History and Physical
An 11-year-old boy presented with a low-grade fever for one month, followed by headache for the past 15 days and altered sensorium over the past week. On day 15 of fever, he experienced an episode of transient right-sided weakness that resolved within 24 hours. The headache was occasionally associated with projectile vomiting and transient relief. Patient and family history were noncontributory.
Clinical examination showed normal vital signs and anthropometry. Blood pressure in supine position was mildly elevated for age. The patient appeared sleepy but arousable. He had neck stiffness, Brudzinski sign, and bilateral Kernig signs. There was no papilledema, restriction of eye movement, facial or motor weakness. The rest of the systemic examination was unremarkable, without organomegaly or lymphadenopathy.
Diagnostic Workup
Lumbar puncture showed elevated CSF pressure with 179 cells (lymphocytes), normal glucose (63 mg/dL), elevated protein (97 mg/dL), and absence of acid-fast bacilli on Ziehl-Neelsen staining. Gram stain, bacterial cultures, and PCR for mycobacterium were negative. Intradermal Mantoux skin test was reactive and showed an induration of 15 × 15 mm. Serology for HIV was negative.
Head CT showed bilateral basal ganglia infarcts, basal exudates, hydrocephalus, and cerebellar tuberculomas ( Fig. 40.1 ). Brain MRI with contrast revealed thick meningeal enhancement along the basal cisterns and bilateral cerebral convexities, basal ganglia infarcts, and moderate obstructive hydrocephalus ( Fig. 40.2 ).
Tuberculous meningitis. Head CT with contrast (A and B) showing communicating hydrocephalus, ring-enhancing lesions ( arrows ) with surrounding vasogenic edema, and leptomeningeal enhancement.
Tuberculous meningitis. Brain MRI, (A) axial and (B) coronal postcontrast T1 show thick irregular meningeal enhancement along basal cisterns and insular regions ( black arrows ) with moderate communicating hydrocephalus ( white arrows ).
Clinical Differential Diagnosis
Chronic neurologic symptoms with fever, increased ICP, and meningismus can be seen in:
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Infection: Tuberculosis, HIV with opportunistic infections, cryptococcosis, neurobrucellosis, invasive fungal infection, granulomatous amebic encephalitis in an immunocompromised host
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Vascular: CNS vasculopathies
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Tumors: primary CNS malignancies and metastases
Imaging Differential Diagnosis
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Meningeal enhancement: Tuberculosis, sarcoidosis, IgG4-related disease, leptomeningeal carcinomatosis.
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Basal exudates: Tuberculosis, neurobrucellosis, granulomatous amebic encephalitis.
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Hydrocephalus: Meningitis, tumors, aqueductal stenosis.
Final Diagnosis
Tuberculous meningitis (TBM) with intracranial tuberculomas.
Discussion
In endemic regions, CNS TB has a prevalence of 2 per 100,000 people and a mortality rate of 40% among hospitalized patients. Mycobacterium tuberculosis is spread via the respiratory tract to the lungs, from which it can disseminate hematogenously to the CNS. Lesions may rupture into the ventricular system and subarachnoid space, with subsequent inflammatory reaction forming thick gelatinous exudates, especially over the brainstem, basal cisterns, and Sylvian fissures. This in turn blocks the flow of CSF with resultant hydrocephalus ( Fig. 40.3 ). Infarcts can occur secondary to perivascular involvement ( Fig. 40.4 ).
