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

The intracerebral microdialysis technique has been used to monitor extracellular levels of noradrenaline, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in the rat hippocampus in vivo in response to focal and generalized seizures induced by hippocampal kindling stimulation. In fully kindled animals a stimulus-induced generalized seizure gave rise to a three-fold increase of noradrenaline levels in the stimulated hippocampus as compared to baseline levels (15-min samples). The maximal increase of noradrenaline levels occurred within the first minutes after onset of seizure activity, as assessed in 2-min sample fractions with the noradrenaline uptake blocker desipramine added to the perfusion medium. After the peak increase, the noradrenaline levels tapered off, reaching baseline after 8-10 min. In 6-hydroxydopamine-treated animals, baseline noradrenaline levels were markedly reduced and there was no significant increase in noradrenaline release in response to a generalized seizure. These data support the hypothesis that the high extracellular levels of noradrenaline measured in seizures are of neuronal origin. There were no significant changes in extracellular 5-hydroxytryptamine or 5-hydroxyindoleacetic acid levels after a generalized seizure. In non-kindled animals the steady state noradrenaline levels during uptake blockade were two-three times higher than in the kindled rats. However, the peak noradrenaline levels measured in both hippocampi after the first two electrical kindling stimulations giving rise to focal epileptiform activity (afterdischarge) were similar to those observed in the kindled animals in response to generalized seizures. The increase of noradrenaline release in the non-kindled animals was significantly correlated to the duration of afterdischarge. In conclusion, the present study demonstrates the usefulness of the intracerebral dialysis technique for monitoring noradrenaline, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid release during seizures. The results indicate that both focal and generalized hippocampal seizures evoked by electrical kindling stimulation lead to a marked increase of transmitter release from noradrenergic but not from serotonergic neurons in the hippocampus. The ability of the noradrenergic system to respond by increased transmitter release to epileptic seizures is thus retained also in the kindled state.
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PMID:Noradrenaline and 5-hydroxytryptamine release in the hippocampus during seizures induced by hippocampal kindling stimulation: an in vivo microdialysis study. 248 Dec 43

Cortical blindness is rarely an ictal manifestation. We report the case of a man who developed transient cortical blindness followed by permanent visual deficits during repeated partial seizures. Intermittent visual impairment began at age 14 years. After he had the first generalized seizure at age 28 years, neurologic, ophthalmologic, angiographic, and brain computed tomographic (CT) examinations were normal. Several EEGs showed almost continuous biposterior spike-waves. Over the next several years, frequent partial seizures were associated with transient visual loss and left body twitching or paresthesias. When he was 32, transient blindness occurred during several days of repeated occipital seizures. Permanent left homonymous hemianopia, right homonymous central scotoma, dyschromatopsia, and altered stereopsis followed these seizures. Brain CT demonstrated a new right occipital lesion. Partial seizures arising posteriorly may cause transient cortical blindness and result in permanent visual deficits.
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PMID:Ictal cortical blindness with permanent visual loss. 249 21

Although older studies have reported elevated plasma taurine concentrations, more recent studies have reported the same or lower plasma taurine concentrations in epileptic than in control subjects. The present study determined plasma taurine concentrations in 114 epileptic and 99 control subjects. In addition, taurine concentrations in platelets, known to be rich in taurine, were assayed. Serum drug concentrations were also determined to detect possible effects on plasma or platelet taurine concentrations. The plasma and platelet taurine concentrations of epileptic subjects were significantly more variable than corresponding control data. Mean platelet taurine was significantly lower for epileptic patients than for controls. Analysis of variance (ANOVA) on data from epileptic patients revealed no significant association between platelet or plasma taurine concentrations and drug or seizure groups. However, t tests revealed a higher mean plasma taurine concentration for patients with primary generalized seizure disorders (group II) receiving valproate (VPA) (p less than 0.004). Utilizing serum drug concentrations, a significant negative correlation (rxy = -0.552) was found between log-converted platelet taurine and serum VPA concentrations (p less than 0.01) among group II patients. Results were interpreted as having potential value for less empiric drug use and as indicating that cellular rather than plasma studies will prove more informative in gaining an understanding of the idiopathic epilepsies.
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PMID:Antiepileptic drugs and plasma and platelet taurine in epilepsy. 249 44

Data from 50 patients with juvenile myoclonic epilepsy (JME) were analyzed retrospectively to assess the response to drug therapy--long-term seizure control, relapse rates, and confounding factors in seizure recurrence. Valproate is the only available antiepileptic drug that has been shown to be effective in controlling the generalized seizure components of JME--myoclonic, tonic--clonic, and absence seizures--without significant side effects. Data were collected using the EpiMonitor software and represented case follow-up from 2 months to 9 years. Forty-three patients (86%) were seizure free for at least 1 year; 25 patients (50%) relapsed at some point during follow-up. Relapses were precipitated most frequently by fatigue, noncompliance, stress, sleep deprivation, and alcohol consumption. With accurate diagnosis and appropriate therapy, seizures in JME can be adequately controlled, although JME is a chronic disorder that may require lifelong therapy. To minimize relapse, patient management must also focus on patient lifestyle to eliminate or control lifestyle-associated precipitants of seizure relapse.
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PMID:Juvenile myoclonic epilepsy: long-term response to therapy. 250 7

Computed tomography of the head performed soon after a generalized seizure demonstrated diffuse bilateral contrast enhancement. The patient had undergone visceral angiography for lower extremity ischemia, and a generalized seizure was observed 90 min afterward. Postictal CT, completed without additional contrast medium administration, demonstrated diffuse patchy contrast enhancement of both cerebral and cerebellar hemispheres. The mechanism of seizure induced contrast enhancement on CT is discussed.
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PMID:Seizure induced disruption of blood-brain barrier demonstrated by CT. 250 56

We reviewed records of 5,000 epileptic patients and identified 154 cases of partial epilepsy with seizure onset in the first 3 years of life. Of these, 35 patients had initial partial seizures. In 57 patients, partial seizures were preceded by a hemiclonic seizure, which manifested as status epilepticus in 70%. Generalized seizures were the initial manifestation in 62 patients: 17 grand mal, 14 clonic or myoclonic, and 31 tonic or atonic seizures. Of the 119 patients, 31 showed a seizure free-interval of several years between the initial seizure and the occurrence of partial epilepsy. The atypical initial clinical presentation and the seizure-free interval before occurrence of more characteristic partial seizures raise the possibility that the diagnosis of partial epilepsies in the first years of life may be missed.
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PMID:Partial epilepsy with seizures appearing in the first three years of life. 251 18

Ultrastructural changes in hippocampal granule cells, mossy fibers and mossy fiber boutons were examined following the administration of picrotoxin in adult rats. Generalized seizures occurred within 5-10 min after the intraperitoneal injection of picrotoxin. The electron-microscopic examination of hippocampal tissues from rats that had been perfused with fixative during the seizure revealed that the large dense-core vesicles increased in number and accumulated on the presynaptic membranes of mossy fiber boutons; some of these vesicles appeared to be fused with the membranes, and omega-shaped exocytotic profiles were frequently seen. Furthermore, greatly increased numbers of coated vesicles (60-90 nm in diameter) were observed on the maturing faces of Golgi fields of granule cells. Thus, our study not only indicates an increased incidence of exocytosis of large dense-core vesicles during picrotoxin-induced seizures, but also suggests that these vesicles are replaced in excess from the perikaryon of the granule cell.
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PMID:Ultrastructural changes in granule cell somata and mossy fibers of the rat hippocampus during picrotoxin-induced convulsions. 253 36

The comparative effect of intracerebral injection of 2-APH, a selective antagonist for N-methyl-D-aspartate (NMDA) receptors, into the substantia innominata (SI) and the amygdala (AM) of AM-kindled rats was examined. The intra-SI injection (ipsilateral to the kindled AM) induced a transient incoordination followed by immobility with loss of the rightening reflex, beginning at about 5 min following the injection and lasting for about 3 h. When the animals were stimulated at the previously established generalized seizure triggering threshold (GST) 45 min after the injection, the kindled seizure regressed to earlier stages although the afterdischarge (AD) duration remained unchanged. At 24 h, kindled seizure was readily activated at the GST. When 2-APH was injected into the kindled AM, no behavioural change occurred but AM stimulation at the GST failed to produce AD 45 min after the injection. Kindled seizure could be elicited, however, when the stimulus intensity was increased. This elevation of the GST lasted for 1-18 days. The findings suggest that NMDA receptors in the AM and SI play a differential role in AM seizure initiation and propagation, respectively. They also provide further support to the role presumed to be played by the SI in transforming the limbic seizure into motor seizure.
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PMID:Suppression of amygdaloid kindled convulsion following unilateral injection of 2-amino-7-phosphonoheptanoic acid (2-APH) into the substantia innominata of rats. 254 69

Transient abnormalities of autonomic nervous system function are observed during almost every generalized tonic-clonic seizure and include disruptions in blood pressure, cardiac arrhythmias and apnea. An increasing body of literature indicates that epileptogenic discharges, even without accompanying clinical seizure activity, can produce a spectrum of autonomic abnormalities. Marked changes in blood pressure and cardiac rhythm occur in patients paralyzed with neuromuscular blocking agents and subjected to electrical shock or intravenous pentylenetetrazol. Similar changes are observed in patients with focal temporal lobe discharges. There is also experimental evidence suggesting that in addition to the well known effects of generalized seizure discharges, interictal discharges can produce effects upon the cardiovascular system. Neurogenic pulmonary edema may be another autonomic dysfunction associated with seizures. The phenomenon of unexplained sudden death in persons with epilepsy, which accounts for up to 15% of mortality in this group, may be a result of some unexplained irreversible disruption of autonomic homeostasis in the face of all these forces of electrical disorganization. Paradoxically, some persons manifest cardiovascular autonomic dysfunction with consequent seizures which are phenomenologically very similar to those of cerebral origin. It is important to consider performing Holter monitoring in patients with epilepsy of unknown cause and 24 h ambulatory electroencephalograms in patients with unexplained cardiac arrhythmias.
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PMID:Paroxysmal autonomic dysfunction, epileptogenic activity and sudden death. 264 19

Picrotoxin (1 mg/kg, i.p.), evoked a single generalized seizure in 75% of ovariectomized rats. Pretreatment of matched pairs with silastic implants containing 100% estradiol had an anticonvulsant effect; it protected all rats against such seizures. Implants containing 10% estradiol in cholesterol were less effective in protecting against picrotoxin-induced seizures. With 2 mg/kg picrotoxin, 85% of the seizure-affected ovariectomized controls had multiple seizures. The incidence of seizures and the ratio of single to multiple seizures induced by the higher dose of picrotoxin were unaffected by estradiol silastic implants, intraperitoneal injections of progesterone (0.5 mg, 4-5 h before convulsant) or the combination of both hormones. At the 2 mg/kg dose, 8/8 intact males had no seizures while all paired ovariectomized females had seizures. By contrast, the incidence of seizures in pairs of gonadectomized males and females did not differ. Testosterone treatment improved the ratio of single to multiple seizures in males but not in females. Males had statistically fewer multiple seizures than did females after testosterone treatment. The distribution of latencies to a single seizure is statistically different from the distribution of latencies to the first of multiple seizures irrespective of dose, sex and hormone treatment. This suggests that the population of rats responding with a single seizure at the higher dose of picrotoxin have a higher threshold for acquiring multiple seizures and that testosterone predisposes males but not females to this population.
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PMID:Steroid hormone effects on picrotoxin-induced seizures in female and male rats. 270 66


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