Trigeminal Herpes Zoster With Longitudinally Extensive Spinal Trigeminal Tract Involvement Presenting as an Isolated Facial Palsy Mimicking Ramsay Hunt Syndrome

Varicella-zoster virus (VZV) is a neurotropic alpha herpesvirus capable of producing a wide spectrum of CNS disease, ranging from aseptic meningitis and vasculopathy to encephalitis and myelitis. Less widely appreciated is its capacity to extend centrally along the trigeminal pathway into the brainstem, producing intra-axial spinal trigeminal tract involvement that may remain clinically silent or manifest only as a cranial neuropathy, particularly when cerebrospinal fluid (CSF) polymerase chain reaction (PCR) is negative. We describe an immunocompetent 41-year-old man who presented with herpes zoster of the left hemiface in a maxillary-mandibular (V2-V3) distribution, followed by an acute left lower motor neuron facial palsy, initially indistinguishable from Ramsay Hunt syndrome. In the absence of encephalopathy, limb weakness, or cerebellar signs, magnetic resonance imaging of the brain demonstrated linear non-enhancing fluid-attenuated inversion recovery (FLAIR) hyperintensity extending across the posterior pons, medulla, and upper cervical cord, corresponding to the course of the spinal trigeminal tract and nucleus. CSF showed lymphocytic pleocytosis with otherwise unremarkable biochemistry; both herpes simplex virus and VZV PCR were negative. The patient was managed with intravenous acyclovir for 14 days, alongside short-course corticosteroids and supportive care. A transient rise in serum creatinine was managed with hydration and close monitoring while full-dose acyclovir was continued, without acyclovir-related neurotoxicity. Recovery was marked, with the House-Brackmann grade improving from V to III over follow-up and corresponding radiological regression of the brainstem signal change. The picture is best understood as sequential trigeminal-then-facial cranial neuropathy with longitudinally extensive spinal trigeminal tract involvement attributable to centripetal VZV spread, rather than a rhombencephalitic clinical syndrome. Such a combination -- trigeminal-territory zoster with longitudinally extensive spinal trigeminal tract involvement and an isolated facial palsy -- has only rarely been reported. This case illustrates the diagnostic dilemma of PCR-negative VZV CNS disease and underscores the value of clinicoradiological correlation, early antiviral therapy, and close neurological surveillance when a peripheral facial palsy emerges in the setting of cephalic herpes zoster.