Background
Headache in patients receiving treatment for multidrug-resistant tuberculosis (MDR-TB) commonly prompts evaluation for central nervous system infection. However, medications themselves may occasionally be responsible for raised intracranial pressure. Chouksey and colleagues describe a rare example of levofloxacin-associated intracranial hypertension in an adolescent with MDR-TB.
The Case
A 14-year-old South Asian boy receiving a multidrug-resistant tuberculosis regimen containing levofloxacin 1000 mg daily developed an 8-day history of holocranial headache that worsened when lying down. Bilateral horizontal diplopia subsequently developed. Neurological examination demonstrated bilateral lateral rectus palsies, and fundoscopy revealed bilateral papilledema.
Brain magnetic resonance imaging showed no parenchymal abnormalities but demonstrated left transverse and sigmoid sinus stenosis. Cerebrospinal fluid analysis was normal apart from an elevated opening pressure of 36 cm H₂O. Infectious studies were negative, making tuberculous meningitis unlikely.
Given the temporal relationship between symptom onset and ongoing levofloxacin therapy, drug-induced intracranial hypertension was suspected. Levofloxacin was discontinued and replaced with pyrazinamide, and a short course of acetazolamide was administered.
Outcome
Clinical improvement was rapid. Headache resolved within one week, cerebrospinal fluid opening pressure normalized, and papilledema resolved within two weeks. There was no recurrence during follow-up while continuing MDR-TB treatment without levofloxacin.
Why This Case Matters
Drug-induced intracranial hypertension is an uncommon but potentially vision-threatening complication. Although tetracyclines and vitamin A derivatives are well-recognized causes, fluoroquinolones are rarely implicated. Previous reports have documented only a handful of cases associated with levofloxacin.
In this patient, a relatively high dose of levofloxacin for body mass index may have contributed to the development of raised intracranial pressure. Recognition of this adverse effect prevented unnecessary treatment for presumed meningitis and led to complete recovery.
Clinical Implications
Clinicians evaluating headache in patients with tuberculosis should think beyond infectious etiologies. Careful review of medications is essential, particularly when papilledema or cranial nerve VI palsies are present. Prompt recognition and withdrawal of the offending agent can prevent permanent visual complications.
Clinical Take-Home Message
In patients receiving levofloxacin, new-onset headache, diplopia, and papilledema should prompt consideration of secondary intracranial hypertension. Drug withdrawal may lead to rapid and complete resolution, emphasizing the importance of considering medication toxicity alongside infectious causes in tuberculosis patients.
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