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

A 34 year old woman developed cerebral infarction, following a tonic-clonic seizure. A vertebral artery dissection was demonstrated and may have been caused by arterial trauma during the seizure. This cause of morbidity following convulsive seizures may have been overlooked in the past and needs to be recognised in view of the potential benefits of anticoagulation.
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PMID:Extracranial vertebral artery dissection following tonic clonic seizure. 190 46

In therapy lasting between 8 and 79 (means = 31) months 22 epileptic dogs had been unsuccessfully treated with phenobarbital and/or primidone. Both drugs had been administered in their maximum dosages. In an add-on therapy, these dogs were given potassium bromide at a rate of 17 to 58 mg/kg daily for a period of 7 to 61 (means = 21) months. We could quantitatively evaluate the seizure data from 19 of the dogs: four became free of seizures; seven showed a greater than 50% reduction in seizure frequency; in two dogs, the seizures were reduced by greater than 50% but the number of seizure-days by less than 50%; in the remaining six dogs the therapy was unsuccessful. We achieved the best therapeutic results in animals that suffered only grand mal seizures. Grand mal in addition to other types of seizures and tonic seizures were affected to a lesser extent if at all. At the beginning of the therapy we saw temporary side effects--weakness in the hind limbs and sedation; these were temporary and dependent on the dosage. Serum concentrations differed even with the same dosage among individual dogs. The therapeutic range of bromide serum concentration was from 0.7 to 2.0 mg/ml. Most of the animals tolerated concentrations up to 1.5 mg/ml quite well. To begin an add-on therapy with potassium bromide we would recommend a daily dose of 30 to 40 mg/kg. During treatment, the dose should be determined for each individual dog.
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PMID:[Effectiveness of bromide in therapy resistant epilepsy of dogs]. 194 87

The prolactin concentration profile over 24 hours was determined in three men, aged 19, 27 and 43 years, who suffered from treatment-resistant complex-partial and (or) grand mal seizures of frontal lobe origin. All three patients were examined in the course of preoperative epilepsy diagnosis, the seizures being classified by video-EEG recordings, including subdural and sphenoidal foramen ovale electrodes. Seizures were recorded in all three patients (4 grand mal; 2 complex-partial), each of them followed by a rise in serum prolactin concentration (over 700 microU/ml). These findings contradict the theory that prolactin concentration rises only after temporal, not after frontal seizures. Knowing the postseizure serum prolactin concentration may help to distinguish frontal epileptic from psychogenic seizures.
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PMID:[Rise in serum prolactin concentration after frontal lobe seizures. Possibilities in differential diagnosis of psychogenic seizures]. 195 86

Sparganosis is a rare infection caused by a tapeworm larva from the genus Spirometra. A 21-year-old Indian man presented with an 18-month history of episodic confusion followed by a grand mal seizure. Computed tomography and magnetic resonance imaging of the brain confirmed the presence of a lesion of the left occipital lobe. Subsequent stereotactic biopsy revealed a plerocercoid larva or sparganum. Surgical resection resulted in cure. This case prompted a review of the literature on central nervous system sparganosis. Altogether, 17 other cases of primary cerebral sparganosis have been reported previously. Seizures, headache, and focal neurologic signs are common at presentation. Neuroradiologic imaging is sensitive but not specific for the identification of lesions. Enzyme-linked immunosorbent assay of cerebrospinal fluid or serum may be diagnostically helpful. However, the diagnosis is generally made after surgical resection, which is usually curative.
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PMID:Cerebral sparganosis: case report and review. 201 16

There are a number of clinical situations where overhydration may occur. If the reduction in plasma osmolality is acute, passive water influx swells brain cells, shrinking the extracellular space around them. It is during this time that susceptibility to generalized tonic-clonic seizure dramatically increases. Common clinical examples include hastened rehydration therapy, the dialysis disequilibrium syndrome, compulsive polydipsia, the syndrome of inappropriate ADH secretion (SIADH) and post-TURP syndrome. Treatments that tend to restore normal cellular volume (dehydration, mannitol infusion) help protect against this form of seizure. Support for a correlation between plasma osmolality and seizure susceptibility is scattered amongst the literature of several medical disciplines and spans almost 70 years. However a cellular basis to explain how overhydration might promote epileptiform activity has been examined only recently. The neocortical and hippocampal brain slice preparations permit an examination of how acute osmotic change alters cortical excitability independent of vascular damage, brain compression or other factors secondary to brain swelling. Electrophysiological evidence indicates that hyposmolality promotes epileptiform activity by strengthening both excitatory synaptic communication in neocortex and field effects among the entire cortical population. Moreover there is little evidence that associated hyponatremia in itself leads to increased CNS excitability. Such findings help in understanding how rapid lowering of plasma osmolality in clinical situations can promote the hyperexcitability associated with generalized tonic-clonic seizure.
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PMID:Seizure and acute osmotic change: clinical and neurophysiological aspects. 202 29

An anticonvulsant action of ketamine, a noncompetitive N-methyl-D-aspartate (NMDA) antagonist (5-40 mg/kg IP), on the bicuculline-induced (3-8 mg/kg IP) or picrotoxin-induced seizures (3-6 mg/kg IP) was assessed in male Wistar rats aged 7, 12, 18, 25 and 90 days. Ketamine alone caused moderate ataxia which was more pronounced in younger animals. In combination with both aforementioned convulsants, ketamine exerted anticonvulsant effects against generalized tonic-clonic seizures in all developmental stages studied. This effect was more pronounced in bicuculline-treated animals. Moreover, ketamine also suppressed the lethality induced by both drugs during all the development. On the contrary, the action of ketamine on minimal (clonic) seizures was moderate or absent. Our results suggest an important role of ketamine-affected transmission in the generation of the generalized tonic-clonic seizure pattern; moreover, an action of high doses of ketamine on GABA-A receptors might be present.
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PMID:Ketamine suppresses both bicuculline- and picrotoxin-induced generalized tonic-clonic seizures during ontogenesis. 209 70

The authors report the clinical and laboratory findings of seven girls with the diagnosis of Rett syndrome seen at the clinic from August 1978 to October 1988. The patient's age varied from two to ten years and they were followed up for 5 years and 9 months in average. The development milestone started to deteriorate between five and twenty-four months. Acquired microcephaly was present in six patients and three cases had hyperventilation. Generalized tonic-clonic seizures were the most frequent type of seizures (6 patients) beginning between one and seven years and effectively controlled with carbamazepine. The EEG's abnormal findings were spike discharges (5 patients) and paroxysmal high-amplitude theta activity (4 patients). The remaining laboratory tests were unremarkable. The pathogenesis of Rett syndrome has not been determined. The clinical evaluation is intended to contribute to the knowledge of that rather uncommon disease.
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PMID:[Rett syndrome: report of 7 cases]. 209 97

Generalized tonic-clonic seizures are a neurologic emergency. Duration of ictal activity has been associated with neurologic sequelae. The purpose of this study was to determine if midazolam, a short-acting benzodiazepine, could effectively ablate ictal activity in an animal model without significant cardiorespiratory compromise. Ten domestic swine (10 to 20 kg) were ventilated and hemodynamically monitored. Bifrontal craniotomies were performed and electrocortical activity was recorded throughout the experiment. Pentylenetetrazol (100 mg/kg) was administered iv to induce seizures. Midazolam (0.1 mg/kg) was administered iv and serum levels were drawn at 1, 2, 5, 10, 15, and 20 min after administration. There was no significant difference between the baseline and postmidazolam vital signs. Seizure activity was seen periodically as generalized spikes, as well as individual spikes for 29 +/- 5 sec after midazolam administration. A period of attenuation of 24 +/- 7 sec was seen before returning to baseline electrocortical activity. Our study demonstrates that midazolam effectively ablated induced ictal activity without significant cardiorespiratory depression and with similar EEG effect as other benzodiazepines.
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PMID:Intravenous midazolam suppression of pentylenetetrazol-induced epileptogenic activity in a porcine model. 210 74

All mentally retarded (MR) subjects in a northern Swedish county were assessed for the occurrence of active epilepsy on a prevalence day. Active epilepsy was found in 299 subjects (20.2% of those with MR) corresponding to a crude prevalence rate of 1.2/1000 inhabitants. The age-specific prevalence for 0-9 years was higher for females than for males, while in other age groups it was slightly higher for males or showed no difference between the sexes. Epilepsy and MR were the only disorders in 129 subjects (43.1%). Cerebral palsy was the most common associated disorder and occurred in 100 (33.4%). A presumable etiology for epilepsy and MR was identified in 73.2% and 71.9%, respectively. The presumable etiological factors which caused MR occurred prenatally in 35%, perinatally in 10% and postnatally in 9%. The pathogenetic period was unknown in 31%. In 15%, the etiological events occurred during more than one of the above periods. The presumable causes were responsible for both epilepsy and MR in all except 7 cases. MR individuals with epilepsy were significantly more retarded than those without epilepsy. The first seizure occurred during the neonatal period in 11.6% and before 1 year of age in 27.7%. Generalized tonic-clonic seizures were the most common type and occurred in 204 subjects (68.2%). Seventy-one of these also had partial seizure manifestations. Daily to weekly seizures occurred in 26.8% and 32.0% had been seizure-free for the past year.
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PMID:Epilepsy in a population of mentally retarded children and adults. 214 25

The anticonvulsant effects of two doses of clonazepam (CZP, Rivotril Roche, 0.1 and 1 mg/kg i.p.) were studied on model motor seizures induced by strychnine, bicuculline, 3-mercaptopropionic acid and metrazol in male laboratory rats (Wistar strain). In the first part the effects of different doses of the convulsants were investigated and for interaction with CZP doses were chosen after which more than 70% of the animals displayed generalized tonic-clonic convulsions (a grand mal seizure). Strychnine induced this type of seizure only: two doses (2 and 3 mg/kg s.c.) were used. CZP reduced the incidence of convulsions only after the larger dose, but plain solvent (propylene glycol, ethanol, water) was equally effective. The other substances first induced a seizure of minimal (mainly clonic) convulsions and only later a grand mal seizure. CZP was highly effective against bicuculline (3 mg/kg s.c.) and metrazol (100 mg/kg s.c.), but was less so against 3-mercaptopropionic acid. The effect on grand mal seizures was more pronounced in every case than on minimal seizures. The decisive role in the anticonvulsant effect of CZP is played by the mechanisms by which the convulsants induce epileptic manifestations. CZP is most effective against substances acting on the supramolecular complex GABA receptor (benzodiazepine receptor) chloride ionophore (bicuculline and probably metrazol).
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PMID:Anticonvulsant effects of clonazepam on chemically induced convulsions. 215 Sep 91


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