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)

This study reports results from experiments designed to test common, clinically useful anti-convulsants for their effectiveness, if any, against the high pressure nervous syndrome (HPNS) in rats. Phenytoin, carbamazepine, phenobarbitone, or diazepam were administered orally to rats before compression. Endpoints used to assess the progression of the HPNS were T1, T3, and T5 (onset of, continuous, and severe tremor), myoclonus, and seizures. Of the four drugs tested, only phenobarbitone increased the onset pressure for tremor and seizures by: T1 33%; T3 11%; T5 14%; seizures 10%. Neither phenytoin, carbamazepine, nor diazepam had any significant effect on any of the endpoints studied. High dose chronic pretreatment with phenytoin also had no effect on the HPNS. These data suggest that conventional anticonvulsant treatment would be of limited value for HPNS in man, and the lack of effect also suggests that HPNS seizures are of an unusual type.
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PMID:Effects of four common anticonvulsants on the high pressure nervous syndrome in the rat. 153 60

Rats were given 75 mg/kg of 5,5-diphenylhydantoin (phenytoin) or vehicle 30 min prior to 75 mg/kg of 1,1,1-trichloro-bis(p-chlorophenyl)ethane (p,p'-DDT) (p.o.) or chlordecone (i.p.) and tremor was measured 12 h later. Rats were then killed, and regional brain levels of biogenic amines and their acid metabolites and amino acids were determined. Pretreatment with phenytoin significantly attenuated the tremor produced by p,p'-DDT but enhanced that produced by chlordecone. p,p'-DDT had significant effects on the levels of aspartate, glutamate, 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG), whereas chlordecone increased glycine, 5-HIAA, and MHPG levels. Pretreatment with phenytoin blocked p,p'-DDT-induced increases of aspartate in the brainstem and spinal cord, 5-HIAA in the hippocampus, and MHPG in the brainstem and hypothalamus. Phenytoin significantly enhanced chlordecone-induced increases of MHPG in the brainstem. These data indicate that organochlorine-induced increases in noradrenergic activity in the brainstem and spinal cord may be directly related to the tremorigenic effects of these chemicals.
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PMID:5,5-Diphenylhydantoin antagonizes neurochemical and behavioral effects of p,p'-DDT but not of chlordecone. 243 63

Phenytoin suspension (PHY-S) is reported to settle, resulting in uneven drug distribution and variable patient dosing. We designed this study to determine the rate of settling and the amount of agitation needed to resuspend the preparation. To determine the rate of settling, we thoroughly shook three bottles of PHY-S and then left them undisturbed. We took samples from the top and bottom of each bottle with a microsyringe at 15 minutes, 1, 6, 12, 24, 48, and 72 hours, and 1, 2, 3, 4, and 5 weeks. We simulated patient administration with daily doses that were measured under good, fair, and poor shaking techniques. We analyzed samples after every tenth dose. After complete resuspension the active ingredient in PHY-S settles at a very slow rate. We found no differences in concentration between the top and bottom until the fifth week in the bottles thoroughly shaken and left undisturbed. Minimal agitation is required to resuspend PHY-S. The well-shaken and poorly shaken bottles in the patient simulation phase exhibited no differences in concentrations whereas the unshaken bottle had differences throughout the study period. Problems thought to be associated with PHY-S may be related to compliance and inaccurate measuring devices.
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PMID:The effects of storage and shaking on the settling properties of phenytoin suspension. 258 85

A patient with recessive generalized congenital myotonia and severe, disabling weakness underwent various forms of treatment while being monitored electrophysiologically. Phenytoin, verapamil, and acetazolamide were ineffective, but tocainide yielded good results. Improvement was dose-dependent, and was limited by irritability and action tremor when the patient was taking 1,600 mg per day.
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PMID:Successful treatment with tocainide of recessive generalized congenital myotonia. 308 70

Pretreatment of rats with hydantoin (75 mg/kg, PO, an anticonvulsant), trihexyphenidyl (10 mg/kg, SC, a muscarinic cholinergic antagonist), or piperonyl butoxide (500 mg/kg, PO, a metabolic inhibitor) had no effect on the whole blood or brain tissue levels of orally administered DDT (75 mg/kg) or its metabolites DDD and DDE. Hydantoin and piperonyl butoxide decreased DDT-induced tremor and hyperthermia due to DDT when measured 12 h after DDT exposure, while trihexyphenidyl augmented some components of DDT-induced tremor. Additional experiments found that pretreatment with piperonyl butoxide increased tremor due to permethrin exposure (120 mg/kg, PO), while having no effect on tremor due to chlordecone administration (60 mg/kg, IP). Pretreatment with ellipticine (30 mg/kg, IP, a metabolic inhibitor) also decreased tremor 12 h after DDT exposure. The effects of piperonyl butoxide and ellipticine on DDT-induced tremor are postulated to occur through direct actions of these compounds on nerve or muscle tissue. Hydantoin-induced attenuation of DDT-induced neurotoxicity may be due to the ability of hydantoin to block repetitive firing of nerves by binding to the inactivation gates of sodium.
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PMID:Pharmacological modification of DDT-induced tremor and hyperthermia in rats: distributional factors. 308 50

The influence of antiepileptic drugs on the wet dog shakes (WDS) induced by intracerebroventricular injections of carbachol (30 micrograms icv) was investigated in rats. Diphenylhydantoin (DPH, 8 and 4 mg/kg), diazepam (0.4, 0.2 and 0.1 mg/kg), phenobarbital (12.5, 6.25 and 3.12 mg/kg), sodium valproate (Depakine, 200, 100 and 50 mg/kg) and trimethadione (200, 100 and 50 mg/kg) given ip inhibited the WDS in a dose-dependent manner. These drugs at the same doses did not change the intensity of shaking behavior induced by lithium chloride or 5-hydroxytryptamine. As the antiepileptic drugs tested in these experiments did not have anticholinergic activity and at used doses were not able to prevent electrical convulsions or pentetrazol-induced seizures, it appears that carbachol-induced WDS could be connected with convulsive activity and could be the initial stage of seizures.
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PMID:Inhibition by antiepileptics of carbachol but not lithium- or 5-methoxytryptamine-induced wet dog shakes in rats. 314 10

In order to elucidate the fundamental differences between alcohol and barbital physical dependence, comparative studies were made on the effect of various drugs on the withdrawal signs developed in alcohol and barbital dependent mice. Ethanol, barbital and diazepam, drugs of alcohol-barbiturate type dependence liability, and ethosuximide, an anticonvulsant, suppressed both withdrawal signs in a dose dependent manner. The effects of these drugs were different from each other only quantitatively and no special difference was observed between the effects on alcohol and barbital withdrawal signs. On the other hand, the effects of phenytoin, an anticonvulsant, and pentylenetetrazol, a convulsant, were only evident in alcohol dependent animals. Phenytoin elicited body tremor and markedly exacerbated the alcohol withdrawal signs, but slightly suppressed the barbital withdrawal signs. Dose-response curves for the convulsive effect of pentylenetetrazol obtained at the peak of the withdrawal signs shifted greatly to the left in alcohol withdrawn animals but less in barbital withdrawn animals. These discrepancies between the effects on alcohol and barbital withdrawal signs may suggest a difference in the underlying mechanisms for the production of alcohol and barbital physical dependence.
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PMID:Differentiation of alcohol and barbital physical dependence. 377 53

Rats given a tremorigenic dose of DDT (75 mg/kg, PO) were treated with pharmacological agents either 30 min prior to DDT or 1-2 h prior to testing at the time of peak effect (12 h postdosing). The administration of mephenesin (a centrally acting muscle relaxant) or Dilantin (an anticonvulsant) prior to DDT significantly attenuated tremor. Pretreatment with pizotifen (a serotonergic receptor antagonist) had no significant effect on tremor. Administration of the same agents 1-2 h prior to measurement had minimal effects. Trihexyphenidyl (a muscarinic cholinergic receptor antagonist) exacerbated the tremor produced by DDT. These data suggest that cholinergic neurotransmitter systems may be involved in DDT-induced tremor. That DDT-induced tremor was significantly attenuated by mephenesin and Dilantin is in accord with the conclusion that DDT-induced tremor is a manifestation of repetitive discharge due to interference with ionic conductance.
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PMID:DDT-induced tremor in rats: effects of pharmacological agents. 392 13

We examined the effects of conventional antiepileptic drugs (AEDs) on absence-like seizures in homozygous tremor rats (tm/tm) to determine if they corresponded pharmacologically to human absence seizures and absence-like seizures in spontaneously epileptic rats (SER: zi/zi, tm/tm) with both tonic convulsive and absence-like seizures. Cortical and hippocampal EEG activity was recorded with chronically implanted electrodes. The effects of AEDS on seizures of the tremor rat showed profiles similar to those observed in human absence seizures and also in absence-like seizures of SER. The absence-like seizures, associated with paroxysmal bursts of 5-7-Hz spike-wave complexes, were inhibited by trimethadione (TMO 200 mg/kg intraperitoneally, i.p.), ethosuximide (ESM 100 and 200 mg/kg, i.p.), valproate (VPA 100 mg/kg, i.p.), and phenobarbital (PB 10 and 20 mg/kg, i.p.). Phenytoin (PHT 20 mg/kg, i.p.) was ineffective. These results are consistent with the conclusion that the tremor rat is a useful model for evaluating new AEDS for human absence seizures.
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PMID:Effect of antiepileptic drugs on absence-like seizures in the tremor rat. 764 34

A case is described of a patient with limb shaking in whom anticonvulsant therapy was effective for inhibiting attacks. A 70 year old female developed rhythmical involuntary limb shaking of the right upper and lower limb in April 1986. She was diagnosed as having transient ischemic attacks and was followed up under treatment with an antiplatelet drug. Subsequently, anticonvulsant therapy was also initiated on an outpatient basis. In August 1991, she was admitted with shaking of the right upper and lower limbs. Low molecular dextran was ineffective for inhibiting limb shaking attacks, but intravenous injection of diazepam was effective. Phenytoin and phenobarbital was used in combination. No limb shaking attacks occurred thereafter. The involuntary movement was the same as that observed at the onset of the disease. Though no changes were observed in the pattern of the involuntary movement, anticonvulsant therapy was effective in preventing and inhibiting attacks. This finding is inconsistent with previous reports. It is possible that epileptic factors are involved in the development of this condition.
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PMID:Effective anticonvulsant therapy in a patient with limb shaking: a case report. 860 39


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