Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence suggests that many cranial nerve syndromes, such as migraine headache, acute vestibular neuronitis, globus hystericus, carotidynia, acute facial paralysis (Bell's palsy), and Meniere's disease, are caused by the neurotropic herpes simplex virus (HSV). Because transitory cranial nerve dysfunction during acute HSV infection can be asymptomatic but often occurs in conjunction with mucocutaneous vesicles, we tested five subjects with herpes labialis for cranial nerve dysfunction. Four of the subjects had hypesthesia of the trigeminal nerve (which recurred in two); four, hypesthesia of the glossopharyngeal nerve; and two, hypesthesia of the second cervical nerve. Three of the subjects had positional or spontaneous nystagmus (which recurred in one); one of the subjects had a unilateral, decreased caloric response of 50%. Unilateral weakness of the cricothyroid muscle or the palate occurred in three of the subjects (and recurred in one). Volitional electromyograms were normal in all the subjects, but two of the subjects had increased facial nerve latency (which recurred in one). Similar findings of an acute, transitory nature should suggest to the clinician a viral polyganglionitis caused by HSV infection.
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PMID:Herpes simplex polyganglionitis. 740 69

Abundant experimental research has shown the potentially damaging effects that the herpes simplex virus (HSV) may have on peripheral or central nervous pathways. Fifty subjects (ages 20-45) with labial herpes virus (HSV-1) and 15 (ages 25-35) with genital herpes virus (HSV-2) were studied through recording spontaneous and optokinetic nystagmus (OKN) and using the eye-tracking-test (ETT) by means of electronystagmography (ENG). Recording was carried out during the first two days after vesicular eruption and seven days later, when cutaneous manifestations had disappeared. Thirty-five of the 50 subjects with HSV-1 showed spontaneous nystagmus, frequently with a vertical component, which in most cases had disappeared by the seventh control day. We recorded qualitative alterations of OKN as well as ETT in 19 patients while in 3 subjects only ETT was abnormal. All the subjects were normal on the seventh control day. At no time did any of the patients with HSV-2 show objective signs involving the peripheral or central vestibular system. Our research shows that HSV infection, especially HSV-1 infection, determines subclinical alterations of the vestibular function, probably due to the involvement of the brainstem. Therefore the virus is to be taken into account in establishing the etiology of "unknown" vertigo.
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PMID:[Herpetic vestibular neuronitis: a hypothesis]. 825 8