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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of the ventral hippocampal dentate granule neurons in the mu opioid receptor agonist-induced motor seizures and wet dog shakes was examined in this study. [NMe-Phe3-D-Pro4]morphiceptin (9.4 nmol) was injected into the left ventral hippocampus of rats 14 days after unilateral or bilateral colchicine (5 nmol/site) lesions of ventral hippocampal dentate granule cells and the subsequent behavioral and neuropathological responses were observed. [NMe-Phe3-D-Pro4]morphiceptin injected into control animals produced convulsions and numerous wet dog shakes that lasted for less than 1 h. [NMe-Phe-D-Pro4]morphiceptin-induced wet dog shakes were significantly reduced in unilateral colchicine-pretreated rats, and completely inhibited in bilateral colchicine-pretreated animals. In contrast, generalized motor seizures evoked by [NMe-Phe3-D-Pro4]morphiceptin were potentiated and prolonged in colchicine-pretreated animals as status epilepticus (sustained clonus of forepaws and head for more than 1 h) was observed in both unilateral and bilateral colchicine-pretreated animals but not in control rats. No morphological damage of granule or pyramidal cells was found in the ventral hippocampus of control animals following [NMe-Phe3-D-Pro4]morphiceptin injection. Colchicine treatment by itself produced a selective lesion of dentate granule cells. In colchicine-pretreated animals, [NMe-Phe3-D-Pro4]morphiceptin induced widespread seizure-related damage of CA3/CA1 pyramidal cells. These results suggest that dentate granule cells in the ventral hippocampus are essential for the elaboration of wet dog shakes. However, these neurons may play an inhibitory role in the spread of seizure activity within the hippocampus or limbic structures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventral hippocampal dentate granule cell lesions enhance motor seizures but reduce wet dog shakes induced by mu opioid receptor agonist. 216 33

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

Prepubescent male rats with an amygdaloid electrode in place were administered kainic acid (KA) intraperitoneally (i.p.) while controls received phosphate-buffered saline (PBS). All KA-treated animals developed status epilepticus with bilateral forelimb clonus and ictal discharges on the EEG. The rats were then tested as adults for learning, memory, emotionality, social interaction, and activity level using the T maze, water maze, handling test, home cage intruder test, and open field test. KA-treated rats learned at a slower rate in the water maze and T maze than the controls. In addition, KA-treated rats had evidence of impaired memory during spatial bias testing in the water maze. In the home cage intruder test, KA-treated animals were more submissive and less aggressive than control animals. Finally, KA-treated animals were significantly more active than control animals in the open field test. This study demonstrates that KA administration to the immature brain, in a convulsant dose, results in permanent changes in behavior, learning, and memory.
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PMID:Behavioral effects of kainic acid administration on the immature brain. 319 87

Electrical stimulation of rat amygdala induced self-sustained steady-state seizures (status epilepticus (SE] within 60 min. These SE states varied in behavioral severity from mere alteration of motility to frank clonic convulsions. Four distinct behavioral states were observed: immobility, exploration, mastication and clonus. These SE states were associated with [14C]2-deoxyglucose (2-DG) autoradiography anatomic patterns that were correspondingly more extensive and complex. Four distinct 2-DG activation patterns were observed: a restricted pattern involving several discrete limbic nuclei, including amygdala; more extensive patterns involving numerous limbic areas, first unilaterally, then bilaterally; finally the most extensive pattern involving widespread areas of forebrain. These data imply a systematic progression of seizure activity: originating in the amygdala, then spreading to some direct amygdala projection areas, and from there to a restricted network of interconnected ipsilateral limbic nuclei. This restricted network then recruits most of the remaining limbic structures, first ipsilaterally, then contralaterally. Finally, most of the basal ganglia, thalamus and neocortex are recruited.
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PMID:Functional [14C]2-deoxyglucose mapping of progressive states of status epilepticus induced by amygdala stimulation in rat. 321 74

Mature DBA/2J (D2) and C57BL/6J (B6) mice aged 9-10 weeks were studied to determine susceptibility to behavioral seizures induced by kainic acid (KA) and the possible influence exerted by differences in metabolism and blood-brain barrier (BBB) transport. Mice were observed for 4 h after subcutaneous (s.c.) KA injection. Behavioral seizure parameters included latency to first seizure (clonus), latency to tonic/clonic seizure, and latency to status epilepticus (SE). At a KA dose of 25 mg/kg, 80% of D2 mice exhibited tonic/clonic seizures, whereas all B6 mice remained seizure-free. At 30 mg/kg, tonic/clonic seizures were observed in 100% of D2 mice and 25% of B6 mice. Of D2 mice exhibiting at least one clonic seizure in response to KA at a dose of 25 mg/kg, 50% entered SE and eventually died. Administration of [3H]KA (6.6 x 10(6) dpm) at doses of 25 mg/kg (convulsive) or 11.1 micrograms (nonconvulsive) to mice of both strains resulted in similar levels of radioactivity in cortex, hippocampus, and cerebellum 30 and 60 min after injection. Bioconversion of [3H]KA to a radiolabeled brain metabolite in vivo could not be documented in mice from either strain. Results confirm previously reported differences between D2 and B6 mice in their relative susceptibility to seizures induced by systemic KA administration and suggest that these differences are not related to strain-specific variation in metabolism or BBB transport of KA. Further studies of these two strains of mice may be useful for investigating genetic influences upon seizure susceptibility.
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PMID:Differential susceptibility to seizures induced by systemic kainic acid treatment in mature DBA/2J and C57BL/6J mice. 761 15

Much remains to be learned about mechanisms underlying entry into, and temporal progression of, status epilepticus (SE). This report describes a non-pharmacologic model of generalized convulsive SE in rat. Pulsed trains of suprathreshold electric current, were administered bilaterally to either of four rostral forebrain sites: orbital cortex, medial precentral cortex, deep prepiriform cortex, or rostral caudate-putamen (n = 8 per site). This induction method resulted in 30/32 animals attaining limb-clonic convulsive SE within a mean of 30-35 min for each forebrain site, with no differences between sites. Subsequent SE proceeded without further interventions, permitting observation of the natural course of progression. A stereotyped behavioral/electrographic sequence occurred, characterized by devolution. Behaviorally, animals progressed from predominantly limb clonus to head clonus, then to subtle twitching, and finally to electrical SE before cessation of spikes. The corresponding electrographic progression was from fast and slow spiking to periodic epileptiform discharges (PEDs). In 20 animals surviving to 48 h, pathologic damage affected mainly limbic sites; damage was related to total convulsive time rather than to clonic activity. High-dose phenobarbital but not phenytoin suppressed SE when given during orbital cortex-induced limb-clonic SE. These findings are compatible with human observations and indicate that this model will enable investigations of generalized SE mechanisms and evaluation of new therapeutic agents for refractory SE.
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PMID:A new, non-pharmacologic model of convulsive status epilepticus induced by electrical stimulation: behavioral/electroencephalographic observations and response to phenytoin and phenobarbital. 781 10

Dural arteriovenous malformations associated with symmetrical calcification of the basal ganglia are rare in children. This report concerns a 22-month-old female infant who was admitted with the problem of acute onset of status epilepticus. Physical examination revealed a grade II/VI heart systolic murmur over the left sternal border, and engorged scalp veins. Neurologically, left side hemiparesis, brisk deep tendon reflexes, bilateral presence of Babinski sign and ankle clonus were present. Brain computed tomography without contrast medium showed cortical atrophy and symmetrical calcification of the basal ganglia. Brain magnetic resonance imaging showed a signal-voided tortuous structure over the right parietal region. Cerebral angiography disclosed a dural arteriovenous malformation, located over the right parietal region, which had two major feeding arteries from the branch of the anterior cerebral artery and the parietal branch of the middle cerebral artery, and had direct venous drainage into the superior sagittal sinus. The patient received craniotomy with ligation of feeding arteries. She became seizure-free, and her neurological deficits improved gradually.
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PMID:Dural arteriovenous malformation with symmetrical calcification of the basal ganglia: a case report. 795 64

Limbic status epilepticus was induced in awake, unrestrained rats by electrically stimulating the olfactory cortex or the basal amygdaloid nucleus for about 40 min. One of four stable forms of status was induced, which were distinguished on the basis of their behavioral and EEG manifestations, and their distinct patterns of 14C-2-deoxyglucose uptake and Fos-like immunoreactivity. Type I status was characterized by sporadic EEG discharges and the activation of the amygdalohippocampal area, but had no overt behavioral manifestation. Type II status involved incessant exploratory behaviors, single EEG discharges, and the additional activation of the basal amygdaloid nucleus, some of its efferent projections, and parts of the olfactory cortex. Type III status included all of these same patterns, plus the episodic development of ictal EEG activity associated with facial and forelimb clonus, and the concurrent recruitment of the entire amygdala, ventral hippocampal formation, prefrontal, insular, and olfactory cortices, and related subcortical structures. Type IV status was characterized by generalized clonus, unremitting ictal EEG discharges, and the additional activation of most of the dorsolateral neocortex, neostriatum, and thalamus. In each case of status type I, II, or III, the same anatomical structures that displayed high levels of 14C-2-deoxyglucose uptake also contained many cells that were immunoreactive for Fos, with the exception of the parataenial and mediodorsal thalamic nuclei and the substantia nigra pars reticularis. Thus, the overall patterns of 14C-2-deoxyglucose uptake and Fos-like immunoreactivity from the same animals displayed a remarkable degree of correspondence. The major results indicate that different levels of status are related to the activation of discrete epileptogenic foci, and the capacity of such foci to interact with a distinct set of interconnected anatomical structures. It is suggested that the behavioral manifestations of limbic status epilepticus may be explained by influences of limbic structures in the ventral forebrain upon lower motor elements in the brainstem and spinal cord, without the participation of the "pyramidal" motor system.
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PMID:The functional anatomy of limbic status epilepticus in the rat. I. Patterns of 14C-2-deoxyglucose uptake and Fos immunocytochemistry. 822 99

Limbic status epilepticus was induced in awake, unrestrained rats by electrically stimulating the anterior piriform cortex or the basal amygdaloid nucleus for about 40 min. As described in the preceding article (White and Price, 1993), one of four stable forms of status may be induced. Each form is characterized on the basis of its behavioral and electroencephalographic manifestations, and its distinct patterns of 14C-2-deoxyglucose uptake and Fos-like immunoreactivity. This study was directed at identifying the epileptogenic foci of the two major forms of status, types II and III, by deactivating the basal amygdaloid nucleus, ventral hippocampal formation, amygdalohippocampal area, or anterior piriform cortex during these seizure states. Infusions of the local anesthetic lidocaine, the GABA agonist muscimol, or a vehicle solution alone were made into each of these structures during ongoing type II or type III status. The major finding is that deactivation of the basal amygdaloid nucleus terminated both types of status. This indicates that the basal nucleus is primarily responsible for the generation of widespread status epilepticus activity. Deactivation of the ventral hippocampal formation did not terminate the subconvulsive levels of status, but did prevent the recurrent development of sustained seizures with facial and forelimb clonus that characterize type III status. These models of status epilepticus may be particularly important for understanding seizure mechanisms that are not dependent upon the hippocampal formation. The possible clinical relevance of these findings is discussed in relation to temporal lobe epilepsy.
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PMID:The functional anatomy of limbic status epilepticus in the rat. II. The effects of focal deactivation. 822

This study investigates some pharmacological effects of the ethanolic extract of the leaves of Desmodium adscendens (Papillionaceae), a medicinal plant in the African traditional medicine, on the central nervous system. The plant extract induced hypothermia and had analgesic effect in mice. D. adscendens suppressed the tonic phase of convulsion and mortality induced by pentylenetetrazole (PTZ) in mice. In addition, the plant extract delayed the onset of PTZ forelimb clonus, and generalized limbic seizures induced by kainic acid. In contrast, the plant extract did not affect either tonic convulsion induced by maximal electroshock in mice or the progression of limbic seizures towards the status epilepticus in rats.
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PMID:Effects of an ethanolic extract of Desmodium adscendens on central nervous system in rodents. 873 51


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