Cerebral microbleeding in varicella-zoster viral meningitis: An early sign of vasculopathy?

Abstract

A 75-year-old man undergoing chemotherapy for prostate cancer for 3 months presented with headache after having blisters in his left ear canal and auricle. His body temperature at presentation was 38°C. Neurologic examination revealed nuchal stiffness and left peripheral facial palsy. We also noted leukocytopenia (2,000/µL) and elevated serum C-reactive protein (8.51 mg/dL). CSF analysis showed no erythrocytes, elevated leukocytes (640/µL; 3% monocytes, 97% neutrophils), an increased protein level (473 mg/dL), and slightly decreased glucose level (51 mg/dL, serum glucose 120 mg/dL). Brain MRI and magnetic resonance angiography (MRA) on the day of admission were normal except for irregular gadolinium (Gd) enhancement of the cerebral sulci and basal meninges consistent with meningitis (figure, A–E). Upon noting Ramsay Hunt syndrome from the patient's clinical history and considering the known predominance of neutrophils in CSF in early cases of varicella-zoster virus (VZV) infection of the nervous system,1 we initiated treatment with IV acyclovir (ACV; 1,800 mg/day) for suspicion of VZV meningitis. The patient's symptoms then gradually improved. Existence of VZV within CSF was later confirmed by PCR testing and high anti-VZV immunoglobulin M (IgM) antibody index (1.68; normal range <0.8) results. Two weeks after ACV treatment initiation, follow-up MRI showed attenuated Gd enhancement of the meninges; unexpectedly, diffusion-weighted imaging (DWI) showed a small acute infarction of the right insula (figure, F), and T2-weighted imaging (T2*WI) showed microbleeding in the left anterior cingulate gyrus (figure, G) and the midbrain interpeduncular fossa (figure, H). MRA revealed no apparent narrowing or malformation of the arteries. Without risk factors for cerebrovascular disease such as arrhythmia, hypertension, or coagulation abnormality, our clinical and radiologic findings taken together with patient history suggested small-vessel vasculopathy associated with VZV infection; therefore, oral dexamethasone (DEX; 1 mg/day) was added to the original treatment. Both ACV and DEX were continued for 2 months until the CSF testing and the anti-VZV IgM antibody index returned to normal. No clinical or radiologic signs of relapse were detected during the therapeutic course.