Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clobazam is a benzodiazepine with special molecular structure (its nitrogen radicals are in positions 1 and 5, rather than 1 and 4 as in all other antiepileptic benzodiazepines), and it is rapidly effective--in a matter of hours or within a few days--against all varieties of epileptic seizures in 52% of subjects treated with it. Its effects are relatively mild. Unfortunately, its outstanding antiepileptic properties are exhausted after only a few weeks in one-third of all cases. The authors discuss the potential significance of this phenomenon, and stress the urgent need for intensive study of the basic mechanism governing exhaustion of the antiepileptic properties of the benzodiazepines in general and clobazam in particular.
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PMID:Antiepileptic properties of clobazam, a 1-5 benzodiazepine, in man. 38 76

The change in paragraph 218 of the criminal code regarding abortion was responsible for new guidelines for the psychiatric evaluation regarding a therapeutic abortion is reported. The commonest indications were medical reasons such as exhaustion, and reactive depression. There was one case of schizophrenia, one case of affective psychosis, two attempted suicides, twenty reactive depressions, one character disorder, and one case of cerebral seizures. Five applications were approved. The follow-up evaluation of the women with the approved and dismissed applications for therapeutic abortions showed no physical or psychic abnormalities. A comparison with 88 German applicants showed similar results. The stringent evaluation of applications for therapeutic abortion is still necessary even after the change of the law.
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PMID:[Desire for therapeutic abortion in the dependents of foreign workers. Outpatients psychiatric evaluation (author's transl)]. 70 Mar 47

The effects of cortisol on the excitability of the dorsal hippocampus, septum, hypothalamus and the pontine reticular formation in unrestrained, unanesthetized rats with permanently-implanted electrodes were investigated. The hormone produced a slowing in the spontaneous activity in these regions. The stimulation of the septum, hypothalamus and reticular formation had no appreciable influence on the local or propagated electrical activity of the brain after cortisol injection; however in 14 out of 29 experiments hippocampal stimulation with the same voltages as before cortisol administration, induced generalized convulsive activity. The attacks consisted of high-voltage spikes and slow-wave activity and were followed by a post-seizure exhaustion in the hippocampus. In half of the rats behavioral convulsions also appeared. The convulsive effects of cortisol on the brain are briefly reviewed and the specificity of hippocampal involvement in the present experiments is emphasized. The possible significance of the present findings in relation to the feedback of glucocorticoids on the brain, in the regulation of ACTH secretion, is discussed. The experiments described may also contribute to our understanding of the mechanisms of the convulsive effects of cortisol on the brain.
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PMID:Effect of cortisol on the excitability of limbic structures of the brain in freely moving rats. 115 57

Transient elevation of serum prolactin frequently follows generalised tonic-clonic and complex partial seizures. However, the levels of prolactin during status epilepticus are not increased above the normal range. Exhaustion of central prolactin supplies has been proposed as a possible mechanism for the absence of prolactin increase during status epilepticus. To test this hypothesis we injected intravenous metoclopramide (10 mg) in eight consecutive patients with status epilepticus. One patient had generalised tonic-clonic status epilepticus. Seven patients had EEG-verified non-convulsive status epilepticus, consisting of one typical absence status, one atypical absence status and five complex partial status epilepticus. Metoclopramide raised the mean (SD) prolactin levels at least five-fold in all patients, from 5.8 (8.0) micrograms/l to 87.0 (39.0) micrograms/l, within 60 minutes after the injection. Thus the mechanism for low prolactin values in status epilepticus is not cellular depletion of stored prolactin, but more likely an altered regulation, presumably induced by prolonged seizure activity.
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PMID:Serum prolactin response to metoclopramide during status epilepticus. 152 38

Paradoxical or "forced" normalization of the EEG of patients with epilepsy was first described by Landolt in 1953. It refers to conditions where disappearance of epileptiform discharge from the routine scalp EEG is accompanied by some kind of behavioral disorder. The best known of these is a paranoid psychotic state in clear consciousness, which is also known as "alternative" psychosis. Thus, the issue is related to much older observations which indicated a "biological antagonism" between productive psychotic symptomatology and epileptic seizures, which led to the therapy of psychoses with artificially induced convulsions. Apart from psychotic episodes, the clinical manifestations of PN comprise dysphoric states, hysterical and hypochondriacal syndromes, affective disorders, and miscellanea. PN can be observed in both generalized and localization-related epilepsies as a rare complication. A subset where it is more frequently seen are in adults with persistent absence seizures when the latter become finally controlled by succinimide therapy. These seem to be the drugs with the highest hazard of precipitation of PN, but all other AEDs have also been suspected. Sleep disturbance by succinimide treatment may play a crucial role, but a variety of other factors are also involved, including psychosocial factors. The pathogenesis of this condition has given rise to some debate but remains still unresolved. Eleven of the most important hypotheses have been discussed and seem to converge into a more comprehensive hypothesis which basically assumes that, during PN, the epilepsy is still active subcortically, perhaps with spread of discharge along unusual pathways. This activity is supposed to provide energy and, possibly, some of the symptoms included in the psychotic syndrome. A critical clinical condition results, usually with a dysphoric symptomatology, where a development towards psychosis is impending but still depends on the presence or absence of a variety of risk factors. Along with neurophysiological factors such as powerful inhibition of the spread of epileptic discharge, these may also include biographic factors such as the repeated experience of ictal sudden, unexpected loss of consciousness. Because during PN there presumably is ongoing epileptic activity, the differences with respect to other psychotic conditions in epilepsy are probably subtle rather than fundamental. Thus, it could be that ictal psychosis is characterized by a direct expression of epileptic activity, whereas in postictal psychosis a momentum of exhaustion may be added; moreover, in PN the prevailing pathogenic factor could be an abnormally high level of balance between excitatory and inhibitory processes.
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PMID:Acute behavioral symptomatology at disappearance of epileptiform EEG abnormality. Paradoxical or "forced" normalization. 200 2

The sensorimotor area of rat cerebral cortex was subjected to repeated electrical stimulation at 10-min intervals, with resultant formation and progressive lengthening of self-sustained after-discharges (SSAD). One and 60 min after the third SSAD ended, we carried out an electron microscopy morphometric analysis of the agranular synaptic vesicles in type I synapses (after Gray) in the second cortical layer of the homotopic area of the unstimulated hemisphere. One minute after the seizure ended, 5.8% enlargement of the synaptic vesicles compared with the control was demonstrated in zone II of the synapse (0.1-0.2 micron from the active zone of the synapse). Neither the size nor the shape of the synaptic vesicles in the other parts of the synaptic apparatus altered. Sixty min after the seizure ended, a 5.5% enlargement of the synaptic vesicles in zone I (0.0-0.1 micron) and a 5.4% enlargement of those in zone II was found. The synaptic vesicles in zone I in the experimental animals were more oval than in the controls. Our findings support the vesicular theory and testify that hyperfunction, up to temporary exhaustion of the synaptic apparatuses, produces a change in the transmitter content of the synaptic vesicles. A raised amount of transmitter in the synaptic vesicles near the active zone could be one of the factors responsible for continued hyperexcitability of the tissue one hour after the seizure had ended. The results likewise support the concept of two mechanisms of synaptic vesicle formation, and hence of the existence of two different vesicle populations.
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PMID:Changes in the size and shape of the synaptic vesicles in the sensorimotor cortex of the rat brain in the initial phases of kindling. 294 5

In order to determine if sickle-cell trait (SCT) represents an inherent adverse effect on response to training, we objectively evaluated exercise performance in 22 healthy, black men with SCT (hemoglobin AS) and 15 controls (hemoglobin AA) before and after seven weeks of army basic training at an altitude of 1270 m. An incremental exercise test to exhaustion on a cycle ergometer was used. Before basic training, peak exercise measurements did not reveal significant differences between groups other than a slightly lower, albeit significant, value for oxygen uptake (VO2) per kilogram (42 +/- 1 vs 45 +/- 1.4 mL/min per kilogram) for the SCT group. Both groups experienced modest overall cardiovascular improvement reflected in both peak and submaximal exercise responses. No statistically significant difference was observed between the SCT and the control groups at the end of basic training for any of the measured variables at peak exercise, including power (258 +/- 6 vs 266 +/- 9W), VO2 (3.24 +/- .06 vs 3.36 +/- .16 L/min), VO2 per kilogram (46 +/- 0.7 vs 46 +/- 1.2), minute ventilation (138 +/- 4 vs 147 +/- 8 L/min), heart rate (185 +/- 2 vs 184 +/- 3 beats per minute), oxygen pulse (17.6 +/- .3 vs 18.4 +/- 1 mL/min per beat), as well as anaerobic threshold (1.81 +/- .04 vs 1.80 +/- .06 L/min), respectively. No medical problems directly attributed to SCT were reported; it remains uncertain, however, whether a seizure experienced by one of the other SCT basic trainees after a two-mile run was SCT related. The results of this study would, therefore, suggest that for the majority of individuals who possess SCT, the response to the moderate training regimen provided by army basic training is not impaired.
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PMID:Effect of Army basic training in sickle-cell trait. 336 81

Specific consequences of cocaine abuse on health and psycho-social functioning were assessed in 55 cocaine-abusing subjects who called a telephone "helpline." REsults showed a high incidence and wide range of adverse consequences including: impairment of job functioning, interpersonal relationships, and financial status; disturbances of mood and cognitive functioning; psychiatric symptoms of depression, paranoia, and increased suicidal/violent tendencies; and physical symptoms of exhaustion, weight loss, sleep problems, and seizures. Cocaine-related automobile accidents, suicide attempts, and violent acts, including a cocaine-related homicide, were also reported. Intranasal users reported no fewer and no less severe adverse consequences than free-base smokers or intravenous users. Our findings challenge popular notions that cocaine is a benign "recreational" drug and that the intranasal route of administration guarantees protection against addictive patterns of use and adverse effects.
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PMID:Adverse effects of cocaine abuse. 643 68

Repeated electrical stimulation of the sensorimotor region of rat cerebral cortex at 10 min intervals led to the development and progressive prolongation of self-sustained after-discharges (SSAD). One minute after the third SSAD ended, an electronoptic morphological analysis of type I synapses after Gray from the second cortical layer of the homotopic area of the unstimulated hemisphere was carried out. In the experimental animals, an 11.7% increase in the area of the presynaptic bag and a 5.5% increase in its perimeter were demonstrated. The number of agranular synaptic vesicles per constant unit area fell by 70.8%. The area of the mitochondria in the presynaptic ending increased by 49.8% and their perimeter by 16.1%. The area of the postsynaptic element increased by 34.1% and its perimeter by 15.7%. Changes in the synapses are evaluated as manifestations of exhaustion and primarily as a manifestation of ion shifts during the epileptic seizure. The findings nevertheless also testify to incipient activation of restitution mechanisms in the structures of the synaptic apparatus within a very short time after termination of the seizure.
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PMID:Changes in some ultrastructural parameters of cortical synapses in the initial phases of kindling. 648 27

Epilepsy is a paroxysmally occurring disturbance of brain function. The neurones directly involved in the epileptic process show characteristic behaviour of the membrane potential, which consists of a rectangular-shaped depolarization recorded in neurones during all experimental models of epilepsy investigated up to now. Occasional recordings in patients have shown a similar reaction of the membrane potential. The membrane potential fluctuation is therefore regarded as the specific reaction of a neurone directly involved in the epileptic process, and the accordingly termed "paroxysmal depolarization shift" (PDS) was found to be the expression of pathophysiologic behaviour by the neuronal membrane. The "epileptic" neurones are hemispherically surrounded by neurones which are simultaneously inhibited. The mechanisms capable of overcoming the surrounding inhibition and thus leading to the spread of epileptic activity are not fully understood as yet: seizure-related changes in the extracellular ionic environment appear to support the spreading process. The termination of an epileptic event is not necessarily the result of metabolic exhaustion of the nerve cells involved. Recent data indicate a prominent role for primary neuronal mechanisms in the termination of a seizure. However, the cortical tissue participating in a partial seizure shows increased vulnerability to hypoxia. Brain damage found in central nervous tissue of epileptics may therefore be the result of secondary cerebral hypoxia consequent on seizure-related disturbances of breathing and circulation.
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PMID:[Pathophysiology of epilepsy]. 649 62


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