Seizures in an immunocompromised adolescent: a case report

Abstract

Introduction: Tuberculosis is a progressive and disabling infection predominantly seen in low-income and middle-income countries. Immunocompromised patients are at a higher risk of contracting tuberculosis than the healthy population. The presentation may also be atypical, leading to delay in diagnosis. We report the first case of tuberculous cerebral vasculitis presenting with epilepsia partialis continua.

Case presentation: A 17-year-old adolescent boy of Sri Lankan Moor heritage was taking long-term immunosuppressants for nephrotic syndrome. He presented to hospital with focal fits affecting his left arm. He later developed choreiform movements of the same arm, progressing to epilepsia partialis continua and weakness. The gradually evolving focal neurological signs and underlying immunosuppression raised the possibility of localized cerebral infection or inflammation. Analysis of his cerebrospinal fluid showed lymphocytosis with normal cellular morphology. Magnetic resonance imaging was suggestive of progressive vasculitic infarctions of the cerebral cortex and basal ganglia. There was no evidence of active autoimmune or viral disease on hematological investigations, but molecular amplification detected Mycobacterium tuberculosis in his cerebrospinal fluid. Although our patient had been established on isoniazid preventive treatment for eight months before the episode, tuberculosis was nonetheless considered to be the most likely cause of the cerebral vasculitis. He was treated with a trial of anti-tuberculosis treatment, including streptomycin and adjunctive steroids, and made an uneventful recovery.

Conclusion: Clinicians should have a high index of suspicion for tuberculosis infection in patients with compromised immunity and other risk factors. The pathophysiological mechanisms underpinning cerebral vasculitis and epilepsia partialis continua are not completely understood. The efficacy of isoniazid prophylaxis in patients with immune suppression warrants further study. We present a regimen that successfully treated tuberculous cerebral vasculitis.

Fig. 1

Magnetic resonance image: transverse section of the brain on the third day of admission. This section shows high T2 signals in the right hippocampal gyrus, right putamen, and the head of the caudate nucleus, suggestive of infarctions

Fig. 2

Magnetic resonance image: transverse section of the brain 1 month after the onset of illness. This section shows new involvement of the right cerebral cortex (right middle meningeal arterial territory) with vasogenic edema

Fig. 3

Magnetic resonance image: coronal section of the brain 1 month after the onset of illness. This section shows the involvement of the right cerebral cortex and hippocampus due to multiple cerebral and basal ganglia infarctions

Fig. 4

Computed tomography image: transverse section of the brain 1 month after the onset of illness. This section shows the infarctions of the right cerebral cortex