'>14</a> </xref>] Despite the many advantages of WEB, a proportion of aneurysms following WEB implantation have required retreatment.[<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>] Retreating recurrent and residual aneurysms with the WEB device is both feasible and associated with a favorable occlusion rate, coupled with a low incidence of complications.[<xref ref-type="bibr" rid="ref5"> <a href='#ref5'>5</a> </xref>,<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>] This case report demonstrates the use of three WEB devices over time to treat basilar tip aneurysm recurrence.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CASE PRESENTATION">CASE PRESENTATION</a></h3><div class="clearfix"></div><div class="hline"></div><h3 class = "title3">Presentation</h3><p>A 56-year-old male patient with a past medical history of hypertension and medication noncompliance presented with the worst headache of his life after being found on the ground at work. He was urgently referred for neuroendovascular treatment for a ruptured cerebral aneurysm. Initial noncontrast head computed tomography (CT) revealed a SAH and CT angiography [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1 </a> </xref>] of the head showed an aneurysm at the basilar tip. His clinical presentation was consistent with a Hunt Hess grade of 4 and imaging with a modified Fisher scale of 4. He was admitted to the neurosurgical service for further management. The patient was intubated and given hypertonic saline as he had a Glasgow Coma Scale (GCS) 8 and a dilated right pupil. An extraventricular drain and arterial line were placed. The patient underwent an unsecured SAH protocol with systolic blood pressure (SBP) maintained <140, seizure prophylaxis with levetiracetam, and vasospasm prevention with nimodipine.</p><p>The patient was taken urgently for digital subtraction angiography, which confirmed the presence of a basilar tip aneurysm measuring 8.9 × 9.1 mm and an incidental 4.6 × 5.8 mm left superior hypophyseal aneurysm. A decision was made to treat the basilar tip aneurysm, deemed the likely source of SAH, with a WEB device. He was taken to the operating/interventional room for placement of a WEB Single-Layer Sphere (SLS) 9 × 7.6 mm. Follow-up angiography [<xref ref-type="fig" rid="F2"> <a href='#F2'> Figure 2 </a> </xref>] showed persistent but slowed filling within the WEB device. The patient was returned to the intensive care unit (ICU) for management of the SAH. He transitioned to a secured protocol. Blood pressure was allowed to autoregulate, and serial cerebral vasculature velocities were monitored by transcranial Doppler as well as neurologic examinations. He required intra-arterial treatment with verapamil for vasospasm on days 5, 6, 7, and 9.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F1'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13499/SNI-16-128-g001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 1:</h3><p>(a and b) Initial computed tomography (CT) of the head at the time of admission, showing subarachnoid hemorrhage. (c) CT angiography of the head showing concern for a basilar tip aneurysm.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F2'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13499/SNI-16-128-g002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 2:</h3><p>(a and b) Digital subtraction angiography pre-treatment. (c and d) High-resolution angiography post-WEB SLS 9 × 7.6 mm embolization, showing good WEB placement within the aneurysm, good lateral device compression, and reduced filling of the aneurysm with contrast stagnation.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>His ICU course was also complicated by tachycardia, likely due to alcohol withdrawal and aspiration pneumonia, for which he received appropriate treatment. He was extubated following WEB embolization. He later required reintubation on day 6 for an increasing oxygen requirement, excess secretions, and airway protection. He subsequently underwent a tracheostomy, which was later downsized, and he was eventually decannulated. Due to challenges in weaning the extraventricular drain, a shunt was placed. He was discharged to inpatient rehabilitation on day 89. He was oriented to self, able to follow commands, and had symmetrical movements in all extremities against gravity. The patient had a significant recovery and returned for follow-up 6 months later. His neurologic examination was intact. There was evidence of interval compaction of the WEB with >50% recanalization measuring approximately 6.5 × 5.9 mm in greatest dimensions. The 4.6 × 5.8 mm left superior hypophyseal aneurysm was stable in size and shape. After a discussion with the patient about treatment options, including a second WEB versus stent-assisted coiling, a decision was made to proceed with a second embolization with WEB SLS 7 × 5.6 [<xref ref-type="fig" rid="F3"> <a href='#F3'> Figure 3 </a> </xref>]. Final angiography revealed good placement within the residual base and contrast stasis within the second WEB. The patient was discharged home the following day.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F3'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13499/SNI-16-128-g003.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 3:</h3><p>(a and b) Digital subtraction angiography pre-treatment. (c and d) High-resolution angiography post-WEB SLS 7 × 5.6 mm embolization, showing good WEB placement within the aneurysm residual, good lateral device compression, and reduced filling of the aneurysm residual with contrast stagnation.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>At 1-year follow-up, the patient’s neurologic examination remained intact, and he was otherwise well. As the patient was stable, he underwent treatment of the incidental 4.6 × 5.8 mm left superior hypophyseal aneurysm with a Pipeline flow diverter. This procedure was uncomplicated, but diagnostic angiography of the posterior circulation showed that there was again a recurrence of the basilar tip aneurysm. The patient was discharged home the following day, with a plan to continue dual antiplatelet therapy for 6 months and re-evaluate both aneurysms at that time.</p><p>At follow-up after another 6 months, the patient expressed a wish to discontinue dual antiplatelet therapy, given easy bleeding and bruising. On angiography, there was minimal residual filling of the left superior hypophyseal artery aneurysm with no evidence of in-stent stenosis or migration. However, there was a persistent recurrence of the basilar tip aneurysm, with residual filling measuring 4.9 × 3.3 mm. There was again consideration of different treatment approaches, including stent-assisted coil embolization. However, the residual filling had a size and shape amenable to the straightforward placement of a third WEB. In addition to the patient’s desire to discontinue dual antiplatelet therapy, another perceived benefit of this approach was avoiding stent placement in the basilar artery. The patient was treated with a third WEB, this time Single-Layer (SL) 5 × 3 [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4 </a> </xref>]. Final angiography revealed good device placement with contrast stagnation within the WEB. He was transitioned to aspirin monotherapy. Overall, the patient remained intact and clinically well status post the third WEB embolization. He complained of only mild lightheadedness and mild right arm tremor, which has been stable since the initial SAH, for which he is seeing outpatient Neurology.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F4'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13499/SNI-16-128-g004.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 4:</h3><p>(a and b) Digital subtraction angiography pre-treatment. (c and d) High-resolution angiography post-WEB SL 5 × 3 mm embolization, showing good WEB placement within the aneurysm residual, good lateral device compression, and reduced filling of the aneurysm residual with contrast stagnation.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="DISCUSSION">DISCUSSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>This case report demonstrates the use of WEB embolization for a ruptured aneurysm and the use of three WEB devices in the same basilar tip aneurysm in the setting of recurrence over time. Aneurysms with a history of prior rupture are recognized for their propensity to exhibit elevated rates of recurrence and need for subsequent treatment.[<xref ref-type="bibr" rid="ref7"> <a href='#ref7'>7</a> </xref>] Although surgical clipping may be utilized to treat ruptured aneurysms, patients with aneurysms involving the posterior circulation or those with poor neurological status may benefit from alternative treatment options, such as endovascular approaches.[<xref ref-type="bibr" rid="ref6"> <a href='#ref6'>6</a> </xref>] Stent-assisted coiling is another treatment option for wide-neck basilar tip aneurysms. Indeed, Nejadhamzeeigilani <i>et al</i>. demonstrated acceptable outcomes using this approach. However, stent-assisted coiling poses risks of thromboembolic complications, possibly more so if a stent is placed in the basilar artery, requires prolonged dual antiplatelet therapy, may increase the risk of bleeding, and carries a risk of recurrence due to technical challenges.[<xref ref-type="bibr" rid="ref18"> <a href='#ref18'>18</a> </xref>]</p><p>As introduced, WEB offers many advantages for ruptured wide-neck aneurysms since it does not necessitate antiplatelet agents due to its intrasaccular placement.[<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>] The patient presented in this case was able to avoid dual antiplatelet therapy in the acute setting, which could have increased his risk of aneurysm re-rupture or complications related to his extraventricular drain. While the most common complication associated with WEB treatment is a thromboembolic event within the periprocedural period,[<xref ref-type="bibr" rid="ref21"> <a href='#ref21'>21</a> </xref>] none occurred in the presented case. Collectively, WEB has demonstrated satisfactory occlusion rates for wide-neck intracranial aneurysms.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>]</p><p>Overall, studies have shown an 87% success rate in treating recurrent aneurysms with the WEB alone.[<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>] A multicenter study demonstrated that adequate occlusion rates using WEB were 86% at the mid-term and 94% at the long-term follow-up.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>] While some neck remnants can be seen after WEB implantation, only 11% of aneurysms had mid-to-long-term recurrence.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>] A systematic review demonstrated that approximately 10.7% of all aneurysms treated with WEB will recur and undergo retreatment.[<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>] Retreatment following basilar aneurysms was 34.1% in one study.[<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>] Furthermore, evidence supports that WEB is effective and safe for retreating wide-neck aneurysms, as the majority of retreated cases had favorable outcomes.[<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>]</p><p>Treatment of recurrent basilar tip aneurysms endovascularly can be challenging due to the aneurysm morphology and proximity and configuration of nearby anatomy.[<xref ref-type="bibr" rid="ref12"> <a href='#ref12'>12</a> </xref>] Aneurysms located in the posterior circulation involving the vertebrobasilar system constitute 12% of intracranial aneurysm cases,[<xref ref-type="bibr" rid="ref13"> <a href='#ref13'>13</a> </xref>] although another study found that basilar tip aneurysms may be even more common (30%).[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>] In addition, basilar tip aneurysms have a high rate of recurrence after treatment.[<xref ref-type="bibr" rid="ref20"> <a href='#ref20'>20</a> </xref>] Since basilar tip aneurysms rank among the most predisposed to rupture within the category of posterior circulation aneurysms, aggressive treatment is warranted.[<xref ref-type="bibr" rid="ref13"> <a href='#ref13'>13</a> </xref>] WEB was approved for wide-neck aneurysms of the basilar tip by the FDA in 2018 due to its safety ad efficacy profile.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>]</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CONCLUSION">CONCLUSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>We present a case study of a patient with a complex clinical course, highlighting the challenges in managing ruptured cerebral aneurysms and recurrent basilar tip aneurysms. This case demonstrates the application of the WEB device for treating a ruptured aneurysm, eliminating the need for dual antiplatelet therapy. In addition, this approach may reduce the risks of re-rupture and extraventricular drain complications. While we do not advocate for the routine use of multiple WEB devices in the same aneurysm, this unique case showcases an example in which it may have provided the safest option by avoiding stent placement in the basilar artery, consistent with patient preferences to discontinue dual antiplatelet therapy, and supports the technical feasibility of this approach, providing another strategy for addressing challenging aneurysm recurrences. The WEB device offers a safe approach for intrasaccular flow disruption, minimizing risks while yielding satisfactory occlusion rates for recurrent aneurysms.</p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Ethical approval">Ethical approval</a></h3><div class="clearfix"></div><div class="hline"></div><p>The research/study was approved by the Institutional Review Boards at the University of New England College of Osteopathic Medicine (0923-05, dated September 28, 2023) and the Massachusetts General Hospital (2017P002427, dated December 14, 2017 and last amended May 22, 2024).</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Declaration of patient consent">Declaration of patient consent</a></h3><div class="clearfix"></div><div class="hline"></div><p>Patient’s consent not required as patients identity is not disclosed or compromised.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Financial support and sponsorship">Financial support and sponsorship</a></h3><div class="clearfix"></div><div class="hline"></div><p>Nil.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Conflicts of interest">Conflicts of interest</a></h3><div class="clearfix"></div><div class="hline"></div><p>Dr. Patel served as consultant for Medtronic, MicroVention, and Penumbra. Dr. Regenhardt served as consultant for Genomadix, on a data and safety monitoring board for a trial sponsored by Rapid Medical, and as site principal investigator for studies sponsored by MicroVention and Penumbra.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Use of artificial intelligence (AI)-assisted technology for manuscript preparation">Use of artificial intelligence (AI)-assisted technology for manuscript preparation</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Disclaimer">Disclaimer</a></h3><div class="clearfix"></div><div class="hline"></div><p>The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.</p></div> </div></div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"></div> </div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a name="References" href="javascript:void(0);">References</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><a href='javascript:void(0);' name='ref1' style='text-decoration: none;'>1.</a> Adeeb N, Dibas M, Diestro JD, Cuellar-Saenz HH, Sweid A, Kandregula S. Multicenter study for the treatment of sidewall versus bifurcation intracranial aneurysms with use of woven endobridge (WEB). Radiology. 2022. 304: 372-82</p><p><a href='javascript:void(0);' name='ref2' style='text-decoration: none;'>2.</a> Alpay K, Nania A, Raj R, Numminen J, Parkkola R, Rautio R. Long term WEB results-still going strong at 5 years?. Interv Neuroradiol. 2022. 30: 517-523</p><p><a href='javascript:void(0);' name='ref3' style='text-decoration: none;'>3.</a> Alpay K, Nania A, Parkkola R, Downer J, Lindgren A, Rautio R. The outcomes of recurrent wide-necked intracranial aneurysms treated with the Woven EndoBridge (WEB): A retrospective bicenter study. J Neuroradiol. 2022. 49: 298-304</p><p><a href='javascript:void(0);' name='ref4' style='text-decoration: none;'>4.</a> Al Saiegh F, Hasan D, Mouchtouris N, Zanaty M, Sweid A, Khanna O. Treatment of acutely ruptured cerebral aneurysms with the woven endobridge device: Experience Post-FDA Approval. Neurosurgery. 2020. 87: E16-22</p><p><a href='javascript:void(0);' name='ref5' style='text-decoration: none;'>5.</a> Booth TC, Parra-Farinas C, deSouza RM, Kandasamy N, Bhattacharya J, Rangi P. Woven endobridge (WEB) Device as a retreatment strategy after unsuccessful surgical clipping. World Neurosurg. 2020. 139: 111-20</p><p><a href='javascript:void(0);' name='ref6' style='text-decoration: none;'>6.</a> Brisman MH, Bederson JB. Surgical management of subarachnoid hemorrhage. New Horiz. 1997. 5: 376-86</p><p><a href='javascript:void(0);' name='ref7' style='text-decoration: none;'>7.</a> Chalouhi N, Bovenzi CD, Thakkar V, Dressler J, Jabbour P, Starke RM. Long-term catheter angiography after aneurysm coil therapy: Results of 209 patients and predictors of delayed recurrence and retreatment. J Neurosurg. 2014. 121: 1102-6</p><p><a href='javascript:void(0);' name='ref8' style='text-decoration: none;'>8.</a> Crinnion W, Bhogal P, Makalanda HL, Wong K, Arthur A, Cognard C. The Woven Endobridge as a treatment for acutely ruptured aneurysms: A review of the literature. Interv Neuroradiol. 2021. 27: 602-8</p><p><a href='javascript:void(0);' name='ref9' style='text-decoration: none;'>9.</a> Dmytriw AA, Dibas M, Ghozy S, Adeeb N, Diestro JD, Phan K. The Woven EndoBridge (WEB) Device for the treatment of intracranial aneurysms: Ten Years of Lessons Learned and Adjustments in Practice from the WorldWideWEB Consortium. Transl Stroke Res. 2023. 14: 455-64</p><p><a href='javascript:void(0);' name='ref10' style='text-decoration: none;'>10.</a> Dibas M, Adeeb N, Diestro JD, Cuellar HH, Sweid A, Lay SV. Transradial versus transfemoral access for embolization of intracranial aneurysms with the Woven EndoBridge device: A propensity score-matched study [published online ahead of print, 2022 Feb 4]. J Neurosurg. 2022. 137: 1064-71</p><p><a href='javascript:void(0);' name='ref11' style='text-decoration: none;'>11.</a> Diestro JD, Dibas M, Adeeb N, Regenhardt RW, Vranic JE, Guenego A. Intrasaccular flow disruption for ruptured aneurysms: An international multicenter study. J Neurointerv Surg. 2023. 15: 844-50</p><p><a href='javascript:void(0);' name='ref12' style='text-decoration: none;'>12.</a> Domingo RA, Ramos-Fresnedo A, Ravindran K, Tawk RG. Combined anterior and posterior circulation approach for stent-assisted coiling of a recurrent basilar tip aneurysm. J Neurointerv Surg. 2023. 15: 512</p><p><a href='javascript:void(0);' name='ref13' style='text-decoration: none;'>13.</a> D’Souza S. Aneurysmal subarachnoid hemorrhage. J Neurosurg Anesthesiol. 2015. 27: 222-40</p><p><a href='javascript:void(0);' name='ref14' style='text-decoration: none;'>14.</a> Gawlitza M, Soize S, Januel AC, Mihalea C, Metaxas GE, Cognard C. Treatment of recurrent aneurysms using the Woven EndoBridge (WEB): Anatomical and clinical results. J Neurointerv Surg. 2018. 10: 629-33</p><p><a href='javascript:void(0);' name='ref15' style='text-decoration: none;'>15.</a> Goertz L, Liebig T, Siebert E, Dorn F, Pflaeging M, Forbrig R. Long-term clinical and angiographic outcome of the Woven EndoBridge (WEB) for endovascular treatment of intracranial aneurysms. Sci Rep. 2022. 12: 11467</p><p><a href='javascript:void(0);' name='ref16' style='text-decoration: none;'>16.</a> Harker P, Regenhardt RW, Alotaibi NM, Vranic J, Robertson FC, Dmytriw AA. The Woven EndoBridge device for ruptured intracranial aneurysms: International multicenter experience and updated meta-analysis. Neuroradiology. 2021. 63: 1891-9</p><p><a href='javascript:void(0);' name='ref17' style='text-decoration: none;'>17.</a> Nawka MT, Lohse A, Bester M, Fiehler J, Buhk JH. Residual flow inside the woven endobridge device at follow-up: Potential predictors of the bicêtre occlusion scale score 1 phenomenon. AJNR Am J Neuroradiol. 2020. 41: 1232-7</p><p><a href='javascript:void(0);' name='ref18' style='text-decoration: none;'>18.</a> Nejadhamzeeigilani H, Buende T, Saleem N, Goddard T, Patankar T. Single centre experience of stent-assisted coiling of wide-necked basilar tip aneurysms. Br J Radiol. 2023. 96: 20220504</p><p><a href='javascript:void(0);' name='ref19' style='text-decoration: none;'>19.</a> Nisson PL, Meybodi AT, Roussas A, James W, Berger GK, Benet A. Surgical clipping of previously ruptured, coiled aneurysms: outcome assessment in 53 patients. World Neurosurg. 2018. 120: e203-11</p><p><a href='javascript:void(0);' name='ref20' style='text-decoration: none;'>20.</a> Peterson C, Cord BJ. Recurrent and residual aneurysms after woven endoBridge (WEB) Therapy: What’s next?. Cureus. 2021. 13: e14404</p><p><a href='javascript:void(0);' name='ref21' style='text-decoration: none;'>21.</a> Pierot L, Spelle L, Molyneux A, Byrne J. clinical and anatomical follow-up in patients with aneurysms treated with the WEB Device: 1-year follow-up report in the cumulated population of 2 prospective, multicenter series (WEBCAST and French Observatory). Neurosurgery. 2016. 78: 133-41</p><p><a href='javascript:void(0);' name='ref22' style='text-decoration: none;'>22.</a> Srinivasan VM, Dmytriw AA, Regenhardt RW, Vicenty-Padilla J, Alotaibi NM, Levy E. Retreatment of residual and recurrent aneurysms after embolization with the woven endobridge device: Multicenter case series. Neurosurgery. 2022. 90: 569-80</p><p><a href='javascript:void(0);' name='ref23' style='text-decoration: none;'>23.</a> van Rooij S, Sprengers ME, Peluso JP, Daams J, Verbaan D, van Rooij WJ. A systematic review and meta-analysis of Woven EndoBridge single layer for treatment of intracranial aneurysms. Interv Neuroradiol. 2020. 26: 455-60</p></div> </div></div>
  7. Hybrid therapy and use of carbon-fiber-reinforced polyetheretherketone instrumentation for management of mobile spine chordomas: A case series and review of the literature

    Fri, 11 Apr 2025 20:09:02 -0000

    Hybrid therapy and use of carbon-fiber-reinforced polyetheretherketone instrumentation for management of mobile spine chordomas: A case series and review of the literature Category: Article Type: Chi Shing Adrian Lam1, Vicente de Paulo Martins Coelho1, Seth Wilson1, Joshua Palmer2, Anas Bardeesi1, Vikram Chakravarthy1Department of Neurological Surgery, The Ohio State University Wexner Medical Center, United StatesDepartment of … Continue reading Hybrid therapy and use of carbon-fiber-reinforced polyetheretherketone instrumentation for management of mobile spine chordomas: A case series and review of the literature
    <div><!DOCTYPE html PUBLIC "-//W3C//DTD HTML 4.0 Transitional//EN" "http://www.w3.org/TR/REC-html40/loose.dtd"> <html><head><meta http-equiv="content-type" content="text/html; charset=utf-8"></head><body><div class="row"><div class="col-lg-9 col-sm-8 col-xs-12"><div class="media-body details-body"> <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13497"><h2 class="media-heading"><h2 class="media-heading">Hybrid therapy and use of carbon-fiber-reinforced polyetheretherketone instrumentation for management of mobile spine chordomas: A case series and review of the literature</h2></h2></a> </div><div class="disp_categories"> <p><label>Category: </label><span></span></p> <p><label>Article Type: </label><span></span></p> </div><a href="mailto:chishing.lam@osumc.edu" target="_top">Chi Shing Adrian Lam</a><sup>1</sup>, <a href="mailto:vicentecoelhojr@yahoo.com.br" target="_top">Vicente de Paulo Martins Coelho</a><sup>1</sup>, <a href="mailto:seth.wilson@osumc.edu" target="_top">Seth Wilson</a><sup>1</sup>, <a href="mailto:joshua.palmer@osumc.edu" target="_top">Joshua Palmer</a><sup>2</sup>, <a href="mailto:anasmohammedwajdia.bardeesi@osumc.edu" target="_top">Anas Bardeesi</a><sup>1</sup>, <a href="mailto:vikram.chakravarthy@osumc.edu" target="_top">Vikram Chakravarthy</a><sup>1</sup><ol class="smalllist"><li>Department of Neurological Surgery, The Ohio State University Wexner Medical Center, United States</li><li>Department of Radiation Oncology, The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, United States</li></ol><p><strong>Correspondence Address:</strong><br>Chi Shing Adrian Lam, Department of Neurological Surgery, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States.<br></p><p><strong>DOI:</strong>10.25259/SNI_53_2025</p>Copyright: © 2025 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.<div class="parablock"><p><strong>How to cite this article: </strong>Chi Shing Adrian Lam1, Vicente de Paulo Martins Coelho1, Seth Wilson1, Joshua Palmer2, Anas Bardeesi1, Vikram Chakravarthy1. Hybrid therapy and use of carbon-fiber-reinforced polyetheretherketone instrumentation for management of mobile spine chordomas: A case series and review of the literature. 11-Apr-2025;16:130</p></div><div class="parablock"><p><strong>How to cite this URL: </strong>Chi Shing Adrian Lam1, Vicente de Paulo Martins Coelho1, Seth Wilson1, Joshua Palmer2, Anas Bardeesi1, Vikram Chakravarthy1. Hybrid therapy and use of carbon-fiber-reinforced polyetheretherketone instrumentation for management of mobile spine chordomas: A case series and review of the literature. 11-Apr-2025;16:130. Available from: <a href="https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13497">https://surgicalneurologyint.com/?post_type=surgicalint_articles&p=13497</a></p></div> </div> <div class="col-lg-3 col-sm-4 col-xs-12"><div class="article-detail-sidebar"><div class="icon sidebar-icon clearfix add-readinglist-icon"><button id="bookmark-article" class="add-reading-list-article">Add to Reading List</button><button id="bookmark-remove-article" class="remove-reading-list-article">Remove from Reading List</button></div><div class="icon sidebar-icon clearfix"><a class="btn btn-link" target="_blank" type="button" id="OpenPdf" href="https://surgicalneurologyint.com/wp-content/uploads/2025/04/13497/SNI-16-130.pdf"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/pdf-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a target="_blank" href="javascript:void(0);" onclick="return PrintArticle();"><img decoding="async" src="https://i0.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/file-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a><a class="btn btn-link" type="button" id="EmaiLPDF"><img decoding="async" src="https://i1.wp.com/surgicalneurologyint.com/wp-content/themes/surgicalint/images/mail-icon.png?w=604&#038;ssl=1" class="no-popup" data-recalc-dims="1"></a></div><div class="date"> <p>Date of Submission<br><span class="darkgray">18-Jan-2025</span></p> <p>Date of Acceptance<br><span class="darkgray">06-Mar-2025</span></p> <p>Date of Web Publication<br><span class="darkgray">11-Apr-2025</span></p> </div> </div></div> </div> <!--.row --><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a href="javascript:void(0);" name="Abstract">Abstract</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><strong>Background</strong>Mobile spine chordomas demonstrate varied surgical risk profiles compared to their sacral analogs. Often, the limitation to performing an <i>en bloc</i> resection of a mobile spine chordoma is tumor violation of the epidural space. Given these limitations, we propose the utilization of carbon fiber-reinforced polyetheretherketone (CFR-PEEK) instrumentation in separation surgery to enhance visualization for stereotactic body radiation therapy (SBRT) planning, allowing an ablative radiosurgical dose to be delivered.</p><p><strong>Methods</strong>We present two illustrative cases highlighting the advantages of hybrid therapy (separation surgery and adjuvant SBRT) with CFR-PEEK instrumentation in the management of mobile spine chordoma.</p><p><strong>Results</strong>Case 1 is a 62-year-old female with an L4 chordoma who underwent separation surgery and L3–5 posterior instrumented fusion using CFR-PEEK instrumentation. Case 2 is a 68-year-old female with a L3 chordoma who underwent revision separation surgery encompassing completion of L3 partial corpectomy and CFR-PEEK screw exchange of prior L2–4 titanium instrumentation. Both patients received postoperative ablative SBRT. At 18-month postoperative time points, both patients were clinically stable, with no signs of tumor recurrence or progression.</p><p><strong>Conclusion</strong>Mobile spine chordomas present a unique challenge in obtaining a margin negative <i>en bloc</i> resection. Separation surgery allows the ability to decrease surgical morbidity and deliver an ablative radiosurgical dose. Furthermore, the incorporation of CFR-PEEK instrumentation allows the utilization of multiparametric magnetic resonance imaging for long-term disease monitoring. Hybrid therapy, a less morbid alternative to standard <i>en bloc</i> spondylectomy, offers a better surgical morbidity profile by combining effectively with SBRT for optimal tumor control.</p><p><strong>Keywords: </strong>Carbon fiber/polyetheretherketone, Chordoma, Hybrid therapy, Magnetic resonance imaging, Mobile spine, Separation surgery</p><p></p></div> </div></body></html> </div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"><p></p><p><inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="SNI-16-130-inline001.tif"/></p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="INTRODUCTION">INTRODUCTION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Chordomas of the mobile spine (C1-L5) are rare primary osseous neoplasms with an annual incidence of 0.05/100,000 people per year.[<xref ref-type="bibr" rid="ref26"> <a href='#ref26'>26</a> </xref>] Epidemiological studies describe 58.3% of cases as male with a mean age of 55 years.[<xref ref-type="bibr" rid="ref55"> <a href='#ref55'>55</a> </xref>] Chordomas most often localize to the skull base (41.1%) or sacrum (31.4%), with the remainder presenting in the mobile spine (27.5%). [<xref ref-type="bibr" rid="ref34"> <a href='#ref34'>34</a> </xref>] Skull base chordomas have a higher median survival at 162 months compared to the sacrum and mobile spine at 87 and 95 months, respectively.[<xref ref-type="bibr" rid="ref34"> <a href='#ref34'>34</a> </xref>] Diagnosis of chordomas is often late in the disease course and requires histologic evaluation through percutaneous biopsy.</p><p>According to the Enneking staging system, chordomas are classified as low-grade malignant tumors, which fall under stages IA and IB.[<xref ref-type="bibr" rid="ref5"> <a href='#ref5'>5</a> </xref>,<xref ref-type="bibr" rid="ref16"> <a href='#ref16'>16</a> </xref>] As such, the standard of care for these patients has been <i>en bloc</i> resection with negative margins, often necessitating resection of the dura, followed by adjuvant radiation and/or chemotherapy. [<xref ref-type="bibr" rid="ref4"> <a href='#ref4'>4</a> </xref>,<xref ref-type="bibr" rid="ref8"> <a href='#ref8'>8</a> </xref>,<xref ref-type="bibr" rid="ref54"> <a href='#ref54'>54</a> </xref>] Mainly influenced by intrinsic anatomic features, arising in the mobile spine typically discourages a more aggressive resection due to an unfavorable morbidity outlook.[<xref ref-type="bibr" rid="ref40"> <a href='#ref40'>40</a> </xref>] These circumstances position separation surgery, where spinal column decompression and tumor resection occur with limited corpectomy, ensuring an adequate target for postoperative radiosurgery, as an appealing strategy for this location.[<xref ref-type="bibr" rid="ref10"> <a href='#ref10'>10</a> </xref>,<xref ref-type="bibr" rid="ref30"> <a href='#ref30'>30</a> </xref>] More recently, Lockney <i>et al</i>. have demonstrated the effectiveness of hybrid therapy, consisting of separation surgery followed by stereotactic body radiation therapy (SBRT), for newly diagnosed chordomas.[<xref ref-type="bibr" rid="ref24"> <a href='#ref24'>24</a> </xref>] In a prospective study with 111 patients, Barzilai <i>et al</i>. demonstrated that hybrid therapy was effective at decreasing pain and improving quality of life for patients with metastatic epidural spinal cord compression.[<xref ref-type="bibr" rid="ref3"> <a href='#ref3'>3</a> </xref>]</p><p>Shifting from therapeutic approaches, radiographic imaging to evaluate chordomas typically involves computed tomography (CT) scans and magnetic resonance imaging (MRI). On CT, these tumors have low density and may have cortical destruction.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>,<xref ref-type="bibr" rid="ref27"> <a href='#ref27'>27</a> </xref>] On T1-weighted imaging, chordomas usually appear hypo- or iso-intense, whereas they are characteristically hyperintense on T2-weighted imaging.[<xref ref-type="bibr" rid="ref11"> <a href='#ref11'>11</a> </xref>] Chordomas can appear with no, mild, or marked enhancement.[<xref ref-type="bibr" rid="ref2"> <a href='#ref2'>2</a> </xref>] Histologically, the World Health Organization[<xref ref-type="bibr" rid="ref51"> <a href='#ref51'>51</a> </xref>] has identified three subtypes of chordoma: conventional, dedifferentiated, and poorly differentiated. Conventional chordomas are the most common,[<xref ref-type="bibr" rid="ref45"> <a href='#ref45'>45</a> </xref>] whereas poorly differentiated chordomas typically occur in the skull base.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'>15</a> </xref>]</p><p>Innovations in surgical technology can assist in the multi-disciplinary nature of standard care for chordoma patients. Titanium-based surgical constructs produce artifacts on follow-up CT and MRI, creating challenges in radiation planning and oncologic surveillance.[<xref ref-type="bibr" rid="ref7"> <a href='#ref7'>7</a> </xref>] Carbon fiber-reinforced polyetheretherketone (CFR-PEEK) is a type of composite material combining the strength and stiffness of carbon fiber with the biocompatibility and resistance to corrosion of polyetheretherketone. It has been used in various medical and surgical applications, including as an alternative to traditional titanium instrumentation in spine surgery.[<xref ref-type="bibr" rid="ref38"> <a href='#ref38'>38</a> </xref>] Notably, CFR-PEEK does not create the same artifact on advanced imaging as titanium instrumentation and, thus, plays an integral role in adjuvant therapy planning. SBRT, compared to conventional radiotherapy, has been shown to provide excellent local tumor control for both primary and metastatic bone tumors.[<xref ref-type="bibr" rid="ref44"> <a href='#ref44'>44</a> </xref>] CFR-PEEK hardware allows for more precise dosimetry contouring of the spinal cord and at-risk organs for patients requiring adjuvant therapy, allowing an ablative dose to be delivered.[<xref ref-type="bibr" rid="ref35"> <a href='#ref35'>35</a> </xref>]</p><p>We report two cases of chordoma in the mobile spine where CFR-PEEK implants were utilized in separation surgery followed by adjuvant SBRT, reporting patient outcomes and benefits of this combined treatment modality.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="MATERIALS AND METHODS">MATERIALS AND METHODS</a></h3><div class="clearfix"></div><div class="hline"></div><p>We describe two cases of mobile spine chordomas [<xref ref-type="table" rid="T1"> <a href='#T1'>Table 1</a> </xref>]. Case 1 is a 62-year-old female with an L4 chordoma who was experiencing back pain, left-sided lower extremity radiculopathy, and paresthesia. The patient then underwent separation surgery, encompassing partial corpectomy at L4 and L3–5 posterior instrumented fusion with CFR-PEEK, followed by adjuvant SBRT.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T1'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13497/SNI-16-130-t001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 1:</h3><p>Demographics overview.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>Case 2 features a 68-year-old female presenting with back pain and bilateral lower extremity radiculopathy impacting ambulation. The patient underwent partial resection of L3 epidural tumor at an outside hospital, with vertebroplasty at the index level and titanium pedicle screw fixation from L2 to 4. Pathology confirmed chordoma and radiation was not performed. Six-month postoperative imaging revealed a residual tumor. The patient then underwent revision surgery with transpedicular L3 partial corpectomy and L2–4 pedicle screw exchange with CFR-PEEK to assist with postoperative radiation therapy planning.</p><p>Patient informed consent was obtained, and this case series has been reported in line with the CARE guidelines (for case reports).[<xref ref-type="bibr" rid="ref36"> <a href='#ref36'>36</a> </xref>]</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="RESULTS">RESULTS</a></h3><div class="clearfix"></div><div class="hline"></div><h3 class = "title3">Case 1</h3><p>A 62-year-old female presented with a 4-month history of axial low back pain with occasional left-sided anterior thigh radicular pain and intermittent paresthesia [<xref ref-type="fig" rid="F1"> <a href='#F1'> Figure 1 </a> </xref>]. Her medical history was significant for hypertension, coronary artery disease, anxiety, osteoarthritis of her knee, and prior hip surgery. She also had a 20-pack year history of tobacco use. On physical examination, she grossly had 5/5 motor strength in all extremities.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F1'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13497/SNI-16-130-g001.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 1:</h3><p>Timeline of important events for case #1.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>Imaging revealed a T2 hyperintense destructive expansile lesion at L4, demonstrating cortical breakthrough into the anterior epidural space and anterior left prevertebral soft tissues [<xref ref-type="fig" rid="F2"> <a href='#F2'> Figure 2 </a> </xref>]. In addition, there was severe stenosis at L4 secondary to epidural tumor extension.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F2'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13497/SNI-16-130-g002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 2:</h3><p>Relevant imaging for Case #1. The first column contains T1-weighted fat-suppressed magnetic resonance imaging (MRI) pre-treatment (top = sagittal, bottom = axial). The second column contains T1-weighted fat-suppressed MRI after surgery (top = sagittal, bottom = axial). The third column contains X-rays after surgery (top = lateral, bottom = anteroposterior). The last column contains the last dynamic contrast-enhanced-MRI (top = overlay, bottom = MR perfusion).</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>Biopsy of the L4 vertebrae demonstrated chordoma consistent with the conventional subtype. Immunohistochemistry confirmed tumor cells positive for pancytokeratin, epithelial membrane antigen (EMA), and weak S100; paired box gene 8 and thyroid transcription factor 1 stain were negative. Expression of p53 was low, where 20% of tumor cell nuclei had intense p53 immunoreactivity, associated with improved prognosis and longer progression-free survival in chordomas.[<xref ref-type="bibr" rid="ref43"> <a href='#ref43'> 43 </a> </xref>]</p><p>Thereafter, she underwent separation surgery, encompassing a partial transpedicular corpectomy of L4 with L3–5 cement-augmented posterior instrumented fusion, using CFR-PEEK instrumentation [<xref ref-type="table" rid="T2"> <a href='#T2'> Table 2 </a> </xref>]. There were no intraoperative complications, the total surgical time was 4.7 h, and the estimated blood loss was 1 L. The patient was discharged home 3 days later without any complications during her stay.</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T2'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13497/SNI-16-130-t002.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 2:</h3><p>Surgical overview.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>At 1-month postoperative, imaging demonstrated adequate neural decompression. Thereafter, she underwent SBRT using 3 volumetric modulated arc therapy (VMAT) at 40 Gy in five fractions with 10 megavolts (MV) photons in a flattening filter-free (FFF) mode [<xref ref-type="fig" rid="F3"> <a href='#F3'> Figure 3 </a> </xref> and <xref ref-type="table" rid="T3"> <a href='#T3'> Table 3 </a> </xref>].</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='T3'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13497/SNI-16-130-t003.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Table 3:</h3><p>Radiotherapy overview.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F3'></a> <br /><img src='https://i2.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13497/SNI-16-130-g003.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 3:</h3><p>Dosimetry mapping for Case #1 (left) and Case #2 (right). This figure highlights typical volumetric modulated arc therapy spinal stereotactic body radiation therapy isocenter planning used in these cases, following consensus contouring guidelines. Of note, no hardware-related imaging artifact at the target volume allowed precise dose delineation.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>Three- and 6-month MRIs were stable, and the patient reported a Karnofsky Performance Scale (KPS) of 100 at 19 months postoperative. Dynamic contrast-enhanced MRI (DCE-MRI) scans were performed postoperatively at 3 weeks, 5 weeks, 4 months, 7 months, 10 months, 13, and 19 months to evaluate for progression. DCE-MRI revealed stable findings consistent with postoperative changes and no evidence of tumor activity or recurrence.</p><h3 class = "title3">Case 2</h3><p>A 68-year-old female presented with worsening back pain with radiation into bilateral lower extremities [<xref ref-type="fig" rid="F4"> <a href='#F4'> Figure 4 </a> </xref>]. Her medical history was significant for melanoma status post excision (deemed cured), hypertension, hyperlipidemia, obesity, gastric sleeve surgery, and ankle repair surgery. The patient did not have a prior smoking history. Lumbar X-ray revealed a worsening sclerotic lesion in her L3 vertebral body and a new L3 compression fracture. In addition, MRI demonstrated an enhancing lesion (4.8 × 4.8 cm) with epidural extension, nearly obliterating the spinal canal at the level of L3 with involvement of the superior and inferior neural foramina [<xref ref-type="fig" rid="F5"> <a href='#F5'> Figure 5 </a> </xref>].</p><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F4'></a> <br /><img src='https://i1.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13497/SNI-16-130-g004.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 4:</h3><p>Timeline of important events for case #2.</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><div class="row"> <div class="col-xs-12 content-figure col-wrap"> <div class="col-xs-2 figure-body col"><a href='javascript:void(0);' name='F5'></a> <br /><img src='https://i0.wp.com/surgicalneurologyint.com/wp-content/uploads/2025/04/13497/SNI-16-130-g005.png?w=604&#038;ssl=1' data-recalc-dims="1" /></div><div class="col-xs-10 col"> <div class="figure-content"><h3>Figure 5:</h3><p>Relevant imaging for Case #2. The first column contains T1-weighted fat-suppressed magnetic resonance imaging (MRI) pre-treatment (top = sagittal, bottom = axial). The second column contains T1-weighted fat-suppressed MRI after her first surgery (top = sagittal, bottom = axial). The third column contains T1-weighted fat-suppressed MRI after her revision surgery (top = sagittal, bottom = axial). The fourth column contains sagittal X-rays before (top) and after (bottom) revision surgery. The last column contains the last dynamic contrast-enhanced-MRI (top = overlay, bottom = MR perfusion).</p></div> </div> </div> </div><div class="clearfix">&nbsp;</div><p>She underwent laminectomy and partial facetectomies of L3 bilaterally, debulking of L3 epidural tumor, L3 vertebroplasty, and L2–4 pedicle screw fixation with titanium instrumentation at an outside institution. Pathology confirmed the diagnosis of chordoma, with tumor cells positive for multiple cytokeratins and the brachyury gene. Cytokeratins AE1/AE3, CAM5.2, and Oscar were found to be diffusely positive in tumor cells. EMA stained positive, while S100 and human melanoma black 45 were focally positive.</p><p>At 3 months postoperative, an MRI lumbar spine demonstrated a persistent marrow placing lesion. At 6 months postoperative, she presented to our institution for evaluation. MRI lumbar spine revealed residual chordoma within the L3 vertebral body with increased right prevertebral extraosseous extension and bilateral L3–4 foraminal tumoral compression. The patient also experienced mechanical back pain, and a CT scan demonstrated loose hardware. On physical examination, she was neurologically intact, with 5/5 motor strength in all extremities.</p><p>Before the revision, KPS was 90. Revision surgery consisted of re-do decompression/epidural tumor debulking with L3 partial corpectomy and L3–5 instrumentation replacement with CFR-PEEK [<xref ref-type="table" rid="T2"> <a href='#T2'> Table 2 </a> </xref>]. Surgical time was 4.4 h, and estimated blood loss was 400 mL, with no intraoperative or postoperative complications. Pathology was consistent with chordoma. Immunohistochemistry was positive for AE1/ AE3, CAM5.2, EMA, S100, HMB45, and Oscar. The patient was discharged home on postoperative day 2 without any complications during her stay.</p><p>The patient then underwent postoperative SBRT, consisting of a cumulative dose of 40 Gy in 5 fractions using 2 VMAT arcs with 10 MV photons in an FFF mode targeting the L3 vertebra [<xref ref-type="fig" rid="F3"> <a href='#F3'> Figure 3 </a> </xref> and <xref ref-type="table" rid="T3"> <a href='#T3'> Table 3 </a> </xref>]. KPS grades pre- and post-radiation therapy were 90. At 18 months post-op, the patient was doing well overall with mild back pain rated 1 out of 10, not requiring medications. The patient elected for conservative measures. The latest MRI and CT imaging demonstrated additional delayed height loss of the L3 vertebral body, which is being followed with interval scans. Her KPS grade was 100. Perfusion sequences at 2, 5, 7, 12, and 18 months postoperative showed “cold” patterns compatible with no metabolic tumor activity.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="DISCUSSION">DISCUSSION</a></h3><div class="clearfix"></div><div class="hline"></div><h3 class = "title3">Overview of the management of mobile spine chordomas</h3><p>Mobile spine chordomas demonstrate a slow, indolent growth rate, often diagnosed at later stages, with patients remaining asymptomatic for a lengthy period.[<xref ref-type="bibr" rid="ref47"> <a href='#ref47'> 47 </a> </xref>] Despite their indolent presentation, chordomas have high rates of metastases and local recurrence.[<xref ref-type="bibr" rid="ref9"> <a href='#ref9'> 9 </a> </xref>] In one of the largest cohorts specific for mobile spine chordomas, a 50-year retrospective study with 52 patients found the overall rate of local recurrence to be 66%, with 75% of recurrences occurring an average of 30 months after excision and radiation.[<xref ref-type="bibr" rid="ref4"> <a href='#ref4'> 4 </a> </xref>]</p><p>Conventionally, chordomas have been thought of as radio- and chemo-resistant tumors that require aggressive surgical control.[<xref ref-type="bibr" rid="ref46"> <a href='#ref46'> 46 </a> </xref>] While <i>en bloc</i> resection with negative margins has been considered the definitive treatment for sacral chordomas,[<xref ref-type="bibr" rid="ref33"> <a href='#ref33'> 33 </a> </xref>] resection of mobile spine chordomas can be more challenging. Since these chordomas are located adjacent to vital structures in the axial skeleton, resection often risks damage to critical neurovascular elements, and anterior and lateral approaches can pose a risk of multiple access morbidity.</p><p>At present, gaps remain in the literature and consensus does not exist regarding the optimal strategy to manage patients with mobile spine chordomas. Debates remain in balancing aggressive surgical resections at the risk of sacrificing neurological function. In a retrospective study of 26 mobile spine chordoma patients who underwent surgical resection, 73% experienced complications, such as deep infection and neurological complications, with 35% requiring reoperation.[<xref ref-type="bibr" rid="ref20"> <a href='#ref20'> 20 </a> </xref>] In the same study, the authors concluded that <i>en bloc</i> resections resulted in better oncological outcomes compared to more debulking-type resections and without an increase in complications.</p><p>Meanwhile, in a multi-institutional study of 32 patients with mobile spine chordomas, Molina <i>et al</i>.[<xref ref-type="bibr" rid="ref29"> <a href='#ref29'> 29 </a> </xref>] showed that <i>en bloc</i> resection of C1–2, chordomas resulted in higher rates of complications and increased tumor recurrence compared to <i>en bloc</i> resection of subaxial cervical spine chordomas. This supports the need to explore additional methods to manage mobile spine chordoma patients with decreased surgical morbidity while maximizing oncological outcomes.</p><p>Furthermore, <i>en bloc</i> resection does not guarantee an R0 resection, and even if an R0 resection is achieved, there could still be microscopic residual disease. Over the years, studies have increasingly highlighted the importance of neoadjuvant or adjuvant high-dose radiotherapy for the management of spinal chordomas.[<xref ref-type="bibr" rid="ref34"> <a href='#ref34'> 34 </a> </xref>] Jin <i>et al</i>.[<xref ref-type="bibr" rid="ref17"> <a href='#ref17'> 17 </a> </xref>] performed a retrospective review of 35 mobile spine and sacral chordoma patients treated with definitive SBRT, intralesional gross-total resection, separation surgery, or <i>en bloc</i> resection. Patients who received high-dose SBRT had a higher 5-year local recurrence-free survival of 89.9% than those who did not undergo SBRT. Thus, even though conventional-dose radiotherapy has been ineffective in these patients, high-dose radiotherapy (SBRT) can help with local control.[<xref ref-type="bibr" rid="ref21"> <a href='#ref21'> 21 </a> </xref>]</p><p>Further studies have suggested coupling intralesional, gross-total resections or separation surgery with postoperative SBRT can be an alternative technique to <i>en bloc</i> resections. In a single-institution study of 12 patients with mobile spine chordomas, Lockney <i>et al</i>.[<xref ref-type="bibr" rid="ref24"> <a href='#ref24'> 24 </a> </xref>] showed those who underwent intralesional resection and SBRT as initial treatment had higher local control rates (80%) at the last follow-up compared to patients who only had initial surgical resection with SBRT at the time of recurrence (57.1%).</p><p>In a single institution study where 16 chordoma patients were treated with varying approaches, Akmansu <i>et al</i>.[<xref ref-type="bibr" rid="ref1"> <a href='#ref1'> 1 </a> </xref>] found subtotal or gross total resection of tumor or radiotherapy dose and techniques were not associated with recurrence. These authors concluded for patients with small or residual tumors, SBRT may be more beneficial.</p><h3 class = "title3">CFR-PEEK benefits over titanium for posttreatment monitoring and radiation effectiveness</h3><p>A key principle in radiation planning is to maximize the tumoricidal dose, or the biologically effective dose while minimizing damage to the surrounding tissues. Having clear visualization for radiation therapy planning is key for radiation oncology treatments, staging scans, and dosimetry protocols.</p><p>As spine surgeons have transitioned away from using traditional autografts, the prevalence of interbody device materials has grown.[<xref ref-type="bibr" rid="ref32"> <a href='#ref32'> 32 </a> </xref>] Two popular hardware materials currently used for pedicle screws, rods, and anterior column reconstruction are titanium and CFR-PEEK. The material and components used to create each construct are largely determined by patient pathology and surgeon experience. [<xref ref-type="bibr" rid="ref14"> <a href='#ref14'> 14 </a> </xref>] Titanium possesses high osseointegrative capacity and elastic modulus,[<xref ref-type="bibr" rid="ref32"> <a href='#ref32'> 32 </a> </xref>] but its radio-opaqueness causes it to generate artifacts on CT and MRI imaging.[<xref ref-type="bibr" rid="ref23"> <a href='#ref23'> 23 </a> </xref>] While titanium has previously been the gold standard, CFR-PEEK poses several unique advantages that enhance surgical outcomes.[<xref ref-type="bibr" rid="ref50"> <a href='#ref50'> 50 </a> </xref>]</p><p>Compared to traditional titanium implants, CFR-PEEK instrumentation provides a radiolucent biomaterial with similar clinical properties to the native spine.[<xref ref-type="bibr" rid="ref39"> <a href='#ref39'> 39 </a> </xref>] This provides a better evaluation of microscopic disease. As such, many studies have advocated for CFR-PEEK instrumentation for postoperative radiation planning in the management of spinal tumors.[<xref ref-type="bibr" rid="ref18"> <a href='#ref18'> 18 </a> </xref>,<xref ref-type="bibr" rid="ref22"> <a href='#ref22'> 22 </a> </xref>,<xref ref-type="bibr" rid="ref42"> <a href='#ref42'> 42 </a> </xref>]</p><p>Out of 1400 patients treated by the National Centre for Oncological Hadron Therapy with proton and carbon therapy, Mastella <i>et al</i>.[<xref ref-type="bibr" rid="ref25"> <a href='#ref25'> 25 </a> </xref>] found seven patients with CFR-PEEK implants, including three mobile spine chordomas. Compared to titanium implants, CFR-PEEK instrumentation was found to cause fewer dose perturbations, CT artifacts, and delineation uncertainties. Although this is not a one-to-one parallel since the patients illustrated in our case studies received photon therapy, the benefits of using CFR-PEEK are similar.</p><p>In a retrospective study of ten patients with spinal metastases who underwent postoperative photon therapy, Müller <i>et al</i>.[<xref ref-type="bibr" rid="ref31"> <a href='#ref31'> 31 </a> </xref>] compared CFR-PEEK to titanium implants for radiotherapy treatment planning. CFR-PEEK was found to cause fewer image artifacts and improved treatment plan quality for intensity modulated radiation therapy, although VMAT plan quality was similar.</p><p>In addition to enhanced visualization for adjuvant treatment, the use of CFR-PEEK instrumentation has demonstrated improved efficacy monitoring for local disease recurrence.[<xref ref-type="bibr" rid="ref48"> <a href='#ref48'> 48 </a> </xref>]</p><p>While beneficial for all primary and metastatic spine diseases, this may play a significant role in the management of chordoma due to high reported rates of local recurrence.[<xref ref-type="bibr" rid="ref13"> <a href='#ref13'> 13 </a> </xref>]</p><h3 class = "title3">Dosimetry for enhanced SBRT efficacy in chordoma treatment</h3><p>Proper dosing of adjuvant radiation therapy is key in chordoma management. Jin <i>et al</i>.[<xref ref-type="bibr" rid="ref17"> <a href='#ref17'> 17 </a> </xref>] demonstrated that patients with high-dose stereotactic radiosurgery had significantly improved 5-year survival compared to those who did not undergo the same treatment. High doses are preferred as chordomas have demonstrated radioresistance.[<xref ref-type="bibr" rid="ref52"> <a href='#ref52'> 52 </a> </xref>]</p><p>In a study completed by Chen <i>et al</i>.,[<xref ref-type="bibr" rid="ref6"> <a href='#ref6'> 6 </a> </xref>] 28 patients with spinal chordomas, including 24 with mobile spine chordomas, were treated with SBRT at a median dose of 4000 cGy in five fractions. Overall, the 2-year survival rate was 92%, and the 2-year local control rate was 96%. This again emphasizes the importance of high-dose hypofractionated SBRT as a tool for local control of these persistent tumors.</p><p>The tumor that is located too close to the spinal cord may indicate the need for proton therapy, as dosing to the spinal cord is one of the main complications of SBRT.[<xref ref-type="bibr" rid="ref19"> <a href='#ref19'> 19 </a> </xref>]</p><p>Although studies have found proton therapy to be advantageous to photon therapy due to the depth-dose characteristics of protons that allow for better sparing of normal tissues,[<xref ref-type="bibr" rid="ref28"> <a href='#ref28'> 28 </a> </xref>,<xref ref-type="bibr" rid="ref41"> <a href='#ref41'> 41 </a> </xref>] there exists limited data comparing the use of proton and photon therapies for mobile spine chordomas.</p><p>Yazici <i>et al</i>.[<xref ref-type="bibr" rid="ref53"> <a href='#ref53'> 53 </a> </xref>] evaluated the impact of spinal implants on dosimetry and concluded care should be taken during adjuvant radiotherapy to avoid implants and that anterior rod instrumentation had the largest impact on unintended spinal cord dosing. Given that proper dosimetry is key in successfully treating chordoma, and it can be impacted by tumor location and the presence of spinal implants, CFR-PEEK can be a valuable tool that allows for more accurate dosing.</p><h3 class = "title3">Multiparametric post-treatment monitoring</h3><p>Radiographic imaging for evaluating chordomas typically involves CT and MRI. On CT, these tumors have low density and may have cortical destruction.[<xref ref-type="bibr" rid="ref15"> <a href='#ref15'> 15 </a> </xref>,<xref ref-type="bibr" rid="ref27"> <a href='#ref27'> 27 </a> </xref>]</p><p>Santos <i>et al</i>.[<xref ref-type="bibr" rid="ref37"> <a href='#ref37'> 37 </a> </xref>] have investigated the limitations of conventional MRI and the advantages of DCE-MRI perfusion imaging in assessing chordoma treatment. They demonstrated that the indolent characteristics of this tumor challenge the monitoring of tumor progression with conventional MRI. In this regard, DCE-MRI perfusion studies provide more insights about underlying tumor vascularity and physiology, better evaluating posttreatment efficacy.</p><p>CFR-PEEK also allows for better disease monitoring. Titanium implants can cause artifacts, leading to an inability to use multiparametric studies reliably. These have shown MRI to be significantly affected by titanium materials.[<xref ref-type="bibr" rid="ref12"> <a href='#ref12'> 12 </a> </xref>] Recent studies suggest that with CFR-PEEK instrumentation, MRI provided similar benefits for treatment planning and monitoring as CT-myelography.[<xref ref-type="bibr" rid="ref49"> <a href='#ref49'> 49 </a> </xref>] Our case studies specifically highlight the strengths of DCE-MRI for multiparametric monitoring. Pre- and post-radiation therapy MRI perfusion can serve as a useful diagnostic modality, especially when patients have CFR-PEEK instrumentation in place.</p><h3 class = "title3">Limitations</h3><p>Optimal management approaches for spine chordomas are debated. Although surgical resection is a mainstay, it is more challenging to obtain negative margin resection in mobile spine chordomas, given the anatomic constraints.</p><p>The present study is limited by its patient volume and longitudinal follow-up; further work will be required to determine whether CFR-PEEK hardware significantly affects the morbidity and mortality of patients with mobile spinal chordomas. Although a small series, early follow-up demonstrates a lack of metabolic activity supporting ablative treatment of the chordoma. Ongoing surveillance with DCE-MRI will confirm absence of active chordoma disease. While many pros of CFR-PEEK instrumentation have been highlighted, other factors for consideration include the cost comparison of titanium versus CFR-PEEK implants.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="CONCLUSION">CONCLUSION</a></h3><div class="clearfix"></div><div class="hline"></div><p>Inherent anatomic differences between the sacrum and mobile spine lead to consequently distinct morbidity outlooks for the traditional <i>en bloc</i> resection dogma. This scenario propels separation surgery as an appealing surgical strategy for this location. With advances in SBRT and the ability to deliver an ablative dose, inducing tumor apoptosis/ necrosis, shifting prior paradigms of radiosensitivity. Hybrid therapy, integrating separation surgery and adjuvant SBRT, has recently demonstrated success in managing chordomas. This integrated approach may be a noteworthy advancement in the comprehensive care of mobile spine chordomas.</p><p></p><p></p><p></p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Ethical approval">Ethical approval</a></h3><div class="clearfix"></div><div class="hline"></div><p>The Institutional Review Board approval is obtained from the Ohio State University and approval number is: 2022C0198 dated 09/07/2023.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Declaration of patient consent">Declaration of patient consent</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors certify that they have obtained all appropriate patient consent.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Financial support and sponsorship">Financial support and sponsorship</a></h3><div class="clearfix"></div><div class="hline"></div><p>Nil.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Conflicts of interest">Conflicts of interest</a></h3><div class="clearfix"></div><div class="hline"></div><p>There are no conflicts of interest.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Use of artificial intelligence (AI)-assisted technology for manuscript preparation">Use of artificial intelligence (AI)-assisted technology for manuscript preparation</a></h3><div class="clearfix"></div><div class="hline"></div><p>The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.</p><h3 class="blogheading Main-Title"><a href="javascript:void(0);" name="Disclaimer">Disclaimer</a></h3><div class="clearfix"></div><div class="hline"></div><p>The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.</p></div> </div></div><div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"><h3 class="blogheading pull-left Main-Title col-lg-9 col-sm-8 col-xs-12"><a href="javascript:void(0);" name="Acknowledgments">Acknowledgments</a></h3><div class="clearfix"></div><div class="hline"></div><p>We would like to thank the patients highlighted in this series whose cases have benefitted neurosurgical research and education.</p></div> </div><div class="row"> <div class="blogparagraph col-lg-9 col-sm-8 col-xs-12"> <h3 class="blogheading pull-left Main-Title"><a name="References" href="javascript:void(0);">References</a></h3> <div class="clearfix"></div> <div class="hline"></div> <p><a href='javascript:void(0);' name='ref1' style='text-decoration: none;'>1.</a> Akmansu M, Kurt G, Demircan V, Senturk E. Results of chordoma patients treated by different approaches in a single institution. Turk Neurosurg. 2020. 30: 366-70</p><p><a href='javascript:void(0);' name='ref2' style='text-decoration: none;'>2.</a> Almefty K, Pravdenkova S, Colli BO, Al-Mefty O, Gokden M. Chordoma and chondrosarcoma: Similar, but quite different, skull base tumors. Cancer. 2007. 110: 2467-77</p><p><a href='javascript:void(0);' name='ref3' style='text-decoration: none;'>3.</a> Barzilai O, Amato MK, McLaughlin L, Reiner AS, Ogilvie SQ, Lis E. Hybrid surgery-radiosurgery therapy for metastatic epidural spinal cord compression: A prospective evaluation using patient-reported outcomes. Neurooncol Pract. 2018. 5: 104-13</p><p><a href='javascript:void(0);' name='ref4' style='text-decoration: none;'>4.</a> Boriani S, Bandiera S, Biagini R, Bacchini P, Boriani L, Cappuccio M. Chordoma of the mobile spine: Fifty years of experience. Spine (Phila Pa 1976). 2006. 31: 493-503</p><p><a href='javascript:void(0);' name='ref5' style='text-decoration: none;'>5.</a> Boriani S. En bloc resection in the spine: A procedure of surgical oncology. J Spine Surg. 2018. 4: 668-76</p><p><a href='javascript:void(0);' name='ref6' style='text-decoration: none;'>6.</a> Chen X, Lo SF, Bettegowda C, Ryan DM, Gross JM, Hu C. High-dose hypofractionated stereotactic body radiotherapy for spinal chordoma. J Neurosurg Spine. 2021. 35: 674-83</p><p><a href='javascript:void(0);' name='ref7' style='text-decoration: none;'>7.</a> Cofano F, Di Perna G, Monticelli M, Marengo N, Ajello M, Mammi M. Carbon fiber reinforced vs titanium implants for fixation in spinal metastases: A comparative clinical study about safety and effectiveness of the new “carbon-strategy. ” J Clin Neurosci. 2020. 75: 106-11</p><p><a href='javascript:void(0);' name='ref8' style='text-decoration: none;'>8.</a> Court C, Briand S, Mir O, Péchoux CL, Lazure T, Missenard G. Management of chordoma of the sacrum and mobile spine. Orthop Traumatol Surg Res. 2022. 108: 103169</p><p><a href='javascript:void(0);' name='ref9' style='text-decoration: none;'>9.</a> Delank KS, Kriegsmann J, Drees P, Eckardt A, Eysel P. Metastasizing chordoma of the lumbar spine. Eur Spine J. 2002. 11: 167-71</p><p><a href='javascript:void(0);' name='ref10' style='text-decoration: none;'>10.</a> Di Perna G, Cofano F, Mantovani C, Badellino S, Marengo N, Ajello M. Separation surgery for metastatic epidural spinal cord compression: A qualitative review. J Bone Oncol. 2020. 25: 100320</p><p><a href='javascript:void(0);' name='ref11' style='text-decoration: none;'>11.</a> Erdem E, Angtuaco EC, Van Hemert R, Park JS, Al-Mefty O. Comprehensive review of intracranial chordoma. Radiographics. 2003. 23: 995-1009</p><p><a href='javascript:void(0);' name='ref12' style='text-decoration: none;'>12.</a> Geibel MA, Gelißen B, Bracher AK, Rasche V. Artifact properties of dental ceramic and titanium implants in MRI. Rofo. 2019. 191: 433-41</p><p><a href='javascript:void(0);' name='ref13' style='text-decoration: none;'>13.</a> Hanna SA, Aston WJ, Briggs TW, Cannon SR, Saifuddin A. Sacral chordoma: Can local recurrence after sacrectomy be predicted?. Clin Orthop Relat Res. 2008. 466: 2217-23</p><p><a href='javascript:void(0);' name='ref14' style='text-decoration: none;'>14.</a> Herzog LN, Traven SA, Walton ZJ, Leddy LR. The use of carbon fiber implants for impending or existing pathologic fractures. J Orthop Trauma. 2022. 36: e260</p><p><a href='javascript:void(0);' name='ref15' style='text-decoration: none;'>15.</a> Hwang S, Hameed M, Kransdorf M. The 2020 World Health Organization classification of bone tumors: What radiologists should know. Skeletal Radiol. 2023. 52: 329-48</p><p><a href='javascript:void(0);' name='ref16' style='text-decoration: none;'>16.</a> Jawad MU, Scully SP. In brief: Classifications in brief: Enneking classification: Benign and malignant tumors of the musculoskeletal system. Clin Orthop Relat Res. 2010. 468: 2000-2</p><p><a href='javascript:void(0);' name='ref17' style='text-decoration: none;'>17.</a> Jin CJ, Berry-Candelario J, Reiner AS, Laufer I, Higginson DS, Schmitt AM. Long-term outcomes of high-dose single-fraction radiosurgery for chordomas of the spine and sacrum. J Neurosurg Spine. 2019. 32: 79-88</p><p><a href='javascript:void(0);' name='ref18' style='text-decoration: none;'>18.</a> Joerger AK, Seitz S, Lange N, Aftahy AK, Wagner A, Ryang YM. CFR-PEEK Pedicle screw instrumentation for spinal neoplasms: A single center experience on safety and efficacy. Cancers (Basel). 2022. 14: 5275</p><p><a href='javascript:void(0);' name='ref19' style='text-decoration: none;'>19.</a> Jung EW, Jung DL, Balagamwala EH, Angelov L, Suh JH, Djemil T. Single-fraction spine stereotactic body radiation therapy for the treatment of chordoma. Technol Cancer Res Treat. 2017. 16: 302-9</p><p><a href='javascript:void(0);' name='ref20' style='text-decoration: none;'>20.</a> Kolz JM, Wellings EP, Houdek MT, Clarke MJ, Yaszemski MJ, Rose PS. Surgical treatment of primary mobile spine chordoma. J Surg Oncol. 2021. 123: 1284-91</p><p><a href='javascript:void(0);' name='ref21' style='text-decoration: none;'>21.</a> Konieczkowski DJ, DeLaney TF, Yamada YJ. Radiation strategies for spine chordoma: Proton beam, carbon ions, and stereotactic body radiation therapy. Neurosurg Clin N Am. 2020. 31: 263-88</p><p><a href='javascript:void(0);' name='ref22' style='text-decoration: none;'>22.</a> Krätzig T, Mende KC, Mohme M, Kniep H, Dreimann M, Stangenberg M. Carbon fiber-reinforced PEEK versus titanium implants: An in vitro comparison of susceptibility artifacts in CT and MR imaging. Neurosurg Rev. 2021. 44: 2163-70</p><p><a href='javascript:void(0);' name='ref23' style='text-decoration: none;'>23.</a> Kumar N, Ramakrishnan SA, Lopez KG, Madhu S, Ramos MR, Fuh JY. Can polyether ether ketone dethrone titanium as the choice implant material for metastatic spine tumor surgery?. World Neurosurg. 2021. 148: 94-109</p><p><a href='javascript:void(0);' name='ref24' style='text-decoration: none;'>24.</a> Lockney DT, Shub T, Hopkins B, Lockney NA, Moussazadeh N, Lis E. Spinal stereotactic body radiotherapy following intralesional curettage with separation surgery for initial or salvage chordoma treatment. Neurosurg Focus. 2017. 42: E4</p><p><a href='javascript:void(0);' name='ref25' style='text-decoration: none;'>25.</a> Mastella E, Molinelli S, Magro G, Mirandola A, Russo S, Vai A. Dosimetric characterization of carbon fiber stabilization devices for post-operative particle therapy. Phys Med. 2017. 44: 18-25</p><p><a href='javascript:void(0);' name='ref26' style='text-decoration: none;'>26.</a> McMaster ML, Goldstein AM, Bromley CM, Ishibe N, Parry DM. Chordoma: Incidence and survival patterns in the United States 1973–1995. Cancer Causes Control. 2001. 12: 1-11</p><p><a href='javascript:void(0);' name='ref27' style='text-decoration: none;'>27.</a> Meyer JE, Lepke RA, Lindfors KK, Pagani JJ, Hirschy JC, Hayman LA. Chordomas: their CT appearance in the cervical, thoracic and lumbar spine. Radiology. 1984. 153: 693-6</p><p><a href='javascript:void(0);' name='ref28' style='text-decoration: none;'>28.</a> Mohan R, Grosshans D. Proton therapy-Present and future. Adv Drug Deliv Rev. 2017. 109: 26-44</p><p><a href='javascript:void(0);' name='ref29' style='text-decoration: none;'>29.</a> Molina CA, Ames CP, Chou D, Rhines LD, Hsieh PC, Zadnik PL. Outcomes following attempted en bloc resection of cervical chordomas in the C-1 and C-2 region versus the subaxial region: A multiinstitutional experience. J Neurosurg Spine. 2014. 21: 348-56</p><p><a href='javascript:void(0);' name='ref30' style='text-decoration: none;'>30.</a> Moussazadeh N, Laufer I, Yamada Y, Bilsky MH. Separation surgery for spinal metastases: Effect of spinal radiosurgery on surgical treatment goals. Cancer Control. 2014. 21: 168-74</p><p><a href='javascript:void(0);' name='ref31' style='text-decoration: none;'>31.</a> Müller BS, Ryang YM, Oechsner M, Düsberg M, Meyer B, Combs SE. The dosimetric impact of stabilizing spinal implants in radiotherapy treatment planning with protons and photons: Standard titanium alloy vs. radiolucent carbon-fiber-reinforced PEEK systems. J Appl Clin Med Phys. 2020. 21: 6-14</p><p><a href='javascript:void(0);' name='ref32' style='text-decoration: none;'>32.</a> Muthiah N, Yolcu YU, Alan N, Agarwal N, Hamilton DK, Ozpinar A. Evolution of polyetheretherketone (PEEK) and titanium interbody devices for spinal procedures: A comprehensive review of the literature. Eur Spine J. 2022. 31: 2547-56</p><p><a href='javascript:void(0);' name='ref33' style='text-decoration: none;'>33.</a> Ozturk AK, Gokaslan ZL, Wolinsky JP. Surgical treatment of sarcomas of the spine. Curr Treat Options Oncol. 2014. 15: 482-92</p><p><a href='javascript:void(0);' name='ref34' style='text-decoration: none;'>34.</a> Pennington Z, Ehresman J, McCarthy EF, Ahmed AK, Pittman PD, Lubelski D. Chordoma of the sacrum and mobile spine: A narrative review. Spine J. 2021. 21: 500-17</p><p><a href='javascript:void(0);' name='ref35' style='text-decoration: none;'>35.</a> Redmond KJ, Lo SS, Fisher C, Sahgal A. Postoperative stereotactic body radiation therapy (SBRT) for spine metastases: A critical review to guide practice. Int J Radiat Oncol Biol Phys. 2016. 95: 1414-28</p><p><a href='javascript:void(0);' name='ref36' style='text-decoration: none;'>36.</a> Riley DS, Barber MS, Kienle GS, Aronson JK, von SchoenAngerere T, Tugwellf P. CARE guidelines for case reports: Explanation and elaboration document. J Clin Epidemiol. 2017. 89: 218-35</p><p><a href='javascript:void(0);' name='ref37' style='text-decoration: none;'>37.</a> Santos P, Peck KK, Arevalo-Perez J, Karimi S, Lis E, Yamada Y. T1-Weighted dynamic contrast-enhanced MR perfusion imaging characterizes tumor response to radiation therapy in chordoma. AJNR Am J Neuroradiol. 2017. 38: 2210-6</p><p><a href='javascript:void(0);' name='ref38' style='text-decoration: none;'>38.</a> Shen FH, Gasbarrini A, Lui DF, Reynolds J, Capua J, Boriani S. Integrated custom composite polyetheretherketone/carbon fiber (PEEK/CF) vertebral body replacement (VBR) in the treatment of bone tumors of the spine: A preliminary report from a multicenter study. Spine. 2022. 47: 252</p><p><a href='javascript:void(0);' name='ref39' style='text-decoration: none;'>39.</a> Shi C, Lin H, Huang S, Xiong W, Hu L, Choi I. Comprehensive evaluation of carbon-fiber-reinforced polyetheretherketone (CFR-PEEK) spinal hardware for proton and photon planning. Technol Cancer Res Treat. 2022. 21: 15330338221091700</p><p><a href='javascript:void(0);' name='ref40' style='text-decoration: none;'>40.</a> Spratt DE, Beeler WH, de Moraes FY, Rhines LD, Gemmete JJ, Chaudhary N. An integrated multidisciplinary algorithm for the management of spinal metastases: An International Spine Oncology Consortium report. Lancet Oncol. 2017. 18: e720-30</p><p><a href='javascript:void(0);' name='ref41' style='text-decoration: none;'>41.</a> Suit H, DeLaney T, Goldberg S, Paganetti H, Clasie B, Gerweck L. Proton vs carbon ion beams in the definitive radiation treatment of cancer patients. Radiother Oncol. 2010. 95: 3-22</p><p><a href='javascript:void(0);' name='ref42' style='text-decoration: none;'>42.</a> Takayanagi A, Siddiqi I, Ghanchi H, Lischalk J, Vrionis F, Ratliff J. Radiolucent carbon fiber-reinforced implants for treatment of spinal tumors-clinical, radiographic, and dosimetric considerations. World Neurosurg. 2021. 152: 61-70</p><p><a href='javascript:void(0);' name='ref43' style='text-decoration: none;'>43.</a> Tauziéde-Espariat A, Bresson D, Polivka M, Bouazza S, Labrousse F, Aronica E. Prognostic and therapeutic markers in chordomas: A study of 287 tumors. J Neuropathol Exp Neurol. 2016. 75: 111-20</p><p><a href='javascript:void(0);' name='ref44' style='text-decoration: none;'>44.</a> Thureau S, Marchesi V, Vieillard MH, Perrier L, Lisbona A, Leheurteur M. Efficacy of extracranial stereotactic body radiation therapy (SBRT) added to standard treatment in patients with solid tumors (breast, prostate and non-small cell lung cancer) with up to 3 bone-only metastases: Study protocol for a randomised phase III trial (STEREO-OS). BMC Cancer. 2021. 21: 117</p><p><a href='javascript:void(0);' name='ref45' style='text-decoration: none;'>45.</a> Tian K, Wang L, Ma J, Wang K, Li D, Du J. MR Imaging grading system for skull base chordoma. AJNR Am J Neuroradiol. 2017. 38: 1206-11</p><p><a href='javascript:void(0);' name='ref46' style='text-decoration: none;'>46.</a> Ulici V, Hart J. A Review and differential diagnosis. Arch Pathol Lab Med. 2022. 146: 386-95</p><p><a href='javascript:void(0);' name='ref47' style='text-decoration: none;'>47.</a> Walcott BP, Nahed BV, Mohyeldin A, Coumans JV, Kahle KT, Ferreira MJ. Chordoma: Current concepts, management, and future directions. Lancet Oncol. 2012. 13: e69-76</p><p><a href='javascript:void(0);' name='ref48' style='text-decoration: none;'>48.</a> Ward J, Damante M, Wilson S, Coelho V, Franceschelli D, Elguindy AN. Impact of instrumentation material on local recurrence: A case-matched series using carbon fiber-PEEK vs. titanium. J Neurooncol. 2025. 171: 155-62</p><p><a href='javascript:void(0);' name='ref49' style='text-decoration: none;'>49.</a> Ward J, Damante M, Wilson S, Elguindy AN, Franceschelli D, Coelho Junior VP. Use of magnetic resonance imaging for postoperative radiation therapy planning in patients with carbon fiber-reinforced polyetheretherketone instrumentation. Pract Radiat Oncol. 2024. p. ???:S1879-8500(24)00296-0</p><p><a href='javascript:void(0);' name='ref50' style='text-decoration: none;'>50.</a> Ward J, Wilson S, Eaton RG, Coelho V, Xu DS, Chakravarthy VB. Emerging role of carbon fiber-reinforced polyetheretherketone instrumentation in spinal oncology: A systematic review. Adv Radiother Nucl Med. 2024. 2: 3130</p><p><a href='javascript:void(0);' name='ref51' style='text-decoration: none;'>51.</a> World Health Organization. Soft tissue and bone tumours. Available from: https://publications.iarc.fr/book-and-report-series/who-classification-of-tumours/soft-tissue-and-bone-tumours-2020 [Last accessed on 2023 Dec 27].</p><p><a href='javascript:void(0);' name='ref52' style='text-decoration: none;'>52.</a> Yamada Y, Gounder M, Laufer I. Multidisciplinary management of recurrent chordomas. Curr Treat Options Oncol. 2013. 14: 442-53</p><p><a href='javascript:void(0);' name='ref53' style='text-decoration: none;'>53.</a> Yazici G, Sari SY, Yedekci FY, Yucekul A, Birgi SD, Demirkiran G. The dosimetric impact of implants on the spinal cord dose during stereotactic body radiotherapy. Radiat Oncol. 2016. 11: 71</p><p><a href='javascript:void(0);' name='ref54' style='text-decoration: none;'>54.</a> York JE, Kaczaraj A, Abi-Said D, Fuller GN, Skibber JM, Janjan NA. Sacral chordoma: 40-year experience at a major cancer center. Neurosurgery. 1999. 44: 74-79 discussion 79-80</p><p><a href='javascript:void(0);' name='ref55' style='text-decoration: none;'>55.</a> Zuckerman SL, Bilsky MH, Laufer I. Chordomas of the skull base, mobile spine, and sacrum: An epidemiologic investigation of presentation, treatment, and survival. World Neurosurg. 2018. 113: e618-27</p></div> </div></div>
  8. Neural (re)organisation of language and memory: implications for neuroplasticity and cognition

    Thu, 10 Apr 2025 15:05:22 -0000

    Background

    In the presence of neurological insult, how language and memory networks jointly reorganise provides insights into mechanisms of neuroplasticity and can inform presurgical planning. As (re)organisation is often studied within a single cognitive modality, how language and memory interact during (re)organisation in response to epilepsy and the implications for memory outcomes is less clear. We investigated (1) the rates and patterns of joint (re)organisation and (2) their associations with pre- and postsurgical memory function.

    Methods

    Individuals with epilepsy (n=162) from three neurosurgical centres underwent the Wada procedure. We examined colateralisation patterns (ie, concordance/discordance) between language and both global and verbal memory (n=34), and associations with clinical characteristics and preoperative and postoperative memory outcomes.

    Results

    Overall concordance between language and memory colateralisation was minimal-to-weak across both global memory and verbal memory (kappa=0.28–0.44). Discordance was primarily observed in individuals with left-lateralised language, of whom 52% and 32% showed discordance in global and verbal memory, respectively. Discordance was most pronounced in left hemisphere epilepsy and mesial temporal sclerosis. Conversely, right-lateralised language consistently predicted right-lateralised memory (95%–100%), regardless of seizure laterality or memory type. While discordance was not associated with presurgical memory function, discordance predicted superior postsurgical memory outcomes following surgery in the language-dominant hemisphere (p<0.05; p 2=0.30).

    Conclusions

    When language dominance is atypical, memory tends to colateralise. However, when language remains typical, concordance with memory is weak, particularly for left hemisphere seizure onset. An interhemispheric shift in language may trigger a shift in memory, possibly to maintain efficient communication between medial temporal and neocortical language networks. In contrast, memory appears able to reorganise in isolation, with discordance predicting better postsurgical memory outcomes without detriment to presurgical function. Our findings support the continued need for separate presurgical mapping of language and memory lateralisation, particularly in the case of typical language dominance and left hemisphere seizures.

  9. “Where Are the Neurosurgeons?”: Reflections from the 79th United Nations General Assembly 

    Wed, 08 Jan 2025 21:16:00 -0000

    The week of September 24-30, 2024, marked the 79th United Nations General Assembly (UNGA), a gathering of representatives from the 193 United Nations (UN) member states at the Headquarters in New York City. Widely regarded as the most important week in the diplomatic calendar year, the UNGA is a unique opportunity to establish and advance […]
    <p>The week of September 24-30, 2024, marked the 79th United Nations General Assembly (UNGA), a gathering of representatives from the 193 United Nations (UN) member states at the Headquarters in New York City. Widely regarded as the most important week in the diplomatic calendar year, the UNGA is a unique opportunity to establish and advance international collaborations, promote high-level policy objectives and promote awareness of critical global issues.&nbsp;</p> <p>One such issue that has garnered particular interest in recent years is “global brain health,” a composite term signifying the summative burden of neurological and psychiatric symptoms throughout the world. In May 2022, the World Health Organization (WHO) released an <a href="https://www.who.int/publications/i/item/9789240076624" target="_blank" rel="noreferrer noopener">Intersectoral Global Action Plan (IGAP)</a> focusing specifically on epilepsy and other neurological disorders (1). While the IGAP outlines overarching objectives to achieve by 2031 and a series of proposed multi-level action items, it is abundantly clear that neurosurgical contributions are required to meet these goals – at both the grassroots and policy levels. Amidst growing interest in brain health, the term &#8220;<a href="https://pubmed.ncbi.nlm.nih.gov/33212057/" target="_blank" rel="noreferrer noopener">brain health diplomacy</a>&#8221; was coined, signifying intersectoral efforts to position brain health as a global public health priority (2).&nbsp;</p> <p>This year’s UNGA followed suit, with a concurrent science summit featuring three “Brain Days” and gathering leaders across diverse fields of brain health. The first of these comprised a brain economy summit that brought together various key stakeholders to evaluate financing solutions for brain health initiatives. The following two days focused on neuroscience and society. Attendees included experts in neuroscience, neurology, psychiatry, mental health, climate science, architecture, design and education, along with representatives from the pharmaceutical and finance sectors and a wide range of government officials. Yet, given the topic at hand, one glaring question arose: <strong><em>where were the neurosurgeons?</em></strong>&nbsp;</p> <p>This is not the first instance in which neurosurgeons have been underrepresented in high-level policy discussions. While some of this is attributable to field-specific demands and time constraints, the relative lack of neurosurgical perspectives in informing neurological policy and investment decisions is concerning. The annual global burden of neurosurgical cases requiring operations amounts to 13.8 million, per a <a href="https://thejns.org/view/journals/j-neurosurg/130/4/article-p1055.xml" target="_blank" rel="noreferrer noopener">2018 estimate</a> (3). Of these needed operations, 80% occur in low and middle-income countries (LMICs), underscoring an already egregious disparity in neurosurgical workforce allocation (3). Among the most salient issues are traumatic brain injuries, stroke-related conditions, tumors, hydrocephalus and epilepsy, all of which are key components of global brain health (3). These conditions often require neurosurgical solutions, and the people trained to provide such services have invaluable perspectives on the corresponding medical needs, resource scarcities and implementation issues.&nbsp;</p> <p>This year, the G4 Alliance, an international civil society organization formed to advocate for safe and affordable surgical, obstetric, trauma and anesthetic (SOTA) care, sent multiple representatives to the UNGA to advocate for neurosurgical inclusion in brain health diplomacy. These included neurosurgeons, policy advocates and the heads of independent civil organizations working as members of the G4 Alliance.&nbsp;</p> <p>Still, this is only a fraction of the neurosurgical representation required to drive sustainable global change. Next year’s high-level meeting of the UNGA will focus on the Prevention and Control of Noncommunicable Diseases (NCDs). This event represents a crucial opportunity for neurosurgeons to help shape the conversations that will set priorities and guide policymaking for UN member states. Though these conversations reach their highest level at the UNGA, brain health diplomacy requires year-round engagement to ensure that high-impact neurological conditions are prioritized and addressed. It is time for neurosurgeons to take their seats at the table.&nbsp;</p> <p><strong>References</strong></p> <ol start="1" class="wp-block-list"> <li>World Health Organization. (2022). Intersectoral global action plan on epilepsy and other neurological disorders (2022-2031).<a href="https://www.who.int/publications/i/item/9789240076624" target="_blank" rel="noreferrer noopener">https://www.who.int/publications/i/item/9789240076624</a>  </li> </ol> <ol start="2" class="wp-block-list"> <li>Dawson et al. Lancet Neurol. 2020 Dec;19(12):972-974. doi: 10.1016/S1474-4422(20)30358-6. PMID: 33212057 <a href="https://pubmed.ncbi.nlm.nih.gov/33212057/" target="_blank" rel="noreferrer noopener">https://pubmed.ncbi.nlm.nih.gov/33212057/</a>  </li> </ol> <ol start="3" class="wp-block-list"> <li>Dewan et al. Global neurosurgery: the current capacity and deficit in the provision of essential neurosurgical care. Executive Summary of the Global Neurosurgery Initiative at the Program in Global Surgery and Social Change. J Neurosurg. 2018 Apr 27;130(4):1055-1064. doi: 10.3171/2017.11.JNS171500. PMID: 29701548. <a href="https://thejns.org/view/journals/j-neurosurg/130/4/article-p1055.xml" target="_blank" rel="noreferrer noopener">https://thejns.org/view/journals/j-neurosurg/130/4/article-p1055.xml</a>  </li> </ol> <figure class="wp-block-gallery has-nested-images columns-default is-cropped wp-block-gallery-1 is-layout-flex wp-block-gallery-is-layout-flex"> <figure class="wp-block-image size-full"><img decoding="async" width="624" height="468" data-id="18667" src="https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga-2.jpg" alt="" class="wp-image-18667" srcset="https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga-2.jpg 624w, https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga-2-300x225.jpg 300w, https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga-2-560x420.jpg 560w, https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga-2-80x60.jpg 80w, https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga-2-265x198.jpg 265w" sizes="(max-width: 624px) 100vw, 624px" /></figure> </figure> <figure class="wp-block-gallery has-nested-images columns-default is-cropped wp-block-gallery-2 is-layout-flex wp-block-gallery-is-layout-flex"> <figure class="wp-block-image size-full"><img decoding="async" width="624" height="499" data-id="18668" src="https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga2.jpg" alt="" class="wp-image-18668" srcset="https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga2.jpg 624w, https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga2-300x240.jpg 300w, https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga2-525x420.jpg 525w" sizes="(max-width: 624px) 100vw, 624px" /></figure> <figure class="wp-block-image size-full"><img loading="lazy" decoding="async" width="624" height="769" data-id="18669" src="https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga3.jpg" alt="" class="wp-image-18669" srcset="https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga3.jpg 624w, https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga3-243x300.jpg 243w, https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga3-341x420.jpg 341w, https://aansneurosurgeon.org/wp-content/uploads/2025/01/unga3-324x400.jpg 324w" sizes="auto, (max-width: 624px) 100vw, 624px" /></figure> </figure>
  10. Cranial Nerve Dysfunction in Patients with an Occipital Condyle Fracture: Underdiagnosis and Clinical Relevance

    Tue, 26 Nov 2024 12:44:09 -0000

    Objectives This study aims to fill in the knowledge gap about patients with occipital condyle fractures (OCFs) and cranial nerve dysfunction (CND) and give advice about when to test the cranial nerves (CNs) and what to do when CND is diagnosed. Design A 14-year period observational, retrospective cohort study. Setting Level-I trauma center study. Participants All 119 surviving cases admitted with an OCF, whereof all 40 cases with either diagnosed CND (confirmed by clinical examination) or expected CND (reported observations high suspicious for CND) were selected for detailed data collection. Early death was the only exclusion criterion because of missing data and clinical irrelevance. Main Outcome Measures One-third of all surviving OCF patients have CND (n = 40/119, 33.6%), where three-quarters had more than one CN affected with a median of three CNs. Of the cases with a concomitant lateral skull base fracture (n = 24/40, 60%), one in three cases (36%, n = 13/36) had facial nerve palsy and nearly two in three cases (61%, n = 22/36) had hearing loss. Results The facial nerve was the most commonly diagnosed CND. Solitary OCF cases often had lower CND (n = 11/14). Fifty-eight percent of all CND cases with follow-up data (n = 19/33)—corresponding to one in six of all surviving OCF cases—had chronic CND sequelae. Conclusions Multiple and chronic CND is common in patients with an OCF. All CNs should be tested in those patients as soon as clinically possible, and testing should be repeated after 3 to 7 days and before discharge. Patients with CND should be counseled about their prognosis and be potentially referred to (e.g.) a speech and language therapist, ophthalmologist, neurologist, or otorhinolaryngologist for early treatment options.
    <p align="right">J Neurol Surg B Skull Base<br/>DOI: 10.1055/a-2461-5391</p><p> Objectives This study aims to fill in the knowledge gap about patients with occipital condyle fractures (OCFs) and cranial nerve dysfunction (CND) and give advice about when to test the cranial nerves (CNs) and what to do when CND is diagnosed. Design A 14-year period observational, retrospective cohort study. Setting Level-I trauma center study. Participants All 119 surviving cases admitted with an OCF, whereof all 40 cases with either diagnosed CND (confirmed by clinical examination) or expected CND (reported observations high suspicious for CND) were selected for detailed data collection. Early death was the only exclusion criterion because of missing data and clinical irrelevance. Main Outcome Measures One-third of all surviving OCF patients have CND (n = 40/119, 33.6%), where three-quarters had more than one CN affected with a median of three CNs. Of the cases with a concomitant lateral skull base fracture (n = 24/40, 60%), one in three cases (36%, n = 13/36) had facial nerve palsy and nearly two in three cases (61%, n = 22/36) had hearing loss. Results The facial nerve was the most commonly diagnosed CND. Solitary OCF cases often had lower CND (n = 11/14). Fifty-eight percent of all CND cases with follow-up data (n = 19/33)—corresponding to one in six of all surviving OCF cases—had chronic CND sequelae. Conclusions Multiple and chronic CND is common in patients with an OCF. All CNs should be tested in those patients as soon as clinically possible, and testing should be repeated after 3 to 7 days and before discharge. Patients with CND should be counseled about their prognosis and be potentially referred to (e.g.) a speech and language therapist, ophthalmologist, neurologist, or otorhinolaryngologist for early treatment options.<br/><a href="/DOI/DOI?10.1055/a-2461-5391">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000181">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/a-2461-5391">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/a-2461-5391">Full text</a></p>
  11. Intraorbital Retrobulbar Salivary Gland Choristoma: Presentation of a Unique Case and Review of the Literature

    Tue, 19 Nov 2024 12:46:52 -0000

    Background A choristoma is defined as the accumulation of normal tissue in an abnormal location. Salivary gland choristomas are a rare entity that is most frequently described in the middle ear. However, there are a few reported cases of salivary gland choristomas in other locations like the pituitary gland and the optic nerve dural sheath. To the best of our knowledge, we present the first case of a patient with an intraconal salivary gland choristoma. A brief but comprehensive review of literature is offered, additionally. Methods A 19-year-old male patient presented with disturbance of ocular motility, ptosis, and exophthalmos of the right eye. The subsequent imaging by magnetic resonance imaging (MRI) demonstrated an intraconal lesion that infiltrated the lateral and medial rectal muscles of the right eye. The lesion showed intensive gadolinium enhancement in T1-weighted sequence and the fluid-attenuated inversion recovery (FLAIR) sequence showed no intracranial edema. The interdisciplinary neuro-oncologic tumor board recommended a biopsy and partial removal of the lesion. Results Partial resection of the choristoma was successfully performed via lateral orbitotomy. No new neurologic or visual deficits occurred postoperatively. During the 2-week follow-up examination, the exophthalmos had completely regressed and the patient only reported a slight retrobulbar pressure sensation. The histopathologic examination of the tissue revealed seromucous glandular tissue. Conclusion Salivary gland choristomas have been occasionally described intracranially before, but this is the first case of an intraconal accumulation of salivary gland tissue. Partial resection was achieved, resulting in complete recovery of the ophthalmologic symptoms.
    <p align="right">J Neurol Surg A Cent Eur Neurosurg<br/>DOI: 10.1055/s-0044-1791974</p><p> Background A choristoma is defined as the accumulation of normal tissue in an abnormal location. Salivary gland choristomas are a rare entity that is most frequently described in the middle ear. However, there are a few reported cases of salivary gland choristomas in other locations like the pituitary gland and the optic nerve dural sheath. To the best of our knowledge, we present the first case of a patient with an intraconal salivary gland choristoma. A brief but comprehensive review of literature is offered, additionally. Methods A 19-year-old male patient presented with disturbance of ocular motility, ptosis, and exophthalmos of the right eye. The subsequent imaging by magnetic resonance imaging (MRI) demonstrated an intraconal lesion that infiltrated the lateral and medial rectal muscles of the right eye. The lesion showed intensive gadolinium enhancement in T1-weighted sequence and the fluid-attenuated inversion recovery (FLAIR) sequence showed no intracranial edema. The interdisciplinary neuro-oncologic tumor board recommended a biopsy and partial removal of the lesion. Results Partial resection of the choristoma was successfully performed via lateral orbitotomy. No new neurologic or visual deficits occurred postoperatively. During the 2-week follow-up examination, the exophthalmos had completely regressed and the patient only reported a slight retrobulbar pressure sensation. The histopathologic examination of the tissue revealed seromucous glandular tissue. Conclusion Salivary gland choristomas have been occasionally described intracranially before, but this is the first case of an intraconal accumulation of salivary gland tissue. Partial resection was achieved, resulting in complete recovery of the ophthalmologic symptoms.<br/><a href="/DOI/DOI?10.1055/s-0044-1791974">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000180">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1791974">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1791974">Full text</a></p>
  12. Sinonasal Plasmablastic Lymphoma: A Systematic Review

    Wed, 13 Nov 2024 13:39:22 -0000

    Objective Plasmablastic lymphoma (PBL) is a type of non-Hodgkin's B-cell lymphoma associated with human immunodeficiency virus and Epstein–Barr virus, commonly located in the oral cavity or gastrointestinal tract. Sinonasal involvement is rare, and there is no consensus on treatment. Data Sources Peer-reviewed published articles served as data sources. Review Methods A systematic review was conducted of the PubMed database for all cases of sinonasal PBL between 1978 and 2023 with the phrase “plasmablastic lymphoma.” Studies not written in English and that did not separate individual cases of sinonasal PBL from aggregated data were excluded. Age, sex, immune status, treatment, and outcomes were collected. Conclusion PBL is a rare malignancy in the sinonasal region usually treated with chemotherapy. It most commonly occurs in immunocompromised adults but has also been diagnosed in immunocompromised children and in immunocompetent adults. It is aggressive and has a poor prognosis. Implications for Practice PBL is a recently described entity with few cases of the sinonasal anatomic variant in the literature. Sinonasal PBL was most frequently treated with chemotherapy alone, closely followed by chemoradiation. The most common chemotherapy regimen utilized in the literature is cyclophosphamide, doxorubicin, oncovin/vincristine, and prednisone, which is also the most common chemotherapy regimen in nonsinonasal PBL. A second commonly used regimen is cyclophosphamide, vincristine/oncovin, doxorubicin/adriamycin, and dexamethasone. However, no treatment has emerged as superior to others with regard to survival. Further data are needed to better understand this rare disease.
    <p align="right">J Neurol Surg Rep 2024; 85: e167-e177<br/>DOI: 10.1055/a-2444-3438</p><p> Objective Plasmablastic lymphoma (PBL) is a type of non-Hodgkin's B-cell lymphoma associated with human immunodeficiency virus and Epstein–Barr virus, commonly located in the oral cavity or gastrointestinal tract. Sinonasal involvement is rare, and there is no consensus on treatment. Data Sources Peer-reviewed published articles served as data sources. Review Methods A systematic review was conducted of the PubMed database for all cases of sinonasal PBL between 1978 and 2023 with the phrase “plasmablastic lymphoma.” Studies not written in English and that did not separate individual cases of sinonasal PBL from aggregated data were excluded. Age, sex, immune status, treatment, and outcomes were collected. Conclusion PBL is a rare malignancy in the sinonasal region usually treated with chemotherapy. It most commonly occurs in immunocompromised adults but has also been diagnosed in immunocompromised children and in immunocompetent adults. It is aggressive and has a poor prognosis. Implications for Practice PBL is a recently described entity with few cases of the sinonasal anatomic variant in the literature. Sinonasal PBL was most frequently treated with chemotherapy alone, closely followed by chemoradiation. The most common chemotherapy regimen utilized in the literature is cyclophosphamide, doxorubicin, oncovin/vincristine, and prednisone, which is also the most common chemotherapy regimen in nonsinonasal PBL. A second commonly used regimen is cyclophosphamide, vincristine/oncovin, doxorubicin/adriamycin, and dexamethasone. However, no treatment has emerged as superior to others with regard to survival. Further data are needed to better understand this rare disease.<br/><a href="/DOI/DOI?10.1055/a-2444-3438">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/10.1055/s-014-60399">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/a-2444-3438">Abstract</a>  |  <span style="font-weight: bold; color: #ff0000;">open access</span> <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/a-2444-3438">Full text</a></p>
  13. Current Applications of the Three-Dimensional Printing Technology in Neurosurgery: A Review

    Wed, 16 Oct 2024 13:18:02 -0000

    Background In the recent years, three-dimensional (3D) printing technology has emerged as a transformative tool, particularly in health care, offering unprecedented possibilities in neurosurgery. This review explores the diverse applications of 3D printing in neurosurgery, assessing its impact on precision, customization, surgical planning, and education. Methods A literature review was conducted using PubMed, Web of Science, Embase, and Scopus, identifying 84 relevant articles. These were categorized into spine applications, neurovascular applications, neuro-oncology applications, neuroendoscopy applications, cranioplasty applications, and modulation/stimulation applications. Results 3D printing applications in spine surgery showcased advancements in guide devices, prosthetics, and neurosurgical planning, with patient-specific models enhancing precision and minimizing complications. Neurovascular applications demonstrated the utility of 3D-printed guide devices in intracranial hemorrhage and enhanced surgical planning for cerebrovascular diseases. Neuro-oncology applications highlighted the role of 3D printing in guide devices for tumor surgery and improved surgical planning through realistic models. Neuroendoscopy applications emphasized the benefits of 3D-printed guide devices, anatomical models, and educational tools. Cranioplasty applications showed promising outcomes in patient-specific implants, addressing biomechanical considerations. Discussion The integration of 3D printing into neurosurgery has significantly advanced precision, customization, and surgical planning. Challenges include standardization, material considerations, and ethical issues. Future directions involve integrating artificial intelligence, multimodal imaging fusion, biofabrication, and global collaboration. Conclusion 3D printing has revolutionized neurosurgery, offering tailored solutions, enhanced surgical planning, and invaluable educational tools. Addressing challenges and exploring future innovations will further solidify the transformative impact of 3D printing in neurosurgical care. This review serves as a comprehensive guide for researchers, clinicians, and policymakers navigating the dynamic landscape of 3D printing in neurosurgery.
    <p align="right">J Neurol Surg A Cent Eur Neurosurg<br/>DOI: 10.1055/a-2389-5207</p><p> Background In the recent years, three-dimensional (3D) printing technology has emerged as a transformative tool, particularly in health care, offering unprecedented possibilities in neurosurgery. This review explores the diverse applications of 3D printing in neurosurgery, assessing its impact on precision, customization, surgical planning, and education. Methods A literature review was conducted using PubMed, Web of Science, Embase, and Scopus, identifying 84 relevant articles. These were categorized into spine applications, neurovascular applications, neuro-oncology applications, neuroendoscopy applications, cranioplasty applications, and modulation/stimulation applications. Results 3D printing applications in spine surgery showcased advancements in guide devices, prosthetics, and neurosurgical planning, with patient-specific models enhancing precision and minimizing complications. Neurovascular applications demonstrated the utility of 3D-printed guide devices in intracranial hemorrhage and enhanced surgical planning for cerebrovascular diseases. Neuro-oncology applications highlighted the role of 3D printing in guide devices for tumor surgery and improved surgical planning through realistic models. Neuroendoscopy applications emphasized the benefits of 3D-printed guide devices, anatomical models, and educational tools. Cranioplasty applications showed promising outcomes in patient-specific implants, addressing biomechanical considerations. Discussion The integration of 3D printing into neurosurgery has significantly advanced precision, customization, and surgical planning. Challenges include standardization, material considerations, and ethical issues. Future directions involve integrating artificial intelligence, multimodal imaging fusion, biofabrication, and global collaboration. Conclusion 3D printing has revolutionized neurosurgery, offering tailored solutions, enhanced surgical planning, and invaluable educational tools. Addressing challenges and exploring future innovations will further solidify the transformative impact of 3D printing in neurosurgical care. This review serves as a comprehensive guide for researchers, clinicians, and policymakers navigating the dynamic landscape of 3D printing in neurosurgery.<br/><a href="/DOI/DOI?10.1055/a-2389-5207">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000180">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/a-2389-5207">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/a-2389-5207">Full text</a></p>
  14. The Role of Electroencephalography in Children with Acute Altered Mental Status of Unknown Etiology: A Prospective Study

    Wed, 04 Sep 2024 06:42:42 -0000

    Introduction Acute altered mental status (AAMS) is often a challenge for clinicians, since the underlying etiologies cannot always easily be inferred based on the patient's clinical presentation, medical history, or early examinations. The aim of this study is to evaluate the role of electroencephalogram (EEG) as a diagnostic tool in AAMS of unknown etiology in children. Materials and Methods We conducted a prospective study involving EEG assessments on children presenting with AAMS between May 2017 and October 2019. Inclusion criteria were age 1 month to 18 years and acute (<1 week) and persistent (>5 minutes) altered mental status. Patients with a known etiology of AAMS were excluded. A literature review was also performed. Results Twenty patients (median age: 7.7 years, range: 0.5–15.4) were enrolled. EEG contributed to the diagnosis in 14/20 cases, and was classified as diagnostic in 9/20 and informative in 5/20. Specifically, EEG was able to identify nonconvulsive status epilepticus (NCSE) in five children and psychogenic events in four. EEG proved to be a poorly informative diagnostic tool at AAMS onset in six children; however, in five of them, it proved useful during follow-up. Conclusions Limited data exist regarding the role of EEG in children with AAMS of unknown etiology. In our population, EEG proved to be valuable tool, and was especially useful in the prompt identification of NCSE and psychogenic events.
    <p align="right">Neuropediatrics<br/>DOI: 10.1055/a-2380-6743</p><p> Introduction Acute altered mental status (AAMS) is often a challenge for clinicians, since the underlying etiologies cannot always easily be inferred based on the patient's clinical presentation, medical history, or early examinations. The aim of this study is to evaluate the role of electroencephalogram (EEG) as a diagnostic tool in AAMS of unknown etiology in children. Materials and Methods We conducted a prospective study involving EEG assessments on children presenting with AAMS between May 2017 and October 2019. Inclusion criteria were age 1 month to 18 years and acute (&lt;1 week) and persistent (&gt;5 minutes) altered mental status. Patients with a known etiology of AAMS were excluded. A literature review was also performed. Results Twenty patients (median age: 7.7 years, range: 0.5–15.4) were enrolled. EEG contributed to the diagnosis in 14/20 cases, and was classified as diagnostic in 9/20 and informative in 5/20. Specifically, EEG was able to identify nonconvulsive status epilepticus (NCSE) in five children and psychogenic events in four. EEG proved to be a poorly informative diagnostic tool at AAMS onset in six children; however, in five of them, it proved useful during follow-up. Conclusions Limited data exist regarding the role of EEG in children with AAMS of unknown etiology. In our population, EEG proved to be valuable tool, and was especially useful in the prompt identification of NCSE and psychogenic events.<br/><a href="/DOI/DOI?10.1055/a-2380-6743">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000041">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/a-2380-6743">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/a-2380-6743">Full text</a></p>
  15. Deskeletonizing the Sigmoid Sinus Is Noncompulsory in Skull Base Surgery: 3D Modeling of the Translabyrinthine Approach

    Wed, 21 Aug 2024 12:45:44 -0000

    Objectives Sigmoid sinus (SS) compression and injury is associated with postoperative SS occlusion and corresponding morbidity. Leaving the SS skeletonized with a thin boney protection during surgery might be favorable. This study quantifies the effect of the SS position on the operative exposure in the translabyrinthine approach and assesses the feasibility of retracting a skeletonized SS. Methods Twelve translabyrinthine approaches were performed on cadaveric heads with varying SS retraction: skeletonized stationary (TL-S), skeletonized posterior retraction (TL-R), and deskeletonized collapsing of the sinus (TL-C). High-definition three-dimensional reconstruction of the resection cavity was obtained. The primary outcome, “surgical freedom” (mm2), was the area at the level of the craniotomy from which the internal acoustic porus could be reached in an unobstructed straight line. Secondary outcomes include the “exposure angle,” “angle of attack,” and presigmoid depth. Results During TL-R, surgical freedom increased by a mean of 41% (range: 9–92%, standard deviation [SD]: 28) when compared to no retraction (TL-S). Collapsing the SS in TL-C provided a mean increase of 52% (range: 19–95%, SD: 22) compared to TL-S. In most cases, the exposure is the greatest when the SS is collapsed. In 40% of the specimens, the provided exposure while retracting (TL-R) instead of collapsing (TL-S) the sinus is equal or greater than 50% of other specimens in which the sinus is collapsed. Conclusion In cases with favorable anatomy, a translabyrinthine resection in which the skeletonized SS is retracted provides comparably sufficient exposure for adequate and safe tumor resection.
    <p align="right">J Neurol Surg B Skull Base<br/>DOI: 10.1055/a-2375-7912</p><p> Objectives Sigmoid sinus (SS) compression and injury is associated with postoperative SS occlusion and corresponding morbidity. Leaving the SS skeletonized with a thin boney protection during surgery might be favorable. This study quantifies the effect of the SS position on the operative exposure in the translabyrinthine approach and assesses the feasibility of retracting a skeletonized SS. Methods Twelve translabyrinthine approaches were performed on cadaveric heads with varying SS retraction: skeletonized stationary (TL-S), skeletonized posterior retraction (TL-R), and deskeletonized collapsing of the sinus (TL-C). High-definition three-dimensional reconstruction of the resection cavity was obtained. The primary outcome, “surgical freedom” (mm2), was the area at the level of the craniotomy from which the internal acoustic porus could be reached in an unobstructed straight line. Secondary outcomes include the “exposure angle,” “angle of attack,” and presigmoid depth. Results During TL-R, surgical freedom increased by a mean of 41% (range: 9–92%, standard deviation [SD]: 28) when compared to no retraction (TL-S). Collapsing the SS in TL-C provided a mean increase of 52% (range: 19–95%, SD: 22) compared to TL-S. In most cases, the exposure is the greatest when the SS is collapsed. In 40% of the specimens, the provided exposure while retracting (TL-R) instead of collapsing (TL-S) the sinus is equal or greater than 50% of other specimens in which the sinus is collapsed. Conclusion In cases with favorable anatomy, a translabyrinthine resection in which the skeletonized SS is retracted provides comparably sufficient exposure for adequate and safe tumor resection.<br/><a href="/DOI/DOI?10.1055/a-2375-7912">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000181">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/a-2375-7912">Abstract</a>  |  <span style="font-weight: bold; color: #ff0000;">open access</span> <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/a-2375-7912">Full text</a></p>
  16. Comparison of Sitting versus Nonsitting Position for the Resection of Brain Metastases in the Posterior Fossa in a Contemporary Cohort

    Tue, 20 Aug 2024 14:12:38 -0000

    Background For surgery of brain metastases, good immediate postoperative functional outcome is of utmost importance. Improved functional status can enable further oncologic therapies and adverse events might delay them. Pros and cons of either sitting or prone positioning for resective surgery of the posterior fossa are debated, but contemporary data on direct postoperative outcome are rare. The aim of our study was to compare the functional outcome and adverse events of surgery for brain metastases in the sitting versus the nonsitting position in the direct postoperative setting. Methods We retrospectively compared surgery of metastases located in the posterior fossa over a 3-year period in two level-A neurosurgical centers. Center 1 performed surgery exclusively in the sitting, while center 2 performed surgery only in the nonsitting position. Results Worse functional outcome (Karnofsky performance scale) and functional deterioration were seen in the “sitting” group. We found significantly more “sitting” patients to deteriorate to a KPS score of ≤60%. In this study, treating patients with brain metastases in the sitting position resulted in a number needed to harm (NNH) of 2.3 and was associated with worse outcome and more adverse events. Conclusion Therefore, we recommend the nonsitting position for surgery of brain metastases of the posterior fossa.
    <p align="right">J Neurol Surg A Cent Eur Neurosurg<br/>DOI: 10.1055/s-0044-1788620</p><p> Background For surgery of brain metastases, good immediate postoperative functional outcome is of utmost importance. Improved functional status can enable further oncologic therapies and adverse events might delay them. Pros and cons of either sitting or prone positioning for resective surgery of the posterior fossa are debated, but contemporary data on direct postoperative outcome are rare. The aim of our study was to compare the functional outcome and adverse events of surgery for brain metastases in the sitting versus the nonsitting position in the direct postoperative setting. Methods We retrospectively compared surgery of metastases located in the posterior fossa over a 3-year period in two level-A neurosurgical centers. Center 1 performed surgery exclusively in the sitting, while center 2 performed surgery only in the nonsitting position. Results Worse functional outcome (Karnofsky performance scale) and functional deterioration were seen in the “sitting” group. We found significantly more “sitting” patients to deteriorate to a KPS score of ≤60%. In this study, treating patients with brain metastases in the sitting position resulted in a number needed to harm (NNH) of 2.3 and was associated with worse outcome and more adverse events. Conclusion Therefore, we recommend the nonsitting position for surgery of brain metastases of the posterior fossa.<br/><a href="/DOI/DOI?10.1055/s-0044-1788620">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000180">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1788620">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1788620">Full text</a></p>
  17. Surgical Management of Ipsilateral Internal Carotid Artery Stenosis and Unruptured Intracranial Aneurysm: Case Review and Treatment Considerations

    Tue, 20 Aug 2024 06:13:26 -0000

    Introduction The coexistence of carotid artery stenosis and a concomitant downstream ipsilateral unruptured intracranial aneurysm requires unique treatment considerations to balance the risk of thromboembolic complications from carotid artery stenosis and the risk of subarachnoid hemorrhage from intracranial aneurysm rupture. These considerations include the selection of optimal treatment modalities, the order and timing of interventions, and potential management of antiplatelet agents with endovascular approaches. We present strategies to optimize treatment in such a case. Case Report We discuss the case of a 69-year-old woman with 90% stenosis of the right internal carotid artery and an ipsilateral, wide-necked, 4.8-mm, irregular-appearing right A1–2 junction aneurysm with an associated daughter sac. Open, endovascular, and mixed treatment strategies were considered. The patient selected and underwent a staged, open treatment approach with a carotid endarterectomy followed by a right craniotomy for microsurgical clipping of the aneurysm 5 days later. Both procedures were performed on daily full-dose aspirin without complications. On follow-up, the right carotid artery was widely patent, the aneurysm was secured, and the patient remained at her neurologic baseline. Discussion The presented strategy for ipsilateral carotid artery stenosis and an unruptured intracranial aneurysm initially optimized cerebral perfusion to mitigate ischemic risks while permitting timely aneurysm intervention without a need for dual antiplatelet therapy or to traverse an earlier procedure site.
    <p align="right">J Neurol Surg Rep 2024; 85: e128-e131<br/>DOI: 10.1055/a-2377-8490</p><p> Introduction The coexistence of carotid artery stenosis and a concomitant downstream ipsilateral unruptured intracranial aneurysm requires unique treatment considerations to balance the risk of thromboembolic complications from carotid artery stenosis and the risk of subarachnoid hemorrhage from intracranial aneurysm rupture. These considerations include the selection of optimal treatment modalities, the order and timing of interventions, and potential management of antiplatelet agents with endovascular approaches. We present strategies to optimize treatment in such a case. Case Report We discuss the case of a 69-year-old woman with 90% stenosis of the right internal carotid artery and an ipsilateral, wide-necked, 4.8-mm, irregular-appearing right A1–2 junction aneurysm with an associated daughter sac. Open, endovascular, and mixed treatment strategies were considered. The patient selected and underwent a staged, open treatment approach with a carotid endarterectomy followed by a right craniotomy for microsurgical clipping of the aneurysm 5 days later. Both procedures were performed on daily full-dose aspirin without complications. On follow-up, the right carotid artery was widely patent, the aneurysm was secured, and the patient remained at her neurologic baseline. Discussion The presented strategy for ipsilateral carotid artery stenosis and an unruptured intracranial aneurysm initially optimized cerebral perfusion to mitigate ischemic risks while permitting timely aneurysm intervention without a need for dual antiplatelet therapy or to traverse an earlier procedure site.<br/><a href="/DOI/DOI?10.1055/a-2377-8490">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/10.1055/s-014-59895">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/a-2377-8490">Abstract</a>  |  <span style="font-weight: bold; color: #ff0000;">open access</span> <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/a-2377-8490">Full text</a></p>
  18. Labyrinthectomy Improves Dizziness in Patients with Vestibular Schwannoma

    Wed, 24 Jul 2024 06:28:27 -0000

    Objective Dizziness is one of the most prevalent and debilitating symptoms associated with vestibular schwannoma (VS), and there are little data on contributing or alleviating factors in the perioperative setting. In this study, we aimed to evaluate whether vestibular nerve sectioning or labyrinthectomy concomitant with surgical resection would improve dizziness in the postoperative period. Methods This is a retrospective study of a consecutive series of VS patients who underwent resection at a large tertiary care center between 2009 and 2023. Dizziness at 6 months was the primary endpoint, whereas facial nerve and hearing outcomes were secondary endpoints. Fisher's exact test was used to identify significant differences between categorical variables, and multivariate logistic regression analysis was performed to identify predictors of dizziness as well as facial nerve and hearing outcomes. Results A total of 333 patients underwent resection of VS at our institution. There was no significant difference in binary reported dizziness based on surgical approach (p = 0.14). However, patients reported significantly less dizziness at discharge (p < 0.01) as well as 6-month (p = 0.02) and 1-year (p < 0.01) follow-up in the translabyrinthine group. On the other hand, patients who underwent labyrinth-sparing approaches reported a significant increase in dizziness that remained up to 1 year from the time of surgery. Conclusions Our data suggest that labyrinthectomy may improve dizziness symptoms in patients with VS. Selective VN sectioning does not appear to affect dizziness or hearing outcomes. Finally, surgical approach does not affect facial nerve outcomes.
    <p align="right">J Neurol Surg B Skull Base<br/>DOI: 10.1055/a-2360-9474</p><p> Objective Dizziness is one of the most prevalent and debilitating symptoms associated with vestibular schwannoma (VS), and there are little data on contributing or alleviating factors in the perioperative setting. In this study, we aimed to evaluate whether vestibular nerve sectioning or labyrinthectomy concomitant with surgical resection would improve dizziness in the postoperative period. Methods This is a retrospective study of a consecutive series of VS patients who underwent resection at a large tertiary care center between 2009 and 2023. Dizziness at 6 months was the primary endpoint, whereas facial nerve and hearing outcomes were secondary endpoints. Fisher's exact test was used to identify significant differences between categorical variables, and multivariate logistic regression analysis was performed to identify predictors of dizziness as well as facial nerve and hearing outcomes. Results A total of 333 patients underwent resection of VS at our institution. There was no significant difference in binary reported dizziness based on surgical approach (p = 0.14). However, patients reported significantly less dizziness at discharge (p &lt; 0.01) as well as 6-month (p = 0.02) and 1-year (p &lt; 0.01) follow-up in the translabyrinthine group. On the other hand, patients who underwent labyrinth-sparing approaches reported a significant increase in dizziness that remained up to 1 year from the time of surgery. Conclusions Our data suggest that labyrinthectomy may improve dizziness symptoms in patients with VS. Selective VN sectioning does not appear to affect dizziness or hearing outcomes. Finally, surgical approach does not affect facial nerve outcomes.<br/><a href="/DOI/DOI?10.1055/a-2360-9474">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000181">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/a-2360-9474">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/a-2360-9474">Full text</a></p>
  19. Understanding the role of surgical intervention for patients with concomitant degenerative spinal disease without deformity and Parkinson’s disease: a meta-analysis

    Mon, 22 Jul 2024 11:21:56 -0000

    .
  20. The Evolution of Skull Base Surgery: A Bibliometric Analysis Spanning Nearly 125 Years

    Mon, 22 Jul 2024 07:41:15 -0000

    Introduction Skull base surgery has evolved from fundamental elements into a distinct multidisciplinary specialty. Using bibliometrics, we appraised the literature pertaining to skull base surgery since 1900 and studied the emergence of the specialty as a scholarly field. Methods We queried Web of Science for all content from past presidents of the North American Skull Base Society (N = 31) and their self-identified forebears, influences, contemporaries, and trainees (N = 115). Statistical and bibliometric analyses were performed using various Python packages on article metadata. Results Our query returned 28,167 articles. The most pertinent works (N = 15,529), identified algorithmically through an analysis of terms in titles, were published between 1900 and 2024 by 15,286 authors. The field exploded in the latter half of the 20th century, concurrently with increased interdisciplinary and international collaboration, and contemporaneously with the formation of centers of excellence and influential societies. Since 1950, prolific contributors to the field from neurosurgery, otolaryngology, radiology/radiation oncology, plastic surgery, and ophthalmology have increasingly subspecialized in skull base topics. The proportion of female authors in the corpus has grown from <1% in 1980 to 17% in 2023. We identify the articles that comprise the historical roots of modern skull base surgery, map the emergence of fundamental terminology within the corpus, and identify the authors who stand as key nodes of collaboration and influence. Conclusion The field of skull base surgery was born from pioneering individuals with training in varied disciplines. The coalescence of skull base surgery into a distinct and diversified subspecialty has been powered by dedicated collaborative efforts on a global scale.
    <p align="right">J Neurol Surg B Skull Base<br/>DOI: 10.1055/s-0044-1788636</p><p> Introduction Skull base surgery has evolved from fundamental elements into a distinct multidisciplinary specialty. Using bibliometrics, we appraised the literature pertaining to skull base surgery since 1900 and studied the emergence of the specialty as a scholarly field. Methods We queried Web of Science for all content from past presidents of the North American Skull Base Society (N = 31) and their self-identified forebears, influences, contemporaries, and trainees (N = 115). Statistical and bibliometric analyses were performed using various Python packages on article metadata. Results Our query returned 28,167 articles. The most pertinent works (N = 15,529), identified algorithmically through an analysis of terms in titles, were published between 1900 and 2024 by 15,286 authors. The field exploded in the latter half of the 20th century, concurrently with increased interdisciplinary and international collaboration, and contemporaneously with the formation of centers of excellence and influential societies. Since 1950, prolific contributors to the field from neurosurgery, otolaryngology, radiology/radiation oncology, plastic surgery, and ophthalmology have increasingly subspecialized in skull base topics. The proportion of female authors in the corpus has grown from &lt;1% in 1980 to 17% in 2023. We identify the articles that comprise the historical roots of modern skull base surgery, map the emergence of fundamental terminology within the corpus, and identify the authors who stand as key nodes of collaboration and influence. Conclusion The field of skull base surgery was born from pioneering individuals with training in varied disciplines. The coalescence of skull base surgery into a distinct and diversified subspecialty has been powered by dedicated collaborative efforts on a global scale.<br/><a href="/DOI/DOI?10.1055/s-0044-1788636">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000181">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1788636">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1788636">Full text</a></p>
  21. Journey to the Centre of the Ovale: A Novel, Combined Percutaneous Fluoroscopic and Image-Guided Approach to Biopsy a Meckel's Cave Lesion

    Thu, 18 Jul 2024 07:00:43 -0000

    Introduction The percutaneous Hartel's technique is a well-described approach to targeting lesions in the Meckel's cave. It is used as the standard approach for all percutaneous trigeminal neuralgia procedures for accessing the Gasserian ganglion through the foramen ovale, be it for a balloon compression, glycerol rhizolysis, or radiofrequency ablation. It has also been described in the literature as an approach to biopsy lesions in the Meckel's cave and cavernous sinus using fluoroscopic guidance; however, there were a significant number of nondiagnostic samples. No one to date has described a combined fluoroscopic and image-guided approach to improve safety and accuracy. Methods The patient had a 3-month history of left-sided facial numbness and a left VIth palsy causing diplopia and a squint. The computed tomography of the chest, abdomen, and pelvis was unremarkable as were the serum tumor markers. We describe the novel approach of using a percutaneous biopsy needle to obtain a cytological sample of a Meckel's cave lesion using a combination of X-ray and electromagnetic image guidance with use of StealthStation S8 System (Medtronic Sofamor Danek, Memphis, Tennessee, United States). The need for a craniotomy and its associated morbidity and technical challenges was therefore obviated. Results The procedure was performed under general anesthesia and eight core samples were sent to neuropathology for analysis. The lesion was histologically confirmed to be lymphoma, and the patient subsequently received oncological treatment. The patient had no immediate or postoperative complications, and the use of the aforementioned combined approach improved safety and accuracy of targeting the lesion in real time. Conclusion A combined percutaneous fluoroscopic and image-guided approach to biopsy a Meckel's cave lesion is recommended, as it improves safety and accuracy.
    <p align="right">J Neurol Surg B Skull Base<br/>DOI: 10.1055/a-2361-4912</p><p> Introduction The percutaneous Hartel's technique is a well-described approach to targeting lesions in the Meckel's cave. It is used as the standard approach for all percutaneous trigeminal neuralgia procedures for accessing the Gasserian ganglion through the foramen ovale, be it for a balloon compression, glycerol rhizolysis, or radiofrequency ablation. It has also been described in the literature as an approach to biopsy lesions in the Meckel's cave and cavernous sinus using fluoroscopic guidance; however, there were a significant number of nondiagnostic samples. No one to date has described a combined fluoroscopic and image-guided approach to improve safety and accuracy. Methods The patient had a 3-month history of left-sided facial numbness and a left VIth palsy causing diplopia and a squint. The computed tomography of the chest, abdomen, and pelvis was unremarkable as were the serum tumor markers. We describe the novel approach of using a percutaneous biopsy needle to obtain a cytological sample of a Meckel's cave lesion using a combination of X-ray and electromagnetic image guidance with use of StealthStation S8 System (Medtronic Sofamor Danek, Memphis, Tennessee, United States). The need for a craniotomy and its associated morbidity and technical challenges was therefore obviated. Results The procedure was performed under general anesthesia and eight core samples were sent to neuropathology for analysis. The lesion was histologically confirmed to be lymphoma, and the patient subsequently received oncological treatment. The patient had no immediate or postoperative complications, and the use of the aforementioned combined approach improved safety and accuracy of targeting the lesion in real time. Conclusion A combined percutaneous fluoroscopic and image-guided approach to biopsy a Meckel's cave lesion is recommended, as it improves safety and accuracy.<br/><a href="/DOI/DOI?10.1055/a-2361-4912">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000181">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/a-2361-4912">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/a-2361-4912">Full text</a></p>
  22. The Impact of the COVID-19 Pandemic and Lockdown on the Outcome of Glioblastoma

    Wed, 03 Jul 2024 13:59:40 -0000

    Background Rapid spread of the SARS-CoV-2 pandemic in 2020 led to an indirect effect on non-COVID patients. Since neuro-oncology cases are unique and brain tumors need a specific therapeutic protocol at proper doses and at the right times, the effects of the pandemic on health care services for patients with glioblastomas (GBs) and their impact on overall survival (OS) and quality of life are not yet known. Methods We conducted a retrospective study of 142 GB patients who underwent surgery, radiation, and chemotherapy before and after the lockdown period, aiming to determine the differences in access to care, treatment modality, and adjuvant therapies, and how the lockdown changed the prognosis. Results The number of procedures performed for GB during the pandemic was comparable to that of the prepandemic period, and patients received standard care. There was a significant difference in the volume of lesions measured at diagnosis with a decreased number of “accidental” diagnoses and expression of a reduced use by the patient for a checkup or follow-up examinations. Patients expressed a significantly lower performance index in the lockdown period with longer progression-free survival (PFS) in the face of a comparable mean time to OS. Conclusion Patients treated surgically for GB during the pandemic period had a more pronounced and earlier reduction in performance status than patients treated during the same period the year before. This appears to be primarily due to lower levels of care in the rehabilitation centers and more frequent discontinuation of adjuvant care.
    <p align="right">J Neurol Surg A Cent Eur Neurosurg<br/>DOI: 10.1055/s-0044-1779262</p><p> Background Rapid spread of the SARS-CoV-2 pandemic in 2020 led to an indirect effect on non-COVID patients. Since neuro-oncology cases are unique and brain tumors need a specific therapeutic protocol at proper doses and at the right times, the effects of the pandemic on health care services for patients with glioblastomas (GBs) and their impact on overall survival (OS) and quality of life are not yet known. Methods We conducted a retrospective study of 142 GB patients who underwent surgery, radiation, and chemotherapy before and after the lockdown period, aiming to determine the differences in access to care, treatment modality, and adjuvant therapies, and how the lockdown changed the prognosis. Results The number of procedures performed for GB during the pandemic was comparable to that of the prepandemic period, and patients received standard care. There was a significant difference in the volume of lesions measured at diagnosis with a decreased number of “accidental” diagnoses and expression of a reduced use by the patient for a checkup or follow-up examinations. Patients expressed a significantly lower performance index in the lockdown period with longer progression-free survival (PFS) in the face of a comparable mean time to OS. Conclusion Patients treated surgically for GB during the pandemic period had a more pronounced and earlier reduction in performance status than patients treated during the same period the year before. This appears to be primarily due to lower levels of care in the rehabilitation centers and more frequent discontinuation of adjuvant care.<br/><a href="/DOI/DOI?10.1055/s-0044-1779262">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000180">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1779262">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1779262">Full text</a></p>
  23. Torticollis with Atlantoaxial Rotatory Subluxation in Children: A Clinical Review

    Wed, 15 May 2024 08:10:22 -0000

    A small proportion of children with a sudden onset torticollis (“wry neck”) presents with an atlantoaxial rotatory subluxation, usually after mild trauma or recent head or neck infection. Torticollis is a clinical diagnosis and imaging is usually not indicated, though often performed in clinical practice. Atlantoaxial rotatory subluxation on imaging is often a physiological phenomenon in torticollis, and concomitant neurological symptoms are therefore rare. Treatment is primarily conservative, with analgesics, a rigid neck collar, and if needed benzodiazepines to counteract muscle spasms and anxiety. In case of treatment failure or chronic subluxation, cervical repositioning and fixation under general anesthesia may be considered. Surgical treatment is only indicated in a small percentage of patients with chronic refractory subluxation, concomitant cervical fractures, or congenital anomalies. Early diagnosis and treatment are important, since this is associated with a more successful conservative outcome than a prolonged approach.
    <p align="right">Neuropediatrics<br/>DOI: 10.1055/a-2312-9994</p><p>A small proportion of children with a sudden onset torticollis (“wry neck”) presents with an atlantoaxial rotatory subluxation, usually after mild trauma or recent head or neck infection. Torticollis is a clinical diagnosis and imaging is usually not indicated, though often performed in clinical practice. Atlantoaxial rotatory subluxation on imaging is often a physiological phenomenon in torticollis, and concomitant neurological symptoms are therefore rare. Treatment is primarily conservative, with analgesics, a rigid neck collar, and if needed benzodiazepines to counteract muscle spasms and anxiety. In case of treatment failure or chronic subluxation, cervical repositioning and fixation under general anesthesia may be considered. Surgical treatment is only indicated in a small percentage of patients with chronic refractory subluxation, concomitant cervical fractures, or congenital anomalies. Early diagnosis and treatment are important, since this is associated with a more successful conservative outcome than a prolonged approach.<br/><a href="/DOI/DOI?10.1055/a-2312-9994">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000041">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/a-2312-9994">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/a-2312-9994">Full text</a></p>
  24. Feasibility and Safety of Bridging Antiplatelet Therapy with Cangrelor in Neuro-Oncology: A Preliminary Experience

    Mon, 15 Apr 2024 13:14:02 -0000

    Antiplatelet therapy is mandatory for prevention of thrombotic events in patients with a recent history of acute coronary syndromes and/or percutaneous coronary interventions. However, if an urgent surgery is required during antiplatelet therapy, a compromise between the ischemic/thrombotic and hemorrhagic risk has to be reached. Different bridging schemes are reported in the literature, but there is no clear consensus on the optimal treatment strategy in terms of efficacy and safety. Although some indications about the perioperative management of antiplatelet therapy regarding specific surgical specializations are available, balancing the thrombotic and hemorrhagic risk on an individual basis, no evidence referring to neurosurgical or neuro-oncologic procedures is reported. Herein, we present our preliminary experience in the perioperative management of a patient who underwent a neurosurgical procedure for the resection of a primary malignant brain tumor using an intravenous P2Y12 inhibitor (cangrelor) as bridging therapy after a recent acute myocardial infarction treated with primary percutaneous coronary intervention and stenting. The oral P2Y12 inhibitor (clopidogrel) was withdrawn 5 days prior to the surgical procedure and continuous infusion of cangrelor was started 3 days before the surgery at a dose of 0.75 μg/kg/min. Cangrelor was discontinued 2 hours before surgery and resumed 72 hours after tumor resection for further 60 hours. Neither cangrelor-related bleeding nor cardiac ischemic events were observed in the perioperative period and the following 90 days, supporting data regarding the feasibility and safety of this bridging scheme. Further studies are needed to confirm our promising results.
    <p align="right">J Neurol Surg A Cent Eur Neurosurg<br/>DOI: 10.1055/s-0044-1785649</p><p>Antiplatelet therapy is mandatory for prevention of thrombotic events in patients with a recent history of acute coronary syndromes and/or percutaneous coronary interventions. However, if an urgent surgery is required during antiplatelet therapy, a compromise between the ischemic/thrombotic and hemorrhagic risk has to be reached. Different bridging schemes are reported in the literature, but there is no clear consensus on the optimal treatment strategy in terms of efficacy and safety. Although some indications about the perioperative management of antiplatelet therapy regarding specific surgical specializations are available, balancing the thrombotic and hemorrhagic risk on an individual basis, no evidence referring to neurosurgical or neuro-oncologic procedures is reported. Herein, we present our preliminary experience in the perioperative management of a patient who underwent a neurosurgical procedure for the resection of a primary malignant brain tumor using an intravenous P2Y12 inhibitor (cangrelor) as bridging therapy after a recent acute myocardial infarction treated with primary percutaneous coronary intervention and stenting. The oral P2Y12 inhibitor (clopidogrel) was withdrawn 5 days prior to the surgical procedure and continuous infusion of cangrelor was started 3 days before the surgery at a dose of 0.75 μg/kg/min. Cangrelor was discontinued 2 hours before surgery and resumed 72 hours after tumor resection for further 60 hours. Neither cangrelor-related bleeding nor cardiac ischemic events were observed in the perioperative period and the following 90 days, supporting data regarding the feasibility and safety of this bridging scheme. Further studies are needed to confirm our promising results.<br/><a href="/DOI/DOI?10.1055/s-0044-1785649">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000180">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1785649">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1785649">Full text</a></p>
  25. Systematic Review: Success Rate of Endoscopic Endonasal versus Combined Endonasal and Transorbital Neuroendoscopic Approach for Nontraumatic Cerebrospinal Fluid Leak Repairs in the Lateral Recess of Sphenoid Sinus

    Mon, 08 Apr 2024 05:44:00 -0000

    Background Cerebrospinal fluid (CSF) leaks from the lateral recess of the sphenoid sinus (LRS) occur due to a skull base defect and are important to treat due to the associated morbidity, e.g., life-threatening meningitis. Nontraumatic CSF leaks have a predilection toward obesity which is a rising phenomenon. LRS is notoriously difficult to access because of its lateral location and its associated neurovascular complications. An alternative surgical corridor has been explored which is the transorbital neuroendoscopic (TONES) approach. Objective To compare the success rate of the endoscopic endonasal with the TONES approaches. Rationale This is the first systematic review on the endoscopic endonasal and combined transorbital approaches to treat CSF leaks from the LRS. Method A PRISMA-concordant systematic review. PubMed, MEDLINE, EMBASE, Web of Science, and SCOPUS were searched. The studies underwent abstract and full-text screening by two reviewers. The data collected included patient demographic, surgical approach, reconstruction method, layers and materials, follow-up period, ROBINS-I bias, complications, and success rate. Results In total, 26 of 4,385 studies were included for further synthesis. Of these studies, a total of 336 patients were identified from a cohort of 910 patients. The endoscopic endonasal approach showed a repair success rate of 95.24% and the combined TONES and endonasal approach showed a success rate of 100%. Conclusion Both the endoscopic endonasal and transorbital approach provide a good success rate. However, due to the small TONES sample, large, randomized control trials are needed.
    <p align="right">J Neurol Surg B Skull Base<br/>DOI: 10.1055/s-0044-1785486</p><p> Background Cerebrospinal fluid (CSF) leaks from the lateral recess of the sphenoid sinus (LRS) occur due to a skull base defect and are important to treat due to the associated morbidity, e.g., life-threatening meningitis. Nontraumatic CSF leaks have a predilection toward obesity which is a rising phenomenon. LRS is notoriously difficult to access because of its lateral location and its associated neurovascular complications. An alternative surgical corridor has been explored which is the transorbital neuroendoscopic (TONES) approach. Objective To compare the success rate of the endoscopic endonasal with the TONES approaches. Rationale This is the first systematic review on the endoscopic endonasal and combined transorbital approaches to treat CSF leaks from the LRS. Method A PRISMA-concordant systematic review. PubMed, MEDLINE, EMBASE, Web of Science, and SCOPUS were searched. The studies underwent abstract and full-text screening by two reviewers. The data collected included patient demographic, surgical approach, reconstruction method, layers and materials, follow-up period, ROBINS-I bias, complications, and success rate. Results In total, 26 of 4,385 studies were included for further synthesis. Of these studies, a total of 336 patients were identified from a cohort of 910 patients. The endoscopic endonasal approach showed a repair success rate of 95.24% and the combined TONES and endonasal approach showed a success rate of 100%. Conclusion Both the endoscopic endonasal and transorbital approach provide a good success rate. However, due to the small TONES sample, large, randomized control trials are needed.<br/><a href="/DOI/DOI?10.1055/s-0044-1785486">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000181">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0044-1785486">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0044-1785486">Full text</a></p>
  26. The Extension of Traumatic Subdural Hematoma into the Interhemispheric Fissure Is Associated with Coagulation Disorders: A Retrospective Study

    Fri, 29 Mar 2024 12:34:18 -0000

    Background This study investigates the correlation of the radiologic sign of interhemispheric subdural hematoma (iSDH) in different injury patterns with clinical coagulation disorders. It is hypothesized that the presence of iSDHs is correlated with clinical coagulation disorders in patients with traumatic brain injuries and subdural hematoma (SDH). Methods Between January 1, 2020 and June 30, 2022, 154 patients with SDH were identified. Coagulation disorders were assessed using chart review and patients were divided into four groups: SDH without iSDH without further injuries (SDH), SDH with iSDH without further injuries (SDH + iSDH), SDH without iSDH with further brain injuries (Combi), SDH with iSDH with further injuries (Combi + iSDH). These four groups were formed under the assumption that isolated SDHs result from a highly specific trauma mechanism (rupture of bridging veins) in predisposed elderly patients, while combined brain injuries with SDH result from a severe global traumatic brain injury combining different pathophysiologic mechanisms often in younger patients. The groups were analyzed for patient demographics, clinical presentation, and association with coagulation disorders. The significance level was set at p < 0.005. Results The presence of an iSDH was associated with a higher likelihood of concomitant coagulation disorder or anticoagulants in cases of isolated subdural hemorrhage (56.8% of the population in SDH vs. 94.7% in SDH + iSDH, p < 0.005). This effect was not significant in the cases with combined traumatic brain injuries (33.3% in Combi vs. 53.6% in Combi + iSDH, p > 0.005). Conclusion Our data indicate a high positive predictive value (PPV = 94.7%) for coagulation disorders in traumatic SDH patients with iSDH without any further focal and diffuse brain injuries. We consider this a relevant finding since it hints at the presence of coagulation disorders and might be used in early hemostaseologic assessment and emergency management.
    <p align="right">J Neurol Surg A Cent Eur Neurosurg<br/>DOI: 10.1055/s-0043-1777859</p><p> Background This study investigates the correlation of the radiologic sign of interhemispheric subdural hematoma (iSDH) in different injury patterns with clinical coagulation disorders. It is hypothesized that the presence of iSDHs is correlated with clinical coagulation disorders in patients with traumatic brain injuries and subdural hematoma (SDH). Methods Between January 1, 2020 and June 30, 2022, 154 patients with SDH were identified. Coagulation disorders were assessed using chart review and patients were divided into four groups: SDH without iSDH without further injuries (SDH), SDH with iSDH without further injuries (SDH + iSDH), SDH without iSDH with further brain injuries (Combi), SDH with iSDH with further injuries (Combi + iSDH). These four groups were formed under the assumption that isolated SDHs result from a highly specific trauma mechanism (rupture of bridging veins) in predisposed elderly patients, while combined brain injuries with SDH result from a severe global traumatic brain injury combining different pathophysiologic mechanisms often in younger patients. The groups were analyzed for patient demographics, clinical presentation, and association with coagulation disorders. The significance level was set at p &lt; 0.005. Results The presence of an iSDH was associated with a higher likelihood of concomitant coagulation disorder or anticoagulants in cases of isolated subdural hemorrhage (56.8% of the population in SDH vs. 94.7% in SDH + iSDH, p &lt; 0.005). This effect was not significant in the cases with combined traumatic brain injuries (33.3% in Combi vs. 53.6% in Combi + iSDH, p &gt; 0.005). Conclusion Our data indicate a high positive predictive value (PPV = 94.7%) for coagulation disorders in traumatic SDH patients with iSDH without any further focal and diffuse brain injuries. We consider this a relevant finding since it hints at the presence of coagulation disorders and might be used in early hemostaseologic assessment and emergency management.<br/><a href="/DOI/DOI?10.1055/s-0043-1777859">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000180">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0043-1777859">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0043-1777859">Full text</a></p>
  27. Stand-Alone Percutaneous Pedicle Screw Lumbar Fixation to Indirectly Decompress the Neural Elements in Spinal Stenosis: A Radiographic Assessment Case Series

    Tue, 19 Dec 2023 11:43:57 -0000

    Background The ideal surgical treatment of lumbar canal stenosis remains controversial. Although decompressive open surgery has been widely used with good clinical outcome, minimally invasive indirect decompression techniques have been developed to avoid the complications associated with open approaches. The purpose of this study was to evaluate the radiologic outcome and safety of the indirect decompression achieved with stand-alone percutaneous pedicle screw fixation in the surgical treatment of lumbar degenerative pathologies. Methods Twenty-eight patients presenting with spinal degenerative diseases including concomitant central and/or lateral stenosis were treated with stand-alone percutaneous pedicle screw fixation. Radiographic measurements were made on axial and sagittal magnetic resonance (MR) images, performed before surgery and after a mean follow-up period of 25.2 months. Measurements included spinal canal and foraminal areas, and anteroposterior canal diameter. Results Percutaneous screw fixation was performed in 35 spinal levels. Measurements on the follow-up MR images showed statistically significant increase in the cross-sectional area of the spinal canal and the neural foramen, from a mean of 88.22 and 61.05 mm2 preoperatively to 141.52 and 92.18 mm2 at final follow-up, respectively. The sagittal central canal diameter increased from a mean of 4.9 to 9.1 mm at final follow-up. Visual analog scale (VAS) pain score and Oswestry Disability Index (ODI) both improved significantly after surgery (p < 0.0001). Conclusion Stand-alone percutaneous pedicle screw fixation is a safe and effective technique for indirect decompression of the spinal canal and neural foramina in lumbar degenerative diseases. This minimally invasive technique may provide the necessary decompression in cases of common degenerative lumbar disorders with ligamentous stenosis.
    <p align="right">J Neurol Surg A Cent Eur Neurosurg<br/>DOI: 10.1055/s-0043-1777751</p><p> Background The ideal surgical treatment of lumbar canal stenosis remains controversial. Although decompressive open surgery has been widely used with good clinical outcome, minimally invasive indirect decompression techniques have been developed to avoid the complications associated with open approaches. The purpose of this study was to evaluate the radiologic outcome and safety of the indirect decompression achieved with stand-alone percutaneous pedicle screw fixation in the surgical treatment of lumbar degenerative pathologies. Methods Twenty-eight patients presenting with spinal degenerative diseases including concomitant central and/or lateral stenosis were treated with stand-alone percutaneous pedicle screw fixation. Radiographic measurements were made on axial and sagittal magnetic resonance (MR) images, performed before surgery and after a mean follow-up period of 25.2 months. Measurements included spinal canal and foraminal areas, and anteroposterior canal diameter. Results Percutaneous screw fixation was performed in 35 spinal levels. Measurements on the follow-up MR images showed statistically significant increase in the cross-sectional area of the spinal canal and the neural foramen, from a mean of 88.22 and 61.05 mm2 preoperatively to 141.52 and 92.18 mm2 at final follow-up, respectively. The sagittal central canal diameter increased from a mean of 4.9 to 9.1 mm at final follow-up. Visual analog scale (VAS) pain score and Oswestry Disability Index (ODI) both improved significantly after surgery (p &lt; 0.0001). Conclusion Stand-alone percutaneous pedicle screw fixation is a safe and effective technique for indirect decompression of the spinal canal and neural foramina in lumbar degenerative diseases. This minimally invasive technique may provide the necessary decompression in cases of common degenerative lumbar disorders with ligamentous stenosis.<br/><a href="/DOI/DOI?10.1055/s-0043-1777751">[...]</a><br/><br/></p><p>Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany</p><p>Article in Thieme eJournals:<br/><a href="https://www.thieme-connect.com/products/ejournals/issue/eFirst/10.1055/s-00000180">Table of contents</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0043-1777751">Abstract</a>  |  <a href="https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0043-1777751">Full text</a></p>
  28. Sequential rupture of two concomitant cerebral aneurysms

    Wed, 12 Jul 2023 01:01:50 -0000

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