Varicella zoster virus reactivation antedating ipsilateral 4brainstem stroke

Abstract

Varicella zoster virus (VZV) infection and reactivation are associated with a number of neurologic conditions. Unifocal large vessel infarcts may follow zoster in the trigeminal or cervical distribution as a result of transaxonal transport of virus from trigeminal or cervical afferent fibers that innervate vessels. Ophthalmic zoster (HZO) might cause ophthalmoplegic syndromes, with secondary optic neuritis. Mechanisms include local orbital muscle inflammation and, viral spread from the ophthalmic branch of the fifth nerve with associated vasculopathy. A 72-year-old man developed a vesicular rash in the territory of C5-T5-6. Within four weeks, the patient developed headache, dysphagia, left facial and extremity ataxic weakness. Magnetic resonance imaging (MRI) revealed a right pontine infarction. A 66-year-old woman presented with right-sided painfull HZO. One week later she developed complete external ophthalmoplegia and blurred vision. MRI showed ill-defined signal alteration in the retrobulbar tissue. Three weeks later, the patient was admitted because of dysarthria, deviated tongue, left-sided limb weakness, and tactile hypoesthesia. Spinal fluid contained 23 lymphocytes/mm3 and increased protein. The serum contained antibodies to VZV IgG and IgM in both cases. The patients received intravenously acyclovir with improvement. This report confirms unusual occurrence of ipsilateral brainstem stroke after VZV reactivation in immunocompetent subjects.