Mitochondrial Stress and Axonal Degeneration in Ramsay Hunt Syndrome: A Bioenergetic Perspective

Abstract

Ramsay Hunt Syndrome was caused by the reactivation of the varicella-zoster virus in the geniculate ganglion. It is a debilitating neurological disorder characterized by facial paralysis, otalgia, and vesicular eruptions. Despite antiviral and corticosteroid therapies, recovery remains suboptimal for many patients. Recent evidence suggests that mitochondrial dysfunction plays a central role in the progression of neural damage in Ramsay Hunt Syndrome. Mitochondria as power house of the cells are critical in maintaining axonal health, energy homeostasis, and redox balance. In Ramsay Hunt Syndrome, viral reactivation initiates an inflammatory cascade that disrupts mitochondrial dynamics, induces oxidative stress, and impairs ATP synthesis. These bioenergetic deficits compromise axonal transport and integrity, leading to degeneration. This review explores the intersection of mitochondrial stress and axonal degeneration in Ramsay Hunt Syndrome, with a focus on the bioenergetic consequences of varicella-zoster virus induced neuroinflammation. By elucidating these mechanisms, we aim to provide a comprehensive understanding of Ramsay Hunt Syndrome pathophysiology and lay the groundwork for novel bioenergetic based interventions to mitigate nerve injury and promote recovery.