Journal of Pediatric Neurosciences
: 2019  |  Volume : 14  |  Issue : 1  |  Page : 57--58

Acute syringomyelia: A complication of tubercular meningitis

Sudipta Mohakud, Nerbadyswari Deep, Suprava Naik 
 Department of Radiodiagnosis, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India

Correspondence Address:
Dr. Sudipta Mohakud
Department of Radiodiagnosis, All India Institute of Medical Sciences, Bhubaneswar, Odisha

How to cite this article:
Mohakud S, Deep N, Naik S. Acute syringomyelia: A complication of tubercular meningitis.J Pediatr Neurosci 2019;14:57-58

How to cite this URL:
Mohakud S, Deep N, Naik S. Acute syringomyelia: A complication of tubercular meningitis. J Pediatr Neurosci [serial online] 2019 [cited 2023 Jan 29 ];14:57-58
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Full Text

Dear Editor,

Syringomyelia is a rare delayed complication of tubercular meningitis (TBM) and develops 7–28 years after the occurrence of TBM.[1] Early syringomyelia during active disease or while continuing antituberculosis therapy (ATT) is even rarer.[2] Multiseptated syringomyelia has been reported in the literature in association with trauma and after spinal surgical procedures for extramedullary lesions and meningomyelocele but not with TBM.[3],[4]

We present a rare case of a 6-year-old boy with TBM developing multiseptated cervico-dorsal syringomyelia during the continuation phase of the ATT.

The child presented with difficulty in walking, blurring of vision, multiple seizure episodes, headache, and intermittent vomiting for 1 month. He had a history of contact with tuberculosis. The contrast-enhanced computed tomography scan of the brain showed basal exudates and communicating hydrocephalus. The cerebrospinal fluid (CSF) analysis revealed increased protein and lymphocytosis. Staining for acid-fast bacilli was negative. He was diagnosed with TBM and was started on ATT. Ventriculoperitoneal shunt surgery was performed after 4 months of starting ATT due to persistent headache and clinico-radiological features of raised intracranial pressure. The patient again presented with paraparesis after a month. On examination, he was afebrile, conscious, and oriented. There was no neck rigidity or cranial nerve palsy. Tone was normal in bilateral upper limbs, and bilateral lower limbs were spastic. All the limbs had power 4/5. The reflexes and the sensory examination were normal. Cerebellar signs and papilledema were absent. Magnetic resonance imaging (MRI) of the brain and the spine was conducted to rule out compressive myelopathy.

The sagittal T2-weighted MRI of the spine showed a long segment, hyperintense, multiseptated intramedullary lesion, involving the cervico-dorsal cord [Figure 1] without cord expansion, which was hypointense on T1-weighted image, suggestive of syringomyelia. No basal exudates or tuberculomas were noted in the brain.{Figure 1}

The patient was continued on ATT and steroid. There was improvement in the tone and power of the limbs during follow-up at 3 months and he was able to walk without support.

The probable mechanisms of syrinx development in TBM are tubercular vasculitis, producing cord ischemia and softening; spinal subarachnoid space scarring, causing reduced compliance of the subarachnoid space; and the patent Virchow-Robin spaces in the spinal cord, providing a channel for the CSF to enter into the central canal and communicating hydrocephalus with acute rise in intracranial pressure.[2],[5] The other spinal complications of TBM are arachnoiditis, vasculitic infarcts, and tuberculomas.

The exact cause of development of septations in our case was not known but could be due to adhesions as a result of inflammation.

Post-tubercular syringomyelia has no medical treatment and may require surgery if a stable clinical state is not achieved.[6]

Onset of neurological symptoms such as paraparesis indicates spinal cord involvement, and the possibility of syringomyelia should be kept in mind as a rare early complication of TBM as seen in our case.

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