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

Some meadow voles (Microtus pennsylvanicus) exhibit prolonged tonic-clonic convulsions, possibly epileptiform seizures, when handled or exposed to a strange environment. These convulsions are often preceded by a period of slow head shaking and/or stiff-legged hopping, but never by the explosively wild running bouts that characterize convulsions in some mammals. Convulsions occasionally occur in meadow voles in response to mild disturbance, as when an individual in its home cage is carried from one room to another. In contrast, they can not be elicited by some of the auditory or olfactory insults used to induce epileptiform seizures in other mammals. Breeding experiments have established the genetic basis of the convulsions seen in meadow voles, and of particular interest here is the fact that some of the convulsing voles were caught in the wild. This raises the interesting possibility that wild voles in natural habitats might be susceptible to convulsions when startled.
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PMID:Tonic-clonic convulsions in meadow voles. 780 Jul 33

Frequent but phasic gnawing of objects is displayed by rats in which severe damage within: 1) the substantia nigra reticulata, 2) all of the amygdaloid nuclei except the central group and 3) multiple thalamic nuclei, was induced by lithium/pilocarpine-induced seizures. Multiple lesions were produced by these rats upon their own tails as well as upon the tails of their cage mates. These behaviors were considered predictable sequela of the disinhibition of compacta dopamine upon orofacial mechanisms that are modulated by the corpus striatum. In a manner similar to tail pinch-induced eating, the usually quick onset of spontaneous gnawing upon food chunks in a test setting was delayed transiently by appropriate dosages of haloperidol.
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PMID:Transient blocking of persistent gnawing by haloperidol in rats with seizure-induced multifocal brain damage. 844 81

L-Deprenyl (selegiline), a selective inhibitor of monoamine oxidase type B, has recently been shown to exert anticonvulsant and antiepileptogenic effects in the kindling model of partial (focal) epilepsy. In the present study, we examined if L-deprenyl exerts anticonvulsant effects in standard rodent models of generalized seizures. In addition to anticonvulsant activity, behavioral effects induced by L-deprenyl were monitored closely. To assess the stereoselectivity of anticonvulsant and behavioral effects of deprenyl, the D-enantiomer was included in the studies. Furthermore, the antiepileptic drug phenobarbital was used for comparison. The following tests were performed in mice: 1) the threshold for tonic electroconvulsions; 2) the maximal electroshock seizure test with fixed supramaximal (suprathreshold) stimulation; 3) the threshold for myoclonic, clonic and tonic seizures in response to i.v. infusion of pentylenetetrazole (PTZ); 4) the s.c. PTZ seizure test, with a fixed dose of PTZ (80 microgram/kg) for seizure induction; 5) the rotarod and chimney tests for determination of motor impairment. Furthermore, animals were observed in cage and open field for stereotyped behavior and other behavioral abnormalities. L-Deprenyl, tested at doses of 1 to 40 microgram/kg i.p., significantly increased myoclonic and clonic PTZ thresholds and the threshold for tonic electroconvulsions, whereas D-deprenyl was either ineffective or exhibited a lower anticonvulsant potency than L-deprenyl. Both drugs were ineffective in the maximal electroshock seizure and s.c. PTZ seizure tests. In contrast to the higher anticonvulsant potency of L-deprenyl in seizure threshold tests, D-deprenyl was more potent than L-deprenyl to induce behavioral abnormalities, such as hyperlocomotion. The data indicate that L-deprenyl exerts anticonvulsant activity against different seizure types. This anticonvulsant activity and the previously reported neuroprotective and cognition-enhancing action of L-deprenyl offer a unique combination of drug effects which might be of clinical benefit in patients with epilepsy.
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PMID:L-deprenyl (selegiline) exerts anticonvulsant effects against different seizure types in mice. 866 4

Alcohol abuse produces a considerable burden of illness in the Canadian population. The diagnosis of alcohol dependence and withdrawal can be difficult, particularly in the setting of covert intake or comorbidity. Two validated scales, the CAGE questionnaire to screen for alcohol abuse and dependence and the Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) scale to assess the severity of withdrawal, are valuable tools for clinicians to use on a regular basis. For the treatment of alcohol withdrawal, compelling anecdotal evidence supports the routine administration of thiamine, but not necessarily other vitamins. Phenytoin has not been shown to be superior to placebo for uncomplicated withdrawal seizures. Neuroleptics are not recommended for routine use. Sedation with benzodiazepines guided by the CIWA-Ar results is recommended. There is good evidence that the management of alcohol withdrawal can be improved with the routine use of the CIWA-Ar scale to assess severity, treatment with adequate doses of benzodiazepines and follow-up monitoring of patients in alcohol withdrawal.
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PMID:Diagnosis and management of acute alcohol withdrawal. 1010 3

Children with hypertension, seizures, lethargy, encephalopathy, headache, and occipital blindness are reviewed. After undergoing antihypertensive therapy, most children improve. Some patients have a similar syndrome associated with chemotherapy, transplantation, transfusion, or human immunodeficiency virus-1 (HIV-1) infection. These latter children can develop symptoms with only minimal or no discernible elevations in blood pressure and improve, in the case of cancer-associated encephalopathy, after discontinuing chemotherapy. The reported children with this distinctive clinical condition are compared to adults with reversible posterior leukoencephalopathy syndrome. Since both gray and white matter are involved, we had suggested previously that the name be changed to (reversible) occipitoparietal encephalopathy syndrome. However, reversible posterior leukoencephalopathy has been used in the adult population and probably should be employed in children for the sake of uniformity, since both children and adults have the same clinical presentation and presumably a similar pathophysiology for the encephalopathy syndrome. The diagnosis is confirmed by reversible posterior abnormalities seen on T2-weighted brain magnetic resonance imaging, and by the presence of either headache, altered mental status, seizures, or visual disturbances.
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PMID:Hypertensive encephalopathy, reversible occipitoparietal encephalopathy, or reversible posterior leukoencephalopathy: three names for an old syndrome. 1034 93

Nutritional secondary hyperparathyroidism (NSH) was diagnosed in six cats during a three-year period, based on clinical, radiographic and laboratory findings. Clinical signs were attributable to severe osteopenia (n = 5) and hypocalcaemia (n = 4), which had resulted in spontaneous fractures of long bones, scapulae, pelvis, nasal bones, or spine, and in excitation, muscle twitching or seizures, respectively. Serum parathormone levels were markedly elevated, and 1,25(OH)2-vitamin D3 mildly elevated, whereas 25(OH)-vitamin D3 was mildly decreased compared to age-matched healthy cats. Treatment was limited to short-term parenteral calcium gluconate injections, as clinically indicated, a balanced diet and cage rest, which resulted in quick clinical recovery in four cases. The remaining two cats had to be euthanased because of progressive neurological deficits secondary to spinal fractures. At the time of writing, a multitude of commercial balanced diets is widely available and diseases secondary to dietary deficiencies have become rare. Nevertheless, NSH is still an important clinical entity, and should be considered in growing cats presenting with spontaneous fractures or seizures.
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PMID:Nutritional secondary hyperparathyroidism in six cats. 1064 98

The present study evaluated the effects of mixed opioid drugs on the severity of cocaine (COCA) toxicity by examining stress-related behavioral alterations in mice. In order to ascertain the strength of the stress, the continuous observation of the behavioral symptoms in the cage and the forced swimming test (Porsolt test) were performed in the COCA (75 mg/kg, i.p.)-treated groups, with or without the mixed mu-kappa receptor-related opioid drugs, buprenorphine (BUP) and pentazocine (PEN). Using the high-sensitivity activity measuring instrument Supermex, both the spontaneous behaviors in the cage and the forced swimming behaviors in the water were assessed as activity counts. The behavioral alterations in the COCA-treated groups were compared with a group of mice given a 10 min immobilization stress (IM group). In the COCA-only group, a prolonged increase in the spontaneous behaviors accompanied by convulsive seizures was observed even in the surviving mice, unlike in the IM group. However, an acceleration of behavioral despair in the Porsolt test similar to that observed in the IM group was observed in the COCA group after the disappearance of the acute toxic symptoms (5 hours after the COCA treatment). Among the opioid-treated groups, the mortality rate was attenuated only in the COCA-BUP (0.25 mg/kg, i.p.) group. In the COCA-BUP group, a prolonged suppression of the morbid hyperactivity in the cage except for the convulsive seizures, and a normalization of the swimming behavior in the Porsolt test were observed in the survivors. On the other hand, in the COCA-PEN (5 mg/kg, i.p.) group, the swimming behavior in the Porsolt test was abnormally increased in addition to the prolonged morbid hyperactivity in the cage. Therefore, the COCA-induced stress-related behaviors were normalized in the group of mice treated with BUP, a group with a good prognosis.
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PMID:Stress-related behavioral alterations accompanying cocaine toxicity: the effects of mixed opioid drugs. 1119 74

1. Trimethylolpropane phosphate (TMPP) is a potent cage convulsant, reported to act through binding to the picrotoxinin and/or benzodiazepine receptor sites of the gamma-aminobutyricA (GABA(A)) ionophore complex. 2. Adult male Fischer-344 rats were pretreated by intraperitoneal (i.p.) injection with either diazepam (DZP) [0.5-5.0 mg/kg], Phenobarbital (PB) [5-20 mg/kg], dizocilpine maleate (MK-801) [0.5-3.0 mg/kg], Tiagabine (TGB) [0.5-5.0 mg/kg], 6,7-dinitro-quinoxaline-2,3-dione (DNQX), [5-20 mg/kg], or scopolamine [SCP] (0.25-1.0 mg/kg) 30 min prior to i.p. injection with a convulsive dose of TMPP (0.6 mg/kg). 3. Rats were rated for occurrence of convulsive activity for 120 min post-injection. Time from TMPP injection to observation of subclinical seizures, generalized (tonic-clonic) seizures, and lethality was rated for each pretreatment group. 4. In general, DZP = PB > TGB in reduction of TMPP subclinical and/or clinical seizures. MK-801, at dose levels inducing near sedation, was also effective in modulation of TMPP-induced seizures. SCP or DNQX were generally ineffective in reducing or eliminating TMPP-induced seizures.
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PMID:Reduction of motor seizures in rats induced by the ethyl bicyclophosphate trimethylolpropane phosphate (TMPP). 1147 48

The present study assessed the effects of repeated subacute exposure to the organophosphorous nerve agent, sarin. Guinea pigs were injected five times per week (Monday-Friday) for 2 weeks with fractions of the established LD(50) dose of sarin (42 microg/kg sc). The animals were assessed for the development of cortical EEG seizures. Changes in body weight, red blood cell (RBC) acetylcholinesterase (AChE) levels and neurobehavioral reactions to a functional observational battery were monitored over the 2 weeks of sarin exposure and for an extended postinjection period. There were dose-related changes in body weight and RBC AChE levels. No guinea pigs receiving 0.3, 0.4 or 0.5 x LD(50) of sarin showed signs of cortical EEG seizures despite decreases in RBC AChE levels to as low as 10% of baseline. Seizures were evident in animals receiving 0.6 x LD(50) of sarin as early as the second day, and subsequent injections led to incapacitation and death. Animals receiving 0.5 x LD(50) sarin showed obvious signs of cholinergic toxicity, which included a significant increase in their angle of gait. Overall, 2/13 animals receiving 0.5 x LD(50) sarin died before all 10 injections were given. By the 10th day of injections, the animals receiving saline were significantly easier to remove from their cages and handle as compared to the first day of injections. They were also significantly less responsive to an approaching pencil and touch on the rump in comparison to the first day of testing. In contrast, the animals receiving 0.4 x LD(50) sarin failed to show any significant reductions in their responses to an approaching pencil and a touch on the rump as compared to the first day. The 0.5 x LD(50) sarin animals failed to show any significant changes to the approach response and touch response and did not adjust to handling or cage removal from the first day of injections to the last day of handling. In summary, the guinea pigs receiving the 0.4 x LD(50) and 0.5 x LD(50) doses of sarin failed to habituate to some aspects of the functional observational battery testing.
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PMID:The dose-response effects of repeated subacute sarin exposure on guinea pigs. 1206 73

OBJECTIVE: To study the sedative effects of Jujuboside A (JuA) on the Central Nervous System of mice. METHODS: Using a novel jiggle-cage test, we compared the sedative effect of JuA with that of Diazepam (DZP) both with a single and cumulative dose of JuA. We also assessed the anticonvulsant effect of JuA on pentylenetetrazol (PTZ)-induced seizures in mice. RESULTS: JuA significantly decreased total activity intensity and increased the quiet state time of mice. The sedative effects of JuA were more stable and more lasting than that of DZP. However, JuA failed to resist and delay the induced seizure activity in mice. CONCLUSION: Though JuA has sedative effects on mice CNS, it has no anticonvulsant effect on PTZ-induced seizures.
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PMID:[Sedative and anticonvulsant effect of jujuboside A] 1253 70


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