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

The effect of right common carotid artery ligation required for arteriovenous extracorporeal membrane oxygenation (ECMO) was investigated in 35 infants. Their neonatal course was reviewed for evidence of right-sided ischemia of the brain, as suggested by the presence of focal seizures, hemiparesis, focal abnormalities on electroencephalography, or infarct or hemorrhage demonstrable on neuroimaging studies. A significant incidence of left focal seizures (9/35) versus right focal seizures (2/35) was noted, suggesting an effect of the carotid ligation on right hemisphere function. Computed tomographic scans (20/35 infants), electroencephalograms (18/35), ultrasound scans (31/35), and neurologic examinations did not reveal an increased incidence of right hemisphere abnormalities. These data suggest that systematic evaluation of the effects of right common carotid ligation should proceed as discussion continues on expanding the use of ECMO.
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PMID:Right common carotid artery ligation in extracorporeal membrane oxygenation. 338 18

The effect of hypoxia on neurological function, compressed spectral array electroencephalography, and histopathology in head-injured rats was evaluated. By itself, an hypoxic insult (PaO2, 40 mm Hg for 30 minutes) caused no neurological deficit. Twenty per cent of rats injured by a 5-atmosphere temporal fluid percussion impact were hemiparetic contralateral to the side of impact, whereas 80% had no deficit 24 hours after injury. Seventy per cent of rats with both fluid impact injury and hypoxic insult, however, either had a definite hemiparesis, showed no spontaneous movement, or died (P less than 0.02). Impact alone produced an initial depression in electroencephalogram power that was prolonged in rats with hypoxic insult; the most dramatic effect was found in the injured hemisphere, with shorter and less profound effects in the contralateral hemisphere. Perfusion staining of injured cerebral tissue in vivo with 2,3,5-triphenyltetrazolium chloride showed an area of extensive ischemia around the impact site in rats with hypoxic insult. This ischemic area was not present in rats with either impact injury or hypoxia alone. We conclude that posttraumatic hypoxia clearly increases the severity of impact injury in this rat model. These findings suggest that hypoxia, which is common in head-injured patients, very likely worsens the effect of impact injury and may account for much of the diffuse neurological dysfunction in patients with severe craniocerebral trauma.
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PMID:Effect of hypoxia on traumatic brain injury in rats: Part 1. Changes in neurological function, electroencephalograms, and histopathology. 361 63

Cerebral ischemia was recorded in 1.9% of 1277 patients with myocardial infarction. In most cases ischemia involved the carotid artery system, usually causing a hemiparesis or hemiplegia. Patients were mostly elderly, and the ischemic episode worsened their prognosis. The pathogenesis was surely often of embolic origin but several facts suggest that other mechanisms were also involved. Anticoagulant therapy, at least in the form in which it was used in these patients, i.e. subcutaneous administration of calcium heparin 5000 I.U. b.i.d. for thrombophlebitis prophylaxis, does not seem to prevent these complications.
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PMID:Cerebrovascular accidents in acute myocardial infarction. 362 75

A retrospective case note survey of 139 cases of carotid territory TIAs was carried out. Angiographic evidence of carotid stenosis was more frequently encountered when the patient's attacks consisted of symptoms suggestive of ischemia of small cortical territories with involvement restricted to the arm or leg or to dysphasia. Attacks of hemiparesis affecting face, arm and leg, or arm and leg were less often associated with carotid stenosis. If patients described any attacks of a restricted nature the chance of finding carotid stenosis was 47%, if not 16%. It is argued that these findings are a reflection of the varied pathogenesis of TIAs, and the relevance of this heterogeneity to the interpretation of clinical trials is briefly mentioned.
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PMID:Clinical identification of TIAs due to carotid stenosis. 371 34

Ischemia causes disturbances of the ionic equilibrium, i.e., Na+ and water influx and K+ efflux. When the ischemic tissue keeps contact with cerebral blood flow, brain tissue equilibrates with systemic circulation and consequently shifts of electrolytes and water are induced. Therefore, brain edema should initiate in the peripheral area of focal cerebral ischemia. To test this hypothesis, we performed the following experiments. Focal ischemia was induced by occlusion of the right common carotid artery in gerbils and by embolization with microspheres in rats. Water and electrolyte content was determined using punched out samples and regional K+ and Ca2+ distribution was visualized by histochemical K+ staining and 45Ca-autoradiography, respectively. Cerebral blood flow and glucose metabolism were evaluated by 14C-iodoantipyrine or 18F-fluoroantipyrine and 14C-deoxyglucose autoradiographies, respectively. Two hours of ischemia in gerbils with definite hemiparesis caused K+ depletion in the ischemic area, often most pronounced in the periphery of the lesion. Water content of cerebral cortex was 79.0 +/- 0.9, 82.0 +/- 1.0, 80.7 +/- 0.9 (%; mean +/- SD) for nonischemic, periphery and center of ischemia, respectively (significantly different with each other). Na+ content was increased and K+ content was decreased most prominently in the periphery of ischemia. Exogenous Ca2+ was also accumulated in the periphery. In the embolized stroke in rats, K+ depletion and Ca2+ accumulation obviously rimmed the ischemic focus. Furthermore the infarcted area was only part of the disturbed area of acute-phase glucose metabolism. Thus water and ionic disturbances were different between in the periphery and in the center of focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain edema initially develops in the periphery of focal cerebral ischemia]. 373 Jan 97

Regional cerebral blood flow (rCBF) and regional cerebral metabolic rate of oxygen (rCMRO2) were measured by positron emission tomography (PET) in four patients with subarachnoid hemorrhage and hemiparesis due to cerebral vasospasm. With resolution of the vasospasm, two patients recovered and two remained hemiparetic. Contralateral to the hemiparesis, rCBF was slightly higher in the two patients who eventually recovered (15.0 and 16.2 ml/100 gm/min) than in the two who remained hemiparetic (12.0 and 11.7 ml/100 gm/min). The rCMRO2 measurements showed similar differences, with values of 1.34 and 2.60 ml/100 gm/min in the patients who recovered, and 0.72 and 1.66 ml/100 gm/min in those who did not. These preliminary findings indicate that with PET studies it may be possible to prospectively differentiate patients with neurological deficits due to reversible ischemia from patients with irreversible infarction.
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PMID:Regional cerebral blood flow and metabolism in reversible ischemia due to vasospasm. Determination by positron emission tomography. 387 46

Periventricular arteriovenous malformations (AVMs) have often been deemed inoperable because of their location in critical structures. Furthermore, the excision of large lesions may be complicated by the potential for serious brain swelling and hemorrhage due to "autoregulation breakthrough." Nonetheless, the unfavorable natural history of the untreated disease in a symptomatic young patient has induced us to approach these lesions using staged microsurgical excision combined with elective barbiturate coma for maximal cerebral protection. Between 1979 and 1983, six patients (four female, aged 12 to 60 years, and 2 male, aged 14 and 29) who harbored large AVMs in the basal ganglia, thalamic, and hypothalamic areas presented with subarachnoid hemorrhage (2 cases), progressive neural deficits (3 cases), and intractable headache (1 case). Nineteen staged operations were performed for the complete excision of these lesions. Among the first three patients, there was one death due to "autoregulation breakthrough" hemorrhage into the lateral ventricle during the excision of a lesion approached through the sylvian fissure using standard anesthesia techniques. This led to the adoption of the transventricular surgical approach and elective barbiturate coma to facilitate exposure of the lesion and to protect the adjacent vital structures from potential ischemia. Three patients were treated in this fashion uneventfully. Of the five successfully treated patients, two have returned to their preoperative status and one has completely recovered from global hemispheric ischemia and hemiplegia. The hemiparesis in one patient worsened as a result of postoperative hypertensive intraventricular hemorrhage, and one patient developed mild dysphasia and hemiparesis. This experience suggests that this approach offers a valid therapeutic regimen for the treatment of this disease. During the same period, three patients--one man (age 23) and two women (aged 29 and 22)--harboring four intraventricular AVMs presented with intraventricular hemorrhage. After the acute effects of chemical ventriculitis and hydrocephalus were overcome with cerebrospinal fluid diversion, all four lesions were excised microsurgically using the transtemporal approach. One patient demonstrated significant and progressive improvement of her preoperative memory deficit. The remaining two patients have both returned to their preoperative employment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Microsurgical excision of paraventricular arteriovenous malformations. 398 6

The activity of the free radical scavenger, superoxide dismutase, was studied in focal cerebral ischemia produced in Mongolian gerbils (Meriones unguiculatus) by occluding the right common and left external carotid arteries under halothane anesthesia. After recovery from anesthesia animals were classified according to their neurologic symptoms. Five animals exhibiting neurologic symptoms such as hemiparesis and rolling seizures were reanesthetized 120 min after vascular occlusion and their brains frozen in situ with liquid nitrogen. A series of 20-micron-thick coronal sections was cut in a cryostat; pictorial representations of tissue pH, ATP, and glucose were obtained using fluorescent and bioluminescent techniques. Using a highly sensitive bioluminescent technique, Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and Mn-superoxide dismutase (Mn-SOD) activities were then measured in samples from both ischemic and nonischemic regions of the remaining tissue block. Cu,Zn-SOD and Mn-SOD activities were, respectively, 13.9 +/- 0.7 X 10(3) units/g and 5.4 +/- 0.3 X 10(3) units/g in the nonischemic tissue, and 13.2 +/- 0.6 X 10(3) units/g and 5.0 +/- 0.2 X 10(3) units/g within the ischemic tissue. Thus focal cerebral ischemia does not lead to a global decrease in SOD activity, as observed by others after heart and liver ischemia.
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PMID:Superoxide dismutase activity in experimental focal cerebral ischemia. 406 77

Ischemic stroke was induced in the Mongolian gerbil by left common carotid ligation. No change in uptake of [3H]dopamine, [3H]gamma-aminobutyric acid ([3H]GABA), or [14C]glutamate in synaptosomes obtained from the ischemic hemisphere was observed for up to 8 h. At 16 h after ligation, marked decrements in uptake were observed in animals showing hemiparesis: Uptake values expressed as a percent of the corresponding control hemisphere were 15.2% for dopamine, 28.9% for GABA, and 47.5% for glutamate. The differential sensitivity of dopamine terminals compared with glutamate terminals was highly significant. Separate experiments performed with synaptosomes isolated from the corpus striatum showed that the greater sensitivity to damage was intrinsic to the dopamine nerve terminal and not the result of regional variations in ischemic damage in brain. No bilateral effect of ischemia on dopamine uptake was evident. In animals exhibiting milder behavioral deficits (circling), a smaller and comparable decrement in uptake of dopamine, GABA, and glutamate was evident at 16 h, whereas animals not affected behaviorally showed no decrement at 16 h. Following uptake, the subsequent fractional release of neurotransmitter stimulated by 60 mM-potassium ions was not affected at any time point studied. Therefore, the loss in uptake at 16 h probably represents overt destruction of nerve terminals. Experiments with urethane used in place of pentobarbital for anesthesia during carotid occlusion showed that "protection" by pentobarbital was not a factor in the delayed response to ischemia. These results show that damage or destruction of nerve terminals is a delayed event following ischemia and that dopamine terminals are intrinsically more sensitive than glutamate terminals.
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PMID:The differential effect of ischemia on the active uptake of dopamine, gamma-aminobutyric acid, and glutamate by brain synaptosomes. 612 Oct 6

A new cerebral syndrome is described which occurs rather frequently with ischemia affecting the common pathway of the internal carotid and middle cerebral arteries. The syndrome consists of contralateral brachiofacial hemiparesis, possibly with hemianopia and/or aphasia, and ipsilateral thermoregulatory hemihypohidrosis with an ipsilateral central Horner syndrome. It is caused by an ischemic lesion of the crossed pathways descending from the cerebrum and the uncrossed hypothalamo-spinal sympathetic pathways descending through the subthalamic region. It is suggested to name the syndrome "telodiencephalic ischemic syndrome".
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PMID:The telodiencephalic ischemic syndrome. 615 86


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