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

Kindling is an experimental model of epilepsy in which periodic brain stimulation induces the progressive development of electrical and behavioral seizures. A kindling-induced electrical seizure (afterdischarge) in the rat hippocampus produces prolonged neuronal supersensitivity to microiontophoretically applied acetylcholine after a latency of 40 to 60 minutes. Neuronal acetylcholine supersensitivity is correlated with the further progression of kindling. A larger hippocampal after-discharge is elicited by a subsequent kindling stimulus delivered in the presence of acetylcholine supersensitivity, but not by one delivered before the onset of the supersensitivity. The results suggest that alteration of synaptic sensitivity to acetylcholine may contribute to kindling and epileptogenesis.
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PMID:Neuronal supersensitivity to acetylcholine induced by kindling in the rat hippocampus. 3 60

Neuronal and potassium activities (ak) were measured in the nucleus ventro-posterolateralis thalami (VPL) during propagated epileptiform activity from the somatosensory cortex of cats. Seizures were induced by repetitive electrical stimulation of the cortical surface or by topical application of penicillin. The recruitment of VPL into a seizure resulted in large increases of ak to levels of up to 11.6 mmoles/l, accompanied by increased in neuronal discharge rate to 300/sec. Sometimes the rise in ak preceded active participation of a given thalamo-cortical relay (TCR) neuron in the seizure. After reaching a peak level, ak and neuronal discharge rate slowly declined during an ictal episode. After cessation of seizures all TCR neurons were inhibited, while ak fell to subnormal levels. The duration of these postictal depressions increased with the amplitude of preceding increases and subsequent undershoots in ak and could last up to 120 sec. During decay and undershoot in ak, relay capability of TCR neurons was reduced. Also the probability that action potentials elicited in intracortical endings of TCR cells would antidromically invade their cell bodies was decreased. The duration of these periods varied with the amplitude of undershoot in ak. Seizure threshold was increased during undershoots. These observations are consistent with a long-lasting postictal hyperpolarization of neuronal membranes. The hyperpolarization may be caused by the action of an electrogenic pump, which is probably involved in termination of seizure discharge.
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PMID:Relation between extracellular potassium concentration and neuronal activities in cat thalamus (VPL) during projection of cortical epileptiform discharge. 9 Jun 4

An unusual neurovisceral lipid storage disorder in two unrelated juvenile patients manifested itself by dystonia and involuntary movements, with facial grimacing, dysarthria, gait difficulty, and impaired manual dexterity. Supranuclear paresis of vertical gaze and splenomegaly were present. Absent were seizures, major intellectual deterioration, spasticity, or blindness. Histiocytes showed lysosomal storage of various phospholipids, cholesterol, neutral lipids, and autofluorescent material. Appendiceal neurons showed only an increse of phospholipids by histochemistry. Neuronal deposits differed ultrastructurally from these in histiocytes. Leukocyte sphingomyelinase activity was normal. The nosology of this disease and its relationship to so-called juvenile types of Niemann-Pick disease is discussed. The primary metabolic defect in these patients remains unknown.
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PMID:Juvenile dystonic lipidosis: an unusual form of neurovisceral storage disease. 18 51

A 13-month-old boy with intractable seizures, left hemiparesis, and psychomotor retardation due to right unilateral megalencephaly, died in hypovolemic shock 1 day after hemispherectomy. The gyral pattern of the hypermegalic hemisphere was simplified and coarse. The cortical cytoarchitecture was disarrayed by a population of giant neurons. Hippocampus and calcarine cortex were cytoarchitectonically normal, as was the entire left cerebral hemisphere. Neuronal heterotopias were present in the right centrum semiovale and both cerebellar hemispheres. Cytomorphometric study of parietal cortex of each cerebral hemisphere revealed a 4-fold increase in neuronal nuclear, and 11-fold increase in neuronal nucleolar, volume in the hypermegalic hemisphere, whereas glial nuclear volume was only one-third as great, in part because of edema of the left hemisphere. Microfluorometric cytochemical analysis demonstrated a 16% increase in neuronal DNA, 40% increase in total neuronal RNA, 12% increase in glial DNA, and 15% increase in glial RNA on the right. Biochemical analysis of tissue extracts disclosed increases in the right hemisphere of 40%, 56%, and 66%, respectively, for DNA, RNA, and protein. The data suggest heteroploidy of chromosomal DNA and enhanced transcription and translation in the hypermegalic hemisphere. Thus, a defect in regulation of cell metabolism may account for the morphologic and clinical abnormalities.
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PMID:Unilateral megalencephaly, cerebral cortical dysplasia, neuronal hypertrophy, and heterotopia: cytomorphometric, fluorometric cytochemical, and biochemical analyses. 41 42

Because of its abundance in the brain, its ability to produce hyperpolarizing inhibition of almost all neurons, its association with benzodiazepines, and the discovery that many convulsants inhibited its synthesis, gamma-aminobutyric acid (GABA) has often appeared to be the key to epilepsy. Many assumed that "primary" or "genetic" epilepsy must be a disorder of GABA synapses and that GABA agonists would be universal anticonvulsants if permeability and drug metabolism were controlled. The GABA synthetic gene was a logical "candidate gene" for epilepsy. However, the GABA-deficiency theory of epilepsy is less convincing today. GABA agonists were found to intensify seizures in some rodent and human cases. Absence and other generalized seizures in humans often worsened when treated with GABA transaminase inhibitors such as gamma-vinyl-GABA. Surprisingly, the GABA transaminase inhibitors appear to be more useful in partial than in generalized epilepsies. Neuronal GABA uptake blockers are proconvulsant. GABA agonists aggravate seizures in several mutants, ranging from the photosensitive baboon to the genetically epilepsy-prone rat. How can this be understood? Muscimol injections into the pedunculopontine nucleus increase seizures due to systematically administered convulsants, while the receptor blocker bicuculline suppresses seizures after injection into several brain regions, including the striatum. The result of inhibiting inhibitory circuits is excitation. Studies with GABA uptake blockers and the GABAB agonist baclofen are presented in which their combined administration provoked seizures in rats. Baclofen was shown also to increase the incidence of seizures evoked by pentylenetetrazole without increasing seizures due to local injections of excitatory amino acids. Baclofen antagonized the myoclonic effect of 5-hydroxytryptophan in rats with serotonin lesions. Baclofen augments some seizures and inhibits others. Selective inhibition of a particular tract, whether GABAergic or not, may have convulsant or anticonvulsant effects, depending on its connections and the state of the organism. GABAA receptor stimulation is usually but not always anticonvulsant. GABAB receptor stimulation may facilitate absence seizures and related primary generalized seizures. GABAB receptors may be abnormal in some forms of nonfocal epilepsy seen in childhood. It is likely that mutations of GABA transporter and GABAA receptor genes will be found in humans but they will probably not be patients with "pure epilepsy."
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PMID:GABA and epilepsy: their complex relationship and the evolution of our understanding. 131 57

The release of somatostatin (somatostatin-like immunoreactivity) from hippocampal slices during the development of hippocampal kindling in rats was measured under resting and depolarizing conditions. Preliminary experiments in naive rats showed that the spontaneous efflux of somatostatin (4.0 +/- 0.3 fmol/ml every 10 min) was independent of external Ca2+ but was reduced to 71.5 +/- 6% of baseline (P < 0.05) during 20 min incubation with 5 microM tetrodotoxin. Neuronal depolarization with 25, 50 and 100 mM KCl induced a Ca(2+)-dependent somatostatin release, respectively 4.3 +/- 0.4, 16.7 +/- 1.6 and 22.0 +/- 1.3 times baseline (P < 0.01). Veratridine caused a dose-dependent Ca2+ and tetrodotoxin (5 microM) sensitive release ranging from 6.5 +/- 0.1 to 13.0 +/- 1.4 times baseline at 1.4 microM and 50 microM respectively (P < 0.01). One week after the last of three consecutive stage 5 seizures (full seizure expression) or 48 h after the last stage 2 stimulation (preconvulsive stage), 50 mM KCl-induced somatostatin release was significantly higher (1.8 +/- 0.1, P < 0.01) than in shams (animals implanted with electrodes but not stimulated) in the stimulated and contralateral hippocampus. Somatostatin release measured under resting conditions was increased by 1.5 times in the stimulated hippocampus at stage 2 (P < 0.05) and by 2.2 and 1.7 times in both hippocampi at stage 5 (P < 0.01). Forty-eight hours after the induction of a single afterdischarge no significant changes were found in either spontaneous or 50 mM KCl-induced release of somatostatin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Somatostatin release is enhanced in the hippocampus of partially and fully kindled rats. 136 Dec 18

A small area of deep prepiriform cortex is uniquely susceptible to convulsant and anticonvulsant drugs in the rat. We have studied the pattern of expression of the non-constitutive stress protein (HSP72) following seizures induced by unilateral microinjection of bicuculline into this area. HSP was seen first in ipsilateral dorsal medial thalamus, amygdala and associated piriform cortex, and with more sustained seizures was seen bilaterally in these structures as well as in other projection sites. Neuronal cell death, as assessed by acid-fuchsin staining, occurred in the same brain regions. Frank necrosis was found in the ipsilateral piriform cortex with prolonged seizures. Behaviorally, the seizures induced are characteristic of involvement of the limbic system and, therefore, may be a model of human complex partial seizures.
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PMID:Distribution of HSP72 induction and neuronal death following limbic seizures. 137 69

Tissues from three cases of hemimegalencephaly (HME) causing intractable seizures treated by cortical resection were studied using immunohistochemical, ultrastructural, and morphometric techniques. Severe cortical dysplasia was seen in all cases and included lesions best characterized as hemilissencephaly and polymicrogyria. Blurring of the cortex-white matter junction, the presence of large neuronal heterotopias, and neuronal cytomegaly were frequent observations. Immunohistochemical analysis demonstrated cellular colocalization of astrocytic markers glial fibrillary acidic protein and vimentin in one case of hemilissencephaly. Morphometric data showed significant increases over controls in neuronal profile area in all cases of HME. Neuronal cell density was increased significantly above controls in one of the cases. The study shows that HME results from severe cortical dysplasia which may be caused by multiple insults, manifest in one of several ways, and reflects abnormal or altered signals that regulate cortical morphogenesis.
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PMID:Neuropathologic findings in surgically treated hemimegalencephaly: immunohistochemical, morphometric, and ultrastructural study. 141 79

Neuronal migration anomalies commonly cause seizures that are partial in type and generally refractory to medical treatment. Epilepsia partialis continua (EPC), an unusual form of epilepsy commonly related to acute damage of the cerebral cortex or to a chronic lesion, has never been described in a patient with neuronal migration anomalies. In 50 children with epilepsy due to neuronal migration anomalies, we observed two cases of EPC. These two children had unilateral neuronal migration abnormalities with partial seizures other than EPC and contralateral hemiparesis. Epilepsia partialis continua appeared two to three years after the onset of partial attacks and was accompanied by a worsening of the children's previous hemiparesis. Although a rare seizure manifestation in children with neuronal migration anomalies, when it does appear, EPC can aggravate the clinical neurological condition and should always be investigated for in these cases. Because its clinical appearance is often subtle, as in these two children, EPC may easily remain undiagnosed.
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PMID:Epilepsia partialis continua and neuronal migration anomalies. 145 92

Multiple morphological and neurochemical changes are found in the dentate gyrus of humans with temporal lobe epilepsy (TLE). Three basically different types of changes will be discussed and some interrelationships considered. Neuronal loss in several regions of the hippocampal formation in human TLE has been recognized for many years, but only recently have the polymorph or hilar neurons been evaluated as a distinct group of neurons, and cell loss in this region is now being documented in many cases with severe TLE. Reorganization of afferents within the molecular layer of the dentate gyrus is also found in a high percentage of TLE specimens. The apparent reorganization of mossy fibers from the dentate granule cells is particularly striking, and aberrant innervation of the inner part of the molecular layer by zinc- and dynorphin-containing mossy fibers has been reported in human tissue by several groups of investigators. In a subpopulation of TLE specimens, there is also disorganization of the granule cell layer. Rather than being arranged in the compact, highly organized layer that is characteristic of control tissue, the granule cell bodies in some TLE cases are dispersed. In some additional cases, a bilaminar pattern of granule cells is observed. Each of these changes could contribute to altered circuitry within the dentate gyrus of humans with TLE, and such alterations could influence seizure susceptibility within the hippocampal formation.
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PMID:Morphological changes in the dentate gyrus in human temporal lobe epilepsy. 146 68


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