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

Migraine, a clinical syndrome of unknown etiology, is a common cause of a variety of visual disturbances. This review describes the visual alterations associated with migraine syndromes of particular interest to the ophthalmologist; acephalgic, ocular, and ophthalmoplegic. Several current theories of migraine pathophysiology are discussed. Migrainous episodes are common and must be differentiated from neurologic dysfunction due to ischemia, inflammation, seizure, and compression. The differentiating characteristics of these conditions as well as a diagnostic algorithm are presented.
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PMID:Visual disturbances of migraine. 265 58

In spite of significant advances made in the technology to image the intracranial contents and to measure the metabolic activity of discrete brain sites, the factor(s) responsible for the death of ischemic neurons remains unresolved. Several potential culprits have been tried: (1) "energy failure", or depletion of high-energy phosphates, occurs very quickly after ischemia, but energy metabolites recover even in tissues where functional return does not occur; (2) "tissue lactacidosis" enhances ischemic cell necrosis, but this factor is not the indispensable cause of neuronal necrosis because acidosis is minimal or nonexistent under conditions of hypoglycemia and seizures; (3) "impairment of the microcirculation" may be a contributing factor, but such microcirculatory impairment cannot be the initiating event as it is known that irreversible neuronal injury precedes the development of microcirculatory abnormalities; (4) the effects of "excitatory neurotransmitters", especially glutamate, may explain the "delayed neuronal death" or the protracted necrosis of neurons in the CA1 sector of the hippocampus; (5) ionic pump alterations: studies of experimental myocardial ischemia tend to support a contributory role of Ca2+ in the aggravation of cell necrosis; however, lack of an experimental model in which steady-state conditions can be maintained has left unresolved the potential participation of calcium ions in ischemic cell necrosis; (6) the same statement, concerning the lack of an experimental model, can be made about the role of free-radical species; oxygen free radicals and superoxides are abundant in the reperfusion stage of ischemic injury, but it is unclear how significant their contribution might be as initiators of ischemic necrosis; and (7) the "ischemic penumbra" is a zone or portion of brain tissue that is sufficiently hypoperfused as to be functionless, but where the cells are likely to recover once normal perfusion is reestablished. Further understanding of the "penumbra" may prove crucial in future studies of brain ischemia.
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PMID:Physiopathology of cerebral ischemia. 265 39

The chemistry, pharmacology, and pharmacokinetics of cocaine are described, and the medical complications of illicit cocaine use are reviewed. Cocaine is readily absorbed from mucous membranes, the gastrointestinal tract, and the vascular beds of the lungs. Thus there are a number of routes for illicit cocaine administration, with the most popular one being intranasal. The most prevalent problems associated with the use of cocaine appear to be route and dose independent and are cardiovascular in nature; they include myocardial infarction and ischemia, sudden death, cardiac arrhythmias, and hypertension. Seizures, cerebrovascular accidents, hepatotoxicity, rhabdomyolysis, pulmonary complications, and obstetrical complications have also been reported. Gastrointestinal complications and acute toxicity may occur in cocaine smugglers who ingest cocaine-filled packets. Route-dependent complications of cocaine use are also of concern. The mechanism underlying the medical complications has not been fully elucidated but appears to be an extension of the drug's pharmacological properties. The treatment of cocaine-related toxicities is supportive and is based on the organ system affected. Drugs such as propranolol, labetalol, and nitrendipine have been advocated for treating the cardiovascular complications, and measures such as maintaining arterial blood pH, monitoring core body temperature, and diazepam therapy have been used to manage seizures. As the number of case reports of cocaine toxicity increases and the underlying mechanism is conclusively defined, management of the medical complications will improve.
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PMID:Medical complications of illicit cocaine use. 266 29

Although much has been written on the response of the heart to various intracerebral events including seizures, ischemia, intracerebral, and subarachnoid hemorrhage, less is known of the cerebral response to altered cardiac rhythm, cardiac failure, and cardiac arrest. The latter may alter central neuronal activity, cerebral blood flow, or cause ischemic damage. Such changes in cerebral function may lead to loss of consciousness, seizures, and focal neurologic deficits at the clinical level.
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PMID:Neurologic manifestations of cardiac disease. 267 32

Adenosine has been proposed as a metabolic factor involved in the regulation of cerebral blood flow. The evidence in support of this hypothesis, presented in this review, includes information on the adenosine receptors associated with cerebral blood vessels, the synthesis and metabolism of adenosine, and the release of adenosine from the brain. Adenosine dilates cerebral blood vessels, acting at an A2 receptor. The critical evidence implicating an involvement of adenosine in cerebrovascular regulation is derived from experiments with adenosine antagonists and potentiators. The antagonists include methylxanthine adenosine receptor antagonists and the enzyme adenosine deaminase. Potentiators include transport inhibitors, enzyme inhibitors, and adenosine precursors. Adenosine has been implicated in vascular regulation during hypoxia/ischemia, hypercapnia, seizures, severe hypotension, and hypoglycemia. Adenosine possesses a number of properties that can be used to minimize neuronal degeneration during cerebral insults, such as ischemia, including vasodilatation, reduction of excitatory transmitter release, reduction of membrane calcium permeability, inhibition of platelets, and neutrophil aggregation. Several recent studies have demonstrated that manipulation of central adenosine tone can alter the extent of cerebral ischemic damage, indicating a potential new therapeutic approach for the treatment of stroke.
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PMID:Adenosine in the control of the cerebral circulation. 270 69

A miniature multiple thin-film recording sensor was used to measure simultaneously the electrical activity, oxygen content and temperature of brain tissue. The chamber-type potential sensor was an Ag/AgCl electrode covered by an Si3N4 (silicon nitride) chamber. The chamber-type oxygen sensor consisted of an Au-Ag/AgCl two-electrode electrochemical cell embedded in an electrolyte-filled Si3N4 chamber. The temperature sensor was a thin-film germanium resistor. The different sensors were spaced 300 microns apart. Anaesthetics (pentobarbital, chloral hydrate, chlornembutal, halothane) were shown to depress electrical activity and to increase local oxygen tension in the hippocampus. Halothane, but not the other anaesthetics, also increased the current output of the oxygen sensor when tested in saline bath, indicating that the apparent increase in measured oxygen levels during halothane anaesthesia was partly due to an electrochemical effect of halothane on the oxygen sensors. The decrease of tissue oxygen consumption produced by the other anaesthetics is likely to be the result of metabolic depression. Cerebral ischemia, evoked by cauterization of the vertebral arteries and occlusion of the carotid arteries for 30 min, resulted in the disappearance of both spontaneous and evoked electrical activity in the hippocampus and a decrease of both local temperature and oxygen tension. There was a marked overshoot of the oxygen tension to above preocclusion level following the release of the carotid arteries. As soon as electrical activity returned, the oxygen tension fell again, often below the lowest level seen during the ischemic period. This secondary decrease of oxygen level could be reversed by administration of supplementary small doses of anaesthetic. The anaesthetic-induced increase in oxygen tension was accompanied by a marked decrease in electroencephalogram amplitude and frequency. During electrically induced seizures a decrease in hippocampal oxygen content occurred and was accompanied by an increase of local temperature. Since the rectal temperature was kept constant, the changes in temperature are likely to reflect changes in blood perfusion of the recorded area. These findings are in agreement with previous observations made with conventional electrodes. In addition, the miniature size of the chamber-type microelectrode assembly allows a correlated monitoring of parallel physiological changes with high spatial and temporal resolution during anaesthesia, ischemia and epilepsy.
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PMID:Simultaneous recording of local electrical activity, partial oxygen tension and temperature in the rat hippocampus with a chamber-type microelectrode. Effects of anaesthesia, ischemia and epilepsy. 271 Mar 29

Glucocorticoids (GCs) are highly pathogenic if secreted in excess. Recent work shows that such deleterious consequences include damage to the hippocampus, a principal neural target site for GCs. Excessive chronic exposure to GCs accelerates senescent hippocampal neuron loss, while the presence of GCs at the time of neurological insults, such as seizure or hypoxia-ischemia, exacerbates hippocampal damage. The present study determines whether GCs endanger hippocampal neurons through the same mechanism by which they damage lymphocytes. GC-induced lymphocytolysis involves cleavage of chromosomal DNA, most likely through steroid induction of a nuclease that produces a characteristic ladder of fragmented DNA. Moreover, inhibition of DNA repair using the poly(ADP-ribose) synthetase inhibitor benzamide exacerbates GC-induced lymphocytolysis. We replicated this GC-induced fragmentation of DNA in thymocytes, but observed the absence of a similar fragmentation in DNA from primary hippocampal cultures under conditions in which GCs exacerbate the toxic effects of the excitotoxin kainic acid. Furthermore, under such conditions benzamide did not worsen the GC/kainic acid toxicity. These observations suggest that GCs endanger hippocampal neurons through a different mechanism, one that seems likely to be less sterotyped and simple than this cascade of apoptosis in lymphocytes.
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PMID:Glucocorticoid endangerment of hippocampal neurons does not involve deoxyribonucleic acid cleavage. 272 59

Unilateral transient cerebral ischemia was produced in Mongolian gerbils by clipping the left common carotid artery for 1 h. About 60% of the gerbils with neurological symptoms had post-ischemic seizures. The majority of those that had seizures died within a few days, and sections of their cerebral cortices contained many dark and shrunken neurons. However, the gerbils that did not have seizures survived without any severe complications. In the cerebral cortex of the latter, the neurons with diffuse or peripheral pallor of the perikarya were seen along with a small number of dark and shrunken neurons. Diffuse pallor occurred within a few hours following ischemia in layers III, V, and VI, and disappeared 1 or 2 days after recirculation. Electron microscopically, these neurons showed dispersion of ribosomes, simple and elongated profiles of rough endoplasmic reticulum (r-ER), clustered vacuoles, and mild to moderate mitochondrial swelling. Occasional net-like tubulomembranous structures, probably derived from r-ER, were observed. On the other hand, peripheral pallor became apparent after 5 days following ischemia, usually involving layer II first and gradually extending to the deeper layers. Concomitantly, the amount of neuropil decreased and the dendrites exhibited tortuosity and irregularity in layer II. Electron microscopically, these neurons showed marked swelling of peripheral perikarya and polyribosomes and organelles were located peripherally to the nuclei. In addition, numerous degenerated axon terminals and distended dendrites were observed around the neurons. These observations indicate that diffuse pallor represents damage directly induced by ischemia and subsequent recirculation, while peripheral pallor is the delayed and remote effect of ischemia, probably due to degeneration of neuronal processes.
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PMID:Morphological studies on cerebral cortical lesions induced by transient ischemia in Mongolian gerbil--diffuse and peripheral pallor of the neuronal perikarya. 273 84

The objective of the present study was to explore metabolic correlates to the appearance of postischemic seizures and the enhancement of brain damage observed in subjects that are made hyperglycemic prior to the induction of ischemia. To that end, transient forebrain ischemia of 10-min duration was induced in normo- and hyperglycemic rats, with subsequent measurements of local CMRglc (LCMRglc) after 3, 6, 12, and 18 h of recirculation. We posed the questions of whether postischemic depression of LCMRglc is exaggerated by preischemic hyperglycemia and whether there are signs of localized increases in LCMRglc in hyperglycemic rats, reflecting subclinical seizure activity. The results confirmed the presence of a long-lasting postischemic depression of LCMRglc in normoglycemic rats. This depression was partially but not tightly related to the degree of reduction of local CBF during ischemia. The depression was most pronounced in neocortical areas and in the hippocampus, but notably it was less pronounced in the densely ischemic caudoputamen. Little or no reduction of LCMRglc was observed in moderately or mildly ischemic structures such as the hypothalamus, red nucleus, and cerebellum. Preischemic hyperglycemia markedly accentuated the postischemic depression of LCMRglc. For example, although the subjects quickly regained wakefulness and motility, they had LCMRglc values in neocortical areas that remained below 50% of control. Corresponding but quantitatively less pronounced reductions in LCMRglc were observed in other areas. Notably, preischemic hyperglycemia reduced postischemic LCMRglc also in areas that showed only moderate to mild reductions in CBF during the ischemia. The results thus demonstrate that preischemic hyperglycemia has pronounced metabolic effects in the postischemic recovery period. The data provide no indication that postischemic seizures, which develop after a recovery period of approximately 24 h, are preceded by the appearance of hypermetabolic "seizure" foci.
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PMID:Preischemic hyperglycemia enhances postischemic depression of cerebral metabolic rate. 273 14

The four-vessel occlusion (4VO) model of Pulsinelli and Brierley (Stroke 1979;10:267-272) has been modified for use in halothane-nitrous oxide-anesthetized, physiologically controlled rats that were ventilating spontaneously. Selection criteria for the classification of severity of ischemia were established by correlating changes in the electroencephalogram and the general physiological status with measurements of regional blood flow and regional energy metabolism. In 13% of animals, 4VO did not cause flattening of the electroencephalogram, and such animals were classified as undergoing only "oligemia." In 65% of rats, the electroencephalogram flattened and blood pressure sharply increased with 4VO, whereas spontaneous respiration continued. This group exhibited almost complete ischemia in autoradiographic blood-flow studies, severe acidosis, and depletion of adenosine 5'-triphosphate and glucose in the forebrain and, hence, was classified as the "ischemia" group. The remaining 22% stopped breathing after vascular occlusion and were rejected for further study. Survival experiments of ischemic animals revealed the typical postischemic sequelae, with primary metabolic recovery after 8 hours of recirculation in all brain structures followed after 8-24 hours by severe biochemical deterioration and neuronal death in the striatum and hippocampus. Postischemic seizure activity was rare. The main advantages of the present modification in comparison with the original method are 1) the application of anesthesia without loss of primary selection criteria, 2) the possibility of invasive physiological monitoring, and 3) the absence of postischemic seizures, which eliminates the necessity for secondary selection criteria.
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PMID:A modified four-vessel occlusion model for inducing incomplete forebrain ischemia in rats. 274 52


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