Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of i.c.v. administration of dodecasodium and dicalcium inositolhexakisphosphate (Na12IP6 and Ca2IP6, respectively) to mice and rats was studied. In mice, Na12IP6 (1-300 nmol) or Ca2IP6 (10-500 nmol) induced: ataxia, ground-hugging, tremor (often continuous), scratching, hyperlocomotion, wild running, myoclonic jerks, jumping, clonic muscle spasms, tonic seizure, followed by death or full recovery. The CD50 values for clonic seizures for Na12IP6 and Ca2IP6 were 16 and 49 nmol, respectively. The convulsant effect of Na12IP6 (15 nmol i.c.v.) was not blocked by pretreatment with D(-)-4-(3-phosphonoprop-2-enyl)-piperazine-2-carboxylate, but was dose dependently reduced by pretreatment with CaCl2 (30-60 nmol i.c.v.) and abolished by coadministration of CaCl2 (30 nmol) with Na12IP6 (i.c.v.). In rats, Na12IP6 (50 nmol i.c.v.) induced severe electroencephalographic seizures in the hippocampus and cortex. The potent convulsant effect of IP6 (administered i.c.v.) depends at least in part on a calcium-chelating action.
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PMID:Inositolhexakisphosphate is convulsant in mice and rats in the nanomolar range. 208 46

The high pressure neurological syndrome (HPNS) occurs when man or animals are exposed to hyperbaric pressure. Four non-competitive N-methyl-D-aspartate (NMDA) antagonists - MK-801, phencyclidine (PCP), SKF 10,047 and ketamine were tested in rats for effects on the HPNS. All drugs were injected i.p. prior to compression; ketamine was also infused i.v. Control rats received saline. Rats were exposed individually to increasing helium pressure (PO2 0.5 atmospheres absolute ATA). Three endpoints were used to assess HPNS: onset pressures for tremor, myoclonus and convulsions. Neither MK-801 (0.03 and 0.3 mg/kg) nor SKF 10,047 (50 mg/kg) had any effect on the onset pressures for tremor, myoclonus or convulsions, although the type of seizure was modified from the clonic/tonic seizure seen in controls to purely clonic. PCP (5 mg/kg) had no effect on the endpoints, but pressure enhanced the excitation and stereotypy seen at 1 ATA. Ketamine (100 mg/kg i.p.) did not affect tremor or myoclonus; ketamine infused i.v. at pressure only prevented tremor and myoclonus at 'anaesthetizing' concentrations. Our results show that these non-competitive NMDA antagonists had little effect on HPNS, in contrast to competitive NMDA antagonists, such as AP7, which are highly effective. Possible explanations for this lack of effect include (1) interactions with NMDA receptor channels are pressure dependent; (2) other actions of these antagonists override their effects on the NMDA receptor channel.
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PMID:The effects of non-competitive NMDA receptor antagonists on rats exposed to hyperbaric pressure. 254 78

Six dogs were, under constant environmental conditions, treated for 7 weeks with clonazepam (0.5 mg/kg b.i.d. orally). Already after 1 week of treatment, slight symptoms of withdrawal could be elicited by intravenous injection of flumazepil (Ro 15-1788). When clonazepam was finally withdrawn, a self-limiting abstinence syndrome was observed in all dogs, consisting of behavioral alterations (listlessness, wet dog shakes, dorsal recumbency), tremor, a severe clonic-tonic seizure in 1 case, hyperthermia, and weight loss. The syndrome was most pronounced on days 2 and 3 after withdrawal, after 1 week all signs of physical dependence had disappeared.
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PMID:Physical dependence on clonazepam in dogs. 308 Jul 62

In common with other dysmyelinating mutants, the myelin-deficient rat displays an action tremor and tonic seizures culminating in the death of the animals at approximately 23-26 days. We find that deep lesions of the cerebellar vermis alleviate the manifestations of the myelin deficiency significantly. Such lesions introduced at 20 days or later eliminate both tremor and seizures for periods up to 10 days. Lifespan is prolonged to nearly 30 days, on average, and to 35 days in some cases. Shallow lesions of the vermis or lateral lobe lesions have relatively little effect. Based on these observations we suggest that the cerebellum contributes not only to the action tremor but also to the tonic seizures characteristic of central myelin deficiency. Spontaneous activity originating in myelin-deficient fiber tracts may be carried to the cerebellum and processed there to produce a highly amplified and/or synchronized output to broad areas of the neuraxis. Deep lesions of the vermis presumably interfere with cerebellar output and compromise the cerebellar contribution to the seizures. Tonic seizures and other 'paroxysmal attacks' also occur commonly in human demyelinating diseases including multiple sclerosis [11]. Manipulation of cerebellar output offers a potential approach to the control of such spontaneous activity.
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PMID:Effects of cerebellar lesions on tonic seizures, tremor and lifespan in myelin-deficient rats. 795 81

Experiments on male Wistar rats and Icr:Icl mice studied the influence of the novel compound--amino acid-containing 1,4-dihydropyridine derivative glutapyrone (G) on acute generalized seizures, arecoline and nicotine tremor, and 45Ca2+ uptake in brain synaptosomes. It was shown that G produced significant antiepileptic effects on models of acute pentylenetetrazole seizures on rats and mice. Efficiency of antiepileptic effect depended on a dose and method of modeling seizures: it was more effective in case of intravenously pentylenetetrazole-induced seizure tested by clonic and tonic seizure components and death. The results suggest the participation of GABAergic system in realization of antiepileptic effect of G. Glutapyrone did not influence the 45Ca2+ uptake by rat cortical synaptosomes (evoked by a 1-min depdariration with 55 mM K+), this suggests that G lacked calcium antagonist properties characteristic of 1,4-dihydropyridine compounds such as nifedipine, nimodipine. In addition, G does not affect N- and M-cholinergic processes.
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PMID:[The anticonvulsant properties of glutapyrone--a new type of derivative of amino acid-containing 1,4-dihydropyridines]. 811 3

Spontaneously epileptic rats (SER) are a double mutant (zi/zi, tm/tm) obtained by mating the tremor rats with another tremulous mutant, zitter rats, and spontaneously exhibit absence-like seizures, tonic convulsions and wild jumping or running episodes. In addition, SER exhibit retardation in learning ability under differential reinforcement at a low rate (DRL)-5 sec schedule of food reinforcement in operant behavior at 14 to 15 weeks of age. We examined the long-term effects of phenobarbital (PB) on total bar presses, reinforcements and inter-response time distribution to assess whether the poorness of learning ability in SER can be ascribed to frequent occurrence of seizures. Food pellets containing 0.1% PB were given ad libitum to male SER from 7 weeks, and operant behavior was examined at 13 to 14 weeks of age. Tonic seizures and wild jumping or running episode were inhibited effectively and poor operant performance was significantly improved by continual intake of PB in SER.
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PMID:Improvement of poor operant performance by continual intake of phenobarbital in spontaneously epileptic rats. 811 37

A 50-year-old man who first noticed shaking of the hands at age of 18 and had previous history of three convulsive episodes was admitted to our department because of the generalized tonic seizure with loss of consciousness. Family history showed that 7 members had similar shaking and one had generalized seizure. On neurological examination, rhythmic myoclonic jerks were noted in the bilateral upper limbs, and was remarkably more severe on the left. Other neurological findings were normal. Based on the benign clinical course, familial history, and the normal range of pyruvate and lactate levels in serum and cerebrospinal fluid, we diagnosed familial essential myoclonus and epilepsy (FEME)/benign adult familial myoclonic and epilepsy (BAFME). After admission, we performed electrophysiological test. EEG showed spike discharge mainly in the left parietooccipital lobe. Jerk-locked back averaging (JLA) showed spikes 30 msec precedings the trigger in the left parietooccipital lobe. Because JLA spikes are commonly found 20 msec precedings the trigger, we consider the subtraction time of 10 msec was due to the conduction through the corpus callosum. Some reports showed that in progressive myoclonus epilepsy patients, transcallosal excitation of one hemisphere by the other was critical for generalized seizure. In cases of FEME/BAFME, epileptic focus in the hemisphere ipsilateral to the myoclonus limbs has not previously reported. Our case suggested that generalization of the seizure was caused by the interhemispheric excitation through the corpus callosum.
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PMID:[A case of familial essential myoclonus and epilepsy with suspected focus in the hemisphere ipsilateral to myoclonus limbs]. 1532 40