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.

CSF and serum levels of soluble fractalkine (CX3CL1) in inflammatory diseases of the nervous system.

The new CX(3)C-chemokine fractalkine (CX(3)CL1) was measured by Western blot in the cerebrospinal fluid (CSF) and serum of patients with inflammatory diseases of the peripheral and central nervous system (Bell's palsy, BP; Guillain-Barré Syndrome, GBS; multiple sclerosis, MS; viral meningitis, VM; bacterial meningitis, BM) and patients with noninflammatory neurological diseases (controls). In controls, fractalkine was detectable at low concentrations in the CSF and, at much higher levels, in serum. In all inflammatory neurological diseases under study, CSF fractalkine levels were significantly (p<0.01) increased vs. controls (BM>>GBS>VM>MS>BP>controls). In serum, fractalkine levels were significantly increased only in MS patients. The fractalkine CSF/serum ratios (a measure of the chemotactic gradient) were significantly elevated in BM, VM and GBS; furthermore, they tended to be increased in BP and to be decreased in MS. The elevated fractalkine CSF/serum ratios in diseases without CSF pleocytosis (GBS, BP) and a lack of correlation between fractalkine levels and CSF leukocyte counts suggested that soluble fractalkine is not a major chemokine in the CSF. There was no evidence of significant intrathecal production of fractalkine as the mean fractalkine indices (fractalkine CSF/serum ratio:albumin CSF/serum ratio) were <1 in all inflammatory diseases and not significantly elevated vs. controls.

Bell's palsy: electrodiagnostics are not indicative of cerebrospinal fluid abnormalities.

Electrodiagnostic testing (electromyography, electroneuronography, and blink reflex) and cerebrospinal fluid (CSF) examination (cell count, immunoglobulins, and antigen-specific intrathecal immunoglobulin G synthesis against herpes simplex virus, varicella zoster virus, cytomegalovirus, and Borrelia burgdorferi sensu latu) were performed in 56 patients with Bell's palsy. The CSF was normal in 45 patients and abnormal in 11 patients. Acute borreliosis was the most common specific pathological CSF finding (4 of 11). Electromyography revealed abolished volitional activity in 22% of patients with normal CSF and in 36% with pathological CSF. Electroneuronographic tests with an amplitude decrease of more than 90% on the affected side or abolished responses were found in 20% of patients with normal CSF and in 18% with pathological CSF. Abolished orbicularis oculi reflexes were seen in 67% of patients with normal CSF and in 82% with pathological CSF Concerning electrodiagnostic testing, no statistically significant difference between patients with normal and abnormal CSF was found, so we conclude that electrodiagnostic testing has no indicative value for abnormal CSF in Bell's palsy.