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

Among 1500 carotid endarterectomies performed between 1975 and 1984, 11 ipsilateral intracranial hemorrhages (IH) occurred between the first and tenth postoperative days for an incidence of 0.7%. The mortality rate among these patients was 36%. The only recognizable predisposing factor was relief of high-grade carotid stenosis (greater than 90%) whereas other factors such as age (58 to 81 years), preoperative hypertension (systolic blood pressure 120 to 160 mm Hg), preoperative head CT scans showing recent infarction (only one in five positive), and preoperative cerebral infarction (only 1 of 11 patients) did not play a role. All patients had normal coagulation studies. No patient required a shunt because all tolerated cross-clamping of the carotid artery. Postoperative systolic blood pressures were 200 to 240 mm Hg in 6 of 11 patients. The time of occurrence of IH extended from the immediate postoperative period to the tenth postoperative day (mean interval 3.3 days). Treatment consisted of craniotomy in five patients; four survived and one recovered completely. Of the six patients treated nonoperatively, three survived and two completely recovered. IH shares equal incidence with recurrent thrombosis, cross-clamping ischemia, and embolization as a cause of perioperative stroke. Although all except IH can be prevented by current practice, the means of preventing IH are not apparent; however, careful monitoring of blood pressure to prevent uncontrolled hypertension deserves consideration.
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PMID:Intracranial hemorrhage after carotid endarterectomy. 333 70

Cerebral infarction and hemorrhage are well-known cerebrovascular complications of eclampsia. A 30-year-old woman with eclampsia developed bilateral posterior parietal and occipital hemorrhages 4 hours after computed tomography demonstrated lucencies indicative of ischemia or infarction within the same regions. The association between infarction and hemorrhage has not been previously documented by computed tomography in eclampsia. Review of the pathophysiological mechanisms and associated risk factors has prompted a more aggressive prophylactic therapeutic approach.
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PMID:Relationships among cortical ischemia, infarction, and hemorrhage in eclampsia. 335 91

Cranial ultrasound (US) through the newborn's open fontanelle can diagnose not only intracerebral hemorrhages but also diffuse and localized hypoxic-ischemic encephalopathies. Sonographically, it was possible to distinguish between different courses of cerebral ischemia in seven neonates: ischemic infarction, usually in the area of the middle cerebral artery: borderline infarction; transient ischemia. The patients showed lateralized seizures during the first days of life with a corresponding focus in the electroencephalogram (EEG). Computed tomography showed areas of partially reduced density corresponding to the regions of increased echogenicity in ultrasound. The course was various; prognosis was good except in one patient. Etiologically, embolism, thromboses or hypoxemia were responsible for cerebral infarction. In some cases secondary bleeding ensued. The prognostic value of cerebral lesions was dependent on the involved area, gestational age, and any concurrent hypoxic cerebral damage.
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PMID:Cerebral infarction in term neonates: diagnosis by cerebral ultrasound. 353 90

To study whether transient ischemia is influenced by hyperglycemia, the middle cerebral artery was occluded for 5, 10 and 15 min in normo- and hyperglycemic rats. Five-minute ischemia induced minor lesions in both groups. After 10-min ischemia a significant greater infarct volume was found in hyperglycemia compared with normoglycemia (29 +/- 9 mm3 vs 4 +/- 4 mm3, P less than 0.001). Fifteen-minute artery occlusion induced even more damage in both hyper- and normoglycemia (63 +/- 20 mm3 vs 13 +/- 12 mm3, P less than 0.006). The lateral part of striatum was infarcted in all hyperglycemic animals exposed to 10 or 15 min of ischemia. In the same area selective neuronal injury occurred in 6 out of 9 normoglycemic animals. The findings show that hyperglycemia increases brain damage during transient ischemia by conversion of selective neuronal injury into cerebral infarction.
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PMID:Transient focal ischemia in hyperglycemic rats is associated with increased cerebral infarction. 359 32

To determine whether treatment with hyperbaric oxygen (HBO) or dimethyl sulfoxide (DMSO) could mitigate the fatal effects of cerebral ischemia, we anesthetized 68 gerbils with ketamine, ligated the right carotid artery (CA), and placed a snare occluder around the left CA. After 48 hours, 30 gerbils that were neurologically normal or had suffered only mild deficits were subjected to left CA occlusion without anesthesia for periods of 2 to 60 minutes. The onset of circling, posturing, falling, and lethargy began immediately; seizures and coma ensued 4 to 5 minutes later and persisted until release of the left CA occluder. All gerbils recovered after 2-minute staged bilateral CA occlusions. The mortality rate was 33% after both 5- and 10-minute occlusions and 100% after 20- and 60-minute bilateral occlusions. Twelve gerbils were placed in an HBO chamber (100% oxygen at 1.5 atmospheres) for 15 minutes during 20-minute bilateral occlusion; only 2 died (16% mortality rate). Thus, HBO therapy conferred significant protection against death from untreated ischemia (P less than 0.001). Histological examination showed that the extent of patchy bilateral ischemic neuronal damage was much less in surviving gerbils that received HBO therapy than in those that died after 20-minute occlusions. Fourteen gerbils were treated with DMSO, 2.5 g/kg intraperitoneally, during 5- or 10-minute bilateral CA occlusion; 12 died (86% mortality rate). Thus, DMSO provided no protection against fatal cerebral infarction; in fact, the results in the 10-minute reperfusion group suggest that DMSO may have a deleterious effect.
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PMID:Effect of hyperbaric oxygen therapy or dimethyl sulfoxide on cerebral ischemia in unanesthetized gerbils. 371 99

The relationship between recovery from aphasia and regional cerebral blood flow (CBF) was compared in 87 patients, 44 with cerebral hemorrhage and 43 with non-embolic cerebral infarction. CBF values correlated poorly with aphasia outcome in patients with cerebral hemorrhage whereas a tight correlation was demonstrated in patients with non-embolic cerebral infarction. A marked variability of CBF values in the acute and subacute stage might account for the poor correlation between CBF and aphasia outcome in patients with cerebral hemorrhage. On the other hand, a sharp discrimination was achieved between those with a good recovery from aphasia and those with a poor recovery by the dimensions of the hematoma on CT. In non-embolic cerebral infarction, a relative frontal ischemia was associated with motor aphasia while a relative temporal ischemia was associated with sensory aphasia. This dichotomy was not demonstrated in the regional CBF values in patients with cerebral hemorrhage.
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PMID:Regional cerebral blood flow correlates of aphasia outcome in cerebral hemorrhage and cerebral infarction. 371 38

We have examined the incidence and size of infarction after occlusion of different portions of the rat middle cerebral artery (MCA) in order to define the reliability and predictability of this model of brain ischemia. We developed a neurologic examination and have correlated changes in neurologic status with the size and location of areas of infarction. The MCA was surgically occluded at different sites in six groups of normal rats. After 24 hr, rats were evaluated for the extent of neurologic deficits and graded as having severe, moderate, or no deficit using a new examination developed for this model. After rats were sacrificed the incidence of infarction was determined at histologic examination. In a subset of rats, the size of the area of infarction was measured as a percent of the area of a standard coronal section. Focal (1-2 mm) occlusion of the MCA at its origin, at the olfactory tract, or lateral to the inferior cerebral vein produced infarction in 13%, 67%, and 0% of rats, respectively (N = 38) and produced variable neurologic deficits. However, more extensive (3 or 6 mm) occlusion of the MCA beginning proximal to the olfactory tract--thus isolating lenticulostriate end-arteries from the proximal and distal supply--produced infarctions of uniform size, location, and with severe neurologic deficit (Grade 2) in 100% of rats (N = 17). Neurologic deficit correlated significantly with the size of the infarcted area (Grade 2, N = 17, 28 +/- 5% infarction; Grade 1, N = 5, 19 +/- 5%; Grade 0, N = 3, 10 +/- 2%; p less than 0.05). We have characterized precise anatomical sites of the MCA that when surgically occluded reliably produce uniform cerebral infarction in rats, and have developed a neurologic grading system that can be used to evaluate the effects of cerebral ischemia rapidly and accurately. The model will be useful for experimental assessment of new therapies for irreversible cerebral ischemia.
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PMID:Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. 371 45

In 100 patients with transient ischemic attacks, correlations between clinical features and CT findings were analyzed. In 77 patients, CT scans were normal. Five percent had mass lesions and 18 had vascular lesions (ischemia, infarction, hematoma) delineated by CT. In two patients whose CT showed a hypodense lesion indicating cerebral infarction, clinical and CT worsening followed carotid surgery. In six patients with isodense enhancing lesions indicating ischemia, there was no clinical or CT deterioration after operation.
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PMID:Computerized tomographic abnormalities in patients with hemispheric transient ischemic attacks. 372 78

During the past decade, nine patients with bacterial endocarditis have required management of mycotic emboli and/or aneurysms in this center. In these patients, 25 separate mycotic emboli or aneurysms were identified. Among these were four visceral, 11 lower extremity, one aortic, one hypogastric, and eight cerebral lesions. Multiple sites were involved in seven of the nine patients (78%). Presenting symptoms were secondary to acute expansion of mycotic aneurysms in three patients and secondary to rupture of aneurysms in four patients. Mycotic emboli produced cerebral infarction in two patients and acute ischemia in six patients. Asymptomatic mycotic aneurysms of the middle cerebral, hepatic, hypogastric, and profunda femoris arteries and asymptomatic emboli to the profunda femoris and tibial arteries were found during angiographic study. Management included resection alone (7 aneurysms), resection and graft replacement (2 aneurysms and 2 emboli), embolectomy (2), or observation. There was no mortality or loss of limb in these patients. This experience underscores the frequent multiplicity of mycotic emboli and/or aneurysms and stresses the importance of empiric angiographic survey to exclude silent yet potentially lethal visceral and cerebral mycotic foci in patients with bacterial endocarditis and peripheral emboli or aneurysms.
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PMID:Mycotic embolism and embolomycotic aneurysms. Neglected lessons of the past. 375 84

Acute ischemia of the brain induces a cascade of biochemical and physiological events. The final consequences depend on the fact whether ischemia is of transient or permanent, total or partial nature. Alteration of extracellular potassium concentration, intracellular calcium and potassium concentration, development of cytotoxic and vasogenic edema, postischemic hyperfusion and no-reflow phenomenon are important factors which decide about the final fate of functional capacity. CO2 reactivity, autoregulation and hemorheology must be considered when therapeutic approaches are used to influence basic flow during ischemic condition. At present there exists no therapy which has been fully accepted and is able to guarantee benefit to the hypoperfused tissue. Since the calcium metabolism is altered by ischemic processes, substances which act on this metabolism might be of value in the treatment of ischemia and its consequences. However, their beneficial effect on cerebral infarction has not been proven yet. In subarachnoid hemorrhage and migraine calcium antagonists are used to prevent and treat ischemia. In epilepsia calcium overload blockers have been tried by one group with promising results.
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PMID:Is there a need for alternative approaches in the therapy of cerebrovascular disorders? 375 10


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