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

The time course of structural change in epilepsy-induced necrosis of the substantia nigra was studied by light and electron microscopy, and was correlated with previous metabolic studies. By light microscopy, tinctorial pallor appeared early, followed by pan-necrosis and macrophage infiltration. Mild lesions showed neuropil vacuolation but sparing of neurons, rather than a selective neuronal vulnerability. Electron microscopy of the evolving necrosis revealed an orderly sequence of structural damage involving first axons, then dendrites, neurons, and glia. No necrotic endothelial cells could be found, even in areas of apparent pan-necrosis by light microscopy. Pericytes near the vascular lumen were spared, whereas those in outer locations were necrotic. Edema, measured densitometrically, was absent. Previous metabolic studies of this lesion have demonstrated a pronounced focal lactic acidosis due to anaerobic hypermetabolism. Although the lesions resemble infarcts, hypermia rather than ischemia has been shown to accompany their development. Structural preservation of endothelial cells and inner pericytes likely stems from proximity to the moving blood stream, away from the site of lactic acid production in the neuropil. The findings indicate that the perfusion of necrotic tissue occurs via a persisting, intact microcirculation. The relative neuronal sparing and the early axonal rather than dendritic lesion show a clear distinction from excitotoxic pathology.
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PMID:Early axonal lesion and preserved microvasculature in epilepsy-induced hypermetabolic necrosis of the substantia nigra. 379 37

Excessive tissue lactic acidosis is considered to be detrimental to the central nervous system (CNS) and may adversely affect recovery from anoxia, ischemia, trauma and epilepsy. Since astrocytes are believed to play a role in pH regulation in the CNS, we studied the effect of this acid on primary astrocyte cultures. Cells exposed to lactic acid showed chromatin clumping, an increase of lipid and dense bodies, a loss of polyribosomal clusters, slightly increased cytoplasmic lucency, swollen mitochondria and tangled intermediate filaments. These alterations progressed with lower pH and longer exposure. Irreversible changes occurred one to two hours after exposure at pH 6; after 30 to 60 minutes (min) at pH 5.5 and after ten to 30 min at pH 5. Comparable results were obtained with the use of other weak acids indicating that the observed changes were due to increased hydrogen ion concentration rather than secondary to lactate per se. Additionally, various concentrations of lactic acid adjusted to identical pH produced similar morphologic alterations. Thus, while lactic acid caused marked and at times irreversible alterations in astrocytes, severe and prolonged acidosis was required to produce such injurious effects. This relative resistance of astrocytes to acidosis is in keeping with their potential role in pH regulation in brain.
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PMID:Effects of lactic acid on astrocytes in primary culture. 381 73

Perinatal asphyxia has been implicated in the pathogenesis of persistent convulsive disorders later in life. Whether epilepsy is the result of oxygen deficiency alone or is due to the combined effect of hypoxia and ischemia is not known. In this report we studied the role of perinatal hypoxia alone on the development of epilepsy. One day and ten days old rat pups were exposed to prolonged hypoxia (6% O2). The subsequent susceptibility to focally elicited (kindled) or generalized (flurothyl) seizures was determined in the fourth week of age. Rats exposed to hypoxia were not more susceptible to the development of either type of seizures when compared to controls. Since the equivalent degree of hypoxia used for the 1 day old rat has previously been shown to result in lasting neurochemical and behavioral alterations and the degree of hypoxia used for the 10 day rat was lethal in over 35% of the animals, it is suggested that oxygen deficiency in and of itself may not be sufficient to lead to the development of epilepsy.
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PMID:Perinatal hypoxia and subsequent development of seizures. 393 75

The clinical picture and investigation of 26 patients (16 males and 10 females) with diagnosis of transient global amnesia (TGA) are reported. Age ranged from 51 to 78 years at the time of TGA, which occurred mor often between 60 and 70 year-old people. Three patients presented more than one episode (3, 4 and 5). Precipitating factors were identified in 8 cases (emotional stress in 7 and physical exercise in 1). Risk factors for cerebrovascular disease were found in 13 cases, mainly hypertension (9 cases) and diabetes (3 cases). EEG was normal in 20 cases and disclosed diffuse delta waves in 2, temporal delta waves in 1 and temporal theta waves in another patient. CAT scan showed no abnormalities in 3 cases and ischemia in the vertebro-basilar system in another 2. Brain angiography was normal in 1 case and showed abnormalities in the vertebro-basilar system arteries in 3. During the follow-up period, which ranged from 1 to 84 months, no neurologic deterioration was seen. The role of risk factors for vascular diseases, epilepsy and migraine in the development of TGA is discussed.
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PMID:[Transient global amnesia: study of 26 cases]. 401 36

Recent investigations at several institutes have demonstrated extensive acute brain pathology in experimental animals exposed to single subcutaneous doses of the chemical warfare nerve agents soman or sarin. Lesions include neuronal and neurophil degeneration, necrosis, and in animals that survive for several weeks, a degenerative encephalopathy characterized by mineralization, encephalomalacia, atrophy, and hydrocephalus. The cerebral cortex, amygdaloid complex, hippocampus, and multiple thalamic nuclei are consistently affected. This pattern of injury resembles that described for epilepsy and ischemic brain injury. Some animals have cardiac lesions characterized by acute necrosis with subsequent mild inflammation and fibrosis. Anticonvulsants protect experimental animals from lesion development. In rats, this encephalopathy causes long-range behavioral changes characterized by hyperactivity during routine handling and variances in traditional behavioral tests. The histopathologic features and distribution of lesions in nerve agent-poisoned animals support the hypothesis that epileptiform seizure activity is a major factor in nerve agent pathology. Other localized insults such as ischemia and hypoxia probably contribute to the pathogenesis.
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PMID:Pathology of nerve agents: perspectives on medical management. 409 82

Positron computed tomography is a noninvasive medical imaging technique. Biologically active, radiolabeled compounds are administered intravenously to patients and the distribution of the radioactivity is quantitatively measured. By using appropriate mathematical models and labeled compounds, quantitative measurements of local metabolism, blood flow and volume, protein synthesis, transport, receptor binding, drug kinetics, and concentrations can be obtained noninvasively. This technique goes beyond medical imaging; it allows local analytic assays of biochemical reactions. In the heart, the technique measures local blood flow as well as myocardial free fatty acid and glucose metabolism, and can clinically evaluate patients with ischemic heart disease or cardiomyopathies. In the brain, positron computed tomography can be used to examine alterations in blood flow and metabolism including ischemia and degenerative disorders (Huntington's disease and Alzheimer's disease), cerebral tumors, and epilepsy. In normal persons, positron computed tomography shows cerebral activations resulting from physiologic stimulation (auditory and visual).
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PMID:Positron computed tomography for studies of myocardial and cerebral function. 621 2

The authors report 31 cases of "vascular epilepsy" among 280 cerebral strokes confirmed by cranial computerized tomography. A high incidence of ischemia (28 cases : 90%) is noted. Epileptic seizures are initial (14 cases) or sequellar (17 cases) manifestations of cerebral stroke. Partial seizures are the most frequent (58%), particularly "Jacksonian" motor fits, which, when initial, often lead to status epilepticus. Frequency and bad prognosis of initial status epilepticus are pointed out.
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PMID:[Vascular epilepsy: clinical, electroencephalographic, and computerized tomographic aspects (author's transl)]. 626 3

Absence spells in adults have been recognized in association with disorders of excessive somnolence, transient ischemia of the temporal lobes, and seizure disorders. A 66-year-old man who presented with a history of absence spells for more than 20 years is described. After diagnosis of a hyperventilation syndrome without an associated seizure disorder, educational and behavioral therapy without the use of medication has produced a long, continuing remission of these spells. The hyperventilation syndrome continues to present in many ways, often without recognition by physicians for prolonged periods. The case presented exemplifies this problem and may be the first report of absence spells caused by hyperventilation.
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PMID:Absence spells. Hyperventilation syndrome as a previously unrecognized cause. 642 1

Regional cerebral blood flow (rCBF) may be measured with a single-photon-emission computed tomograph (SPECT) after inhalation of xenon 133. Our SPECT studies of rCBF in a group of 18 patients with seizure disorders, when compared with studies in 32 normal control subjects, have shown enhanced flow to an active seizure focus and ischemia of brain areas in certain subjects between seizures. Thus, SPECT determination of rCBF has demonstrated a number of findings recently observed with positron-emission tomography and may become a useful modality in the study of patients who have epilepsy.
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PMID:Single-proton tomographic study of regional cerebral blood flow in epilepsy. A preliminary report. 660 42

A patient with an unusual "compulsion" to induce syncope over a period of years by bilateral compression of the carotid arteries subsequently had recurrent seizures. The EEG showed patterns typical of cerebral ischemia during the syncope and epileptogenic foci in both temporal lobes after sleep deprivation. It is difficult to distinguish between seizure and syncope associated with involuntary movements when making a differential diagnosis. We hypothesize that the frequent self-induced ischemic insult to the brain caused a cicatrix to develop, which in turn caused the frequent seizure disorder; and that because this ischemia functioned as a stimulus to the reward site in the limbic system, the patient repeatedly induced it.
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PMID:Repeated self-induced syncope and subsequent seizures. A case report. 663 12


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