Varicella zoster presenting as cranial polyneuropathy.

Cranial polyneuropathy is commonly caused by Lyme disease. We discuss the case of a man who presented with cranial nerve deficits causing dysphagia, dysphonia and facial weakness. This diagnostic dilemma stemmed from a workup that ruled out Lyme and vascular causes leading to an expanded search for infectious explanations, which revealed varicella zoster in the cerebrospinal fluid. On review, this phenomenon is rarely reported, but has been observed with a number of herpes family viruses. In emergency department settings, clinical suspicion should be raised for VZV infection even in the absence of rash in patients that present with multiple cranial nerve palsies.

Detection of herpes simplex and varicella-zoster viruses in patients with Bell's palsy by the polymerase chain reaction technique.

OBJECTIVES: Infectious causes of peripheral facial paralysis are well known. Bell's palsy, however, is an idiopathic facial paralysis, and the genesis is still unknown. Herpes simplex virus type 1 (HSV-1) and varicella-zoster virus (VZV) have been suggested as etiologic agents. METHODS: Twenty consecutive adult patients with Bell's palsy were included in the study. Ten adult patients operated on for chronic otitis served as controls. A biopsy specimen from the posterior auricular muscle was resected within 72 hours after the onset of Bell's palsy and was analyzed together with cerebrospinal fluid (CSF) by nested polymerase chain reaction for HSV-1 and VZV DNA. Serum samples were analyzed for antibodies to HSV-1 and VZV. RESULTS: HSV-1 DNA was found in the muscle biopsy specimen from 1 of the 20 patients, but was not found in any of the CSF samples. VZV DNA was detected in the muscle biopsy as well as the CSF from 1 other patient. All controls were negative. Seventeen of 19 patients had stationary serum antibody concentrations to HSV-1, and none displayed an antibody titer rise. A significant antibody titer rise to VZV was found in 1 of 19 patients, whereas 17 of 19 had stationary antibody levels. CONCLUSIONS: HSV-1 or VZV DNA was detected in 10% of patients with Bell's palsy in the present study. Viral replication might already have declined in many cases at the onset of the palsy. Use of an HSV-1/VZV polymerase chain reaction on a muscle biopsy specimen or CSF does not seem to be the method of choice for rapid etiologic diagnosis in the acute phase of Bell's palsy.

Bell's palsy and Herpes simplex virus: fact or mystery?

HYPOTHESIS AND BACKGROUND: In recent years, progress has been made in the understanding of Bell's palsy, the most common form of acute facial weakness. Herpes simplex virus (HSV) reactivation within the geniculate ganglion with subsequent inflammation and entrapment of the nerve at the meatal foramen has been proposed to be the pathogenetic mechanism. We challenged its accuracy by analyzing our own data on the presence of viral genomic DNA of HSV-1 and 2, human herpes virus (HHV)-6A/B, as well as varizella zoster virus (VZV) in patients with Bell's palsy and in control patients without the disease. METHODS: Polymerase chain reaction was performed with primer sets specific for viral genomic DNA of HSV-1, HSV-2, and VZV in facial muscle biopsy specimens from patients with Bell's palsy. As control specimens, the Scarpa's ganglion of patients with Meniere's disease and the geniculate ganglion harvested at autopsy from patients without history of facial palsy. In a second study, we used polymerase chain reaction with primers specific for HSV-1, -2, and HHV-6A, -6B to analyze for the presence of these viruses in tear fluid samples from control patients and patients with acute Bell's palsy. RESULTS: HSV-1 and VZV genomic DNA were detected in 86 and 43%, respectively, of geniculate ganglion preparations from control specimen. We were not able to detect the presence of HSV-1, HSV-2, or VZV genomic DNA in ganglion scarpae or muscle biopsy results in control and Bell's palsy patients. HHV-6A could be detected in tear fluid samples in 40% of control patients and 30% of Bell's palsy patients. CONCLUSIONS: The sole presence of HSV genomic DNA within the sensory ganglion along the facial nerve does not explain the direct association with Bell's palsy. The missing link would be the identification of an active replicating virus, an investigation that has not yet been carried out.