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Tumor necrosis factor‐α response and herpesvirus infection in bell's palsy
Author(s) -
Larsson Christina,
BernströmLundberg Christina,
Edström Staffan,
Bergström Tomas
Publication year - 1998
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1097/00005537-199808000-00013
Subject(s) - bell's palsy , medicine , palsy , polymerase chain reaction , cerebrospinal fluid , immunology , tumor necrosis factor alpha , serology , cytokine , herpesviridae , herpes simplex virus , pathology , antibody , gastroenterology , virus , viral disease , biology , biochemistry , alternative medicine , gene
Objectives : To attempt early diagnosis of patients with Bell's palsy by detection of herpesviral DNA in body fluids, and to investigate whether tumor necrosis factor‐α (TNF‐α), a cytokine associated with demyelination, is involved in the inflammatory response in this disease. Study Design : Eleven patients with acute facial palsy admitted within 1 week after onset of the disease were followed in a consecutive prospective study. Methods : Antibodies reactive to herpesviruses were determined by enzyme‐linked immunosorbent assay in serum samples from acute and convalescent (> 2‐week interval) cases. Intrathecal antibody response was investigated by immunoblotting. Polymerase chain reaction amplification of herpesviral DNA was attempted from samples of serum, cerebrospinal fluid, tear fluid, and saliva. TNF‐α and its soluble receptors (types I and II) were assessed in serum and cerebrospinal fluid samples. Results : Ten of the 11 patients demonstrated serologic evidence of herpesviral primary infection or reactivation, supporting the evidence that herpesviruses are the most prevalent etiologic agents in Bell's palsy. Despite this, DNA amplifications by polymerase chain reaction were negative for herpesviruses in the body fluids tested. TNF‐α concentrations were significantly elevated in serum, as compared with controls. Only one patient had a remaining facial nerve dysfunction at follow‐up after 3 months. Conclusion : The absence of herpes DNA in body fluids in the acute stage of serologically confirmed Bell's palsy suggests that viral replication is transient in cases with an early restoration of the facial nerve function. The elevated serum levels of TNF‐α indicate that this cytokine might be a pathogenetic factor related to the demyelination in this disease.