Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Loss of consciousness is rare in the absence of transient or persistent insult to the diencephalon or mesencephalon. We found three patients with severe atherosclerotic stenosis or occlusion of both internal carotid arteries who experienced brief loss of consciousness. Common characteristics were the absence of clinical or electroencephalographic seizure activities, significant cardiovascular disease, or a history suggestive of vasovagal syncope. Angiographically, the patients had widely patent vertebrobasilar circulation and collaterals from vertebrobasilar to carotid circulation. Episodic loss of consciousness disappeared after carotid endarterectomy. We concluded that bilateral hemispheric ischemia caused brief loss of consciousness, but selective focal ischemia in the subcortical structures superimposed on widespread bihemispheric ischemia may have been responsible. Since loss of consciousness is rare in carotid occlusive diseases, systemic and vertebrobasilar causes must be carefully ruled out in each instance.
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PMID:Brief loss of consciousness in bilateral carotid occlusive disease. 275 25

Gerbils were subjected to bilateral carotid artery occlusion for either 15 or 20 min. After ischemia the animals were injected i.p. with oligo-prostaglandin B (oligo-PGB; trimer of 16,16'-dimethyl-15-dehydro-prostaglandin B1) dissolved in 4% sodium-bicarbonate, or with the vehicle. The dosing regimen of oligo-PGB was 0.5, 1, 2, 5, 10 mg/kg injected 5 min postischemia, or 1 mg/kg injected 30, 60, 90, 120 min after ischemia, or 10 mg/kg injected 5 min and 24 h postischemia. Behaviour of the animals and their mortality were studied for 14 days after ischemia. Administration of the drug did not affect recovery of the electrical activity in the brain and did not reduce the number of postischemic seizures. Following 15 min ischemia, administration of oligo-PGB resulted in statistically valid improvement of survival (P less than 0.04 or better) in all treatment groups. After 20 min ischemia only the double injection (10 mg/kg at 5 min and 24 h postischemia) resulted in a substantial survival improvement (64%, P less than 0.005). The mechanism of the drug action is unknown but, based on the available data, the authors believe it to be related to the modification of arachidonic acid metabolism in the late postischemic period.
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PMID:Cerebral ischemia in gerbils: improvement of survival after postischemic treatment with oligo-prostaglandin B. 276 15

In this study, the cerebral hemisphere content of calcium as well as selected parameters of oxidative metabolism and electrophysiological function were assessed in normoglycemic and hyperglycemic rats that were exposed to ischemia produced by electrocautery of the vertebral arteries and reversible occlusion of the carotid arteries. In hyperglycemic animals, 0.5 h of ischemia was associated with large accumulations of lactate (27 mmol/kg), whereas normoglycemic animals showed lesser lactate accumulation (17 mmol/kg). At this sampling time (0.5 h of ischemia), both groups of ischemic animals showed tissue calcium contents that were unchanged from preischemic control levels. In normoglycemic animals, release of the carotid clamps and recirculation for 1.5-24 h was associated with normalization of lactate, ATP and phosphocreatine, clinical behavior, and EEG. During this 24 h of recirculation, cerebral calcium levels showed no changes. Hyperglycemic ischemic animals recirculated for 1.5-24 h showed a persistent lactic acidosis, depressed ATP and phosphocreatine, gross EEG abnormalities, seizures, and a high mortality rate. Again, during this 24 h period, cerebral calcium content showed no changes from preischemic control or from the matched saline-treated group. These data suggest that significant accumulation of calcium in brain tissue is not an early event in ischemic-hyperglycemic brain damage, and thus does not provide support for a role of calcium in the production of this form of ischemic damage.
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PMID:Influence of lactate accumulation on calcium content of ischemic and postischemic brain. 277 33

Nonsynaptic mitochondria isolated from rat brain hippocampus were compared with those obtained by means of the same preparative procedure from cerebral cortex and striatum. Protein recovery, marker enzyme activities (lactate dehydrogenase, citrate synthase, and acid phosphatase), state 4 respiration, and response to hypoosmotic shock showed no difference among the three cerebral regions, suggesting homogeneous behavior during the subfractionation procedure. Cholinergic markers--choline acetyltransferase, acetylcholinesterase activities, and high-affinity choline uptake--evaluated on synaptosomes showed the classic regional pattern with an enrichment in the striatum (striatum much greater than hippocampus). The coupling state of the mitochondrial fractions was maintained (respiratory control ratios ranging from 3.62 to 5.08 with glutamate + malate as oxidizable substrates), showing a metabolic competence sufficient to perform metabolic studies. Regional differences were found in state 3, uncoupled state of respiration, and cytochrome oxidase activity. Hippocampus showed the lower values (hippocampus less than striatum less than cortex). A possible role of this lower capacity of mitochondrial energy metabolism in determining the sensitivity of hippocampal neurons to ischemia or epileptic seizures is suggested.
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PMID:Oxidative metabolism of nonsynaptic mitochondria isolated from rat brain hippocampus: a comparative regional study. 283 1

Intracerebral dialysis in conscious freely moving rats was used to examine the involvement of the N-methyl-D-aspartate (NMDA) receptor in the formation of lactic acid and its consequent appearance in extracellular fluid. Local administration of NMDA in the striatum of conscious, freely moving rats was found to produce a transient increase in extracellular lactate. Alternatively, administration of the NMDA antagonists 2-amino-7-phosphonoheptanoic acid or 2-amino-5-phosphonopentanoic acid delayed the onset of and attenuated the magnitude of the lactate production induced by an electroconvulsive seizure. Pretreatment of the striatum with either of these antagonists reduced the total amount of lactate observed in extracellular fluid following ischemia induced by cardiac arrest, but did not affect the time course of the appearance of lactate in the extracellular space.
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PMID:N-methyl-D-aspartate receptor involvement in lactate production following ischemia or convulsion in rats. 285 69

In this chapter, the pathophysiology and neurochemical pathology of epileptic brain damage is discussed on the basis of an integrative approach in which a comparison is made to cell necrosis resulting from ischemia and hypoglycemia. Two main questions are asked. First, is the brain damage resulting from these three disorders of cerebral energy metabolism similar in distribution and structural characteristics, as previously proposed? Second, is it possible to identify one or several neurochemical events, at the cellular and subcellular level, that qualify as the final common pathways leading to neuronal necrosis? A related question is, will seizures cause structural damage even if they do not critically curtail cellular oxygen supply? A review of the literature and of recent results obtained in animals with long-term recovery following status epilepticus of known duration suggests that although brain damage caused by epilepsy shows some similarities to that incurred due to ischemic and hypoglycemic insults, it is far from identical. In well oxygenated animals with an adequate cardiovascular function, 2 hr of status epilepticus causes moderate neuronal necrosis in the cerebral cortex (layers 3-4), the hippocampus (CA4 and CA1 pyramidal cells), and the thalamus (ventromedial nuclei). In rats, status epilepticus of 30 min duration or longer invariably causes infarction of the substantia nigra (pars reticularis), with some affectation of globus pallidus as well. Notably, CA3 pyramids and dentate neurons are spared, as is the pars compacta of the substantia nigra. Neurochemical events in ischemia, hypoglycemia, and status epilepticus show some striking dissimilarities, yet all three conditions lead to neuronal necrosis. In complete or near-complete ischemia, in which metabolic rate virtually ceases; deterioration of tissue energy state is rapid and extensive, with dramatic loss of ion homeostasis; cellular redox systems are reduced; and acidosis is marked to excessive. In hypoglycemic coma, oxygen consumption continues, albeit at a reduced rate; loss of high energy phosphates is extensive but less than complete, as is loss of ion homeostasis; cellular redox system become oxidized; and acidosis is absent. In epileptic seizures, finally, metabolic rate is markedly enhanced; perturbation of tissue energy state and of ion homeostasis is minimal to small; and acidosis is moderate. Results obtained in experimental animals suggest that neuronal necrosis, when incurred, is unrelated to energy failure and occurs in spite of adequate cellular oxygenation. Four neurochemical events are common to all three conditions discussed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epileptic brain damage: pathophysiology and neurochemical pathology. 287 25

EEG was continuously recorded from Mongolian gerbils for 4 days after transient bilateral forebrain ischemia, to determine whether ischemic brain damage in this species is necessarily associated with seizures. Gerbils were chronically implanted with EEG recording electrodes in hippocampal area CA1, striatum and frontal neocortex and were subjected to a 5-10 min occlusion of both common carotid arteries. During the first few hours after the occlusion, the EEG was dominated by slow waves similar to those recorded from human brain after a damaging episode of cerebral ischemia. Amplitudes of the hippocampal and striatal EEG declined markedly with time, presumably as a result of neuronal degeneration. Ictal activity was never recorded, even from animals that suffered extreme damage to the hippocampal formation and striatum. Therefore ischemic brain damage in the gerbil does not result from seizure activity.
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PMID:Absence of electrographic seizures after transient forebrain ischemia in the Mongolian gerbil. 291 13

The role of spinal cord injury in the pathogenesis of abnormal motor signs (depressed tone and reflexes) following severe perinatal hypoxia-ischemia was prospectively evaluated by clinical, electrophysiological, and neuropathological examinations in 18 asphyxiated neonates. All infants had an abnormal mental status (lethargy or coma), and seizures were present in 12. Neuromuscular examinations revealed hypotonia or flaccidity and hyporeflexia or areflexia in all infants. Neuropathological examinations of the cerebrum and spinal cord were conducted in the 12 neonates who expired. Cerebral pathological findings included cortical neuronal necrosis in 10 of 12 and subcortical white matter injury in 5 of 12. All infants with coma or seizures displayed diffuse cortical injury, but no injury conformed to a parasagittal "watershed" distribution. Spinal cord gray matter displayed prominent ischemic necrosis in 5 patients who were typically flaccid and areflexic. Electromyographic examinations of all 6 survivors were abnormal, consistent with recent injury to the lower motor neuron above the level of the dorsal root ganglion. We conclude that ischemic injury to anterior horn cells within spinal cord gray matter is relatively common among hypotonic-hyporeflexic neonates following severe perinatal hypoxia-ischemia. Although the acute neurological syndrome of neonatal asphyxia is often overshadowed by prominent cerebral signs such as coma and seizures, the motor abnormalities may be partially attributed to concurrent spinal cord injury.
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PMID:Hypoxic-ischemic spinal cord injury following perinatal asphyxia. 291 67

The effect of insulin-induced hypoglycemia following 10.5 minutes of forebrain ischemia was studied in the rat. All groups received preischemic glucose loading (2 gm/kg) to promote brain infarction. Following completion of ischemia, rats received either 2 to 3 IU/kg (low-dose group) or 8 to 20 IU/kg (high-dose group) insulin. During the survival period, blood glucose concentrations were maintained in the ranges of 1.2 to 2.9 mM and 2.9 to 4.9 mM, respectively, for the low-dose and high-dose insulin groups. Control rats were given 2 gm/kg glucose immediately following ischemia. During the recovery period, until perfusion at 7 days, they were given glucose, 2 gm/kg, twice daily by intraperitoneal injection, and their drinking water was supplemented with 25% glucose. Mortality (p less than 0.05) and postischemic seizure incidence (p less than 0.01) were significantly reduced in the low-dose insulin group compared to the control group. Mortality was increased in the high-dose insulin group compared to the control group and was associated with an increased incidence of postischemic seizures. Neuropathological examination revealed no cortical infarction in the low-dose or high-dose insulin-treated rats compared to a 60% incidence of cortical infarction in the control group. In addition, the high-dose insulin-treated group showed a significant reduction in striatal and hippocampal CA1 selective neuronal necrosis compared to control rats with comparable survivals (p less than 0.05). The findings suggest that postischemic blood glucose concentrations play an important role in modulating both ischemic infarction and selective neuronal necrosis.
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PMID:The effect of postischemic blood glucose levels on ischemic brain damage in the rat. 305 89

Perinatal asphyxia is associated with an increased risk of cerebral palsy and significant mortality. We investigated the use of flunarizine, a calcium antagonist and MK-801, an excitatory amino acid antagonist, in preventing the sequelae of severe hypoxic/ischemic insults. Flunarizine was neuroprotective in the infant rat subjected to unilateral carotid ligation and 2 h of hypoxia. Preliminary analysis of experiments in a novel model of cerebral ischemia in the fetal sheep suggests that prophylactic treatment with flunarizine greatly modified the outcome after 30 min of total ischemia. Treatment with MK-801 prevented post-ischemic seizures. The background to these developments is outlined and future prospects considered.
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PMID:Perinatal cerebral asphyxia: pharmacological intervention. 307 20


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