Acute Hepatitis E Virus Infection Presenting as Stimulus-induced Status Epilepticus
Nsser Abdelall1, Farah Alkilani2, Abdulradha Alqallaf3
1Neurology, LSU Health Sciences Center - New Orleans, 2Internal Medicine, University of Miami/Jackson Memorial Hospital, 3Neurology, Adan hospital
Background:
Hepatitis E virus (HEV) is a leading cause of acute hepatitis worldwide, with an expanding range of extrahepatic manifestations involving both central and peripheral nervous systems. Neurological complications such as Guillain-Barré syndrome, neuralgic amyotrophy, encephalitis, and myelitis have been described; however, status epilepticus has not been previously associated with HEV infection. We report the first documented case of acute HEV-induced stimulus-triggered status epilepticus, highlighting the virus’s neurotropic potential and underscoring the importance of considering infectious causes in unexplained seizures accompanied by hepatic dysfunction and elevated liver enzymes.
Design/Methods:
A 58-year-old previously healthy woman presented with new-onset focal seizures that progressed to bilateral clonic status epilepticus, refractory to multiple antiseizure regimens. Continuous EEG monitoring confirmed persistent electrographic seizures reproducibly provoked by tactile and auditory stimuli. Laboratory studies showed markedly elevated aminotransferases (AST 621 IU/L, ALT 491 IU/L) and positive HEV IgM confirmed by real-time PCR. Other infectious, autoimmune, metabolic, and toxic evaluations were unremarkable. Brain MRI demonstrated right mesial temporal hyperintensity consistent with focal cortical edema due to prolonged seizures, while cerebrospinal fluid analysis revealed mild protein elevation with normal cell counts, suggesting non-encephalitic cortical involvement without inflammatory changes.
Results:
The patient developed super-refractory status epilepticus requiring mechanical ventilation, anesthetic infusions, and therapeutic hypothermia. Despite eventual resolution of electrographic seizures and normalization of hepatic enzymes, she evolved into a vegetative state. This course supports a possible direct or immune-mediated neuroinvasive mechanism of HEV infection, consistent with evidence of viral replication within the central nervous system and disruption of the blood–brain barrier in experimental animal models.
Conclusions:
This case broadens the recognized neurological spectrum of HEV to include stimulus-induced status epilepticus. Incorporating HEV serology and PCR into the diagnostic work-up of unexplained seizures or encephalitis with abnormal liver enzymes may facilitate earlier diagnosis, targeted management, and improved neurologic outcomes.
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