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

The effects of four neural excitants (damphetamine, cocaine, nicotine, and strychnine) on myoclonic and clonic seizure susceptibility were investigated in two age groups (30 and 120 days) of short-sleep mice. Amphetamine and cocaine decreased susceptibility to myoclonus in young mice and increased susceptibility in mature mice. These effects were attenuated by pretreatment with haloperidol, indicating mediation by a dopaminergic system. Amphetamine did not alter clonic susceptibility in either age group of mice, whereas cocaine affected clonic susceptibility and myoclonus. These effects were not attenuated by haloperidol, indicating mediation by systems other than dopamine. Nicotine decreased susceptibility to myoclonus and increased susceptibility to clonus, whereas strychnine increased susceptibility to both types of seizure. Haloperidol, however, failed to alter any of these effects. These results are consistent with our previous work which suggests that a dopaminergic mechanism in these mice undergoes marked developmental changes between 30 and 120 days of age.
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PMID:Maturational changes related to dopamine in the effects of d-amphetamine, cocaine, nicotine, and strychnine on seizure susceptibility. 11 67

Clinical, electrical and biochemical studies in an eight years old boy with movement-induced seizures were reported. The attack was usually triggered by sudden initiation of movement, but rarely occurred without any apparent movement. Repeated jumping provoked attacks constantly, which was recorded cinematographically. No abnormality was found either in ictal or interictal EEGs. Haloperidol aggravated the condition, but 1-DOPA had no effect, while DPH (100 mg/day) controlled attacks perfectly with the serum DPH concentration of just 2.0 ug/dl. In overnight sleep analysis, sleep rhythms and characters of REM sleep were not differed significantly from the standard. After DPH therapy, stabilization of sleep in general was noticed; that is, total sleep time prolonged, number of sleep stages decreased and interrupting awakening disappeared. Probenecid loading test revealed that 5-HIAA was normal, HVA high, and large amount of octopamine was detected in CSF.
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PMID:Overnight sleep EEG and cerebrospinal fluid monoamines in seizures induced by movement. 22 8

The patient was a 35-year-old, unmarried male whose epileptic psychomotor fits persisted since the age of 13. The author has observed the case for about 12 years, so that incomplete information concerning epileptic symptoms was considered to be compensated considerably by longitudinal observation, including ictal seizure and ictal EEG's. In this patient seizure with impaired consciousness which correspond rhythmic slow waves of EEG tracing might be a nuclear sign; several kinds of automatism then might be considered as postictal phenomenon. The most important of all was tonic seizure of psychomotor epilepsy particularly in the face which was not seen in the petit mal epilepsy. With observation of ictal period as well as ictal EEG, differential identification of centrencephalic epilepsy and psychomotor epilepsy may not be totally impossible. The case also showed a typical productive psychotic episodes of Landolt, which could be treated favorably by 10 mg of intravenous Haloperidol. This method, named as "pathologization" of Helmchen, was found by the present author as a useful treatmental means of choice.
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PMID:Ictal clinical patterns and ictal EEG in a case of partial seizures of frontotemporal origin associated with complex symptomatology. 59 Aug 79

In experiments with pentylenetetrazol convulsion model it has been found that L-DOPA in a dose of 50 mg/kg has no influence, while 500 mg/kg potentiate convulsions. Amantadine in a dose of 25 mg/kg and particularly markedly in a dose of 100 mg/kg potentaites convulsive seizures. Amphetamine in a dose of 0.5 mg/kg has no effect, while 5 mg/kg potentiate convulsive seizures, which is particularly pronounced in mice. Apomorphine in doses of 0.5 and 5 mg/kg has no marked effect on convulsions. Haloperidol in doses of 0.2 and 2 mg/kg does not have a pronounced effect on convulsive-seizure reactions and does not influence the effect of L-DOPA and amantadine on these reactions. The results obtained suggested a rather indirect effect of the dopaminergic system on convulsive-seizure reactivity. It is possible that the effects of some of the dopaminergic agents studied are realized through influencing the relationships between the dopaminergic system and other neurotransmitter systems (especially cholinergic, GABA-ergic and serotonin-ergic).
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PMID:On certain effects of dopaminergic agents in pentylenetetrazol convulsions. 75 52

Behavioural analyses have been made of effects brought about by both single and combined injections of dopamine, haloperidol, carbachol and atropine into the caput nuclei caudati of rhesus monkeys. High doses of dopamine produced the subsequent development of three types of behavioural changes: an increase in the number of skilled manipulation movements (the dynamic phase); the appearance of a dystonic torticollis (the dystonic phase); and, finally, the appearance of an oro-lingual-facial dyskinesia and a number of dyskinetic activities in the extremities (the dyskinetic phase); low doses of dopamine solely produced the dynamic phase. Haloperidol only inhibited the dopamine-induced dynamic and dystonic phase: it did not suppress the dyskinetic phase. High doses of carbachol produced the subsequent development of four phases: a dynamic, dystonic, dyskinetic and epileptoid phase; the last one was marked by the appearance of secondary generalized epileptic seizures. Low doses of carbachol solely produced the dynamic phase. Atropine inhibited the carbachol-induced dynamic, dystonic and epileptoid phase; it did not suppress the dyskinetic phase. High doses of dopamine strongly modified the carbachol-induced phases: dopamine intensified the dystonic phase on the one hand, but it abolished the generalized epileptic seizures on the other hand. Apart from the fact that the data presented have confirmed that both dopaminergic and cholinergic mechanisms within the basal ganglia of rhesus monkeys are involved in the elicitation and modulation of both normal and abnormal motor activities, they have also revealed that the simple concept of a stristal acetylcholine-dopamine "see-saw" has to be revised. Furthermore, the data have suggested that development of supersensitive dopamine-sensitive sites is not the only mechanism that underlies the elicitation of the oro-lingual-facial dyskinesia. And finally, the present experiments have given clearcut evidence that an intrastriatal acetylcholine-dopamine "see-saw" fulfils and essential role in the process involved in the generalization of epileptic seizures.
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PMID:The acetylcholine-dopamine balance in the basal ganglia of rhesus monkeys and its role in dynamic, dystonic, dyskinetic, and epileptoid motor activities. 115 71

The quantitative 2-[14C]deoxyglucose autoradiographic method was applied to measure local cerebral metabolic rates of glucose (LCMRglc) in a model of genetic petit-mal-like seizures in a strain of Wistar rats. During the experimental period, epileptic rats exhibited synchronous spike-and-wave discharges, whereas the EEG pattern of control animals was normal. Overall, LCMRglc was consistently higher in epileptic rats than in the non-epileptic controls. The increase in LCMRglc was widespread and concerned all cerebral functional systems studied, whether they exhibit spike-and-wave discharges (neocortex and thalamus), or not (limbic system). These results are in good accordance with positron-emission tomography measurements in humans with typical childhood absence epilepsy. There appears to be a lack of anatomical correlation between areas demonstrating hypermetabolism and areas where spike-and-wave discharges are recorded. The administration of 200 mg/kg ethosuximide completely suppressed spike-and-wave discharges in epileptic rats and did not change the EEG pattern in controls. However, LCMRglc were increased to the same extent over control values in epileptic rats whether they were injected with ethosuximide or untreated. By contrast, when epileptic rats were given 2 mg/kg haloperidol, the frequency and the length of spike-and-wave discharges increased, inducing almost a permanent petit-mal status epilepticus. Haloperidol did not change EEG pattern in controls. In haloperidol-treated epileptic rats, LCMRglc decreased to levels comparable to those measured in untreated control rats. In the presence of haloperidol, LCMRglc were similar in both control and epileptic rats. Thus, the diffuse increase in cerebral energy metabolism in epileptic rats as compared to controls is not directly related to the occurrence of spike-and-wave discharges, and may rather be associated with inhibitory mechanisms involved in their termination and suppression, as well as their spread to limbic and motor structures.
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PMID:Mapping of cerebral energy metabolism in rats with genetic generalized nonconvulsive epilepsy. 151 92

Chronic pharmacological experiments were conducted to evaluate the relationship between sensitization induced by repeated administration of amphetamine (AMPH) and electrical stimulation of the amygdala. While AMPH withdrawal did not influence the kindling process, AMPH administered during the kindling procedure increased the rate at which seizures evolved, and under these conditions withdrawal from chronic AMPH further facilitated the propensity to kindle. Haloperidol (HAL) treatment failed to block the stimulant-induced increase in kindling acquisition indicating that changes in dopamine (DA) are not necessary for the AMPH/kindling synergism to develop. Scopolamine dose-dependently retarded kindling evolution irrespective of prior AMPH pretreatment also ruling out a cholinergic mechanism in the kindling sensitization. Subsequent experiments assessed the interactive effects of AMPH and desipramine (DMI) on the kindling process. Animals chronically exposed to AMPH and switched to DMI treatment during the kindling procedure kindled faster than control subjects. In addition, withdrawal from DMI preexposure advanced the AMPH-induced increase in kindling rate. These results were discussed in terms of the role of norepinephrine-mediated inhibition of the kindling process, and were related to drug-elicited alterations in beta-adrenergic receptor functioning. Taken together, these findings implicate the amygdala as an important structure in the development of non-DA forms of AMPH sensitization.
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PMID:Amphetamine sensitization and amygdala kindling: pharmacological evaluation of catecholaminergic and cholinergic mechanisms. 164 66

The functional significance of the interaction between serotonergic and dopaminergic neurotransmission is still uncertain. To document this interaction further, specific behavioral responses of rats to tryptamine and apomorphine were studied. The sequential injection of these agonists, at time intervals with minimal direct behavioral interference, was used to observe response changes with respect to a single challenge. The antagonists haloperidol, ritanserin and risperidone, with known actions on serotonin-S2 (5-HT2) and dopamine-D2 (D2) receptors were used to evaluate effective antagonism of single and sequential challenges. When tryptamine was preceded by an apomorphine challenge the effective doses of the 5-HT2 antagonists ritanserin and risperidone for 50% inhibition of the seizures increased by a factor of 2.5. The dose-response curve of haloperidol remained virtually unchanged, apparently because of the potent dopamine-D2 antagonism associated with these doses which may block the potentiating effect of apomorphine. When apomorphine was preceded by a tryptamine challenge, the total agitation score of the control animals increased by 59% on the average. Haloperidol was equally effective against the enhanced as against the unenhanced apomorphine response. Ritanserin reduced agitation only by the part corresponding to the tryptamine enhancement. Risperidone's activity against the enhanced agitation started at very low doses and was complete at a dose still about 2.5 times lower than that required against the single apomorphine challenge. Mutual enhancement of tryptamine and apomorphine appears to occur even at a time when the behavioral effects of the first agonist are no longer manifest. The enhanced agitation remains largely dopamine-D2-specific and the enhanced seizures serotonin 5-HT2-specific.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Functional interaction between serotonin-S2 and dopamine-D2 neurotransmission as revealed by selective antagonism of hyper-reactivity to tryptamine and apomorphine. 169 23

We assessed the effects of chronic treatment with haloperidol (0.5-2 mg/kg/day, p.o., 17 days) and methamphetamine (1-2 mg/kg/day, p.o., 17 days; 4 mg/kg/day, p.o. 9 days) on hippocampal kindled seizures using a kindling procedure with low-frequency (about 3 Hz) electrical stimulation in cats. The number of stimulating pulses required to trigger epileptic afterdischarge (pulse-number threshold, PNT) was considered an indicator of seizure threshold. Haloperidol, 0.5 and 1.0 mg/kg, reduced the duration of epileptic afterdischarge (afterdischarge duration, ADD) without affecting PNT, and 2.0 mg/kg strongly reduced PNT and ADD. Methamphetamine, 2.0 mg/kg, reduced PNT and ADD, and 4.0 mg/kg preferentially reduced PNT. The effects of the two drugs on hippocampal kindled seizures were found to be partially opposite to those on amygdala kindled seizures, suggesting the different response of these limbic structures to dopamine receptor manipulation.
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PMID:Effects of chronic treatment with haloperidol and methamphetamine on hippocampal kindled seizures in the cat. 186 21

Administration of reserpine, trifluperidol, chlorpromazine, haloperidol, spiroperidol, and thioproperazine to adult mice shortened the latency and increased the number of animals with clonic seizures induced by 1-kynurenine sulfate or its metabolite quinolinic acid. Haloperidol dose-dependently intensified kynurenine-induced seizures and did not alter pentylenetetrazole seizures. Dopamine abolished the effect of haloperidol while serotonin was ineffective. Pretreatment with 6-hydroxydopamine potentiated kynurenine-induced seizures, but not quinolinic acid-induced seizures. The seizure thresholds of kynurenine and quinolinic acid were not affected by pretreatments with yohimbine, clonidine, piperoxan, phentolamine and tricyclic antidepressants. Apomorphine and amphetamine (i.p.), noradrenaline and adrenaline (i.c.v.) possess anticonvulsant action against kynurenine and not against quinolinic acid. The data obtained suggest a similarity of kynurenine and known convulsants in the involvement of the catecholaminergic processes in their convulsant action. Quinolinic acid markedly differs from kynurenine in its mechanism of action as indicated by their interactions with numerous endogenous substances.
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PMID:Effect of catecholaminergic drugs on quinolinate- and kynurenine-induced seizures in mice. 214 73


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