Showing papers on "Cerebral infarction published in 1970"
TL;DR: Different differences in outcome were noted in specific subgroups in the frequency and pattern of transient attacks and in the occurrence and location of cerebral infarction.
Abstract: A series of 316 patients with transient cerebral ischemic attacks and no neurological deficit were randomly allocated to surgical or nonsurgical treatment categories in a controlled manner. The total group was divided by anatomical patterns of lesions (carotid stenosis, unilaterally; carotid stenosis, bilaterally; and unilateral occlusion with opposite stenosis). During an average 42-month follow-up, distinct differences in outcome were noted in specific subgroups in the frequency and pattern of transient attacks and in the occurrence and location of cerebral infarction.
452 citations
TL;DR: Modifications to a previously devised method for induction of cerebral infarct are herein described and this new surgical approach has made it possible to conduct detailed and sequential ultrastructural analysis of experimental cerebralinfarctions.
Abstract: An appropriate surgical technique for the production of cerebral infarction must fulfill, among others, the following criteria in order to be suitable for electron microscopy (EM) studies: (1) the method of arterial occlusion should yield a high percentage of infarcts with predictable average size; (2) there must be avoidance of surgical manipulation (i.e., retraction) of the cerebral tissues or exposure of the same to the atmosphere; and (3) the method for occluding the artery must be one that permits fixation by perfusion of the ischemic and nonischemic brain.
Modifications to a previously devised method for induction of cerebral infarct are herein described. This new surgical approach has made it possible to conduct detailed and sequential ultrastructural analysis of experimental cerebral infarctions.
245 citations
TL;DR: Clinical and anatomic findings suggested that increased intracranial pressure probably did not develop until later in the course of the illness and should not be overlooked in the management of patients with severe strokes.
Abstract: All cases of acute supratentorial cerebral infarction which came to postmortem examination over the past 10 years at the Philadelphia General Hospital were reviewed. Of a total of 353 such cases, 45 showed severe brain swelling. Seventy-eight percent of these 45 patients died within seven days of the acute infarction. The rapidly fatal outcome appeared to be directly related to the acute brain swelling with transtentorial herniation and brain-stem edema or hemorrhage. In those patients who survived longer than one week following onset of the ictus (22%), clinical and anatomic findings suggested that increased intracranial pressure probably did not develop until later in the course of the illness. A second massive infarct was probably superimposed upon an earlier one and produced the acute brain swelling noted at the time of postmortem examination. Complicating visceral diseases were more common in this group and seemed to contribute to death in the majority of these patients. Although it has been establis...
191 citations
TL;DR: HEDT-RASMUSSEN and Skinhoj 1,2 were the first to report bilateral reduction of hemispheric blood flow (HBF) in patients with unilateral cerebral infarction.
Abstract: HOEDT-RASMUSSEN and Skinhoj 1,2 were the first to report bilateral reduction of hemispheric blood flow (HBF) in patients with unilateral cerebral infarction. They measured HBF by means of intracarotid injection of a bolus of radioactive inert gas and an uncollimated detector placed over each hemisphere and found the HBF to be reduced on the "healthy" side as well as in the diseased hemisphere. They did not measure cerebral metabolism but hypothesized that unilateral infarction reduced metabolism, and consequently, resulted in reduced blood flow in the contralateral hemisphere due to transneural depression. There were only six patients with unilateral cerebral infarction in their series, three of whom had thrombosis or embolic occlusion of the internal carotid artery. The smallness of their series was complicated further by the fact that one of the requirements of their method is that the bolus be injected into the internal carotid artery to avoid extracranial
165 citations
TL;DR: The combined total of 81 cases of transient complications that were collected from the literature and from the series showed that such deficits occur frequently from 10 minutes to six hours after the occlusion of the vessel.
Abstract: The immediate postoperative cerebral complications of 65 carotid occlusions were evaluated. The occlusions were done in all but one case for intracranial saccular aneurysms and were performed by either direct ligation (quick type) or slow turning down of a Silverstone clamp or similar device (slow occlusion). Cerebral complications occurred in 21 patients. The quick type of occlusion of the artery resulted in a complication rate of 24% whereas the slow type had a rate of 38%. A total of 123 cases involving cerebral complications after carotid ligation were collected from the literature and evaluated. The combined total of 81 cases of transient complications that were collected from the literature and from our series showed that such deficits occur frequently from 10 minutes to six hours after the occlusion of the vessel.
68 citations
TL;DR: The preliminary results to be reported here suggest that the circulatory dynamic abnormalities characteristic of acute infarction vary in severity with distance from the vascular occlusion and the time elapsing after it occurs.
Abstract: AN IMPORTANT CONCEPT about the cerebral circulation which has emerged in the past decade is that vascular reactivity to changes in blood pressure and $0, is altered in and around a cerebral infarction resulting from a major vessel occlusion. There is general agreement that the circulation in an ischemic region tends to become passively responsive to changes in systemic blood pressure and unresponsive to changes in systemic pC0,. These phenomena have been studied qualitatively in animals with proximal middle cerebral artery ligation by measurement of cannulated pressure in its distal branches,l and by heat clearance,, and quantitatively by measurement of cortical clearance of radioactive isotopes injected into the carotid arteries, correlated with direct observation of the cortical microvasculature.3 This study was undertaken to examine some of these phenomena for ourselves. We have employed the technique of chronically implanted polarographic electrodes, used by one of us (L.C.C.) for several years in a continuing study of cerebral oxygen m e t a b ~ l i s m . ~ The method permits continuous recording in the awake, unrestrained animal and is, therefore, suitable for serial studies during and following cerebral infarction. The preliminary results to be reported here suggest that the circulatory dynamic abnormalities characteristic of acute infarction vary in severity with distance from the vascular occlusion and the time elapsing after it occurs.
55 citations
TL;DR: The case of a 35-year-old man in whom spontaneous dissecting aneurysm of the internal carotid artery in the neck was the cause of its sudden occlusion and resultant massive cerebral infarction is reported, emphasizing the role of medial necrosis in the pathogenesis of the dissection.
Abstract: OCCLUSION of the internal carotid artery is a common cause of cerebral ischemia or infarction. Occlusion usually results from thrombosis secondary to atherosclerosis at or near the origin of the artery.1Internal carotid artery occlusion is therefore more common in older patients (arbitrarily defined as persons above the age of 40) in whom arteriosclerosis is a frequent finding.2In younger patients the causes of internal carotid artery occlusion are more variable. Humphrey and Newton3listed trauma, hypertension, blood dycrasias, various vascular inflammatory diseases, and the postpartum state, in that order, as the main contributing and precipitating factor in nearly half of the cases in the below-40 age group. In the remaining cases no precipitating or contributory factors could be found. The purpose of this paper is to report the case of a 35-year-old man in whom spontaneous dissecting aneurysm of the internal carotid artery in the neck was the cause of its sudden occlusion and resultant massive cerebral infarction. Study of this case and review of the literature of this rare condition emphasize the role of medial necrosis in the pathogenesis of the dissection, although considerable doubt persists concerning the etiology of the medial necrosis.
46 citations
TL;DR: Injection of silicone rubber cylinders into the internal carotid system permits selective occlusion of the proximal middle cerebral artery segment in the dog and, therefore, may be a function of patent meningocerebral anastomoses.
Abstract: Injection of silicone rubber cylinders into the internal carotid system permits selective occlusion of the proximal middle cerebral artery segment in the dog. Occlusions of this segment obstruct the mouths of the lenticulostriate arteries and result in deep cerebral hemisphere infarctions. Surface vessels distal to the occluded segment remain patent and the cortex of the hemisphere is spared, due to efficient collateral circulation. Hemorrhage in cortical infarctions may occur distal to the point of vascular occlusion and, therefore, may be a function of patent meningocerebral anastomoses. Hemorrhage into a deep infarction, however, occurred only when there was clinical and pathological evidence of distal migration of the embolus after an initial proximal occlusion. Infarctions of deep hemisphere structures were otherwise bland or "ischemic," probably because of the paucity of anastomoses among the penetrating blood vessels of the brain.
40 citations
Journal Article•
33 citations
TL;DR: It is shown that patients with cerebrovascular disease have platelets which are significantly more adhesive to glass than those of control subjects, and a good linear correlation was found between platelet adhesiveness values obtained by using the two methods simultaneously in 89 subjects.
32 citations
TL;DR: The original diagnosis of “CNS vascular” could not be substantiated in 25 patients and the prognosis was, in general, unfavorably affected by older age, further cerebrovascular events, and abnormal electrocardiograms.
Abstract: As an initial step in studying the characteristics of cerebrovascular disease in a geographically limited segment of population, the hospital records of 285 patients coded as "CNS vascular" in the Elkhart General Hospital (Indiana) were reviewed for the years 1963, 1964 and 1965 by a team of neurology residents, under the supervision of the author. Information from examination of almost half the group by a team of neurologists and data from relatives, family physicians, hospital records and death certificates concerning the remainder led to the conclusion that the original diagnosis of "CNS vascular" could not be substantiated in 25 patients (9%), was cerebral infarction in 125 (53%), cerebral hemorrhage in 40 patients (14%), subarachnoid hemorrhage in 21 patients (7%), generalized atherosclerosis in 24 patients (8%), and transient focal cerebral ischemic attacks in 25 patients (9%).
Disorders such as diabetes, hypertension, heart disease, myocardial infarction, auricular fibrillation and genitourinary disease were significantly more frequent in patients with cerebral infarction than in a group of similar age and sex patients collected from the same hospital in an attempt to form a "contrast group." However, hypertension was the only disorder significantly more often associated with cerebral hemorrhage.
Cigarette consumption was increased at a highly significant level in the males who had infarction and the prognosis was, in general, unfavorably affected by older age, further cerebrovascular events, and abnormal electrocardiograms. Eighty-three percent of the patients with cerebral hemorrhage died during initial hospitalization.
TL;DR: It is indicated that age was a more important factor than chronic cerebrovascular disease in producing the deterioration of circulatory reflexes, and combined ischaemia in both carotid and vertebrobasilar territories significantly impaired the cardioaccelerator but not the vasoconstrictor response to Valsalva9s manoeuvre.
Abstract: 1. Circulatory reflex function was assessed in a series of subjects with chronic ischaemic cerebrovascular disease and compared with a group of subjects with no known cerebrovascular disease by intra-arterial pressure responses to Valsalva9s manoeuvre. 2. Circulatory reflexes were impaired in the patients with cerebrovascular disease as compared with controls, but statistical analysis indicated that age was a more important factor than chronic cerebrovascular disease in producing the deterioration. 3. No significant difference was found in the circulatory reflex function of subjects with ischaemia in the internal carotid territory when compared with those having ischaemia in the vertebrobasilar territory. 4. Combined ischaemia in both carotid and vertebrobasilar territories significantly impaired the cardioaccelerator but not the vasoconstrictor response to Valsalva9s manoeuvre. 5. No significant difference was found in circulatory reflex function in subjects who had suffered cerebral infarction as opposed to transient ischaemic attacks.
TL;DR: The right middle cerebral artery was occluded in cats, and Paoo2 was increased by increasing the amount of oxygen inhaled by the animals at atmospheric pressure as discussed by the authors, which had no apparent effect on CBF or arteriolar caliber of the ischemic cerebral hemispheres.
Abstract: The right middle cerebral artery was occluded in cats, and Paoo2 was increased by increasing the amount of oxygen inhaled by the animals at atmospheric pressure. Cortical blood flow (CBF) was measured with Krypton-85, and observations and photographs of the superficial cortical microvasculature were made bilaterally. In two of five animals, increasing the Paoo2 caused constriction of surface arterioles of the nonischemic hemispheres, with an associated decrease of CBF; in the three other animals, there were no circulatory responses to the increased Paoo2. In seven animals, increasing the Paoo2 had no apparent effect on CBF or arteriolar caliber of the ischemic cerebral hemispheres. In four animals, at Paoo2 greater than 400 torr, reactivity to increases of PaCOCO2 was preserved in nonischemic cortex but impaired in ischemic cortex. Reddening of venous blood of the microvasculature of ischemic cerebral cortex occurred when Paoo2 was increased, indicating that more oxygen was made available to the ischemic ...
TL;DR: These two pathoanatomic processes associated with necrosis of the cerebral tissues most likely account for the abnormal accumulation of radionuclide tracer in brain scans of patients with cerebral infarction.
Abstract: A combined histological and radioautographical study was made to determine the mechanism for the selective localization of Hg-203-labelled Chlormerodrin in the brain of 13 cats with experimentally induced cerebral infarction. The presence of the radioactive tracer in the infarcted areas was noted within a few days after the onset of the lesions and was increased by hemorrhage into the tissues. The radioautograms revealed the radioactive material to be localized mostly within macrophages and in areas surrounding capillary proliferation. These two pathoanatomic processes associated with necrosis of the cerebral tissues most likely account for the abnormal accumulation of radionuclide tracer in brain scans of patients with cerebral infarction.
TL;DR: Data may be viewed as lending support to the thesis that nonembolic cerebral infarction and the diseases that are frequently found with it are related in their occurrence and mortality to aging and may truly be concurrent events and not etiologically related one to the other.
Abstract: The frequency of occurrence of nonembolic cerebral infarction is linearly related to age.
The sexual frequency of nonembolic cerebral infarction is directly related to the age group of the sample studied.
The mortality of nonembolic cerebral infarction and its prognosis are most closely related to the age of the patient at the time of stroke. The older the patient, the higher is the mortality and the poorer the prognosis.
The cause of death in nonembolic cerebral infarction is as much a function of age-related concurrent diseases, especially cardiac disease, as it is of stroke itself. The natural history of stroke is more related to the natural history of cardiac disease than it is to cerebral vascular disease.
These data may be viewed as lending support to the thesis that nonembolic cerebral infarction and the diseases that are frequently found with it, such as diabetes, cardiac disease and hypertension, are related in their occurrence and mortality to aging and may truly be concurrent events and not etiologically related one to the other.
TL;DR: Patients who had transient cerebral attacks in association with subacute bacterial endocarditis had manifestations of general illness, particularly fever, malaise, and elevated sedimentation rate, and a definite relationship between anticoagulant therapy and hemorrhage could not be established.
Abstract: The case histories are given of 12 patients who had transient cerebral attacks in association with subacute bacterial endocarditis. The attacks are similar to those that accompany atherosclerotic occlusive cerebrovascular disease. All patients had manifestations of general illness, particularly fever, malaise, and elevated sedimentation rate. Subsequently, cerebral infarcts occurred in three patients and cerebral hemorrhages in four patients. A definite relationship between anticoagulant therapy and hemorrhage could not be established.
TL;DR: It would seem that vasodilators may be contraindicated in most cases of complete internal carotid artery occlusion and that probably before they are used in any patient CBF, CMRO2, and CVR responses to 5% carbon dioxide should be determined.
Abstract: SUMMARYA group of 10 patients with complete occlusion of one internal carotid artery (COG) were compared with a group of 12 patients with cerebral infarction and severe atherosclerosis but no complete occlusion of an internal carotid artery (IOG) The two groups were closely matched clinically and by age, degree of atherosclerosis, time from infarction, cerebral blood flow, and metabolic studies while breathing room air After breathing 5% carbon dioxide, the COG had significantly less increase in CBF and decrease in CVR CMRO 2 decreased in the completely occluded group and increased in the incompletely occluded group It is postulated that in the area normally supplied by the occluded internal carotid artery there is a large area that functions because the arterioles are maximally dilated Under normal conditions, cerebral blood flow is maximal but may be decreased to the point where oxygen supply is at a critical level When 5% CO 2 is inhaled, the increased PaCO 2 directly affects the large amount of brain not involved and dilates the arterioles, so that blood that would normally be shunted into the area of maximum need is now stolen from the collaterals As this area of brain is already receiving the maximum amount of oxygen that it needs for normal metabolism, the CMRO 2 in this region does not change In the area of maximum need, however, the flow has decreased far below the critical level, and as oxygen is not available for normal metabolism, the CMRO 2 decreases in this area Thus, the average cerebral blood flow may not be affected, but the average CMRO 2 will be significantly reduced It would seem that vasodilators may be contraindicated in most cases of complete internal carotid artery occlusion and that probably before they are used in any patient CBF, CMRO 2 , and CVR responses to 5% carbon dioxide should be determined
TL;DR: Cerebral ischemia is caused by occlusive arterial disease anywhere along the course of the blood supply to the brain, and is usually preceded by premonitory symptoms of transient neurologic handicaps or minor strokes heralding the catastrophic event.
Abstract: Cerebral ischemia is caused by occlusive arterial disease anywhere along the course of the blood supply to the brain. Irreversible damage is most likely to occur when there is inadequate collateral circulation due to (a) involvement of multiple vessels; (b) inadequacy of anastomoses of the vascular structures at the base of the brain due to congenital variation or occlusive disease; or (c) when an artery terminal to the circle of Willis becomes occluded. The fact that cerebral infarction may result from disease in the surgically accessible portion of the cervical carotid artery is well known. The Joint Study of Extracranial Arterial Occlusion reports that 75% of 3,788 patients had accessible lesions, often combined with inaccessible lesions, but existing alone in 41%. 1 It is equally well known that cerebral infarction is usually preceded by premonitory symptoms of transient neurologic handicaps or minor strokes heralding the catastrophic event. These symptoms may
TL;DR: This vascular spasm or thrombosis of major intracranial vessels is a rare but serious complication of head injuries and should be suspected in patients in whom progressive neurological signs develop after head injuries.
Abstract: The case of a Marine in whom a vertex epidural hematoma developed, depressing the superior sagittal sinus as a result of a fracture of the vertex of the skull, is presented. The hematoma was removed, and the patient did well until signs of progressive right hemiparesis suddenly developed two days after the hematoma removal. Serial carotid angiography demonstrated the interval development of spaism of the left internal carotid, anterior cerebral and middle cerebral arteries, and occlusion of the posterior parietal branch of the left middle cerebral artery. Prior to the development of the arterial spasm an earlier angiogram had shown these vessels to be of normal diameter.
This delayed or "spate" spasm and thrombosis of major intracranial vessels is a rare but serious complication of head injuries.
In addition to the usual causes of post-traumatic hemiplegias, this vascular spasm or thrombosis should be suspected in patients in whom progressive neurological signs develop after head injuries.
Journal Article•
TL;DR: Data may be viewed as lending support to the thesis that nonembolic cerebral infarction and the diseases that are frequently found with it, such as diabetes, cardiac disease and hypertension, are related in their occurrence and mortality to aging and may truly be concurrent events.
Abstract: The frequency of occurrence of nonembolic cerebral infarction is linearly related to age. The sexual frequency of nonembolic cerebral infarction is directly related to the age group of the sample studied. The mortality of nonembolic cerebral infarction and its prognosis are most closely related to the age of the patient at the time of stroke. The older the patient, the higher is the mortality and the poorer the prognosis. The cause of death in nonembolic cerebral infarction is as much a function of age-related concurrent diseases, especially cardiac disease, as it is of stroke itself. The natural history of stroke is more related to the natural history of cardiac disease than it is to cerebral vascular disease. These data may be viewed as lending support to the thesis that nonembolic cerebral infarction and the diseases that are frequently found with it, such as diabetes, cardiac disease and hypertension, are related in their occurrence and mortality to aging and may truly be concurrent events and not eti...
TL;DR: This case suggests that the treatment of cerebral ischemia by surgical removal of stenotic lesions in the extracranial cerebral arteries may produce only temporary relief of symptoms and emphasizes the need, following endarterectomy, for medical therapy of the underlying atherosclerotic disease.
Abstract: A patient is described in whom an obstructive atherosclerotic plaque recurred in the cervical portion of the internal carotid artery five years after endarterectomy. The lesion appeared to be a new formation of atheromatous material contiguous to the site of the previous arteriotomy and resulted in neurological symptoms almost identical to those experienced by the patient five years before. This case suggests that the treatment of cerebral ischemia by surgical removal of stenotic lesions in the extracranial cerebral arteries may produce only temporary relief of symptoms and emphasizes the need, following endarterectomy, for medical therapy of the underlying atherosclerotic disease.
TL;DR: It did not appear likely that there was any significant difference between blood pressure lability in subjects who had had cerebral infarction and those who hadHad transient ischaemic attacks.
Abstract: 1. In a survey of blood pressures taken over 24-hr periods by automatic monitoring in a series of men with ischaemic cerebrovascular disease, the variances of the readings were used to compare the lability of blood pressure in subjects subdivided according to the territory of the vascular disorder. 2. The findings that diastolic variance during the daytime in vertebrobasilar ischaemia was significantly higher than in controls and that in both carotid and vertebrobasilar ischaemia, but not controls, daytime variance was higher than night variance, were explicable on the basis that variance is directly related to the height of the blood pressure. 3. There was no evidence that cerebral ischaemia itself, whether in the carotid or vertebrobasilar territories, was associated with abnormal blood pressure lability. 4. It did not appear likely that there was any significant difference between blood pressure lability in subjects who had had cerebral infarction and those who had had transient ischaemic attacks.
TL;DR: From results, some consideration to the pathogenesis of vascular lesions in CVD and coronary heart disease was conducted and generally, intracerebral arterial lesions had no relation with atherosclerosis, but in the atherosclerotic lesions between brain and heart close correlation was noted in individual cases.
Abstract: The present study was undertaken to define the etiologic mechanism of CVD and coronary heart disease and to detect their relation. In a series of 328 autopsies (37 cases of cerebral hemorrhage, 60 of cerebral infarction, 51 of myocardial infarction and 180 of miscellaneous disease), macroscopic and microscopic studies of intracerebral arteries, cerebral basilar arteries and coronary arteries were carried out. Generally, intracerebral arterial lesions had no relation with atherosclerosis, but in the atherosclerotic lesions between brain and heart close correlation was noted in individual cases. From these results some consideration to the pathogenesis of vascular lesions in CVD and coronary heart disease was conducted.
TL;DR: In six patients with Parkinson's disease, three with cerebral tumors, and three with progressive focal encephalopathy presumed to be arteriosclerotic, shoulder pain was the sole presenting complaint.
Abstract: To the Editor.— Immobility of an upper limb, the most common cause of periarthritis of the shoulder, is especially likely to occur in association with spasticity or rigidity. A typical cause is the spastic hemiparesis ensuing from cerebral infarction. It is well known that shoulder pain often occurs with cervical root compression from spinal degenerative arthropathy or spinal tumor. Shoulder pain also may be the first warning of cerebral disease, an association that does not seem to be widely recognized. Pain in the shoulder warrants the clinician's concentration on the neurologic findings not only in regard to the radicular signs, but also the evaluation of cerebral function. In six patients with Parkinson's disease, three with cerebral tumors, and three with progressive focal encephalopathy presumed to be arteriosclerotic, shoulder pain was the sole presenting complaint. The common finding in the painful limb was hypertonicity of either clasp-knife spasticity or plastic rigidity