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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 36-week controlled study, the efficacy of clonazepam administered with phenytoin and phenobarbital was evaluated in twenty-four epileptic mental patients suffering from major motor seizures. The patients were distributed in two strata according to the presence or the absence of chlorpromazine. As compared with placebo treatment in the chlorpromazine-free patients, a significant reduction in the frequency of the tonic-clonic seizures was observed during the 24-week clonazepam treatment. This effect could not be observed in the patients requiring the antipsychotic drug. The EEG performed before and at the end of the experimental period did not show any significant change. The most common adverse reactions to clonazepam were drowsiness and ataxia; they diminished with continued treatment.
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PMID:Clonazepam: its efficacy in association with phenytoin and phenobarbital in mental patients with generalized major motor seizures. 35 72

The anticonvulsant and CNS-depressant activities of 16 commercially available antiepileptics were subjected to regression analysis. For the maximal electroshock seizure test and pentylenetetrazol seizure threshold test, good correlations were obtained only after diazepam, clonazepam, and carbamazepam were deleted; for the median toxic dose (rotorod ataxia), all 16 compounds can be included in one single equation using log MW, log P, and dipole moment (mu) terms. For the anticonvulsant activities of 7-substituted 1,4-benzodiazepinones, a parabolic equation of pi combined with the Hammett sigma constant gave fair correlations for most derivatives examined in three different tests. Based upon the correlations obtained, further molecular modifications are suggested. The dipole moments of seven clinically used antiepileptic drugs were measured in 1,4-dioxane for the first time.
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PMID:Quantitative structure-activity relationships and dipole moments of anticonvulsants and CNS depressants. 43 70

Six cats with chronic progressive neurologic signs of ataxia, paresis, tremors, pupillary abnormalities and seizures had polioencephalomyelitis of probable viral origin. Lesions were most severe in the spinal cord. The uniformity in distribution and nature of the lesions in all six cats strongly suggested a common cause. The condition was compared with other viral infections of known and unknown cause.
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PMID:Polioencephalomyelitis in cats. 45 15

Two dogs that had been given phenytoin for control of seizures for approximately 1 year developed signs of phenytoin toxicosis (postural ataxia an d a hypermetric gait) when chloramphenicol was added to the therapeutic regimen. The signs of toxicosis disappeared within 24 hours after cessation of chloramphenicol treatment. Oral treatment of laboratory dogs with chloramphenicol (50 mg/kg, TID for 3 days) prior to intravenous injection of phenytoin increased the half-life of phenytoin from 3 hours to 15 hours. Dogs infused with phenytoin during pentobarbital anesthesia had little or no change in serum phenytoin concentration during a 2-hour postinfusion observation period, which was unexpected for the intravenous route of administration.
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PMID:Interaction of phenytoin with chloramphenicol or pentobarbital in the dog. 50 Apr 38

Eleven dogs with signs of lead poisoning were examined. The principal clinical signs were neurologic and included ataxia, tremors, clonic-tonic seizures, amaurosis, and deafness. Basophilic stippling and circulating nucleated red cells were not common findings in blood films. Blood lead values varied from 0.22 ppm to 0.63 ppm before treatment. Electroencephalographic changes in nonsedated dogs were marked by intermittent high-amplitude slow wave activity.
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PMID:Clinical, clinicopathologic, and electroencephalographic features of lead poisoning in dogs. 50 Apr 42

We have compared the sleep-producing effects of thalidomide and pentobarbital. In a dose range that did not produce ataxia, thalidomide increased slow wave sleep and rapid eye movement sleep in cats (2-8 mg/kg p.o.) and rats (16 mg/kg p.o.). Pentobarbital had hypnotic activity in the same dose range but produced ataxia also at these doses. Thalidomide reduced spontaneous activity of both mice and rats. This occurred over a dose range of 8 to 1000 mg/kg p.o., but plateaued at a level of activity well above the complete inactivity of anesthesia that occurred with pentobarbital at well above the complete inactivity of anesthesia that occurred with pentobarbital at doses (greater than or equal to 32 mg/kg p.o.) above the hypnotic range. Several simple screens for thalidomide-like activity have been described which, together, could facilitate the search for thalidomide-like hypnotics. Pentobarbital, at doses 3 to 10 times the hypnotic range, prevented audiogenic seizures in physically dependent rats withdrawn from sodium barbital but thalidomide did not substitute for barbiturates even at doses 30 times those that increased sleep. Thalidomide, but not pentobarbital, enhanced the sleep-producing effect of electrical stimulation of basal forebrain in cats. The latter two findings suggest that thalidomide probably has a mechanism of action different from that of pentobarbital and that this may involve the activation of a sleep center in the forebrain.
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PMID:A comparison of thalidomide and pentobarbital - new methods for identifying novel hypnotic drugs. 56 42

A boy with mild hand tremor since age 2 1/2 was found at 4 to have cherry-red spots and mild trucal ataxia without seizures or dementia. Biochemically, he had striking hexosaminidase deficiency (serum: 4.6 percent of normal, 88.9 percent heat-labile; leukocyte: 2.2 percent of normal, 84.6 percent heat-labile; fibroblast 12.8 percent normal, 93.1 percent heat-labile). The residual hexosaminidase activity migrated electrophoretically in two bands. The major band comigrated with hexosaminidase A, the minor with hexosaminidase S. Hexosaminidase B was totally absent. The parents had partially reduced hexosaminidase with a decreased heat-stabile fraction. This disorder may result from a new mutation closely related to that causing Sandhoff-Jatzkewitz disease.
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PMID:A new juvenile hexosaminidase deficiency disease presenting as cerebellar ataxia. Clinical and biochemical studies. 56 95

Clonazepam, a new anticonvulsant, appears to be useful for childhood minor motor seizures and for petit mal refractory to Ethosuximide and Trimethadione. It appears less effective in infantile spasms though may be beneficial when there is no response to steroids. It is variably effective in partial complex and focal epilepsy and may exacerbate tonic seizures. A transient disadvantage is the high incidence of side effects, especially lethargy and ataxia, though these may be transitory. Aggressivity and hyperkinesis may necessitate medication withdrawal. Some children who initially respond to therapy and then relapse may respond again to a higher dosage.
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PMID:The utility of clonazepam in epilepsy of various types. Observations with 22 childhood cases. 61 1

Studies were conducted on a colony of purebred beagle dogs. Animals with spontaneous seizures were classed as epileptic beagles (EB). Those without spontaneous seizures were termed nonepileptic beagles (NEB). The median convulsant current for maximal electroshock seizure (MES) threshold was 175(194-158)mA for EB and 390 (417-364) mA for NEB. Similarly the median convulsant dose of pentylenetetrazol (PTZ) was 7.9 (10.1-6.2) mg/kg for EB and 20.2 (24.2-17.6) mg/kg for NEB. Following pretreatment with graded doses of ropizine (SC 13504), the median protective dose against MES was 6.0(9.2-3.9) mg/kg in EB and 3.2(4.8-2.1) mg/kg in NEB. Based on the incidence of ataxia, EB had a median toxic dose (TD50) of 14.0(16.5-11.9) mg/kg, while in NEB it was 18.0(23.6-13.7)mg/kg. The TD50 doses were unable to protect against a convulsive dose of PTZ. It is concluded first that ropizine may have anti-grand mal activity but apparently lacks an anti-petit mal action. Secondly, EB are more sensitive than NEB to the convulsive effects of electric current and PTZ, yet less responsive to the anticonvulsant actions of ropizine.
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PMID:Anticonvulsant properties of ropizine in epileptic and nonepileptic beagle dogs. 63 71

A fatal case of toxic encephalopathy due to ingestion of bismuth salts is reported in a twenty year old female patient. The clinical features were characterized by a confusional state, ataxia, myoclonic jerks, and epileptic seizures. Despite supportive therapy and administration of chelating agents, there was an irreversible evolution towards coma. The immediate cause of death was an intercurrent septicaemia. The anatomo-pathological study showed non specific anoxic lesions including a widespread loss of Purkinje cells in the cerebellum. Despite a drastic decrease of bismuth levels in blood, the concentration of bismuth in visceral organs and different parts of the central nervous system remained very high.
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PMID:Bismuth encephalopathy. A clinical and anatomo-pathological report of one case. 71 34


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