Case Presentation: A 31-year-old male with past medical history of narcolepsy, migraine, anxiety, depression, and motor tics disorder presented to the hospital complaining of headache, left sided weakness and intermittent left upper extremity paresthesia for 3 days. Physical examination was remarkable for decreased left upper extremity sensation; motor strength was 5/5 in all 4 extremities. Computed tomography (CT) of the head showed new age-indeterminate small areas of hypodensity in the right caudate nucleus tail. CT of the cervical spine showed nonspecific prominent upper cervical lymphadenopathy. Echocardiography showed left ventricular ejection fraction of 55 to 60% with mild to moderate left atrium dilatation. Magnetic resonance imaging (MRI) of the brain showed focal areas of the right middle cerebral artery (MCA) infarction with local mass effect. Magnetic resonance angiography (MRA) of the brain showed focal moderate to severe stenosis of distal M1 and proximal M2 segments of right MCA. MRA of the neck was normal. Hypercoagulable panel was negative, 24-hour electroencephalogram was negative. Patient was started on dual antiplatelet therapy. MRI and MRA of the brain were repeated one month later and revealed a new right frontal infract and marked progression of the disease. Patient was readmitted to the hospital for a diagnostic cerebral angiogram which revealed severe right MCA stenosis with post stenotic dilation of M2 segment with significant collaterals. Lumbar puncture showed 37 WBC/microliter with lymphocytic predominance (74%) and mildly elevated protein of 67 mg/dl. VZV was detected in CSF. Serum serology of VZV IgM was less than 0.91 index but IgG was elevated to 3,864 index. HIV, RPR, ANA and ANCA serology was negative. Patient was discharged home on intravenous acyclovir 750 mg three times daily for 14 days.
Discussion: Varicella zoster virus (VZV) is the only known human virus isolated from arteries and responsible for vascular inflammation resulting in cerebral ischemia. Here we describe a case of a young immunocompetent male who presents with stroke symptoms due to VZV vasculopathy.
Conclusions: VZV vasculopathy has a unique and uncommon stroke mechanism that has been underrecognized. Diagnosis of VZV vasculopathy can be missed in the absence of the rash and therefore antiviral treatment is not administered timely. Intracerebral VZV vasculopathy is potentially treatable so one should have a high index of suspicion in young patients even without preceding rash who present with a new stroke and high-grade intracerebral artery stenoses.