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

Cortical laminar necrosis is a histopathological entity, related to conditions of cerebral energy depletion. Clinical correlates are supposed to be spastic motor deficits, decreased intellectual capacity and epilepsy. A study was performed in 45 children with cortical laminar abnormalities in signal intensity on MRI. The purpose of the study was to evaluate causes and clinical consequences of these cortical abnormalities on MRI in order to find indirect evidence for the hypothesis that they may represent cortical laminar necrosis. In view of the frequently present concomitant white matter damage, two contrast groups were formed: one group of 40 children with periventricular white matter abnormalities, part of them with subcortical extensions of the white matter damage; and another group of 53 children without abnormalities on MRI. Data concerning history, present clinical condition and final diagnosis were collected. The presence of cortical laminar abnormalities on MRI was found to be strongly associated with a history of cerebral energy depletion, especially hypoxia-ischemia, either in the perinatal period or later in life. Whereas white matter abnormalities tended to be more frequent in premature children, cortical laminar abnormalities tended to occur more frequently in term neonates and older children. The presence of cortical laminar abnormalities on MRI was correlated with an increased risk of spasticity in children without concomitant white matter abnormalities. In children with white matter lesions, cortical laminar abnormalities did not contribute to the risk of spasticity, which was already highly increased by the presence of white matter damage. No association was found between cortical abnormalities on MRI and epilepsy or psychomotor retardation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cortical laminar abnormalities--occurrence and clinical significance. 835 19

New highly-accurate stereological methods for estimating the total numbers of neurons in brain structures have been used to test for age-related neuron loss in the human hippocampal formation. Across the age range of 13 to 85 years, there was a substantial loss of neurons in the subiculum (52%) and in the hilus of the dentate gyrus (31%); the three remaining hippocampal subdivisions showed no significant change. These losses qualify as potential morphological correlates of senescent decline in relational memory in that they can be expected to compromise the functional integrity of a region of the brain known to be intimately involved in this type of memory. The regional pattern of neuron loss is similar in certain respects to the patterns of cell loss seen during the initial phases of ischemia and epilepsy and is fundamentally different from the pattern associated with Alzheimer's disease.
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PMID:Regionally specific loss of neurons in the aging human hippocampus. 836 10

Brain is a logical target of free radical damage, considering the large lipid content of myelin sheaths and the high rate of brain oxidative metabolism. Thus, the hypothesis that free radicals may be involved in the pathogenesis of certain CNS diseases has gained increasing popularity in recent years. In CNS ischemia-reperfusion injury, the role of free radicals appears to be well established, however, involvement of other factors, such as excitatory amino acids and prostaglandins, may also contribute to the production of neuronal necrosis following ischemia. Liberation of free iron appears to play a crucial role in the generation of reactive oxygen species in posttraumatic epilepsy. Although there is no direct evidence to indicate free radical involvement in the pathogenesis of Alzheimer's disease, brain trauma with release of iron, amyloid angiopathy and disturbances in blood-brain barrier function all appear to contribute to the development of ischemic episodes with free radical generation and neuronal degeneration. In Parkinson's disease, the substantia nigra appears to be under oxidative stress as evidenced by the findings of increased lipid peroxidation, reduced GSH levels, high concentration of iron and free radical generation via autocatalytic mechanisms within neuromelanin-containing catecholaminergic neurons. Regardless of the initial insult, a cascade of events involving both reactive oxygen radicals and mitochondrial metabolism is likely to contribute to cell injury.
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PMID:Oxygen, antioxidants and brain dysfunction. 837 80

The high mortality associated with status epilepticus (SE) has been hypothesized to result partially from neurologically induced changes in cardiac function. To test this hypothesis, we reviewed electrocardiograms of 60 patients presenting in status epilepticus. Sequential electrocardiograms before, during and after ictal episodes were compared to define changes from baseline studies. 58.3% of the SE patients (N = 35) exhibited significant abnormalities on electrocardiograms obtained within 24 h of status epilepticus. Specific electrocardiographic changes included arrhythmias, axis changes, conduction abnormalities and ischemic patterns. All of these abnormal ECG changes met generally accepted cardiologic standards for a high risk of myocardial dysfunction or ischemia. The association of ECG changes with mortality was statistically significant. These results indicate that a significant proportion of SE patients are at risk for cardiac dysfunction and that close monitoring of cardiac function is indicated during and after SE.
Epilepsy Res 1993 Jan
PMID:Analysis of electrocardiographic changes in status epilepticus. 844 82

NeuroSPECT of regional cerebral blood flow (rCBF) with Tc-99m HMPAO demonstrated left temporoparietal hyperemia in two patients with acute receptive aphasia. This finding prompted further testing with electroencephalography that added to the impression of ictal dysphasia. The differential diagnosis in one case included complicated migraine. NeuroSPECT depicts blood flow abnormalities in acute aphasic disorders, either due to ischemia, which is most commonly the cause, or due to hyperemia secondary to migraine or epilepsy. The treatment and prognosis of these latter conditions differ from stroke, and thus SPECT plays a role in patient management.
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PMID:Hyperemic receptive aphasia on neuroSPECT. 850 76

Bilateral long-term surface cortical cerebral blood flow (CBF) and electrocorticographic (ECoG) monitoring were performed in eight patients with complex partial seizures. In each patient, the epileptic temporal lobe was localized using ictal ECoG. Mean seizure interval (frequency-1) off anticonvulsant medication, a clinical measure of epileptogenicity, was 1.0 +/- 0.3 h (range: 0.4 to 2.5 h). During 13 interictal hyperventilation periods, 3.6 +/- 0.6 min in duration, the mean decrease in epileptic and nonepileptic temporal cortical CBF was 13.7 +/- 2.3 versus 6.4 +/- 1.9 ml/(100 g min) (t = 2.230, d.f. = 16, P < 0.05), representing 20.9% and 10.8% reduction from baseline CBF during hyperventilation, respectively. Seizure interval decreased (i.e. frequency increased) with increasing magnitude of seizure focus CBF reduction during hyperventilation. Seizure interval was significantly correlated with epileptic temporal lobe CBF decrease during hyperventilation (R = 0.763, d.f. = 5, P < 0.05). The data suggest that, compared to nonepileptic brain, epileptic temporal lobe is particularly prone to hypoperfusion during hyperventilation. Epileptogenicity is a function of this seizure focus susceptibility to ischemia. The finding of abnormal seizure focus autoregulation during hyperventilation has implication for epileptic focus localization with cerebral blood flow analysis.
Epilepsy Res 1995 Jul
PMID:Response of human epileptic temporal lobe cortical blood flow to hyperventilation. 853 75

In-vivo microdialysis has been used extensively to study the neurochemical mechanisms of ischemia, epilepsy and hypoglycemia. It is also being increasingly used to document the response of neurons to various medications. Most of the work to date has been done in small animals. In the last 2 years, the technique has been adapted for use in patients with subarachnoid hemorrhage, head trauma, Parkinson's disease, brain tumors and epilepsy. Two of the major limiting factors are the invasiveness of the technique and the resultant potential for CNS infection. We describe a simple, safe and reliable method to measure neurochemical changes in the human brain with in-vivo microdialysis. We were able to easily monitor for 4-6 h daily for up to 4 days in awake or comatose patients with subarachnoid hemorrhage or head trauma. Cerebral concentrations of glutamate, GABA, other amino acids and catecholamines were measured. This technique thus has a potential for on-line measurements of neurotoxins in patients with unstable neurological conditions.
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PMID:A new method of in-vivo microdialysis of the human brain. 854 74

Organotypic cultures provide a unique strategy with which to examine many aspects of brain physiology and pathology. Long-term slice cultures from the hippocampus, a region involved in memory encoding and one that exhibits early degeneration in Alzheimer's disease and ischemia, are particularly valuable in this regard due to their expression of synaptic plasticity mechanisms (e.g., long-term potentiation) and responsiveness to pathological insults (e.g., excitotoxicity). Long-term slices can be prepared from hippocampi at the second or third postnatal week of development and thus incorporate a number of relatively mature features; further signs of maturation and the preservation of adult-like characteristics occur over succeeding weeks. The stability of the cultured slice renders it an appropriate model for studying 1) prolonged regulation/stabilization events linked to synaptogenesis and certain forms of plasticity, 2) temporal patterns of cellular atrophy associated with pathogenic conditions such as ischemia and epilepsia, and 3) slow processes associated with aging and age-related pathologies.
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PMID:Long-term hippocampal slices: a model system for investigating synaptic mechanisms and pathologic processes. 858 97

Cerebrovascular disease is one of the most common causes of epilepsy in the elderly. Most of the studies published relate to cortical infarction, subarachnoid, and intracranial hemorrhage, whereas the incidence of epilepsy from subcortical ischemia, i.e. deep lacunar infarctions and diffuse white matter lesions, is obscure. Therefore, we prospectively examined 18 patients with the precisely defined diagnosis of subcortical vascular encephalopathy (SVE), who were admitted to our hospital due to epileptic seizures (group A), and compared them to a similarly selected group matched for age, sex, risk factors, and neurological deficits with an equivalent severity of SVE but without seizures (group B). Subcortical lacunar infarctions were significantly more frequent in group A than group B (15/18 versus 4/18, p < 0.001), whereas neither the extension, degree, distribution of periventricular white matter changes, nor the presence of internal hydrocephalus, focal or diffuse cortical atrophy showed any statistical significance. However, a temporal constant theta or delta EEG focus was present in 10/18 patients in group A but only in 1/18 patients from group B (p < 0.005). 10/18 patients developed epilepsy with further seizures during follow-up. The association of SVE, multiple subcortical lacunas, and temporal EEG abnormalities are suggestive for an increased risk for epileptic seizures, which is particularly important for the treatment of patients with SVE if uncertain paroxysmal episodes occur, e.g. transient ischemic attacks, seizures, or cardiac syncope.
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PMID:Epileptic seizures in subcortical vascular encephalopathy. 858 82

Central nervous system has a low antioxidative capacity, which is formed mainly by ascorbic acid. Therefore the cerebral tissue is threatened by the increased formation of free radicals and their metabolites (ROS--reactive oxygen species). ROS are formed such as in reperfusion phase after ischemia and in catecholamine metabolism, in oxidative stress due to hyperglycaemia. Polyunsaturated fatty acids (PUFA) are peroxidased by ROS; proteins and DNK are damaged as well. Free radicals are involved in etiology and pathogenesis of many CNS diseases, such as neuritis, Alzheimer disease, Parkinson disease, Huntington disease, aging and atherosclerosis of the brain, epilepsy, etc. During the antioxidant therapy it is necessary to consider the types of ROS, their origin and their mode of action, whether to administer hydrophilic or lipophilic antioxidants, eventually chelate agents, etc. Hydrophylic antioxidants are acting very soon after the administration, whereas the lipophilic ones reach their target tissues with a great delay. Therefore it is better to apply them preferentially like a prevention, if possible. Enzymatic antioxidants (SOD, GSPHx and catalase and others) are usually acting only for a short time. The methods of estimation of free radicals attacks are discussed as well their possible pathophysiological effects.
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PMID:[Free radicals in the central nervous system]. 866 12


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