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

Using facial and forelimb (F&F) clonus (a proposed forebrain marker) and running-bouncing (R/B) clonus and tonus (proposed brain-stem markers), the responsiveness of forebrain and brain-stem to electroshock or pentylenetetrazol seizures was assessed in GEPRs. The most striking finding was the failure of GEPR-9s to display F&F clonus in response to transcorneal electroshock at any stimulus intensity. Indeed, GEPR-9s displayed only R/B clonus or tonus indicative of brain-stem seizure discharge. GEPR-3s and normal rats, on the other hand, displayed F&F clonus in response to the least effective electroshock stimulus, and R/B clonus and tonus at higher stimulus intensities. After treatment with phenytoin (50 mg/kg) to inhibit the tonic seizure, the least effective electroshock stimulus also produced F&F clonus in GEPR-9s. These findings suggest that the threshold for triggering brain-stem seizure discharge by electroshock is lower than that for triggering forebrain seizure discharge in GEPR-9s, whereas the reverse relationship is true in normal rats and GEPR-3s. The rank ordering of the electroshock thresholds was: normals greater than GEPR-3s greater than GEPR-9s. Both GEPR-3s and GEPR-9s were found to be hyper-responsive to pentylenetetrazol as evidenced by shorter latency for the tonic seizure and a greater seizure severity than normal rats. The rank ordering of seizure severity in response to pentylenetetrazol was: GEPR-9 greater than GEPR-3 greater than normal rats.
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PMID:Electroshock- and pentylenetetrazol-induced seizures in genetically epilepsy-prone rats (GEPRs): differences in threshold and pattern. 235 51

Propofol and thiopentone were compared as anaesthetic agents for electroconvulsive therapy in 31 patients on four occasions in a repeated measure crossover study. Discomfort on injection was significantly more common with propofol (51.6% of anaesthetics) compared to thiopentone (1.6% of anaesthetics). The duration of seizure was shorter with propofol in both treatments but there was significant drug-time interaction. Propofol gave a milder tonus and clonus during seizure when both treatments were considered together. The increase in systolic and diastolic arterial pressures and heart rate after treatment were significantly higher with thiopentone. Apnoea was significantly longer with propofol. The times to sitting up unaided and opening the eyes on command were the same for both drugs. The ability to walk 10 m 20 minutes after anaesthesia was significantly better with propofol (p less than 0.0001).
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PMID:Comparison of propofol and thiopentone as anaesthetic agents for electroconvulsive therapy. 240 70

It has been hypothesized that the Long-Sleep and Short-Sleep mouse lines were bidirectionally selected for high and low brain excitability, and further, that these differences are mediated by the benzodiazepine/gamma-aminobutyric acid (GABA) receptor-chloride channel complex. Hence, mice from both lines were administered seven convulsants (bicuculline, pentylenetetrazol, 3-carbomethoxy-beta-carboline, picrotoxin, caffeine, flurothyl and strychnine) and myoclonic and clonic seizure latencies recorded. Supporting the original hypothesis, the results show that the two lines were differentiated by all of the convulsants and that in response to the drugs, three distinct convulsive patterns were found. Nevertheless, a simple genetic model accounting for these results was not evident. To further clarify these susceptibility patterns, a convulsant representing each of these patterns (bicuculline, pentylenetetrazol or caffeine) was administered in conjunction with the anticonvulsant-barbiturate phenobarbital or the benzodiazepine antagonist Ro 15-1788. Irrespective of the convulsant given, phenobarbital attenuated both myoclonus and clonus subsequent to all convulsants, while Ro 15-1788 had a more discrete anticonvulsant profile.
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PMID:Patterns of convulsive susceptibility in the long-sleep and short-sleep selected mouse lines. 250 42

The convulsant potency of bicuculline, a GABA antagonist, was shown to be greater in Short-Sleep (SS) mice than in Long-Sleep (LS) mice. LS mice, selectively bred for lengthy ethanol-induced narcosis, had longer latencies to myoclonus and clonus following administration of bicuculline and picrotoxin than did ethanol-resistant SS mice. SS mice were also more susceptible to pentylenetetrazol-induced myoclonus, but not clonus. F1 hybrids showed bicuculline seizure sensitivity intermediate to the two parent lines. Ethanol weakly inhibited bicuculline-induced myoclonus in both LS and SS mice. Clonus was clearly antagonized by ethanol in both lines, but to a similar degree. These data provide evidence for a GABAergic role in genotype-dependent sensitivity to ethanol.
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PMID:Convulsant properties of GABA antagonists and anticonvulsant properties of ethanol in selectively bred long- and short-sleep mice. 250 97

The effect of the focal injection of N-methyl-D-aspartate (NMDA) and 2-amino-7-phosphonoheptanoate (APH) into the substantia nigra pars reticulata (SNR) and entopeduncular nucleus (EP) on behavioural signs of the high pressure neurological syndrome (HPNS) in rats was studied. Doses of 1, 5 and 10 nmoles of NMDA or APH were injected into the SNR or EP, 10-30 min prior to the exposure of animals to a high pressure. Injection of NMDA into either SNR or EP results in a lowering of the threshold pressure for tremor by about 30%. Injection of NMDA into the SNR has no significant effect on clonic seizures whereas its injection into the EP results in a decrease of threshold pressure for clonic seizures. NMDA also facilitates the occurrence of forelimb clonus when injected into the EP. Injection of the NMDA antagonist, APH, into the SNR or EP significantly increases the threshold pressure of tremor (32.8 and 48.2% respectively). Seizure threshold is also increased by the injection of APH into either area, but nigral injections (especially the higher doses) are more protective against seizures than the EP injections. Comparing the two sites blockade of NMDA receptors within the EP is more protective against tremor, whereas in the SNR NMDA blockade is more protective against seizures.
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PMID:Studies on the role of the NMDA receptor in the substantia nigra pars reticulata and entopeduncular nucleus in the development of the high pressure neurological syndrome in rats. 255 89

The purpose of the present study was to examine whether doses of phenytoin and phenobarbital that blocked kindled seizures in rats also disrupted operant behavior. Subjects initially were exposed to a kindling procedure in which repeated electrical stimulation of the amygdala evoked generalized seizures. After kindling, they were trained under a multiple fixed-ratio 30 interresponse-time-greater than 10-sec schedule of food delivery. Once each day, 6 days per week, 30-min exposures to this schedule were followed immediately by amygdaloid stimulation which occurred at no other time. Response rate, reinforcement rate and duration of forelimb clonus were recorded. When response rates were stable, 5 rats were tested with phenytoin (25, 50, 75 and 100 mg/kg) and 5 others were tested with phenobarbital (10, 25 and 40 mg/kg). Results indicated that doses of phenytoin that controlled kindled seizures also affected operant behavior. For this drug, the ED50 for forelimb clonus was 62 mg/kg. For response rate under the fixed-ratio and interresponse-time components, it was 48 and 58.2 mg/kg, respectively. Dose-response curves for the behavioral and antiseizure effects of phenobarbital were similar. However, for this drug the ED50 for forelimb clonus (18.9 mg/kg) was significantly lower than for response rate under the fixed ratio component (37.4 mg/kg).
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PMID:Effects of phenytoin and phenobarbital on schedule-controlled responding and seizure activity in the amygdala-kindled rat. 270 79

Kainic acid (KA, 8-15 ng) was injected into the amygdala of conscious freely moving rats via chronically implanted fused silica cannulas. At 15-25 min after the injection, most rats suffered a limbic seizure attack of short duration, consisting of mastication, forelimb clonus, and raising on hind limbs, behaviorally indistinguishable from kindled seizures. Typically, the attack was followed by stereotypies, intense exploration, and by 1 or 2 more attacks. About 60 min after the injection, most rats appeared normal again and histopathological changes in their brains did not exceed those seen in vehicle-injected rats. In 3 cases, however, recurrent seizures culminated in behavioral status epilepticus 60-90 min after the injection. The status epilepticus was stopped by i.p. injection of diazepam (10 mg/kg) after a duration of 10 min (1 case) and 30 min (2 cases), respectively. After 10 min status epilepticus, we observed marginal neuronal damage with slight gliosis in both hippocampi (CA3 and CA1); after 30 min, hippocampal histopathology was more pronounced, with additional necrosis of the ipsilateral piriform cortex. After 0.8 microgram KA, a hundredfold higher dose, the incidence of limbic seizures during the first 40 min was not significantly higher (9/12) than after the lower KA doses (13/19). However, a significantly higher proportion of rats exhibited long-lasting seizure activity, associated with confluent destruction of CA3 pyramidal cells and additional seizure-related brain damage. Our results show that limbic motor seizures do not inevitably lead to histopathological changes in the brain, provided they do not culminate in a state of permanent seizure activity.
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PMID:Limbic seizures without brain damage after injection of low doses of kainic acid into the amygdala of freely moving rats. 274 56

Male Long-Evans rats were kindled by stimulation of the pyriform cortex using an afterdischarge (AD) threshold procedure that triggered one AD every 24 h. AD threshold dropped rapidly as long as the seizures remained localized, reaching an asymptote of 30% of its initial value by the 6th AD. In contrast, AD threshold rose progressively across the first six generalized seizures (i.e. ADs accompanied by forelimb clonus). This elevation in threshold was dependent upon the daily elicitation of a generalized seizure, and the threshold returned to its previous low value after 4 seizure-free days. This indicates that post-seizure inhibition in the pyriform cortex is a transient response produced by generalized seizures and is not related to the relatively permanent changes that underlie kindling.
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PMID:Twenty-four-hour post-seizure inhibition during limbic kindling requires seizure generalization. 274 13

The effect of kainic acid on extracellular [K+], [Ca2+], and [Na+] in the rat piriform cortex and hippocampus was studied by means of intracranial microdialysis. Either a dialysis fiber loop or horizontal Vita fiber were stereotaxically implanted within the piriform cortex or hippocampus, respectively. About 24 h later, fibers were perfused (1 ml/min) with Krebs-Ringer bicarbonate solution. Effluent samples were collected before (four at 30 min intervals), and after (six at 30 min intervals) administration of kainic acid (16 mg/kg, i.p.) or kainic acid vehicle. Kainic acid induced sequential signs of lethargy, staring, "wet-dog shakes," forepaw clonus, and tonic-clonic convulsions. In these awake free-moving rats, kainic acid induced a rapid and prolonged increase in extracellular [K+] and an apparent, but not statistically significant, decrease in extracellular [Ca2+] within the hippocampus. In the piriform cortex, kainic acid induced increases in extracellular [K+] and [Na+], which were associated with early pre-convulsive signs. In contrast to the pronounced ion changes commonly seen when the brain is activated by factors such as local application of excitatory substances or when the brain is made ischemic or hypoxic, extracellular ion concentrations are relatively well maintained during parenteral kainic acid-induced seizures.
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PMID:Kainic acid-induced seizures: changes in brain extracellular ions as assessed by intracranial microdialysis. 277 Apr 22

Kindling of the deep prepyriform cortex (DPC), a recently identified sensitive site to chemoconvulsants, was compared to kindling of the amygdala in rats. Although the two kindled sites were very similar in their initial responses, electroencephalographic changes during kindling stimulation, kindling seizure development, and growth of afterdischarge, they differed in that the deep prepyriform cortex showed a significantly lower final threshold, a significantly higher frequency of afterdischarge and a significantly shorter latency to bilateral forelimb clonus than the amygdala. Significant bidirectional transfer was found during secondary kindling of either of the two sites, suggesting a close interrelation between them. Rhythmic synchronous discharge was directly induced in the deep prepyriform cortex by ipsilateral amygdala stimulation, but not in the amygdala by ipsilateral cortical stimulation. Local application of both muscimol (0.45 nM) and 2-amino-5-phosphonovaleric acid (25 nM) into the cortical site reduced the afterdischarge duration of amygdala-kindled seizures by approximately 20% without changing the type or duration of the motor seizure. We suggest that the deep prepyriform cortex is "downstream" from the amygdala in the preferential routes of afterdischarge propagation, and that, although the deep prepyriform cortical neurocircuits of GABA and excitatory amino acids may be involved in the maintenance of amygdala-kindled, self-sustained afterdischarge, they are not essential in the expression of amygdala-kindled motor convulsions.
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PMID:Deep prepyriform cortex kindling and its relation to amygdala kindling in the rat. 287 99


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