Showing papers on "Cerebral infarction published in 1971"
TL;DR: Extravasation of the tracer during the first 3 weeks after MCA occlusion is therefore related to thesize of the resulting brain necrosis, but restitution of the BBB occurs thereafter irrespective of infarct size.
Abstract: A study was made on the blood-brain barrier (BBB) to protein tracers in focal cerebral ischemia and infarction caused by permanent or temporary occlusion of the middle cerebral artery (MCA) in the rhesus monkey.
167 citations
TL;DR: The records of the Mayo Clinic have been used as the primary basis for the study of stroke in the population of Rochester, Minnesota, from 1945 through 1954, and information from these studies confirmed the high degree of accuracy of the clinical appraisals.
Abstract: The records of the Mayo Clinic have been used as the primary basis for the study of stroke in the population of Rochester, Minnesota, from 1945 through 1954. The incidence rate for first stroke of all types was 1947/100,000/year. The rates increased with age, and at age 65 to 74 years, about 1% of the population was affected annually. No significant differences were noted between men and women. The rate for cerebral thrombosis was 146/l00,000/year for all ages. Cerebral hemorrhage represented less than 10% of all strokes and occurred in less than 15% of those who died; this is contrary to what is published in the U.S. Mortality Statistics. The prevalence rate was 547/100,000 on January 1, 1955. Twenty-one percent of these persons who had previously had a stroke were functioning with no incapacity on the date of prevalence determination and only 3% were bedridden. Death certificates were reviewed for all those who died after a stroke. Among those who died within a month after a stroke, some type of stroke ...
157 citations
TL;DR: Hyperemia, or “luxury perfusion,” manifested by red venous blood, appears to be related to failure of cerebral tissue to utilize available oxygen as well as to “reactive” hyperemian flow in regions previously ischemic.
Abstract: Correlative studies of cortical blood flow measured by the 85Kr washout technique and observations of the cortical blood vessels of 10 squirrel monkeys subjected to temporary occlusion of the middle cerebral artery are described. During occlusion, cortical blood flow in core areas of ischemia decreased to 0.12 to 0.90 ml/g/min (20 to 50% of preocclusion values) and became pressure dependent with failure of autoregulation. After release of the occluding clip, cortical blood flow was restored. Correlation between degree of vascular reaction judged by observation of the cortex and degree of hyperemia as determined by cortical blood flow was poor. There was incomplete correlation between the degree of hyperemia and the degree of preceding ischemia. Hyperemia, or "luxury perfusion," manifested by red venous blood, appears to be related to failure of cerebral tissue to utilize available oxygen as well as to "reactive" hyperemia, or supernormal blood flow, in regions previously ischemic. There was no demonstrabl...
146 citations
TL;DR: For purposes of stroke screening alone the most efficient and practical method would be to determine casual blood pressure, although it must be stated that as yet there is uncertainty concerning the change in the risk if such blood pressure is treated.
Abstract: Although large gaps in our knowledge concerning the epidemiology of cerebrovascular disease are apparent, careful inspection of all existing data now makes it possible to see certain patterns emerging which suggest certain risk factors for stroke. While the problem of differential diagnosis of the various categories of cerebrovascular disease presents a major obstacle to obtaining an undistorted picture of the epidemiological features of stroke from death certificate mortality data, the addition of evidence from prospective studies, including those in Framingham, Massachusetts, reveals that various types of arterial occlusion with cerebral infarction are by far the most prevalent type of stroke. Any specific origin of atherosclerosis remains obscure, as possible etiological candidates including dietary alterations in salt, fat and refined carbohydrate, sedentary living, excessive calories promoting obesity, the cigarette habit and even the mineral content of water in addition to marital status have all be...
145 citations
TL;DR: Pathophysiological and pathogenetic concepts, particularly in occlusive cerebrovascular disease, are reviewed and discussed with emphasis on the results of current research and therapy is discussed in the context of these concepts.
Abstract: Pathophysiological and pathogenetic concepts, particularly in occlusive cerebrovascular disease, are reviewed and discussed with emphasis on the results of current research. Therapy is discussed in the context of these concepts. When focal ischemia, with or without cerebral infarction, is not associated with definable arterial occlusion, studies of regional cerebral blood flow strongly support the thromboembolic theory; the arterial defect is relatively transient and is caused by an embolus or thrombus which rapidly disappears (fragments or is lysed). The treatment of transient ischemic attacks by the administration of anticoagulant or surgical reconstruction of the appropriate artery is discussed. When cerebral infarction is caused by arterial occlusion there is vasomotor paralysis (loss of autoregulation and of reactivity to carbon dioxide). In some instances hypercapnia apparently causes only the vessels in nonaffected brain to dilate so that an increased amount of blood streams to these parts while bl...
126 citations
117 citations
TL;DR: Oral or intravenous administration of glycerol was nontoxic and caused a diuresis even in patients with advanced cardiorenal disease, and Glycerol administration decreased cerebrospinal-fluid pressure without rebound.
114 citations
TL;DR: Hypoxemia, as judged by the relative structural integrity of mitochondria, does not seem to be the most important pathogenetic factor in the development of cerebral ischemic necrosis.
Abstract: Structural evaluation of cerebral infarction in twelve squirrel monkeys was conducted for the purpose of elucidating some aspects of the pathogenesis of regional cerebral ischemia.
93 citations
TL;DR: It is concluded that vasodilator therapy presumably decreased flow in pathological tissue and that such treatment should not be employed in the therapy of cerebrovascular disease.
Abstract: The effect of intracarotid injection of 10 mg of papaverine on regional cerebral blood flow was measured in 27 patients. Most of the patients had cerebral infarction or intracranial neoplasm. The intra-arterial 133Xenon injection method was used and 16 or 35 regions of the diseased hemisphere were monitored. In patients without focal flow abnormalities an average flow increase of 93% followed the injection. In patients with focal abnormalities of cerebral blood flow the intra-arterial injection of papaverine produced a decrease in focal flow or less increase in flow than normal. It is concluded that vasodilator therapy presumably decreased flow in pathological tissue and that such treatment should not be employed in the therapy of cerebrovascular disease.
92 citations
TL;DR: It is concluded that anticoagulant therapy significantly decreased the risk of cerebral infarction in patients who had attacks of transient focal cerebral ischemia.
Abstract: Precise use of categorical terms and definitions is mandatory in discussing the use of anticoagulants in treating occlusive cerebrovascular disease The components of the temporal profile of the disease are described Six reports have appeared which describe the results of anticagulant therapy in transient cerebral ischemic attacks From these six studies it is concluded that anticoagulant therapy significantly decreased the risk of cerebral infarction in patients who had attacks of transient focal cerebral ischemia In the few carefully performed investigations of the use of anticoagulant for acute progressing stroke the evidence points to the lack of progression in patients receiving treatment when compared to individuals not getting such drugs There continues to be a definite difference of opinion about the results of anticoagulant therapy in completed stroke If anticoagulant is to be administered on a long-term basis, it must be considered dangerous and every effort made to control the level of anti
64 citations
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TL;DR: Of 407 consecutive patients with cerebrovascular disease seen from July 1967 to June 1969 in a prospective study of stroke being conducted by the Department of Neurological Sciences at Christian Medical College Hospital, Vellore, South India, 127 (32%) patients were between the ages of 11 and 40.
Abstract: Of 407 consecutive patients with cerebrovascular disease seen from July 1967 to June 1969 in a prospective study of stroke being conducted by the Department of Neurological Sciences at Christian Medical College Hospital, Vellore, South India, 127 (32%) patients were between the ages of 11 and 40. Using the standard criteria for diagnosis, 50% of the patients had cerebral thrombosis, 13% had cerebral embolism, 13% had internal carotid artery thrombosis (a subcategory of cerebral infarction), and the remainder were distributed through the other categories of cerebrovascular disease. Hypertension appeared to be a factor in about 19% of the patients (angiography revealed that the small intracranial vessels were more commonly abnormal than the larger extracranial arteries). Less than 10% of the patients had intracerebral hemorrhage or subarachnoid hemorrhage. The question was raised as to the possible role of arteritis secondary to common tropical diseases in the pathogenesis of these "strokes in the young."
TL;DR: Neither hypocapnia nor hypercapnia was associated with a smaller size or higher CBF of regions of cerebral ischemia produced by occlusion of a middle cerebral artery, althoughhypercapnia inhibited the development of hyperemia.
Abstract: To assess the effects of PaCOCO2 on cerebral ischemia and reactive hyperemia, the right middle cerebral artery was occluded in 18 cats. Four to six hours later, PaCO2 was adjusted by mechanical ventilation, with or without CO2, to less than 20 torr in four cats, 31 to 38 torr in six, and 46 to 68 torr in eight. Regional cerebral blood flow (CBF) then was measured at multiple sites in each hemisphere by autoradiography. In regions of brain tissue outside the distribution of the occluded middle cerebral artery, log10 CBF correlated positively with PaCOCO2. In ischemic regions, CBF was higher in normocapnic cats. Reactive hyperemia occurred in two cats of the hypocapnic group, in four cats of the normocapnic group, but in only one hypercapnic cat (PaCOCO2 = 46 torr). Hyperemia also was found outside potentially ischemic regions in five cats. Multiple hyperemic foci developed in six cats. Neither hypocapnia nor hypercapnia was associated with a smaller size or higher CBF of regions of cerebral ischemia produc...
TL;DR: In patients with acute unilateral cerebral infarction, there was reduction of hemispheric blood flow (HBF) and metabolism in the healthy hemisphere (phenomenon of diaschisis) as well as in the diseased hemisphere in patients in all age groups.
Abstract: In 44 patients with acute unilateral cerebral infarction, there was reduction of hemispheric blood flow (HBF) and metabolism in the healthy hemisphere (phenomenon of diaschisis) as well as in the diseased hemisphere in patients in all age groups (30 to 70 years of age). In patients with symptoms present for three weeks or longer, the decrease in HBF in the healthy hemisphere was less than during the acute stage of infarction. The HBF in the healthy hemisphere of the younger patients approached normal values months or years after the stroke but remained reduced in older patients, probably reflecting diffuse as well as focal cerebrovascular disease. When the severity and outcome of the neurological deficit was correlated with the blood flow and metabolism of the diseased hemisphere, it was apparent that HBF in patients with transient ischemic attacks and more prolonged but reversible neurological deficit was greater than in those who had sustained severe, permanent neurological deficit.
TL;DR: Direct evidence for a platelet contribution in experimental vascular occlusive stroke and subarachnoid hemorrhage was sought and occlusion or puncture of the middle cerebral artery invariably produced a prompt and striking fall in the platelet count of venous blood draining the affected side.
Abstract: There is increasing evidence that platelets play a key role in the development of arterial occlusive lesions and in the tissue response to them. Direct evidence for a platelet contribution in experimental vascular occlusive stroke and subarachnoid hemorrhage was sought. Platelet counts were done on jugular blood before and after production of the vascular lesion. Craniectomy had little or no effect but occlusion or puncture of the middle cerebral artery invariably produced a prompt and striking fall in the platelet count of venous blood draining the affected side. Some implications of this observation are discussed.
TL;DR: An unusual syndrome is described consisting of right hemiplegia, right hemisensory loss, mild naming disturbance, and severe alexia coupled with normal expressive language and ability to write, strongly suggesting involvement of the left posterior cerebral artery.
Abstract: An unusual syndrome is described consisting of right hemiplegia, right hemisensory loss, mild naming disturbance, and severe alexia coupled with normal expressive language and ability to write. The clinical syndrome of alexia without agraphia strongly suggests involvement of the left posterior cerebral artery. A study of the territory of distribution of the posterior cerebral artery would appear to confirm the possibility that occlusion of this vessel could produce the entire symptom picture. Of particular interest was the unusual hemiplegia, involving both limbs and face equally, but with a minimum of spasticity.
TL;DR: Speculation that hyperventilation with resultant hypocarbia might increase flow in the ischemic region by increasing vascular resistance in the normal brain and improving collateral perfusion to the isChemic area is led to.
Abstract: THE TRADITIONAL MEANS for increasing blood flow to an area of localized cerebral ischemia has been the use of cerebral vasodilating agents, e.g., carbon dioxide. Recently, investigators1,2 have demonstrated a reduction in cerebral blood flow in ischemic areas with hypercarbia, suggesting that the employment of this method of treatment for stroke may be detrimental. They theorize that in the presence of ischemia, there is already maximal dilatation of the vascular bed, probably due to a local increase in lactate with a reduction in pH and an increase in tissue CO,. Therefore, an increase in PaCO, would not cause further vasodilatation in the ischemic area but would serve only to dilate arterioles in the surrounding nonischemic brain and shunt blood away from the ischemic area. This paradoxical situation has been termed the “intracerebral steal syndrome.”3 These findings have led to speculation that hyperventilation with resultant hypocarbia might increase flow in the ischemic region by increasing vascular resistance in the normal brain and improving collateral perfusion to the ischemic area. In support of this concept, it has been demonstrated in the experimental animal that hyperventilation initiated prior to cerebral artery occlusion will reduce the area of infarction.4.3
TL;DR: The luxiiry perfnsioii syndrome, a state of hyperemia occurring on the periphery of a focal ischemic lesion, has been demonstrated in man with angiography?
Abstract: THE “LUXURY PERFUSION” SYNDROMEI-~ and the “no-reflow” phen0menon7.~ are two microvascular phenomena that are currently undergoing extensive investigation in the process of cerebral ischemia and infarction. The luxiiry perfnsioii syndrome, a state of hyperemia occurring on the periphery of a focal ischemic lesion, has been demonstrated in man with angiography? and with the xenon133 method of regional cerebral blood flow measurement.“ Luxury perfusion is apparently a transitory event lasting only a few hours or a few days. Enhanced blood flow is believed to occur in ;ireas of low oxygen demand, and blood therefore rapidly traverses the area, giving off very little oxygen.’-4 Evidence of luxury perfusion in experimental cerebral ischemia is thus far rather Experimental studies on global ischemia of the brain have revealed that a transient arrest of the cerebral circulation may be followed by an impaired recirculation of blood after ischemia; this is the no-reflow phenomenon. With the cnrbon-black perfusion technique, Anics and his collaborators have demonstrated nonpatency of cerebral capillaries immediately after global ischemia of more than five minutes’ duratioii.7 This is probably due to increased blood viscosity and occlusive changes in the terminal blood vessels. Chiang et :Lx presented electron-microscopic data which indicate that swelling of the endothelium and the perivascular glial cells occurring during ischemia may
TL;DR: A complete postmortem examination of a patient with a symptomatic cerebral vascular anomaly associated with hereditary hemorrhagic telangiectasia (HHT) has not been recorded previously as discussed by the authors, and the patient reported in this paper presented with seizures and underwent surgical resection of infarcted brain tissue associated with a venous angioma.
Abstract: While neurological symptoms are often mentioned in reports of families with hereditary hemorrhagic telangiectasia (HHT) and are frequently assumed to be due to vascular anomalies of the central nervous system, documentation of such anomalies is surprisingly rare. Two cases of surgically treated symptomatic cerebral vascular malformations in HHT have been published previously. In addition, there are three descriptions of vascular anomalies discovered at autopsy in the brains of neurologically asymptomatic patients with HHT available in the literature. A complete postmortem examination of a patient with a symptomatic cerebral vascular anomaly associated with HHT has not been recorded previously.
The patient reported in this paper presented with seizures and underwent surgical resection of infarcted brain tissue associated with a venous angioma. He died six months later and, at autopsy, was found to have multiple "cryptic" venous angiomas of the brain. Hypoxic damage to brain tissue related to small venous angiomas is one mechanism whereby these lesions may become symptomatic. Hemorrhage may also occur. Neurological symptoms in patients with HHT cannot be assumed to be due to cerebral vascular anomalies, and consideration must be especially given to the complications of pulmonary arteriovenous fistula such as polycythemia, embolism, and abscess.
TL;DR: Data is presented indicating that improvement in function of a paralyzed extremity may occur in the early phase after stroke but was extremely unlikely to continue during long-term follow-up from three months to five years.
Abstract: The problems involved in measuring improvement as well as the conceptual difficulties in considering this phenomenon were considered in general terms. Data on 300 patients with nonembolic cerebral infarction followed from five to nine years are presented, indicating that improvement in function of a paralyzed extremity may occur in the early phase after stroke but was extremely unlikely to continue during long-term follow-up from three months to five years. It was concluded that improvement in function might be determined more by retraining of the nonaffected muscles and particularly of the unaffected side rather than by recovery of the area paralyzed.
TL;DR: The preserved CO2 responsiveness of the flow indices in these six patients is in support of the theory that intermittent platelet microembolization is an important cause of TIA.
Abstract: Cerebral blood flow and its ability to increase in response to inhalation of 6% CO2 was measured in six patients with a history of transient ischemic attacks in the internal carotid distribution and in ten normal control subjects. Flow was measured with a method which uses time concentration curves made with intravenously injected radioactive indicator and externally placed radiation detectors. It permits measurement of flow, expressed in arbitrary units as a flow index, within the range of a detector placed against the side of the head. Resting flow indices and the increases in flow indices in response to CO2 inhalation did not differ significantly between the TIA patients and the normal control subjects. These results are discussed in terms of possible mechanisms of TIA, and it is concluded that the preserved CO2 responsiveness of the flow indices in these six patients is in support of the theory that intermittent platelet microembolization is an important cause of TIA.
TL;DR: In cats subjected to middle cerebral artery occlusion, the resulting ischemia was unaffected by the blood pressure at the time of Occlusion when arterial PCO2 was normal or low, and this conclusion suggests that proper analysis of the pathogenesis of cerebral infarction requires consideration of immediate ischemía separately from the subsequent course of the ischemic lesion.
Abstract: In cats subjected to middle cerebral artery occlusion, the resulting ischemia was unaffected by the blood pressure at the time of occlusion when arterial PCOCO2 was normal or low. At normal and elevated blood pressures, hypercapnia established prior to occlusion minimized the ischemia and hypocapnia aggravated it. Re-occlusion during postischemic reactive hyperemia resulted in ischemia of the same severity as during the initial occlusion, provided PCOCO2 and blood pressure were not changed. These observations suggest that a general determinant of the severity of immediate ischemia in this preparation is the competence of the collateral circulation. This conclusion suggests that proper analysis of the pathogenesis of cerebral infarction requires consideration of immediate ischemia separately from the subsequent course of the ischemic lesion. There are so many variables bearing on the pathogenesis of cerebral infarction that a rational therapy of acute stroke can only be visualized when there is knowledge o...
Journal Article•
TL;DR: Data is presented indicating that improvement in function of a paralyzed extremity may occur in the early phase after stroke but was extremely unlikely to continue during long-term follow-up from three months to five years.
Abstract: The problems involved in measuring improvement as well as the conceptual difficulties in considering this phenomenon were considered in general terms. Data on 300 patients with nonembolic cerebral infarction followed from five to nine years are presented, indicating that improvement in function of a paralyzed extremity may occur in the early phase after stroke but was extremely unlikely to continue during long-term follow-up from three months to five years. It was concluded that improvement in function might be determined more by retraining of the nonaffected muscles and particularly of the unaffected side rather than by recovery of the area paralyzed.
Journal Article•
TL;DR: The value of A-mode echoencephalography was studied in a series of patients with Cerebrovascular disease of various types and proved to be restricted value limited to those situations in which a midline shift was obtained and the midlineshift was observed within 36 hours after the onset of symptoms.
Abstract: The value of A-mode echoencephalography was studied in a series of patients with Cerebrovascular disease of various types. The procedure proved to be restricted value limited to those situations in which (1) a midline shift was obtained, and (2) the midline shift was observed within 36 hours after the onset of symptoms.
Whereas after 36 hours some patients with cerebral infarction showed a midline shift (presumably due to edema), such a shift was not noted in patients with cerebral infarct who were examined within 36 hours after its occurrence. Those patients showing a midline shift before this interval should be suspected of having an intracerebral hemorrhage or other intracranial space-occupying process.
01 Jan 1971
Journal Article•
01 Jan 1971
TL;DR: There were 45 false negative brain scans among the last 3,600 consecutive scans obtained between January 1966 and December 1968 at the Henry Ford Hospital, andEleven of these cases were of cerebral infarction and other intracranial disease was diagnosed in 34.
Abstract: There were 45 false negative brain scans among the last 3,600 consecutive scans obtained between January 1966 and December 1968 at the Henry Ford Hospital. Eleven of these cases were of cerebral infarction. Other intracranial disease was diagnosed in 34 on or shortly after the date of the false negative scan, and no explanation can be offered for 18 of these false negatives. Explanations suggested for the remaining 16 cases include head position during scanning, location of the lesion, repair of the damaged blood-brain barrier, and diffuse character of the disease.
TL;DR: Of the many comments received following publication of the 'Joint Study of Extracranial Arterial Occlusion' (211:1993, 1970), none has been from a surgeon, undoubtedly due in part to the fact that surgeons interested in cerebral ischemia are convinced of the validity of certain conclusions and inferences derived from this important study.
Abstract: To the Editor.— Fields stated (216: 1199, 1971) that "of the many comments received following publication [of the 'Joint Study of Extracranial Arterial Occlusion' (211:1993, 1970)], none has been from a surgeon." This is undoubtedly due in part to the fact that surgeons interested in cerebral ischemia are convinced of the validity of certain conclusions and inferences derived from this important study. Some of these are almost axiomatic, as follows: (1) Extracranial arterial occlusive disease is a competent cause of cerebral ischemia and infarction. (2) Untreated extracranial arterial occlusive disease leads to cerebral infarction in many instances. (3) Many patients with cerebral ischemia can be recognized before infarction occurs. (4) Operation is effective in correcting extracranial arterial lesions. (5) The operation is being done with ever-decreasing morbidity and mortality. (6) Survivors of operation show a decreased incidence of cerebral ischemic symptoms. (7) Survivors show a decreased incidence of cerebral