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

1. The effects of some centrally acting muscle relaxants on the post-rotatory nystagmus induced by rotatory stimulation were investigated in the rabbit, to examine the action of the drugs on vestibular function. 2. Tolperisone-HCl (5-10 mg/kg, i.v.) and baclofen (1-3 mg/kg, i.v.) decreased the number of post-rotatory nystagmus beats dose-dependently, whereas mephenesin (40-80 mg/kg, i.v.) and diazepam (0.5-1.0 mg/kg, i.v.) prolonged it dose-dependently. 3. The inhibitory effects of tolperisone-HCl and baclofen may provide some suggestions as to the mechanisms and sites of actions of centrally acting muscle relaxants, while the significance of the prolonging action of mephenesin remains unclear. 4. The prolonging action of diazepam is discussed with reference to GABAergic mechanisms.
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PMID:Effects of centrally acting muscle relaxants on post-rotatory nystagmus in the rabbit. 270 72

1. To determine how the GABAergic mechanism operates in the generation of post-rotatory nystagmus, an experiment was performed with GABAergic drugs in rabbits. 2. Subconvulsive doses of picrotoxin (0.3-0.6 mg/kg, i.v.) and bicuculline (0.1 mg/kg, i.v.) decreased the number of post-rotatory nystagmus beats, whereas strychnine sulphate, at a subconvulsive dose (0.1 mg/kg i.v.), increased it. 3. Diazepam (1 mg/kg, i.v.) remarkably increased the number of post-rotatory nystagmus beats. Pretreatment with picrotoxin (0.45 mg/kg, i.v.), bicuculline (0.1 mg/kg, i.v.) or semicarbazide-HCl (180 mg/kg, i.v.) antagonized the effects of diazepam (1 mg/kg, i.v.). 4. GABAergic mechanisms may play a modulatory role in the production of nystagmus rhythm. Strychnine-sensitive neurons involved in the vestibular mechanism may behave in a different manner from picrotoxin-sensitive neurons.
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PMID:Modulatory roles of GABAergic mechanisms in post-rotatory nystagmus in the rabbit. 271 19

Dextrorphan HCl (Ro 01-6794/706) is an NMDA receptor antagonist with clinical potential for administration in an elderly population of acute ischemic stroke patients. In vivo experience with such patients demonstrated a consistent pharmacologic effect/adverse experience profile that is typical of an NMDA receptor antagonist (e.g., nystagmus, nausea, vomiting, agitation, somnolence, hallucinations and hypertension). For the most part, these pharmacologic effects were mild to moderate in severity; short-lived; reversible; not life-threatening and subjectively tolerated. The most serious pharmacologic effect produced by dextrorphan administration was hypotension, which occurred within a well-defined window of 90 minutes from the start of the loading dose infusion in patients who received 200 mg/hr or greater loading dose infusions. In all cases it was reversible without neurologic sequelae. Careful review of demographic and pharmacokinetic parameters did not demonstrate any overriding factor(s) to the production of hypotension other than the rate of the loading dose infusion. Severe hypotension, severe decreased levels of consciousness and respiratory depression should not be generally expected at loading doses less than 200 mg/hr. In summary, dextrorphan can be safely given to an elderly population of ischemic stroke patients as a loading dose rate below 200 mg/hr and as a maintenance dose rate between 50-90 mg/hr for 24 hours when patients are monitored carefully for pharmacologic effects.
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PMID:Safety, tolerability and pharmacokinetics of the N-methyl-D-aspartate antagonist Ro-01-6794/706 in patients with acute ischemic stroke. The Dextrorphan Study Group and Hoffmann-La Roche. 748 11

Following a double-blind, four-way crossover design, 32 healthy volunteers (20 males and 12 females) each consumed lactose placebo, or 80, 120 or 160 mg quinine HCl daily for 21 days. Before dosing and at regular intervals during dosing, blood and urine samples were collected and analysed for quinine HCl. Electrocardiography, heart rate, blood pressure, audiometry, peripheral field, funduscopy, colour vision, visual acuity, electronystagmography (ENG) and test for optokinetic nystagmus were all evaluated before dosing and at selected times during dosing. The results showed that daily consumption of up to 80 mg quinine HCl did not significantly alter physiological, ophthalmic or audiometric responses. ENG determination showed that 12.5% of volunteers given lactose placebo or 80 mg quinine HCl exhibited at least one transitory period of ocular motor oscillations. This phenomenon was observed in 18.8% (P < 0.05) of volunteers with a daily intake of 120 mg quinine HCl or more. However, there was not a significant dose-related correlation between nystagmus and daily intake of quinine HCl. Five volunteers consuming lactose placebo displayed an aberrant ocular flutter that decreased significantly (P < 0.05) as the daily intake of quinine HCl increased. One volunteer showed a change in perception of red/green colour vision after taking 160 mg quinine HCl for 21 days. This study demonstrated that the no-untoward-effect level of quinine HCl is at least 80 mg/day.
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PMID:Toxicity threshold of quinine hydrochloride following low-level repeated dosing in healthy volunteers. 847 13

Previous studies have demonstrated that vestibular compensation, the process of behavioural recovery which occurs following unilateral deafferentation of the vestibular labyrinth (UVD), is correlated with changes in in vitro phosphorylation of various protein substrates in the brainstem vestibular nucleus complex (VNC). The aim of the present study was to investigate the possible causal relationship between protein kinase activity and the induction of the vestibular compensation process, by delivering inhibitors of protein kinase C (PKC) or Ca(2+)/calmodulin-dependent kinase II (CaMKII) into the ipsilateral VNC at the time of the UVD and determining their effects on three static symptoms of UVD, spontaneous nystagmus (SN), yaw head tilt (YHT) and roll head tilt (RHT) in guinea pigs. Infusion of the PKC inhibitor, 3-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-4-(1H-indol-3-yl)-1H-pyrr ole-2,5-dione, HCl (bisindolylmaleimide I, HCl/GF 109203X, HCl) ('Bis I'), at a concentration of 5 or 50 microM, significantly increased SN frequency at the earliest time points (6 and 8 h post-UVD) compared to vehicle controls and the less selective analogue, 2,3-bis(1H-indol-3-yl)-N-methylmaleimide (bisindolylmaleimide V) ('Bis V'). However, the compensation of YHT and RHT was unaffected by the PKC inhibitor. By contrast, the cell-permeable CaMKII inhibitor, myristoylated autocamtide-2 related inhibitory peptide (N-Myr-Lys-Lys-Ala-Leu-Arg-Arg-Gln-Glu-Ala-Val-Asp-Ala-Leu-OH) ('myr-AIP') or the cell-impermeable analogue, autocamtide-2 related inhibitory peptide (N-Lys-Lys-Ala-Leu-Arg-Arg-Cln-Glu-Ala-Val-Asp-Ala-Leu-OH) ('AIP'), failed to alter the compensation of SN, YHT or RHT at any dose compared to vehicle controls. These results implicate PKC-, but not CaMKII-, signal transduction pathways in the initiation of SN compensation in guinea pig.
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PMID:The effects of protein kinase C and calmodulin kinase II inhibitors on vestibular compensation in the guinea pig. 1105 83