摘要:

Ten histologic sections were sampled from similar cortical regions in each of 84 autopsy brains removed from patients aged 60 to 97 years. The sections were stained by the Congo-red method and examined under polarized light for the presence of cortical (parenchymal) cerebral amyloid angiopathy (CAA). Some degree of CAA was found in 36% of all brains examined, with a higher proportion of patients affected in each successive decade of life. Angiopathy was seen most frequently and was of greater severity in the parietal and occipital gray matter. Overall, it was often a patchy and asymmetric lesion. There was sparing of subcortical white matter and the hippocampi. CAA was most severe in cases of Alzheimer's disease, but occurred in the absence of this condition.

ISSN:0039-2499    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

To investigate the relationship between neuropathologic damage and cerebral metabolic alterations during hypothermia in the neonatal animal, 7 day old Sprague-Dawley rats were subjected to unilateral common carotid artery ligation and hypoxia at 37 degrees C, 29 degrees C, and 21 degrees C. At 37 degrees C, animals had extensive infarction of tectum and ipsilateral cerebral hemisphere, and marked depletion of brain ATP. At 29 degrees C, there was no significant change in brain ATP; neuropathologic damage was limited to a few areas of necrosis in the deeper layers of cerebral cortex. No histologic injury was seen in the 21 degrees C group of rats. Profound hypothermia may prevent cerebral edema and visible neuropathologic damage associated with hypoxic-ischemic injury by decreasing cerebral metabolic demands. Moderate hypothermia confers a partial, but incomplete degree of protection; whereas during normothermia, the full extent of hypoxicischemic injury is manifest.

ISSN:0039-2499    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Frequency of cerebrovascular diseases (CVD) and their underlying vascular lesions were analyzed in 724 autopsy cases, aged 40 years and over, in the community of Hisayama, Japan during the period 1961 to 1981. Cerebral infarction (CI) was more frequently found at autopsy than cerebral hemorrhage (CH) with a ratio of infarction and hemorrhage of 4.4. Small CI occupied 75.7% of the cases with CI. The cases with any type of CVD showed more severe atherosclerosis of the major cerebral arteries than did those without CI or CH. Cerebral atherosclerosis of those with large and medium CI was the greatest, and with decreasing severity in those with small CI and with CH sequentially. Fibrinoid necrosis of the intracerebral small arteries was frequently found in cases with hypertension and particularly associated with CH. The decline in frequency of CH was confirmed; however, changes in frequency of CI were not evident. Fibrinoid necrosis was also reduced, although the severity of cerebral atherosclerosis showed no definite change. The decline of CH seemed to be ascribed to the reduction of fibrinoid necrosis of the intracerebral small arteries.

ISSN:0039-2499    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Radioactive microspheres (15 mu) were used to measure regional cerebral blood flow during intravenous infusion of nicotine (36 micrograms/kg/min) in anesthetized, open chest dogs. Experiments were conducted with uncontrolled mean aortic pressure and intact autonomic receptors (Series I; n = 9), and in four groups of dogs with mean aortic pressure held constant (Series II); 1) with intact autonomic receptors (n = 6), 2) after beta adrenergic blockade (n = 8), 3) after alpha and beta adrenergic blockade (n = 6), 4) after alpha and beta adrenergic and cholinergic blockade (n = 4). In Series I, nicotine raised mean aortic pressure (+ 72%) and increased flow in cerebral cortex (+ 67%), cerebellum (+ 38%), pons (+ 46%), medulla (+ 39%), and spinal cord (+ 48%). In all regions, but cortex, increases in vascular resistance limited nicotine-induced increases in flow. In Series II, nicotine changed flow only in cortex. Without blockade, nicotine increased cortical flow (+ 38%); but beta blockade abolished this increase in flow. After alpha and beta blockade nicotine again raised cortical flow (+ 29%), and additional cholinergic blockade had no effect on this response. It is concluded that nicotine causes predominant beta receptor mediated vasodilation in cerebral cortex, although it also activates alpha (vasoconstrictor) receptors and a non-adrenergic, non-cholinergic vasodilator mechanism in this region of brain.

ISSN:0039-2499    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

We report two patients with large subcortical hemispheric infarctions, located in areas prone to the development of lacunes, who had occlusion of the middle cerebral artery demonstrated by arteriography. The cortical vessels were perfused by leptomeningeal collaterals. We suggest that large vessel arterial disease should be considered as a possible etiology of large subcortical infarctions and propose that the term lacune should not be used in cases in which neither the size nor the pathophysiologic mechanism of the lesion conform to C.M. Fisher's description.

ISSN:0039-2499    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Occlusion of the anterior cerebral artery is a rare condition. A review of CT scans from 413 patients with ischemic infarction confirmed this low relative incidence: only 3% of CT scans evidencing infarction involved the territory of the anterior cerebral artery. Four major mechanisms of anterior cerebral artery occlusion have been identified in this series: Emboli in unusual hemodynamic circumstances such as patients presumed to have increased flow through the anterior communicating artery because of unilateral internal carotid artery occlusion. Propagation of thrombotic material from an occluded internal artery into the intracranial branches. Spasm, emboli or propagating thrombosis associated with anterior communicating aneurysm.

ISSN:0039-2499    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

The extent of edema related to infarction assessed by computed tomography was compared with the CSF-lactate concentration in patients with middle cerebral artery (MCA) infarction on the first, third and seventh day following the stroke. A linear correlation between the extent of infarction edema and CSF-lactate level was most distinct on the third day. CSF-lactate concentration on the third day can be considered as a measure of the extent of the accompanying edema which in our study reached its maximum at this time in comparison to the first and seventh day.

ISSN:0039-2499    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

In 31 hypertensive patients the effect of chronic oral administration of the beta blocking agent propranolol on regional cerebral blood flow (rCBF) was studied, using the non-invasive 133Xenon inhalation technique. The results of the measurements were compared to the rCBF obtained in an age-matched normal control group. Our study shows that during long-term therapy with low doses of propranolol (less than 120 mg/daily) the rCBF is unaffected, but it is increased significantly if higher doses (greater than 120 mg/daily) are used. In all six patients who served as their own control, as they had basic rCBF measurements before or during low-dose propranolol, the rCBF on high-dose propranolol became significantly increased. The possible mechanisms which may cause the increased rCBF on high-dose propranolol are discussed.

ISSN:0039-2499    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

A 44-year-old woman with prolonged coma and hypotension following drug overdosage developed bilateral hemorrhagic infarcts in the dorsolateral brainstem. The regional distribution of these paired lesions corresponds to the area of confluence of penetrating arteries in the brainstem. It is suggested that under exceptional circumstances brainstem arterial end-zones may be vulnerable to anoxic-ischemic insult.

ISSN:0039-2499    

出版商:OVID    

年代:1983

数据来源: OVID

摘要:

Previously we found that 1,3-butanediol-treated mice live longer during hypoxia. We hypothesized that 1,3-butanediol could reduce the brain's accumulation of potentially cytotoxic lactate and/or elevate brain substrate availability (ketones or glucose) and thus maintain the brain's energy producing capability even during reduced oxygen availability. To test these hypotheses, whole brain metabolites from normoxic and hypoxic mice, pretreated with 1,3-butanediol or insulin, were compared to saline controls. During hypoxia both pretreated groups had lower brain lactate than controls. If lactate accumulation was the sole factor responsible for hypoxic tolerance, insulin should have increased brain lactate since insulin has been shown previously to reduce hypoxic tolerance. In normoxic mice the ratio of lactate to pyruvate and the level of malate and fumarate were not changed by 1,3-butanediol as is found with other agents known to protect the hypoxic animal. When substrate availability was directly elevated by beta-hydroxybutyrate and glucose administration hypoxic survival time increased thus implicating substrate availability as an important factor in hypoxic tolerance. We conclude that reduced brain lactate and augmented substrate availability both contribute to 1,3-butanediol-enhanced hypoxic tolerance in this animal model.

ISSN:0039-2499    

出版商:OVID    

年代:1983

数据来源: OVID