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| NEUROIMAGES |
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| Year : 2018 | Volume
: 66
| Issue : 3 | Page : 886-888 |
An unusual cause of combined cauda equina and conus medullaris syndrome
Suraj Sajeev, R Krishnakumar
Department of Spine Surgery, VPS Lakeshore Hospital, Ernakulam, Kerala, India
| Date of Web Publication | 15-May-2018 |
Correspondence Address:
Dr. Suraj Sajeev
VPS Lakeshore Hospital, Ernakulam - 682 040, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.232280
How to cite this article:
Sajeev S, Krishnakumar R. An unusual cause of combined cauda equina and conus medullaris syndrome. Neurol India 2018;66:886-8 |
A 38-year old lady developed insidious onset of asymmetric weakness of both lower limbs, sphincteric paralysis and saddle anesthesia. Magnetic resonance imaging [Figure 1], [Figure 2], [Figure 3] with contrast revealed a lobulated intramedullary lesion from D11 to L1 levels involving the conus medullaris with no metastases in the brain. | Figure 1: T2 sagittal image showing a 5.6 × 1.5 cm intramedullary lesion involving the conus medullaris region, extending to the filum terminale with a prominent syrinx (arrow) proximal to the tumor
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 | Figure 2: T2 axial image showing expansion of the cord with tumor (arrow) abutting the dura
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 | Figure 3: T1 sagittal image with contrast showing the heterogeneous enhancement of the tumor (arrow)
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The tumor was excised with a T11-L1 laminectomy under neuromonitoring guidance. Intraoperatively, the lesion was found to infiltrate the cauda equina roots [Figure 4] and [Figure 5]. Histopathology revealed glioblastoma WHO grade IV [Figure 6], [Figure 7], [Figure 8]. Immunohistochemical study revealed cells strongly positive for glial fibrillary acid protein (GFAP), S-100 with a high Ki-67 proliferation index. Cluster of differentiation (CD) 34 was negative.[1],[2],[3] The patient did not develop further neurological deficit and received concurrent chemoradiation with temozolamide and 50 Gy radiation in 25 fractions over 5 weeks.[4] | Figure 4: Photomicrograph (hematoxylin and eosin ×200 magnification) of the glioblastoma showing a brisk mitotic activity (black arrows), pleomorphism, and hyperchromatism
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 | Figure 5: Photomicrograph (hematoxylin and eosin ×100 magnification) of the glioblastoma showing palisading necrosis (black box) and bizarre multinucleated tumor giant cells (black arrow)
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 | Figure 6: Immunohistochemistry study (×100 magnification) showing diffuse strong positivity to GFAP (glial fibrillary acidic protein)
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 | Figure 7: Immunohistochemistry study (×100 magnification) showing diffuse strong positivity to S-100
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 | Figure 8: Immunohistochemistry study (×100 magnification) for Ki-67 showing a high proliferation index
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Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
Informed consent was obtained from the patient and there were no conflicts of interest.
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| 2. | Singh PK, Singh VK, Tomar J, Azam A, Gupta S, Kumar S. Spinal glioblastoma multiforme: Unusual cause of post-traumatic tetraparesis. J Spinal Cord Med 2009;32:583-6. [ PUBMED] |
| 3. | Prasad GL, Borkar SA, Subbarao KC, Suri V, Mahapatra AK. Primary spinal cord glioblastoma multiforme: A report of two cases. Neurol India 2012;60:333-5. [Full text] |
| 4. | Mallick S, Madan R, Julka PK. Primary spinal glioblastoma treated with adjuvant radiation and temozolomide: Report of two cases. J Can Res Ther 2015;11:654. [ PUBMED] [Full text] |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
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