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)

This article reports an investigation into the vestibuloocular reflex (VOR) recorded in rats during acute nontoxic treatment with phenytoin (PHT). In animals adapted to the dark, latency and duration of postrotatory nystagmus (VAN), cumulative trend of slow phases (CTSP), slow-phase velocity, temporal trend of the frequency and amplitude of the nystagmic beats, and mean frequency-amplitude ratio were analyzed. Observations were correlated with plasma and brain levels of the drug. Results showed that an acute nontoxic dose of PHT impairs some parameters of the VAN. At low concentrations (8.24 +/- 2.56) (microgram/ml in plasma and 6.02 +/- 3.24 micrograms/g in brain), only CTSP and slow-phase velocity were remarkably modified in each animal. At higher concentrations but still subthreshold for evoking the appearance of evident signs of drug toxicity (17 +/- 6.13 micrograms/ml in plasma and 11.4 +/- 5.28 micrograms/g in brain), all parameters were modified in each animal. In the same animal, VOR impairment was always linearly correlated to the plasma and brain drug levels. A considerable individual biovariability in the drug response appeared, and an individual subtoxic threshold for each animal was evident. Thus, when results of all experiments were averaged, the statistical significance of the differences of the greater part of the VOR parameters disappeared. However, VOR analysis performed before and after drug administration, i.e., with each subject as its own control, proved to be an excellent diagnostic pointer to the approach of the particular subject's toxic threshold before the appearance of spontaneous nystagmus or postural impairments.
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PMID:Postrotatory nystagmus during phenytoin treatment. 372 Jun 97

In humans the influence of prior vestibular stimulation (3, 6, 9, 12, and 18 degrees/second2 for 10 seconds) and subsequent whole-field optokinetic stimulation (30, 60, 90, 120, and 180 degrees/second for 1 minute) or the presentation of a stationary pattern on after-nystagmus (AN) was studied. For comparison, pure vestibular and pure optokinetic stimuli also were employed. The presentation of a stationary pattern resulted in suppression of vestibular nystagmus, which recovered after the termination of fixation. Fixation during the period of AN I did not inhibit an AN II. During the combinations of vestibular and optokinetic stimuli when the elicited vestibular (VN) and optokinetic nystagmus (OKN) had the same direction, there was a weak AN I toward the direction of the preceding VN and OKN, and a strong AN II toward the opposite side. When VN had been opposite to the subsequent OKN, there was a strong AN I toward the direction of OKN; AN II toward the opposite direction was small or mostly absent. Thus, AN was always stronger into the direction opposite to the previously elicited VN, indicating that the vestibular afference is the predominant input to the VAN II-integrator.
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PMID:Aftereffects of vestibular and optokinetic stimulation and their interaction. 697 40