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LETTER TO EDITOR
Year : 2019  |  Volume : 14  |  Issue : 1  |  Page : 57-58
 

Acute syringomyelia: A complication of tubercular meningitis


Department of Radiodiagnosis, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India

Date of Web Publication18-Jun-2019

Correspondence Address:
Dr. Sudipta Mohakud
Department of Radiodiagnosis, All India Institute of Medical Sciences, Bhubaneswar, Odisha
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JPN.JPN_16_19

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How to cite this article:
Mohakud S, Deep N, Naik S. Acute syringomyelia: A complication of tubercular meningitis. J Pediatr Neurosci 2019;14:57-8

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 2019 Jul 16];14:57-8. Available from: http://www.pediatricneurosciences.com/text.asp?2019/14/1/57/260613




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 sagittal T2-weighted MRI of the spine showing a long segment, hyperintense, multiseptated intramedullary lesion, involving the cervico-dorsal cord without cord expansion, suggestive of syringomyelia

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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.



Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Moghtaderi A, Alavi-Naini R, Rahimi-Movaghar V. Syringomyelia: an early complication of tuberculous meningitis. Trop Doct 2006;36:254-5.  Back to cited text no. 1
    
2.
Caplan LR, Norohna AB, Amico LL. Syringomyelia and arachnoiditis. J Neurol Neurosurg Psychiatry 1990;53:106-13.  Back to cited text no. 2
    
3.
Castillo M, Quencer RM, Green BA, Montalvo BM. Syringomyelia as a consequence of compressive extramedullary lesions: postoperative clinical and radiological manifestations. AJR Am J Roentgenol 1988;150:391-6.  Back to cited text no. 3
    
4.
Van Hall MH, Beuls EA, Wilmink JT, Boiten J, Vles JS. Magnetic resonance imaging of progressive hydrosyringomyelia in two patients with meningomyelocele. Neuropediatrics 1992;23:276-80.  Back to cited text no. 4
    
5.
Pandey S, Nayak R, Mehndiratta MM. Early syringomyelia in tubercular meningitis: a rare occurrence. J Neurol Res 2013;3:46-8.  Back to cited text no. 5
    
6.
Ramanathan SR, Ahluwalia T. Rare complication: acute syringomyelia due to tuberculoma and tubercular meningitis. J Neurosci Rural Pract 2010;1:123-5.  Back to cited text no. 6
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