Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bell's palsy or idiopathic palsy is the most common disorder affecting the facial nerve. Diagnosis is primarily one of exclusion. There is typically an acute unilateral facial paresis that evolves in 24 to 48 hours. Etiology and pathophysiology are heavily disputed, and as of yet unknown. The natural history of Bell's palsy is favorable. Eight-four percent show satisfactory recovery without any treatment, however 16% suffer moderate to severe sequelae. Prognosis is influenced by degree of paresis, age of patient, and time until first signs of recovery. Prognostic testing currently involves various electrophysiological tests. More than 90% degeneration of the facial nerve carries a poor prognosis for recovery; these are the patients who may benefit from facial nerve decompression surgery. If surgery is performed it should be done early (< 21 days from onset of palsy) and should include a middle cranial fossa decompression. Steroids are generally agreed to be beneficial. Acyclovir would seem to be a promising drug; however studies have not adequately assessed its use.
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PMID:Management of Bell's palsy. 881 19

Delayed facial palsy after acoustic neuroma resection may occur in up to 15% of cases. Prognosis is generally good if the palsy does not progress to total paralysis. However, a delayed palsy with subsequent total paralysis has a more variable final outcome, which ranges from normal function to permanent total paralysis. This delayed paralysis has been attributed to edema from surgical manipulation of the facial nerve. Steroids and intraoperative decompression of the meatal foramen have been used with some success, but some cases remain refractory to these measures. Herpes simplex virus and varicella-zoster virus are ubiquitous in the population and remain in a latent state in neural ganglia. These viruses are reactivated during times of stress. Trigeminal nerve surgery (partial sensory rhizotomy and microvascular decompression) stimulates reactivation of herpes simplex with manifestations in the sensory distribution of the trigeminal nerve in 38-94% of procedures. Prevention of this reactivation has been demonstrated in placebo-controlled trials by using prophylactic acyclovir. We present a patient who underwent translabyrinthine resection of an intracanalicular acoustic neuroma and in whom developed otalgia, vesicles on the ear canal and the ipsilateral buccal mucosa, and progressive facial palsy the week after surgery. Serologic evaluation confirmed the diagnosis of herpes zoster oticus. Reactivation of latent virus apparently occurred as a result of surgical manipulation of the facial nerve. This parallels viral reactivation seen in trigeminal nerve surgery. We propose a new theory for an additional cause of delayed facial palsy after acoustic neuroma resection-reactivation of latent herpesvirus resulting from surgical trauma. Acyclovir should be evaluated in clinical trials for a prophylactic role in patients undergoing acoustic neuroma resection or a therapeutic role in patients in whom a delayed postoperative facial palsy develops.
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PMID:Delayed facial palsy after acoustic neuroma resection: the role of viral reactivation. 884 11