Showing papers on "Cerebral infarction published in 1972"
TL;DR: The present study was undertaken to determine the reproducibility of the modcl and to document for the first time the natural cc)urse of events following ligation, which can then be used to evaluate the efficiency of theraupeutic agents in modifying morbidity and mortality.
Abstract: The study of any disease process is greatly advanced by the availability of an animal model for laboratory investigation. Cerebral infarction has been difficult to reproduce experimentally because of the efficiency of the collateral circulation. It has recently been demonstrated that a unilateral hemispheric infarction can be produced i n the Mongolian gerbil (Meriones unguiculatus) by ligation of a single common carotid artery.' This unique characteristic of the gerbil is due to an absence of connecting a r t e r i e s between the basilar and carotid systems.* The present study was undertaken to determine the reproducibility of the modcl and to document for the first time the natural cc)urse of events following ligation. These base-line data can then be used to evaluate the efficiency of theraupeutic agents in modifying morbidity and mortality.
283 citations
TL;DR: Hemoglobin level had only a modest residual effect, and the pathogenetic, preventive and therapeutic implications of the interrelationship of blood hemoglobin, blood pressure and the cigarette habit and their association with cerebral infarction require further exploration.
Abstract: Risk of cerebral infarction over 16 years was ascertained in 5,185 men and women classified according to their hemoglobin, blood pressure and cigarette habit on entry to the Framingham Study. Within the normal range of hemoglobin values, risk was found to be proportional to the blood hemoglobin concentration in both sexes. Men with hemoglobin values of 15 gm or greater and women with 14 gm or more had twice as many cerebral infarctions as did their cohorts with lower values. The risk of initial development of 82 cerebral infarctions was also strikingly related to antecedent blood pressure status in both sexes and to the cigarette habit in men. When allowance is made for associated blood pressure and cigarette habit--factors found to correlate with both blood hemoglobin values and incidence of cerebral infarction--hemoglobin level had only a modest residual effect, no longer statistically significant. The pathogenetic, preventive and therapeutic implications of the interrelationship of blood hemoglobin, bl...
282 citations
TL;DR: Patients with cerebral infarction treated with glycerol showed significant improvement in neurological status compared to the patients treated with placebo, and the neurological status was evaluated by use of a neurological scoring system.
257 citations
TL;DR: Short-term hypocapnic-hyperventilation can be lifesaving in the treatment of acute intracranial hypertension, but prolonged hyperventilation has not been convincingly shown to benefit patients, whether with severe head injury or cerebral infarction, or during carotid endarterectomy without bypass.
Abstract: Hypocapnic-hyperventilation has a profound, but probably temporary, effect on CBF, producing approximately a 2% decline in CBF for each 1 torr decline in Pcoco2. This effect appears to be mediated through changes in perivascular pH of the cerebral resistance vessels acting directly on the vessel wall. At low Pcoco2 the vasoconstrictor effect of short-term hypocapnic-hyperventilation is attenuated by resultant cerebral hypoxia. During prolonged hyperventilation CBF returns toward normal as the pH in the CSF is restored. Short-term hypocapnic-hyperventilation can be lifesaving in the treatment of acute intracranial hypertension. On the other hand, prolonged hyperventilation has not been convincingly shown to benefit patients, whether with severe head injury or cerebral infarction, or during carotid endarterectomy without bypass.
171 citations
TL;DR: The role of arterial Pressure seems to be greatest in the malignant phase and least in atheroma, and when high arterial pressure is reduced by the administration of drugs, atheromas becomes increasingly the common cause of death.
163 citations
TL;DR: A double blind study of the effects of dexamethasone on acute stroke was conducted at the Neurological Institute of New York and found that 17 patients had been treated with placebo and 14 patients had be treated with dexamETHasone.
Abstract: A double blind study of the effects of dexamethasone on acute stroke was conducted at the Neurological Institute of New York. At the end of the study, it was found that 17 patients had been treated with placebo and 14 patients had been treated with dexamethasone. The dose of steroid was 16 mg daily for 10 days followed by tapering doses from 12 mg to zero over the ensuing 7 days.
130 citations
TL;DR: A transitory outflow of polymorphonuclear neutrophilic leukocytes (PNL) was found in 70% of the patients with hemorrhagic infarction and lobar hematoma, with a peak three to four days after onset, and the strongest PNL reaction was recorded in CSF from patients with lobarHematoma.
Abstract: Cerebrospinal fluid (CSF) samples obtained by consecutive lumbar puncture of 26 patients with presumed pale cerebral infarction, 66 with presumed hemorrhagic infarction, 16 with lobar hematoma, and 18 with cerebral infarction verified at autopsy, were examined with a cytological method permitting a total and differential cell count A transitory outflow of polymorphonuclear neutrophilic leukocytes (PNL) was found in 70% of the patients with hemorrhagic infarction and lobar hematoma, with a peak three to four days after onset The strongest PNL reaction was recorded in CSF from patients with lobar hematoma In 75% of patients with pale infarction, no PNL or only a few PNL were found In the autopsy group the PNL reaction in the brain as well as in the CSF was stronger in patients with hemorrhagic infarcts than in those with pale infarcts
76 citations
TL;DR: Mycotic aneurysm with hemorrhage was an extremely dramatic complication of emboli infected with the virulent pathogens, Staphylococcus aureus and Escherichia coli, while brain abscess developed insidiously in ischemic areas, after embolism with the opportunistic pathogens, Streptococcus viridans and Enterococcus.
Abstract: In order to study the effects of septic embolism on neurovascular structures, cerebral infarction was produced in a series of dogs by injecting silicone rubber cylinders through an internal carotid artery cannula. Each embolic particle was first incubated with one of four known bacterial pathogens. Death occurred in three animals on the second postoperative day, at which time ten other moribund dogs were sacrificed. Eleven animals made apparently uneventful recoveries from early hemiplegia and appeared well when sacrificed electively one to five weeks after embolism. Autopsies revealed subarachnoid and acute subdural hemorrhages in the early group with gross and microscopic evidence of mycotic aneurysm in each instance. Chronically surviving animals showed histological lesions in the putamen or temporal pole consistent with brain abscess. In this series, mycotic aneurysm with hemorrhage was an extremely dramatic complication of emboli infected with the virulent pathogens, Staphylococcus aureus and Escheri...
50 citations
TL;DR: A functioning blood channel ran through the laminated thrombus within the aneurysm, and operative injury to this blood channel caused serious cerebral infarction.
Abstract: ✓ An enormous globoid aneurysm arising from the right middle cerebral artery is reported. A functioning blood channel ran through the laminated thrombus within the aneurysm, and operative injury to this blood channel caused serious cerebral infarction.
49 citations
TL;DR: Evidence is presented that cerebral edema was caused by loss of autoregulation of cerebral blood flow concomitant with hyperemia and an increase of water and chloride content of brain tissue.
Abstract: ✓ Severe cerebral ischemia was produced in 25 baboons by clamping the carotid and vertebral arteries bilaterally for 10 minutes. Cerebral hemodynamics and metabolism were monitored throughout. Cerebral anoxia was less severe in animals in which a marked pressor response occurred due to ischemia of the vasomotor center, and a reversible type of brain swelling was usual. In those with more severe ischemic anoxia, progressive cerebral edema was a pathological entity. Evidence is presented that cerebral edema was caused by loss of autoregulation of cerebral blood flow (CBF) concomitant with hyperemia and an increase of water and chloride content of brain tissue. Cerebral edema began when CBF was reduced during occlusion and progressed for several hours after termination of occlusion. Evidence is adduced that uncoupling of oxidative phosphorylation may be an important concomitant of cerebral edema.
41 citations
TL;DR: Cerebral infarction was produced in the gerbil by ligation of one common carotid artery and the mortality from the lesion was significantly reduced by the daily administration of dexamethasone in the first 48 hours after surgery.
Abstract: Cerebral infarction was produced in the gerbil by ligation of one common carotid artery. The mortality from the lesion was significantly reduced by the daily administration of dexamethasone in the first 48 hours after surgery.
TL;DR: It is demonstrated that if massive experimental cerebral infarction is accompanied by progressive cerebral edema and greatly increased intracranial pressure, inhalation of 5% COz does indeed reduce rCBF, and Meyer et a1.6 proposed the term “intracerebral squeeze” to describe this phenomenon.
Abstract: Following the description of Brawley et al.’ of reduction of blood flow in the ischemic area in 5 of 7 dogs following occlusion of the middle cerebral artery (MCA), much controversy arose concerning the use of COz inhalation versus hyperventilation in treating patients with acute cerebral infarction (stroke). This phenomenon, termed the “intracerebral steal,” though rare, has been described in numerous clinical and experimental investigations. Various methods, including external monitoring from the head with diffusible isotopes following intracarotid injection,’ > 3 heat clearance methods, and oxygen electrode^,^ were employed to estimate regional cerebral blood flow (rCBF). The underlying factors responsible for such paradoxical reactions of rCBF to changes in the partial pressure of arterial COz (PaCO,) have never been determined, but vasomotor response or capacitance to COz was assumed to be lost. Brock et were the first to postulate that changes in intracranial pressure (ICP) induced by COz inhalation or hyperventilation might influence regional tissue perfusion pressure (PP) in zones with impaired autoregulation. They proposed that inhalation of COz may decrease rCBF by increasing intracranial pressure and that hyperventilation increases rCBF by decreasing intracranial pressure. Meyer et a1.6 demonstrated that if massive experimental cerebral infarction is accompanied by progressive cerebral edema and greatly increased intracranial pressure, inhalation of 5% COz does indeed reduce rCBF. They proposed the term “intracerebral squeeze” to describe this phenomenon. In the present series of experiments rCBF was measured in 18 monkeys ( 6 baboons and 12 Macacus monkeys) by inserting hydrogen electrodes into the brain. These electrodes are similar to those described by Aukland et al.’ who measured regional blood flow in the kidney. Fieschi et al.’ attempted to use such electrodes in their acute preparations; however, it is known that the responses of acutely implanted platinum electrodes to hydrogen inhalation are unreliable and, furthermore, that accurate rCBF values cannot be calculated unless the arterial hydrogen desaturation curve is also recorded. Both of these drawbacks were overcome in our experiments by chronically implanting the electrodes from four to twenty-five days until their response to hydrogen was consistent and by injecting the hydrogen gas as a bolus, saturated in saline, via the carotid artery.
TL;DR: During a 72-hour period of study, large doses of dexamethasone did not favorably affect survival, severity of brain edema, brain electrolyte shifts, or alterations in cerebral red blood cell, albumin, and pertechnetate spaces.
Abstract: Ischemic brain injury was produced in rats by the intracarotid injection of microspheres. During a 72-hour period of study, large doses of dexamethasone did not favorably affect survival, severity of brain edema, brain electrolyte shifts, or alterations in cerebral red blood cell, albumin, and pertechnetate spaces. The role of steroid therapy in cerebral infarction requires critical clinical appraisal.
TL;DR: Cerebral revascularization using a recently developed intracranial bypass procedure for the occluded internal carotid artery was found effective in increasing rCBF in selected cases where the procedure was successful.
Abstract: Regional cerebral blood flow (rCBF), hemispheric blood flow (HBF), extracranial blood flow, and regional cerebral blood volume (rCBV) have been measured in a series of patients using a gamma camera equipped with a magnetic tape system for storage and retrieval. This method eliminates the need for multiple probes in measuring these parameters. 133Xe and 99m Tc injected into the carotid arteries were used as radioactive indicators. These measurements were carried out in patients with cerebral infarction, intracerebral hematoma, brain tumor, arteriovenous malformation, and dementia. The HBF values obtained with this method were in excellent agreement with those using the hydrogen bolus method in the same patients. The effects of 5% CO2 inhalation, intravenous infusion of glycerol, and vasodilator drugs on rCBF and rCBV were evaluated and were found useful from diagnostic and therapeutic points of view. “Intracerebral steal” or “intracerebral squeeze” were demonstrated only in patients with space-occupying lesions such as intracerebral hematoma or brain tumor. Cerebral revascularization using a recently developed intracranial bypass procedure for the occluded internal carotid artery was found effective in increasing rCBF in selected cases where the procedure was successful.
TL;DR: Six autopsied cases of rare cerebrovascular diseases of childhood have been presented, including arteriosclerosis, alternating hemiparesis (“moyamoya” syndrome), and a reasonable classification of cerebral arterial diseases during childhood (based on tissue diagnoses) is presented and discussed.
Abstract: Six autopsied cases of rare cerebrovascular diseases of childhood have been presented, including arteriosclerosis, alternating hemiparesis (“moyamoya” syndrome), phyototic aneurysm caused by an awn of grass, arterio-occlusive infarct occurring near the time of birth, necrotizing arteritis predominantly affecting the nervous system and infantile thrombosis with cerebral infarction associated with tuberous sclerosis. These cases have raised some important but difficult questions with regard to the pathogenesis of strokes during childhood as compared to adulthood, especially whether cerebral arteriosclerosis is a response to diverse injuries during childhood and young adulthood, and whether there is a factor which protects the cerebral arteries during infancy and childhood such that the systemic arteries bear the brunt of vascular disease as compared to adulthood. In addition, a reasonable classification of cerebral arterial diseases during childhood (based on tissue diagnoses) is presented and discussed.
TL;DR: It is demonstrated that acute cerebral ischemia constitutes a severe stress in the gerbil which is reflected, almost quantitatively, by temporal changes in such blood constituents as enzymes, lipids, glucose, and adrenal stress hormones.
Abstract: The left carotid artery of healthy, male gerbils was surgically ligated to induce a state of cerebral ischemia. The animals were sacrificed two, four, six, 12, 24 and 48 hours postligation to determine whether the induced cerebral ischemia would be reflected by changes in blood chemistry. The gerbil, unlike the rat, has a well-defined circle of Willis and cerebral arterial branches which resemble the arrangement of cerebral arteries found in man. The gerbils withstood the induced cerebral ischemia relatively well with few overt signs of cerebral damage, e.g., muscular paralysis, and a low mortality rate. However, intense lipid mobilization accompanied by depletion of peripheral adipose tissue sites and fatty infiltration of the liver developed very promptly. Marked cerebral edema and definitive foci of cerebral infarction occurred in both the frontal and medial lobes of the brain. The adrenal cortices of the gerbil were markedly depleted of lipid concomitant with severe thymus gland involution indicative ...
TL;DR: Though the possibility of systemic fat embolism was considered in this case, evidence for it was not found in vivo, and pathological evidence was readily obtained by microscopy.
Abstract: Gresham et al. (1971) described an association between Thompson's replacement arthroplasty using methylmethacrylic cement and a high incidence of fatal fat embolism in the immediate postoperative period, and suggested that fat embolism occurs more often than is recognized. Though the possibility of systemic fat embolism was considered in this case, evidence for it was not found in vivo. Pathological evidence, however, was readily obtained by microscopy.
Journal Article•
TL;DR: The morphologic findings suggest that separation of the internal elastic lamina from the endothelial basement membrane is a consistent change and probably an initiating mechanism in the pathogenesis of atherosclerosis of the cerebral arteries.
Abstract: Prolonged feeding with an atherogenic diet can induce occlusive disease of the intracranial arteries and cerebral infarction in dogs. The morphologic findings suggest that separation of the internal elastic lamina from the endothelial basement membrane is a consistent change and probably an initiating mechanism in the pathogenesis of atherosclerosis of the cerebral arteries.
TL;DR: In cats being subjected to surgical occlusion of the middle cerebral artery, regional oxygen availability (O2a) was monitored continuously from four open-tip platinum electrodes in the ischemic hemisphere and one in the control hemisphere and the recovery of regional O2a was slower and less complete.
Abstract: In cats being subjected to surgical occlusion of the middle cerebral artery, regional oxygen availability (O2a) was monitored continuously from four open-tip platinum electrodes in the ischemic hemisphere and one in the control hemisphere. Extradural pressure over the convexity of the ischemic hemisphere was measured hourly. The animals were killed 24 hours after occlusion. Ten animals developing substantial increases in extradural pressure as a consequence of cerebral infarction were compared with ten which did not. The two groups did not differ in severity of the initial ischemic insult resulting from the arterial ligation, in blood pressure following occlusion, or in hematocrit, PCOCO2, or oxygen saturation.
The most important difference between the two groups was in the course of regional O2a in the ischemic hemispheres following occlusion. In the animals which ultimately developed increased intracranial pressure the recovery of regional O2a was slower and less complete. After the ninth hour postocclusion O2a declined progressively, clearly related to rising intracranial pressure. In the animals which developed increased extradural pressure, it rose progressively to a mean of 40 mm Hg by 24 hours postocclusion. The intracranial pressure changes during the first few hours seemed insufficient to account for the early failure of recovery of regional O2a, unless they are viewed as averages which obscure important regional intracerebral pressure changes.
TL;DR: In this article, representative enzymes in brain were studied by histochemical techniques at intervals varying between 6 hours and 8 weeks after permanent middle cerebral artery occlusion in 18 cats and showed progressive axonal changes, after the period of reversibility, bordering the core area of ischemia.
Abstract: ✓ Representative enzymes in brain were studied by histochemical techniques at intervals varying between 6 hours and 8 weeks after permanent middle cerebral artery occlusion in 18 cats. Unequivocal enzyme changes did not develop until 12 hours after occlusion, and no specific enzyme system was demonstrated to fail prior to others. That the ischemia of the first 6 hours is reversible in the cat was further substantiated by histological studies in a separate group of animals subjected to temporary middle cerebral artery occlusion for 6 hours. This study demonstrated progressive axonal changes, after the period of reversibility, bordering the core area of ischemia and resembling neural tissue reaction to injury in the spinal cord. Correlation of this study with previous biochemical determinations suggests that a self-induced and self-perpetuated toxicity might explain, in part, progressive changes in ischemic areas.
TL;DR: Six cases are presented to show that the intracranial arterial spasm accompanying subarachnoid hemorrhage can be associated with an abnormal brain scan beginning 1 to 3 weeks after the onset of the spasm, presumably due to cerebral infarction.
Abstract: ✓ Six cases are presented to show that the intracranial arterial spasm accompanying subarachnoid hemorrhage can be associated with an abnormal brain scan beginning 1 to 3 weeks after the onset of the spasm. The scan abnormality gradually disappears over a few months, and is presumably due to cerebral infarction.
TL;DR: Two unusual brain scan patterns were found among 38 abnormal scans in 84 patients with cerebral infarction, and three cases involved laminar or pseudolaminar necrosis, resulting in a crescent sign in the coronal plane projection.
Abstract: Two unusual brain scan patterns were found among 38 abnormal scans in 84 patients with cerebral infarction. Nine demonstrated a borderland infarction in which the abnormal uptake overlapped the territory supplied by two or more of the major cerebral vessels. Three cases involved laminar or pseudolaminar necrosis, resulting in a crescent sign in the coronal plane projection. The pathophysiology of these lesions is correlated with the scan findings.
01 Jan 1972
TL;DR: The role of intracranial pressure gradients in the development of neurologic deficits after cerebral infarction has not been evaluated adequately, partly because of technical problems with measurements of regional intrac Cranial pressure (ICP).
Abstract: The role of intracranial pressure gradients in the development of neurologic deficits after cerebral infarction has not been evaluated adequately, partly because of technical problems with measurements of regional intracranial pressure (ICP). The presumed cause of post-infarction ICP gradients is ischemic cerebral edema; as a preliminary to a study of edema and its modification by treatment, ICP was measured in cats after occlusion of one middle cerebral artery (MCA).
TL;DR: Baseline and follow-up measurements of cerebral hemodynamics were performed in hypertensive patients by the N2O method with a certain time interval, and a tendency for some decrease in the CBF was noted, but the difference was not statistically significant.
Abstract: Baseline and follow-up measurements of cerebral hemodynamics were performed in hypertensive patients by the N2O method with a certain time interval. A tendency for some decrease in the CBF was noted, but the difference was not statistically significant. Twelve hypertensive patients suffered from a stroke during the period of observation. The CBF values prior to the stroke varied so widely that there was no predictive value from these measurements. The decrease in CBF in a mild case of cerebral infarction is slight and is followed by little fluctuation. The decrease in a case of moderate severity is marked but returns to normal in two to five months. Clinically severe cases of infarction and hemorrhage are also characterized by a marked decrease in CBF, but this decrease of infarcted cases may be irreversible. A higher incidence of recurrent infarction is noted in those patients in whom recovery of CBF following a stroke is poorest. This is most apparent in those patients suffering a recurrence within one ...
TL;DR: Evidence for abnormal cerebral metabolic patterns, such as anaerobic glycolysis, in patients with cerebrovascular disease, and oxidation of nonglucose substances such as β-hydroxybutyrate, are discussed.
Abstract: Hemispheric blood flow (HBF) and metabolism were studied in 46 patients with various types and stages of ischemic cerebrovascular disease and were found to be abnormal in all patients, including those with transient ischemic attacks. Bilateral depression of HBF and metabolism was observed in association with acute unilateral cerebral infarction. Hemispheric respiratory quotient (HRQ) was higher in the ischemic hemisphere than in the healthy side. The degree of elevation of HRQ on the diseased side correlated well with the acuteness of infarction, increasing age of the patients, and the severity of the neurological deficit. However, the HRQ in the healthy hemisphere was lower than unity, which suggests that substances other than glucose were being metabolized. The high hemispheric glucose:oxygen ratio (HG:O) correlated well with the severity of infarction and the age of the patient. Patients with brain stem ischemia had the lowest HBF values, suggesting that central neurogenic vasomotor control had been im...
01 Jan 1972
TL;DR: The effects of dexamethasone were investigated in experimental brain edema induced by triethyl tin intoxication and cerebral microembolism, and steroids had no effect on mortality, severity of edema, brain electrolyte changes, or cerebral isotope spaces.
Abstract: The effects of dexamethasone were investigated in experimental brain edema induced by triethyl tin intoxication and cerebral microembolism Large doses of steroid (125 mg/kg/day) significandy reduced brain water and sodium in triethyl tin poisoned rats However, in experimental microembolism, steroids had no effect on mortality, severity of edema, brain electrolyte changes, or cerebral isotope spaces
TL;DR: The reactivity of the higher autonomic centers to hypoglycemia prior to and after the treatment with pyrithioxin or caffeine in patients with cerebral infarct was studied.
Abstract: The reactivity of the higher autonomic centers to hypoglycemia prior to and after the treatment with pyrithioxin or caffeine in patients with cerebral infarct was studied. Before treatment a hyporeact
TL;DR: This study failed to demonstrate any beneficial effect in men with cerebral infarction from estrogens given in moderate amounts for as long as five years, and there was, on the other hand, no evidence to support current reports that prolonged estrogen use in these dosages produced an increased mortality from thromboembolism.
Abstract: Estrogenic Therapy in Men With Ischemic vascular Disease: on Recurrent Cerebral Infarction and Survival • A cooperative clinical investigation was undertaken in 15 Veterans Administration Hospitals to determine whether long-term therapy with conjugated equine estrogens prevented recurrent cerebral infarction or death due to atherosclerotic vascular disease. Follow-up observations were made for periods up to five years in 572 men with cerebral infarction who were assigned on a random basis to placebo or to treatment with 1.25 to 2.5 mg of Premarin daily. Estrogen administration failed to reduce the incidence of cerebral infarction, transient cerebral ischemia or death due to vascular disease. Although use of hormones was associated with an overall higher death rate, this excess mortality was due largely to cancer and various other diseases and could not be attributed directly to the medication. Occurrences of and deaths from myocardial infarction were less in treated than control patients, but vascular disorders, such as pulmonary embolism, mesenteric thrombosis and heart failure were more frequent in the former group. This study failed to demonstrate any beneficial effect in men with cerebral infarction from estrogens given in moderate amounts for as long as five years. There was, on the other hand, no evidence to support current reports that prolonged estrogen use in these dosages produced an increased mortality from thromboembolism.