Tuberculous meningitis complicated with thoracic cord myelitis; a diagnostic conundrum

Tuberculosis is known as the great masquerader for its ability to present atypically. We report a case of a young man presented with progressive tuberculous meningitis and subsequently developed paraplegia due to thoracic cord myelitis, where diagnosis was confirmed bacteriologically. We highlight the presence of acute gastric dilatation as a warning sign of thoracic cord involvement and the place for CSF examination and spinal imaging in arriving at a clinical diagnosis, as treatment needs to start without delay to avoid permanent sequelae. Patient showed a good response to a combined approach of anti-tuberculosis treatment, systemic steroids and intravenous immunoglobulin.


Tuberculosis (TB) is an airborne infection caused by
Mycobacterium tuberculosis with a history of more than four thousand years. In Sri Lanka, the prevalence rate is 103 per 100,000 populations which show that it is one of the low TB prevalence countries in the region [1]. Central nervous system TB is common in TB prevailing developing countries. Within the wide spectrum of presentations of Central nervous system TB, paraplegia due to thoracic cord myelitis is an uncommon presentation which leads to diagnostic dilemma. Delay in initiating treatment causes poor outcome with permanent neurological sequelae.

CASE REPORT
We report a case of a 31-year-old male, presented to Teaching Hospital Peradeniya with headache, fever and vomiting for 3 days. He had mild occipital headache associated with photophobia which has been worsening over one week. He had loss of appetite and weight for two months, but no cough, abdominal pain, altered urinary or bowel habits. He was a teetotaler and non-smoker and had no past history or contact history of tuberculosis. He had taken treatments from general practitioner which partly subsided his symptoms without improving his general ill-health.
On examination he was thin-built, ill looking, mildly dehydrated and febrile. There were no rash or enlarged lymph nodes. His cardiovascular and respiratory system examination were unremarkable except for mild tachycardia (104/min). He had soft abdomen without organomegaly or renal angle tenderness. He was conscious, cranial nerves and bilateral upper and lower limb examinations were normal and had good bladder and bowel continence. He had mild neck stiffness, but Kernig's and Brudzinski's signs were negative.
His serology was normal (Table 1) and cerebrospinal fluid (CSF) analysis (Table 2) showed turbid appearance with lymphocytosis, high proteins and low sugars. CSF pyogenic culture revealed no growth along with negative blood and urine cultures. Patient was treated with intravenous Ceftriaxone 2g twice daily and intravenous Acyclovir 500 mg twice daily for possible partially treated bacterial meningitis.  Contrast enhanced computed tomography (CECT) of brain and cerebral venogram showed no features suggestive of venous sinus thrombosis, infarctions or haemorrhage and Electroencephalogram (EEG) revealed generalized slowing with intermittent seizures suggestive of encephalitis. Nerve conductions on bilateral common peroneal and posterior tibial nerve were normal, but delayed F waves and conduction blocks suggestive of severe demyelinating polyneuropathy were noted. Chest radiograph was poorly inflated and abdominal X ray showed marked gastric dilatation. His erythrocyte sedimentation rate in first hour was 105mm, CSF adenosine deaminase became positive, though CSF PCR was negative for TB. His retroviral screen was negative.
With the high clinical suspicion on tuberculous meningitis, patient was started on standard anti TB medication and Intravenous dexamethasone, followed by intravenous immunoglobulin (IVIG) 0.4g/kg daily due to progressive neuropathy. Gastric decompression achieved with nasogastric tube. Meanwhile patient developed poor respiratory effort which warranted intubation and mechanical ventilation for five days.
Patient underwent magnetic resonance imaging (MRI), which showed normal MRI brain (figure-1) with a segment of dilated thoracic central canal/syrinx (T8-T9) with thoracic cord atrophy at T6, T7, representing chronic changes of TB myelitis (Figure-2). There were no abnormalities seen in vertebral bodies, intervertebral disks or paraspinal soft tissues. CSF culture was positive for Mycobacterium tuberculosis after 10 weeks of incubation which bacteriologically confirmed the diagnosis.
Anti TB treatment is planned to continue for 12 months, with 4-6 weeks of steroids. Limb physiotherapy and ambulatory rehabilitation was continued. Patient was discharged after six weeks of inward care, where he was able to walk with support on discharge.   10] and no change in neurological status [11] may occur. The time taken for recovery is usually few months but it can be vary from few days to months [5,6] where our patient was able to engage in activities of daily living independently at the end of six months follow up.

CONCLUSION
In conclusion, tuberculous myelitis is an uncommon complication of TB meningitis which needs to be suspected in a meningitis patient with features of myelopathy. Along with anti-TB medications and steroids, IVIG can be considered as a treatment option in a patient with progressive symptoms.