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 paper describes the EEG profiles, observed in rabbits, of drugs which affect GABA synaptic activity at GBB complex. Drugs which enhance GABA synaptic activity induce sedation associated with EEG synchronization. However, muscimol, THIP, GHB and baclofen induce signs of CNS stimulation (light tremors of the forelimbs, chewing, light nystagmus and hyperpnea) associated with EEG spikes. Signs of light stimulation (chewing and jerks of the head) also occur after BDZs and barbiturates, and are associated with the presence of 12-24 and 20-25 Hz waves, respectively. Drugs which reduce GABA synaptic activity (bicuculline, inverse BDZ agonists, PTZ, picrotoxin and Ro 5-3663) induce three dose-dependent stages of EEG changes: trains of slow waves, trains of spike-and-wave complexes and paroxysmal activity in the rostral encephalic structures without apparent changes of the electrical activity in the spinal cord. The first two stages are associated with a behavioral state of alert and the third stage with tonico-clonic convulsions. Among the inverse BDZ agonists, DMCM and beta-CCM elicit all three stages, whereas FG 7142 and beta-CCE induce only the first two and CGS 8216 only the first. The BDZ antagonists Ro 15-1788 and Ro 15-3505 (0.2-30 mg/kg IV) do not significantly affect the EEG pattern. However, they selectively inhibit the effects of diazepam and of the inverse BDZ agonists. In both cases, the inhibition is observed with doses as low as 0.2 mg/kg IV and leads to an EEG desynchronization. The possible involvement of the modifications of GABA synaptic activity in the etiology of both petit mal and grand mal epilepsies is discussed.
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PMID:Electroencephalographic investigations in rabbits of drugs acting at GABA-benzodiazepine-barbiturate/picrotoxin receptors complex. 299 34

Obstructive cardiomyopathy has been reported in cases of male and female Turner phenotype with normal chromosomes. We report here a case of a male dwarf with bilateral undescended testes and biventricular obstructive cardiomyopathy. Clinical features included choreoathetoid movements, chorioretinitis, bilateral nystagmus, and unusual red color of the hair, associated with some features of Turner phenotype. Endocrine studies were normal except for a lack of thyrotrophic stimulating hormone (TSH) stimulation. Propranolol removed the gradient during cardiac catheterization and relieved the exertional chest pain clinically.
Clin Cardiol 1982 Apr
PMID:Obstructive cardiomyopathy in a male dwarf with cryptorchidism. 612 97

We studied the antiarrhythmic effect of oral Mexiletine in 20 patients with stable high-frequency ventricular arrhythmias refractory to therapeutic doses of conventional antiarrhythmic therapy. Arrhythmias were classified according to modified grading system of Lown and Wolf. The efficacy of Mexiletine was assessed with use of both the arrhythmic modified classification of Lown and Wolf and count of premature ventricular beats (PVB) from 24 hours ambulatory electrocardiographic recordings. The dose of Mexiletine was 300 mg every 8 hours; 24 hours ECG recordings were obtained in each patient on days 5,15 and 20 during Mexiletine therapy. The worst of tracings before and during Mexiletine therapy was compared. Mean decrease in PVB was 57% (P less than 0.001). The decrease in PVB was more than 80% in 11 patients. Comparison of the grade of arrhythmias disclosed a favorable effect of Mexiletine in 13 patients, a worsening in 1, and no effect in 6. Classification of the most severe arrhythmia revealed a significant decrease from an average grade of 3.05 to 1.75 (P less than 0.01). Before Mexiletine therapy, 40% of our patients were in Class 0 to II and 60% were in Class III or V, whereas during Mexiletine therapy the corresponding proportions were 75% and 25% respectively. Side effects (confusion, tremors, gastro-intestinal complaints) prompted reduction of the dose in 3 patients. Three additional patients had transient minor side effects (dizziness, nystagmus and gastrointestinal disorders) that did not necessitate a change in therapy and 14 patients reported no side effects. In conclusion our data suggest that Mexiletine is an effective agent in the long-term treatment of serious ventricular arrhythmias refractory to other agents. Since Mexiletine therapy is not associated with severe long-term side effects, it should now be possible to determine its role as a first-line drug for treating ventricular arrhythmias.
G Ital Cardiol 1981
PMID:[Mexiletine in treatment of chronic ventricular refractary arrhythmias (author's transl)]. 616 80