Herpes Simplex Virus Encephalitis With Cerebellar Infarction and Cortical Laminar Necrosis

TL;DR

This case report describes a rare instance of herpes simplex virus encephalitis involving the cerebellum, leading to infarction and cortical laminar necrosis.

Contribution

The paper presents a rare clinical manifestation of HSV encephalitis with cerebellar infarction and cortical laminar necrosis.

Findings

HSV encephalitis can present with acute vestibulocerebellar syndrome and cerebellar infarction.

Follow-up imaging showed curvilinear T1 hyperintensities consistent with cortical laminar necrosis.

Early neuroimaging and lumbar puncture are critical in febrile patients with peripheral vertigo.

Abstract

Herpes simplex virus (HSV) encephalitis typically involves the temporal lobes, and cerebellar involvement with stroke and cortical laminar necrosis (CLN) is rare. A 40-year-old man with no prior comorbidities presented with 10 days of positional vertigo, vomiting and intermittent fever. Initial otorhinolaryngology assessment showed bilateral nystagmus and a positive fistula test, and he was treated as having a peripheral vestibular disorder. He re-presented with persistent vertigo and new confusion; on admission, he was febrile, hypertensive and ataxic, and within 24 hours, he developed worsening encephalopathy, focal deficits and generalised tonic-clonic seizures. Cerebrospinal fluid (CSF) analysis demonstrated lymphocytic pleocytosis, elevated protein, normal glucose, raised opening pressure and red blood cells, and polymerase chain reaction (PCR) for HSV DNA was positive, confirming HSV encephalitis. Brain magnetic resonance imaging (MRI) revealed an acute infarction in the right greater than the left cerebellar hemisphere with corresponding diffusion restriction on diffusion-weighted and apparent diffusion coefficient sequences. Follow-up imaging in the subacute phase showed curvilinear T1 hyperintensities along the cerebellar cortical ribbon consistent with CLN. The patient was treated with intravenous acyclovir, high-dose corticosteroids, antiepileptic drugs, osmotherapy, blood pressure control and supportive care. Over a three-week admission, his sensorium normalised, and seizures ceased, but truncal and appendicular ataxia persisted. At early outpatient review, he was ambulant with a cane, with mild residual truncal ataxia and no further seizures. This case highlights that HSV encephalitis can present with an acute vestibulocerebellar syndrome and be complicated by cerebellar infarction and CLN and emphasises the need for early neuroimaging and lumbar puncture in febrile patients with ‘peripheral’ vertigo.

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