Abstract

IntroductionWe present a case of herpes zoster infection (shingles) precipitated by surgical manipulation of the trigeminal nerve root during an attempted microvascular decompression procedure. The pathogenesis of this phenomenon, as well as the importance and role of prophylactic acyclovir in its management, are discussed.Case presentationA 54-year-old Caucasian man with a classical long-standing left-sided V2 and V3 division primary trigeminal neuralgia refractory to medical management, underwent posterior fossa exploration for microvascular decompression via a standard retromastoid craniectomy. The patient had immediate and complete relief from pain. Three days after the operation, he developed severely painful vesicles with V2 and V3 dermatomal distribution. Rather than the classical paroxysmal, lancinating type of trigeminal neuralgia, the pain experienced by the patient was of a constant burning nature. A clinical diagnosis of herpes zoster (shingles) was made after smear confirmation from microbiological testing. The patient was commenced on antiviral treatment with acyclovir. His vesicular rash and pain gradually subsided over the next two weeks. He remains asymptomatic one year later.ConclusionsPostoperative shingles precipitated by trigeminal nerve manipulation during surgery for trigeminal neuralgia can be a distressing and demoralizing experience for the patient. A careful preoperative history, early recognition, and prompt antiviral therapy is necessary.

Highlights

  • Introduction: We present a case of herpes zoster infection precipitated by surgical manipulation of the trigeminal nerve root during an attempted microvascular decompression procedure

  • Case presentation A 54-year-old Caucasian man with a classic long-standing, left-sided maxillary and mandibular (V2 and V3) division primary trigeminal neuralgia, refractory to medical management, underwent a posterior fossa exploration aimed at performing a microvascular decompression (MVD) via a standard retromastoid craniectomy

  • The most widely accepted theory explaining the aetiopathogenesis of trigeminal neuralgia (TN) is that of vascular compression and arterial pulsations resulting in demyelination at the dorsal root entry zone (DREZ)

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Summary

Introduction

The herpes zoster virus is known to be associated with trigeminal neuralgia (TN). In some cases it is implicated in the etiology of TN [1]. The trigeminal nerve was identified and exposed from its origin to its entry into the Meckel’s cave. Both the sensory and motor nerve rootlets were displayed. The pain was characteristically different from the original pain of neuralgia This pain was of constant burning nature rather than the classical paroxysmal lancinating type of TN, which had completely subsided following surgery. The patient was immunocompetent with no other predisposing factor for developing shingles He had no history of chickenpox or herpes zoster.

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