Acute development of syringomyelia following TBM in a pediat
A 12-year-old boy was admitted with the chief complaints of low-grade fever, cough for over a month, and headache, vomiting, progressive disturbance of consciousness for 3 weeks. He suffered from several generalized seizures throughout the course of the illness. His parents reported that he was previously healthy. On examination, his temperature was 37.8 °C, his heart rate 74/min, and his respiration rate 20/min. No BCG scar was observed on his upper arms. The patient was confused and lethargic and had neck stiffness and positive Kernig’s sign. The lower limbs had normal muscle tone and can be lifted off the bed when giving pain stimulation. The Babinski sign was absent. There were crackles in the left lung.

Xpert MTB/RIF test on bronchoalveolar lavage fluid demonstrated a diagnosis of rifampicin-sensitive tuberculosis. The patient was diagnosed with pulmonary TB and TBM and commenced on standard anti-tubercular therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) with dexamethasone 0.6 mg/kg.d. In the following days, the patient became conscious and oriented and experienced no recurrence of seizure or vomiting. Other symptoms including fever and headache were gradually relieved. However, seventeen days after treatment, he developed right upper quadrant pain and lumbodorsal pain, and thereafter, he developed spastic paraplegia of the lower limbs with fecal and urinary retention. On examination, there was motor weakness in the lower extremity (manual muscle testing assessed 1/5) as well as impaired sensation in right lower limb. Hypertonia and hyperreflexia were detected in the lower limbs. MRI of the spine demonstrated generalized inflammation of the spinal cord and meninges with enlarged syringomyelic cavities. Syrinx formation was exceptionally notable from C1 to T1 with a maximum width of 5.9 mm in the central canal of the cervical cord. T2-weighted images showed hyperintense signals within the spinal cord parenchyma. Contrast-enhanced MRI demonstrated significant thickening and enhancement of the arachnoid, with narrow and even, disappeared subarachnoid space. Hyperintense signals on T2 and isointense signals on T1-weighted images were shown in the subarachnoid space. There was atrophy of the spinal cord from T6 to T8, and nodular enhancement of conus medullaris was shown.

The clinical deterioration and the spinal involvement were unexpected since the patient was receiving effective anti-tubercular treatment with initial improvement. After discussion with the pediatric neurosurgeon, surgery was believed to be unrewarding given the extensive arachnoiditis with no obvious cord compression. The development of spinal cord complications was thought to be caused by the exaggerated cell-mediated immune response against mycobacterial antigens, while other etiologies, like superimposed bacterial infection and drug-resistant TB, were thoughtless likely. High-dose intravenous immunoglobulin (IVIG, 2 g/kg) was given to the patient given the progressive deterioration of the symptoms and potential efficacy of IVIG as an immunoregulatory and anti-inflammatory drug. The patient responded well and went on for a steady recovery. Seven days after the use of IVIG together with anti-tubercular drugs and dexamethasone, the patient was not complaining of any urinary disturbance, back pain, headache, or vomiting. Manual muscle testing assessed 4/5 in his lower extremities and he was able to walk under assistance. Repeat MRI showed radiological improvement of syringomyelia and other spinal lesions. He was then discharged for further rehabilitation at a local hospital.