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PubMed1983

[Pathology of cerebral infarction].

Classification of cerebral infarctions is presented in connection with their etiology and pathogenesis. The zones of cerebral infarction, the ultrastructural and synthesizing characteristics of clear, dark, and pyknomorphic neurons are described in detail. The results of pathological examinations of cerebral infarctions are compared with experimental data obtained in hypoxia conditions of the nervous system by means of electron microscopy and ultrastructural autoradiography.

Animals↗
PubMed1985

Beagle puppy model of perinatal cerebral infarction. Acute changes in cerebral blood flow and metabolism during hemorrhagic hypotension.

Asphyxia, with its attendant hypotension, is by far the most common cause of neonatal cerebral infarction and frequently results in lesions of the parieto-occipital white matter. This study examines the effects of hypotension on regional cerebral blood flow (CBF), local cerebral glucose utilization (LCGU), and serum prostaglandin levels in newborn beagle pups. The animals (24 to 96 hours old) were anesthetized, tracheotomized, and paralyzed. Pups were randomly divided into two groups: one was subjected to hemorrhagic hypotension and the other received no insult. Hypotension was induced by slow venous hemorrhage to maintain a mean arterial blood pressure of 20 to 30 mm Hg. Autoradiographic determinations of LCGU using carbon-14 (14C)-2-deoxyglucose were performed 45 minutes after randomization to groups. Autoradiographic determinations of CBF were performed using 14C-iodoantipyrine on a second group of pups 15 minutes after randomization. Prostaglandins were measured immediately before and 15 minutes after insult or control manipulation. There were no significant differences in the values for thromboxane B2 or 6-keto-prostaglandin F1 alpha, the stable breakdown products of thromboxane A2, and prostacyclin. Prostaglandin E2 levels significantly increased in response to hemorrhagic hypotensive insult. In addition, although regional CBF was maintained in cortical and central gray matter structures during hypotension, CBF to the periventricular temporal and parietal white matter zones significantly decreased, and LCGU was increased in these same regions during hypotensive insult. The uncoupling of CBF and metabolism in these periventricular white matter regions may be responsible for the neuropathological sequelae of perinatal asphyxia.

Animals↗
PubMed2000

Age-dependent increase in infarct volume following photochemically induced cerebral infarction: putative role of astroglia.

This study demonstrates that the photochemically induced model of stroke is an extremely viable method of inducing cerebral infarction in old animals. The lesions are reproducible both in terms of location and size and compatible with long-term survival of the animal. With this model we demonstrated, one week following surgery, a significantly larger infarct in rats 20 and 24 months of age compared to 4-month-old rats. The older rats also sustained greater neurologic deficits as assessed on a rotarod task. Older rats also were characterized by a glial response that was far less intense than in young animals. While the precise relationship between glia activation and cerebral damage remains to be determined, it would appear that a better understanding of those factors that contribute to the astrocytic response in the aged rat may be of particular benefit in designing therapeutic strategies aimed at reducing the pathologic consequences of cerebral infarction in elderly humans.

Aging↗
PubMedDate not supplied

Cerebral infarction after middle cerebral artery occlusion in progenies of spontaneously stroke-prone and normal rats.

A differential outcome results from rapid middle cerebral artery (MCA) occlusion in young normotensive Wistar (NW) rats as compared to the spontaneously hypertensive stroke-prone (SHRSP) rat. The SHRSP invariably infarcts; the NW usually does not. To determine if segregation at a single autosomal locus explains the difference between strains, a NW male was crossed with several SHRSP females to produce F1 rats. The segregation of the strain difference was studied in the F2 and backcrosses to the NW and SHRSP parental strains. The relative frequency of infarcting and noninfarcting animals in the segregating progenies supported a single locus recessive model of inheritance for susceptibility to infarction after sudden occlusion of the MCA. Mean infarct size was largest for SHRSP and proportional to the SHRSP gene dosage in the segregating progenies. Variation in the size of the infarct within segregating classes may be attributable to the segregation of polygenes and/or environmental influences during the initial formation of the cerebral anastomoses.

Animals↗
PubMed1991

Early spontaneous hematoma in cerebral infarct: is primary cerebral hemorrhage overdiagnosed?

We identified 15 patients (63 +/- 8 years) in whom CT showed no bleeding within 6 hours of stroke onset but showed ganglionic or lobar hemorrhage less than 18 hours later, without visible underlying infarct (early spontaneous intra-infarct hematoma [ESIH]). No patient had antithrombotic therapy or a coagulation disorder, but eight had hypertension. The second CT was prompted by rapid worsening (in 10) or because the first CT was not available (in five). Prior transient ischemic attacks, silent infarcts on CT, and a potential cardiac source of embolism were more common in patients with ESIH than in 200 patients with primary cerebral hemorrhage (PCH) admitted during the same period. Distal occlusions were present in four of five patients who underwent intracranial studies within the first 2 days. Most of these patients probably had embolism with early and extensive bleeding in the ischemic area. Our findings suggest that ESIH may be under-recognized, while PCH may be overdiagnosed.

Aged↗
PubMed1993

Dexamethasone prevents cerebral infarction without affecting cerebral blood flow in neonatal rats.

BACKGROUND AND PURPOSE: We recently demonstrated that pretreatment with the synthetic glucocorticoid dexamethasone prevents hypoxic-ischemic brain damage in neonatal rats. Presently, we examine whether this protective effect of dexamethasone is due to an improvement in local cerebral blood flow. METHODS: Neonatal rats were treated with either vehicle or 0.1 mg/kg i.p. dexamethasone 24 hours before hypoxia-ischemia (right carotid artery occlusion +3 hours of 8% O2). Cerebral blood flow was measured with [14C]iodoantipyrine autoradiography after either 2 (n = 17) or 3 (n = 15) hours of hypoxia-ischemia. Additional animals (n = 20) were perfusion-fixed 3 days after hypoxia-ischemia. The area of cerebral pathological changes was measured from hematoxylin and eosin-stained coronal sections taken at three different levels. RESULTS: Pathological outcome differed between groups. In vehicle-treated rats, sections from anterior, mid, and posterior portions of the cerebrum all had extensive infarction or cellular necrosis ipsilateral to the occlusion (mean areas of damage were 62.6 +/- 10%, 70.2 +/- 9%, and 54.2 +/- 8%, respectively). However, in dexamethasone-treated animals, brain damage in sections at corresponding levels was minimal (0%, 1.6 +/- 2%, and 1.5 +/- 1%, respectively; p < 0.0002). In contrast to the pathological results, cerebral blood flow was equivalent in the dexamethasone- and vehicle-treated groups. After either 2 or 3 hours of hypoxia, cerebral blood flow was reduced 60-80% ipsilateral to the carotid artery occlusion in animals treated with either vehicle or dexamethasone. CONCLUSIONS: Despite ischemic levels of cerebral blood flow, pretreatment with dexamethasone prevents cerebral damage in neonatal rats. Instead of improving local cerebral perfusion, dexamethasone presumably acts via peripheral or central glucocorticoid receptors to produce some alteration in the brain that decreases its susceptibility to hypoxia-ischemia.

Animals↗
PubMed2006

Acute physiological derangement is associated with early radiographic cerebral infarction after subarachnoid haemorrhage.

BACKGROUND: Cerebral infarction after aneurysmal subarachnoid haemorrhage (SAH) is presumed to be due to cerebral vasospasm, defined as arterial lumen narrowing from days 3 to 14. METHODS: We reviewed the computed tomography scans of 103 patients with aneurysmal SAH for radiographic cerebral infarction and controlled for other predictors of outcome. A blinded neuroradiologist reviewed the angiograms. Cerebral infarction from vasospasm was judged to be unlikely if it was visible on computed tomography within 2 calendar days of SAH or if angiography showed no vasospasm in a referable vessel, or both. RESULTS: Cerebral infarction occurred in 29 (28%) of 103 patients with SAH. 18 patients had cerebral infarction that was unlikely to be due to vasospasm because it was visible on computed tomography by day 2 (6 (33%)) or because angiography showed no vasospasm in a referable artery (7 (39%)), or both (5 (28%)). In a multivariate model, cerebral infarction was significantly related to World Federation of Neurologic Surgeons grade (odds ratio (OR) 1.5/grade, 95% confidence interval (CI) 1.1 to 2.01, p = 0.006) and SAH-Physiologic Derangement Score (PDS) >2 (OR 3.7, 95% CI 1.4 to 9.8, p = 0.01) on admission. Global cerebral oedema (OR 4.3, 95% CI 1.5 to 12.5, p = 0.007) predicted cerebral infarction. Patients with cerebral infarction detectable by day 2 had a higher SAH-PDS than patients with later cerebral infarction (p = 0.025). CONCLUSIONS: Many cerebral infarctions after SAH are unlikely to be caused by vasospasm because they occur too soon after SAH or because angiography shows no vasospasm in a referable artery, or both. Physiological derangement and cerebral oedema may be worthwhile targets for intervention to decrease the occurrence and clinical impact of cerebral infarction after SAH.

Acute Disease↗
PubMed2000

[CT perfusion imaging in acute ischemic cerebral infarct: comparison of cerebral perfusion maps and conventional CT findings].

PURPOSE: To evaluate the findings of acute brain ischemia on different functional maps of cerebral perfusion CT in stroke patients and to compare the results with early ischemic changes on conventional CT. METHODS: The baseline CT scans of 45 acute stroke patients were retrospectively evaluated with respect to early CT findings. For each patient the extent of cerebral ischemia as shown on the maps of cerebral blood flow (CBF), cerebral blood volume (CBV), and "time to peak" (TP) was compared and the severity of ischemia was assigned to one of three levels based on the findings of the CBF image. RESULTS: In 75% of all patients conventional CT was performed within 2 hours from symptom onset. 29 of 45 patients showed early signs of ischemia on conventional CT, whereas perfusion CT revealed cerebral ischemia in all patients. Severe ischemia was found in approximately the same rate of incidence in patients with early CT changes (55.2%) and in those with normal findings (43.8%). If the perfusion impairment was judged as mild or moderate the extent of the hypoperfused area was significantly larger on the CBF and TP images than on the CBV map. This was significantly different in patients with severe hypoperfusion where a complete correspondence of the affected area between the three functional maps was found. DISCUSSION: The use of conventional CT for the assessment of stroke in the hyperacute phase is limited. Perfusion CT yields excellent information regarding the severity and extent of ischemia. The use of various perfusion maps helps to differentiate the core of infarction from the ischemic penumbra zone.

Acute Disease↗
PubMed2003

Zonal frequency analysis of the gyral and sulcal extent of cerebral infarcts. Part III: Middle cerebral artery and watershed infarcts.

We tested the hypothesis that frequency analysis of the anatomic zones affected by single anterior (A), posterior (P), and middle (M) cerebral artery (CA), multivessel, and watershed infarcts will disclose specific sites (peak zones) most frequently involved by each type, sites most frequently injured by multiple different types (vulnerable zones), and overlapping sites of equal relative frequency for two or more different types of infarct (equal frequency zones). We adopted precise definitions of each vascular territory. CT and MRI studies of 50 MCA, 20 ACA-MCA, three PCA-MCA, and 30 parasagittal watershed infarcts were mapped onto a standard template. Relative infarct frequencies in each zone were analyzed within and across infarct types to identify the centers and peripheries of each, vulnerable zones, and equal frequency zones. These data were then correlated with the prior analysis of 47 ACA, PCA, dual ACA-PCA, and ACA-PCA-MCA infarcts. Zonal frequency data for MCA and watershed infarcts, the sites of peak infarct frequency, the sites of vulnerability to diverse infarcts, and the overlapping sites of equal infarct frequency are tabulated and displayed in standardized format for direct comparison of different infarcts. This method successfully displays the nature, sites, and extent of individual infarct types, illustrates the shifts in zonal frequency and lesion center that attend dual and triple infarcts, and clarifies the relationships among the diverse types of infarct.

Aged↗
PubMed1992

Reduction by delayed hypothermia of cerebral infarction following middle cerebral artery occlusion in the rat: a time-course study.

The effect of hypothermia on neuronal injury following permanent middle cerebral artery (MCA) occlusion in the rat was examined. Moderate hypothermia (body temperature 24 degrees C) was induced before MCA occlusion (0-minute delay group) in six rats, at 30 minutes in eight rats, and at 1 (seven rats), 2 (seven rats), and 3 (nine rats) hours after occlusion. The rats were kept at a 24 degrees C body temperature for 1 hour, then allowed to rewarm over 90 minutes. The animals were sacrificed 24 hours after MCA occlusion, and infarction was visualized by staining of coronal sections with 2,3,5-triphenyltetrazolium chloride. Infarct volumes were compared to matched normothermic control rats (body temperature 36 degrees C). Additional groups of 0-minute delay hypothermic (10 rats) and control animals (nine rats) were sacrificed 72 hours after MCA occlusion to examine the effects of prolonged survival. A significant reduction in the percentage of infarcted right hemisphere was seen in the animals sacrificed after 24 hours with 0-minute, 30-minute, and 1-hour delays in inducing hypothermia (mean +/- standard error of the mean: 2.2% +/- 0.7%, 4.4% +/- 0.9%, and 3.6% +/- 1.1%, respectively) as compared to normothermic control rats (10.8% +/- 1.5%, p less than 0.01 by Student's t-test). In the 2- and 3-hour delay groups, the percentage of infarcted right hemisphere was 17.1% +/- 2.4% and 12.0% +/- 2.7%, respectively, and no decrease in infarct volume was observed. The 0-minute delay hypothermia group sacrificed after 72 hours also displayed a significant reduction in right hemisphere infarct compared to their respective controls (4.8% vs. 11.7%, p less than 0.05). These findings indicate that, in the setting of permanent MCA occlusion, hypothermia markedly decreases brain injury even when its induction is delayed for up to 1 hour after the onset of ischemia. Ischemic damage does not appear to be merely retarded but permanently averted.

Animals↗
PubMedDate not supplied

The effect of cerebral infarction on the regional cerebral blood flow of the contralateral hemisphere.

Regional cerebral blood flow (rCBF) measurements were performed over the contralateral hemisphere by the 133Xe intracarotid injection method in 20 patients with acute cerebral infarction in the territory of the internal carotid artery. The rCBF was found to be reduced, sometimes remarkably, in all of the patients. The mean reduction was 30 percent to 36 percent from the lowest normal value for the mean age of these patients. In the younger age group (40 to 59) the reduction was greater, 40 percent to 47 percent from the lowest normal value for this age. tthe rCBF depression was not related to cerebral dominance, previous hypertension or arterial PCO2 levels. The occurred in both patients who were fully alert and those with disturbances or consciousness, although it tended to be more diminished in the latter. tit can be assumed that the flow reduction in the nonaffected hemisphere is part of a general phenomenon affecting the entire brain and caused by globally reduced cerebral metabolism.

Acute Disease↗
PubMed1987

Time study of macroscopic identification of experimental cerebral infarction in rat.

Cerebral infarctions were induced in rats by injection of Sephadex G-200 into the internal carotid artery. Unfixed slices of brain were stained with nitro blue tetrazolium (nitro-BT). Tissue dehydrogenase in normal regions reacts with this chemical and changes from a pale yellow color to dark blue consequent to formation of formazan. However, the color changes do not develop in infarcted tissue as there is depletion of tissue dehydrogenase in these regions. Ischemic lesions are identifiable by this method in over half the brain 2 to 4 hours after the embolization, but are seen in all brains 6 hours or more following the embolization. The procedure is simple, requires 30 minutes, and is useful for identification of small or acute cerebral infarction.

Animals↗
PubMed1981

Cholesterol embolism as a cause of transient ischemic attacks and cerebral infarction.

Although cerebral cholesterol embolism is a well-known process, the range of clinical manifestations has not been established. In the present case, the occurrence of transient ischemic attacks in association with cerebral cholesterol embolism is described for the first time. A 69-year-old man experienced multiple 5- to 8-minute spells of numbness or weakness involving one or the other hand in 3 years. The attacks continued despite warfarin therapy. When the left arm became permanently paralyzed, an ulcerative plaque was removed from the right internal carotid artery, but the neurologic deficits increased. Progressive renal failure developed, and he died 5 months after the initial medical evaluation. Neuropathologic examination disclosed multiple small infarcts in both cerebral hemispheres, predominantly in the border-zone territory on the right side. Many small cerebral arteries were occluded by cholesterol emboli. Anticoagulant therapy appeared to exert an adverse affect.

Aged↗