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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Advances in imaging hardware for positron emission tomography and single-photon emission CT, coupled with a wide variety of radiopharmaceutical agents, have allowed these techniques to be used in the evaluation of neoplasm, stroke, epilepsy, and dementia. Cerebral perfusion agents continue to be the mainstay of single-photon emission CT imaging but, in addition to the evaluation of ischemia, it has seen an increasing role in the study of dementia, neuropsychiatric disorders, and seizures. Positron emission tomography scanning has had similar applications but it is playing a greater part in the evaluation of neoplasms, including primary gliomas and pituitary adenomas. Stable-xenon CT has shown value in the study of ischemia associated with meningitis, sickle cell disease, chronic subdural hematomas, and cerebral arteriovenous malformations. MR diffusion imaging shows promise in the evaluation of white matter pathology and some tumors.
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PMID:Physiologic imaging of the brain. 173 6

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

A new case of neonatal seizures due to arterial ischemia is reported and the symptoms and prognosis of this condition are discussed. Arterial ischemia should be routinely considered in neonates who develop seizures a few days after an uneventful birth. Seizure recurrences exhibit unchanging features, in particular consistent focalization. The value of cerebral CT scan studies is underlined. Transfontanellar ultrasonography is not helpful in this condition. MRI may be especially informative for monitoring anatomical lesions over time and Doppler studies may be of value when performed at a very early stage. The outcome in the case reported herein and in previous reports is fairly favorable.
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PMID:[Cerebral artery ischemia and neonatal convulsions]. 175 Jul 42

A review of a series of 56 patients with a giant intracranial aneurysm showed that 28 presented with signs related to the mass effect and 19 with subarachnoid hemorrhage (SAH). Additional clinical signs observed were seizures, ischemia, and endocrinological disturbances. Fourty-five aneurysms involved the carotid artery territory and eleven the vertebrobasilar system. On computed tomography (CT) images partially thrombosed aneurysms (23 cases) showed 1) a marginal or central "target" appearance on contrast enhanced scans corresponding to the non-thrombosed lumen as demonstrated by angiography, 2) capsular enhancement in 16 cases and 3) calcifications in 9. SAH occurred in 13 and 6 cases of non-thrombosed and partially thrombosed aneurysms, respectively. Magnetic resonance imaging (MRI) in 6 cases showed several layers of thrombosis in 4 cases and a small signal void close to the parent artery. In one case of a non-thrombosed aneurysm, thrombosis was mimicked by flow artifacts of MRI.
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PMID:Clinico-radiological spectrum of giant intracranial aneurysms. 179 40

Of 737 patients with Down syndrome, newborn to 22 years of age, 47 had a history of at least one seizure. Of those, 24 children had seizures with an identifiable etiology, usually related to a common medical complication of Down syndrome: neonatal hypoxia-ischemia, hypoxia from congenital heart disease, or infection. These acute medical illnesses may precipitate seizures in brains already predisposed to hyperexcitability because of abnormal neuronal development. It is recommended that all Down syndrome children with seizures undergo investigations to determine the etiology of the seizure.
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PMID:Seizures in children with Down syndrome: etiology, characteristics and outcome. 182 17

Two patients with Down's syndrome undergoing intracardiac operations had segmental and generalized myoclonic movements postoperatively and eventual brain death. Electroencephalography in 1 patient showed no seizure despite the presence of the myoclonic movements. Computed tomographic scan showed possible cerebellar hemorrhage. Ultrasound showed cerebral edema when the pupils became fixed and dilated. Because known postoperative neurologic complications could not fully explain the clinical course, and the myoclonic movements suggested spinal origin, we considered the possibility of atlantoaxial instability causing spinal cord damage related to perioperative head and neck positioning. Postmortem study on the second patient revealed 50% reduction of the spinal canal with hyperextension and 90-degree external rotation of the head and neck. In contrast, similar maneuvers in 3 infants without Down's syndrome resulted in only mild spinal canal narrowing. Although the myoclonic movements could be explained by spinal cord compression at the atlantoaxial level, the explanation for the eventual brain death is unclear. However, kinking of the vertebral arteries related to the positioning could have caused cerebellar ischemia, hemorrhage, and increased intracranial pressure. We believe that attention to the problem might bring further answers in the future.
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PMID:Perioperative spinal canal narrowing in patients with Down's syndrome. 183 20

Preischemic hyperglycemia aggravates brain damage following transient ischemia, and adds some special features to the damage incurred, notably a high frequency of postischemic seizures, cellular edema, and affectation of additional brain structures, such as the substanta nigra pars reticulata (SNPR). We raised the question whether mild intra-ischemic hypothermia (32-33 degrees C), known to reduce selective neuronal vulnerability in normoglycemic subjects, also ameliorates the characteristic damage observed in hyperglycemic animals. To that end, two series of experiments were performed. In the first, normo- and hypothermic animals were subjected to 10 min of ischemia during hyperglycemic conditions (plasma glucose 20-25 mmol.l-1), and allowed either 15 h or 1 week of recovery. In the second, both normo- and hyperglycemic animals were subjected to 15 min of ischemia (at normal or reduced temperature) and surviving animals were studied after 1 week of recovery. All normothermic, hyperglycemic animals developed postischemic seizures and died within the first 24 h. Mild hypothermia afforded substantial protection. Thus, 6/7 hypothermic animals subjected to 10 min of ischemia survived 1 week of recovery and none developed post-ischemic seizures. Of the hypothermic animals subjected to 15 min of ischemia 6/11 survived for 1 week, only one of which developed seizures. Protection by hypothermia was also shown by the histopathological analysis. Experiments with 10 min of ischemia and 15 h of recovery showed the expected damage in normothermic, hyperglycemic subjects. Hypothermia markedly reduced damage in all vulnerable structures, including the cingulate cortex and SNPR. The protection was most pronounced in the caudoputamen, where no affected neurons were seen in the hypothermic subjects. The experiments with 15 min of ischemia confirmed previous findings that mild hypothermia protects normoglycemic animals against the insult. The results also showed that hypothermia prevented most of the exaggeration of damage caused by hyperglycemia. However, under hypothermic conditions hyperglycemia still augmented damage in the cingulate cortex, medial and lateral venteroposterior thalamic nuclei, and SNPR, structures specifically damaged under hyperglycemic, normothermic conditions. This suggests that hypothermia has less of a protective effect on mechanisms causing such damage than on neuronal damage in the classic selectively vulnerable regions, particularly the caudoputamen.
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PMID:Influence of moderate hypothermia on ischemic brain damage incurred under hyperglycemic conditions. 185 66

We have previously demonstrated that hypoxia is acutely epileptogenic in the immature rat but not in the adult. The window during which hypoxia induces seizures in the rat ranges from postnatal day (P) 5-17, with the most severe seizures occurring at P10-12. Perinatal hypoxia resulted in significantly more acute seizure activity than perinatal anoxia. The present study evaluates the long term effects of perinatal hypoxia versus anoxia. Animals were exposed to hypoxia (3%O2) or anoxia (0%O2) at P10 and challenged later in adulthood (P55-60) with administration of pentylenetetrazol (PTZ) (45 mg/kg subcutaneously). Compared to normal littermate controls, the animals which had been exposed to perinatal hypoxia had a significantly higher frequency of generalized convulsions (GC) and a significantly shorter latency to the first myoclonic jerk (MJ) after PTZ. In contrast, perinatal anoxia did not alter long term seizure susceptibility. These results are discussed in context of previous studies which have shown variable long term effects using different models of perinatal hypoxia and/or ischemia.
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PMID:Differential effects of perinatal hypoxia and anoxia on long term seizure susceptibility in the rat. 185 88

A case of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes, in which a pituitary growth hormone (GH) secretion deficiency of hypothalamic origin was revealed through neuro-endocrinological examinations, was described. The case was a 10-year-old girl, who had been suffering from generalized tonic seizures since age 5, four episodes of alternating hemiplegia since age 6, stunted growth since age 7, and simple partial motor seizures as well as gelastic seizures since age 8. Marked elevation of lactate and pyruvate in both serum and CSF, abundant ragged red fibers in biopsied muscle, and low density areas in the left occipital lobe and bilateral globus pallidus in addition to diffuse brain atrophy on CT scan and MRI of the head were demonstrated, although the activities of muscle enzymes complex I-IV were within normal ranges. Pituitary GH secretion was deficient under the loadings with insulin, L-DOPA, sleep, and a single growth hormone releasing factor (GRF) administration, but normal GH response was registered under the repetitive stimulation with GRF. Activities of other hormonal axes were normal. It is likely that short stature commonly observed in MELAS patients is due to hypothalamic dysfunction, which might be brought out by chronic ischemia and energy deficiency of the diencephalon based upon mitochondrial abnormality of that region. It is likely that gelastic seizure in this case is due to hypothalamic dysfunction.
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PMID:[Hypothalamic GH Deficiency and gelastic seizures in a 10-year-old girl with MELAS]. 187 57

An examination of the cellular and molecular mechanisms of neuronal cell damage may lead to the design of pharmacologic interventions during presumed or actual fetal asphyxia. Hypoxia-ischemia in its severest form results in insufficient adenosine 5'-triphosphate production. The most important effect of this is failure of adenosine 5'-triphosphate-dependent membrane functions, which maintain ionic homeostasis, that is, ionic pumping. There is K+ efflux and Na+ influx across the cell membrane, depolarization of the cell membrane, opening of the voltage-dependent calcium channels, and entrance of Ca++ into the cell. Cytosolic Ca++ is also increased by Ca++ efflux from the mitochondria and the sarcoplasmic reticulum. Ca++ is a toxin in high cytosolic concentrations; it activates phospholipases A and C, which cause membrane breakdown and release of free fatty acids, including arachidonic acid. The membrane is damaged, lysis occurs, and the neuron dies. High cytosolic Ca++ also causes release of excitatory amino acids (especially glutamate), which overwhelm the suppressant neurotransmitters, causing seizures, increased metabolism, and aggravation of the insufficient adenosine 5'-triphosphate availability. Thromboxane A2 is generated from arachidonic acid, increasing smooth muscle tone and thereby worsening the ischemia. Cyclooxygenase activity also results in formation of oxygen-free radicals that contribute to cell membrane damage, lysis, and death. Possibilities for pharmacologic interventions include (1) calcium channel blockers and antagonists, (2) excitatory neurotransmitter blockers, (3) oxygen-free radical scavengers (e.g., superoxide dismutase), (4) cyclooxygenase or prostaglandin synthesis inhibitors, and (5) seizure suppressants (e.g., phenobarbital). Some of these treatments have been shown experimentally to limit neuronal death in the adult and fetus, and after more investigative work they may be applicable to clinical practice.
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PMID:Mechanisms of asphyxial brain damage, and possible pharmacologic interventions, in the fetus. 190 82


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