Virus Induced Voracity: Uncovering Hyperphagia Post Herpes Simplex Virus Type 1

Abstract

Herpes simplex virus type 1 (HSV-1) is the leading cause of sporadic fatal encephalitis, typically presenting with temporal lobe abnormalities. We report a 25-year-old woman with a 10-day history of fever, headache, and vomiting, progressing to confusion, visual hallucinations and drowsiness. She had a history of meningoencephalitis at age eight and well-controlled focal seizures. Upon admission, her GCS score was E3V5M3, and the MRI showed hyperintensities in both temporal lobes with diffusion restriction. EEG indicated generalised slowing, and CSF analysis revealed lymphocytic pleocytosis with elevated protein levels. Viral encephalitis was suspected, and intravenous acyclovir was initiated. CSF PCR confirmed HSV-1. By the end of 1st week, she became afebrile and showed improved awareness but developed hyperphagia for both edible and non-edible objects. She received 21 days of acyclovir with significant improvement in consciousness but only partial improvement in over eating. HSV-1 affects the bilateral medial temporal lobes, insular cortex, and cingulate gyrus. An MRI confirmed these findings in this patient. Hyperphagia, a rare complication of HSV encephalitis, is a part of Kluver-Bucy Syndrome (KBS), typically associated with other cognitive dysfunctions. Despite early treatment, hyperphagia persisted partially, emphasising the need for rapid diagnosis and treatment to prevent severe outcomes. The case highlights that acute onset hyperphagia can be an isolated complication of HSV encephalitis, requiring tailored therapeutic strategies. Follow-up showed significant weight gain with moderate improvement in hyperphagia, underscoring the challenges in managing this condition.