Showing papers on "Cerebral infarction published in 1984"

Local interrelationships of cerebral oxygen consumption and glucose utilization in normal subjects and in ischemic stroke patients: a positron tomography study

Abstract: With the use of positron emission tomography (PET) and the 15O steady-state-[18F]fluorodeoxyglucose combined method, the local interrelationships between the cerebral metabolic rate for oxygen (CMRO2) and the cerebral metabolic rate for glucose (CMRGlc) were investigated in control subjects and in stroke patients. In addition to the classic in vivo autoradiographic approach, a kinetic method was used to measure CMRGlc because it was expected to be more reliable in cerebral ischemia. In control subjects local coupling between CBF, CMRO2, and CMRGlc was confirmed, and acceptable values for the CMRO2/CMRGlc ratio were found; the latter, however, was lower in white matter than in gray. Uncoupling between CMRO2 and CMRGlc was observed in all stroke patients, suggesting that (1) enhanced anaerobic glycolysis occurred both in reperfused recent infarcts and in chronically ischemic tissue, and (2) substrates other than blood-borne glucose were being oxidized at the borders of recent infarcts. However, methodologic...

Cerebral infarction in systemic lupus: association with anticardiolipin antibodies.

Abstract: We report fifteen patients, thirteen with systemic lupus and two patients with a "lupus-like" illness who developed cerebral infarction. All fifteen patients were shown to have elevated anticardiolipin antibody levels using a newly devised solid phase radioimmunoassay. The lupus anticoagulant was detected in all eleven patients tested. It is proposed that anticardiolipin antibodies and the lupus anticoagulant make up a population of antiphospholipid antibodies capable of causing cerebral vascular injury and thrombosis resulting in cerebral infarction. These antibodies may also play a pathogenic role in autoimmune disorders other than lupus where cerebral thrombotic disease is a prominent feature.

Experimental ischemic stroke: a review.

Abstract: Pour ameliorer les connaissances de l'accident vasculaire cerebral ischemique on passe en revue la bibliographie sur ce type d'accident sous diverses sections: modele le plus approprie et reproductible, methodes experimentales de production, evolution, tentatives pour modifier l'evolution d'infarctus cerebral en cours de constitution

Myocardial damage from acute cerebral lesions.

Abstract: Autopsy findings in 58 patients with intracranial lesions were compared with those in 50 control patients for myocardial damage, characterised by a change from a myofibrillar to a granular staining pattern, using a histochemical method for succinic dehydrogenase. Transmurally scattered foci of damaged myocardial fibres were significantly more common (p less than 0.01) in patients with intracranial lesions (62%) compared to controls (26%). No victims of sudden violent deaths showed these cardiac lesions. Focal myocardial damage required at least six hours to develop after onset of the acute neurological event and was not observed after the second week. It was associated with lesions producing a rapid increase in intracranial pressure and was usually absent in patients with slowly enlarging or small cerebral lesions. Similar myocardial changes were seen in patients in the control group dying from prolonged shock or other forms of acute circulatory or metabolic failure. The postulated mechanism of cardiac damage in these patients is increased levels of plasma catecholamines secondary to rapidly increasing intracranial pressure, irrespective of the cerebral pathology.

The decline of stroke.

Abstract: Stroke mortality in the United States has declined since 1900. The mortality rates from stroke in Rochester, Minnesota, have declined 76% since 1950, and the primary cause for the declines is a decrease in the incidence of new cases of cerebral infarction and cerebral hemorrhage. There are no data on the incidence of stroke prior to 1945 to confirm the US mortality trend. The decline in incidence was noted in women 10-15 years before it was seen in men. Hypertension is the most important risk factor for stroke. Hypertension surveys have shown an increasing effectiveness of antihypertensive medication in lowering blood pressure, and the effect was noted earlier in women. Available evidence is consistent with the idea that treatment of hypertension is the only significant contributor to the decline of stroke.

Cerebral infarction associated with lupus anticoagulants--preliminary report.

Abstract: Hypercoagulability may contribute to stroke in young adults. Lupus anticoagulants (LA) were identified in six patients (4%) of 145 young adults with cerebral infarction. The clinical features of the 6 patients in this survey plus an additional patient from another institution with LA-associated stroke are presented. Four had systemic lupus erythematosus and 3 had idiopathic LA; all had mild thrombocytopenia. In 2 patients, no other conditions associated with stroke were discovered after thorough evaluation. Recurrent arterial thrombosis occurred in 4 of 7 patients during an average of two years of follow-up. Evidence suggests that inhibition of prostacyclin formation may occur with LA, promoting a prothrombotic state.

Anticardiolipin antibodies: occurrence in Behçet's syndrome.

Abstract: Anticardiolipin antibodies have recently been described in association with arterial and venous thrombosis, and with neurological symptoms, in connective tissue diseases. In a study of 70 patients with Behcet's syndrome 13 patients had these antibodies. Of these 13 patients eight had a history of either retinal vascular pathology, cerebral infarction, or thrombophlebitis. The association of retinal vascular disease and the presence of anticardiolipin antibodies was statistically significant.

Perinatal cerebral infarction.

Abstract: The diagnosis of perinatal cerebral infarction, although frequently suggested clinically, has been made most commonly at postmortem examination; few infants surviving stroke are reported in the literature. We evaluated 18 infants with perinatal cerebral infarction in a recent twelve-month interval. Seven were preterm neonates, 6 of whom had experienced neonatal intraventricular hemorrhage. Three full-term infants were thought to have experienced cerebral infarction in utero and had evidence of well-defined strokes on computed tomographic scans performed shortly after birth. Eight infants developed stroke at term. The most common cause of cerebral infarction in our series was perinatal asphyxia. Fourteen of the infants were seen with neonatal seizures. Fourteen of the 18 have died or are faring poorly at 4 to 12 months of age (corrected).

Cerebrospinal fluid enolase in stroke.

Abstract: This study relates the level of alpha and gamma enolase in cerebrospinal fluid sampled within 4 days of a stroke to the volume of the cerebral infarct measured on the CT image and to the clinical outcome of the patient. Twenty-eight patients were studied, two with transient ischaemic attacks and 26 with completed stroke due to infarction. The cerebrospinal fluid enolase was raised in the two patients with transient ischaemic attacks and 23 with completed stroke. There was a positive correlation between the volume of the infarct and the level of cerebrospinal fluid alpha and gamma enolase. A high cerebrospinal fluid enolase was always associated with a poor prognosis.

Clinical and neuroradiological analysis of thrombotic and embolic cerebral infarction.

Abstract: The clinical and neuroradiological characteristics of cerebral thrombosis and cerebral embolism were established in 109 cases with nonembolic and 120 cases with embolic arterial occlusion of the brain. Cases with cerebral thrombosis due to occlusion of perforating branches were excluded from the study, to equalize the size of the involved arteries in the two groups. More than 60% of patients with cerebral embolism showed a level of consciousness lower than stupor, while less than 15% did so in the thrombotic group. Cortical signs such as aphasia, agnosia, conjugate deviation, etc., were more frequently seen in the embolic group. A mean size of the infarct on CT (Infarct-Index) was significantly larger, and a shift of the midline structure was more frequently noticed in the embolic group than in the thrombotic group. Accordingly, the patients with cerebral embolism showed more unfavorable outcome than those with thrombosis. Hyperdense area developed in 40% of cerebral embolism during the period of observation, while in only 2% of cerebral thrombosis. Recurrence of the attack was very common in cerebral embolism. Forty-four percent experienced more than two episodes of cerebral and/or systemic embolization; of these recurrences 51% (27% of all cases) occurred within 2 weeks before and/or after the present episode that caused the admission. The importance of atrial fibrillation as the source of emboli was reemphasized.

Risk of ischemic heart disease in patients with TIA

Abstract: A prospective study was made of the morbidity and mortality from ischemic heart disease in 390 patients with focal TIA caused by atherosclerotic vascular disease. The 5-year cumulative rate of myocardial infarction or sudden death in these patients was 21.0%, a rate only slightly less than that of fatal or nonfatal cerebral infarction (22.7%). Risk factors including diabetes, angina, and ECG abnormalities were associated with an increase in morbidity and mortality from ischemic heart disease. A major factor associated with these cardiac events was the presence of atherosclerotic obstructive or ulcerative lesions in the carotid arteries. These observations indicate that focal TIA caused by carotid atherosclerosis is a predictor not only of cerebral infarction, but also of serious cardiac disease and death.

Crossed Cerebellar Diaschisis in Ischemic Stroke: A Study of Regional Cerebral Blood Flow by 133Xe Inhalation and Single Photon Emission Computerized Tomography

Abstract: Seventy measurements of CBF were performed in 12 stroke patients by 133Xe inhalation and a rapidly rotating single photon emission computerized tomograph. CBF was measured every other day during the acute phase and at 2- and 6-month follow-up visits. A persistent contralateral cerebellar blood flow depression was evident in five patients with severe hemispheric low flow areas, which correlated with large, hypodense lesions on the computerized tomographic scan. In a sixth patient with a small, deep infarct, a transient crossed cerebellar low flow was observed, while the clinical symptoms persisted. It is concluded from this serial study that crossed cerebellar diaschisis is a common finding in completed stroke. It is probably caused by disconnection of the corticopontine pathways, a disconnection that tends to persist. The phenomenon is in fact less variable than the stroke-related CBF changes in the infarcted hemisphere, in which a period of relative hyperemia is frequently seen.

Intracranial Hemorrhage in the Term Newborn

Abstract: • Over a five-year period we identified 22 term newborns with intracranial hemorrhage by computed tomography in an intensive care unit for newborns. Primary subarachnoid hemorrhage (diffuse or focal) was the most common type of hemorrhage. Diffuse subarachnoid hemorrhage was caused either by traumatic delivery or severe hypoxic-ischemic encephalopathy and caused seizures on the first day. Focal subarachnoid hemorrhage was associated with cerebral infarction. Intraventricular hemorrhage was always accompanied by bloody CSF. Somewhat more than half the newborns with intraventricular hemorrhage had a history of traumatic delivery. In the remainder there were no associated risk factors for the hemorrhage. Hemorrhage into the cerebral hemispheres occurred without any identifiable risk factors. Hemorrhage into the cerebellum was associated with traumatic delivery.

Declining incidence and mortality of stroke

Abstract: The incidence and mortality from stroke in Espoo-Kauniainen, Finland, in 1972-73 were compared to the incidence and mortality from stroke in the same area 1978-80. The factors at the acute stage influencing case fatality were also analyzed. A declining trend in age-adjusted incidence of stroke was observed, though failing to reach statistical significance. The greatest decline was seen in the incidence of cerebral hemorrhage in men, with a statistically significant difference. The incidence of subarachnoid hemorrhage also decreased, and in women the decline was significant. There was no decrease at all of the incidence of cerebral infarction. The total mortality displayed no clear declining trend. However, the mortality from cerebral hemorrhage after three months from stroke had gone down from 72% to 59%. The most important factors responsible for increased case fatality were: lowered level of consciousness, cerebral hemorrhage and old age. The case fatality was also higher for women than for men. Previous heart diseases increased the mortality, but hypertension, diabetes, pure myocardial infarction and previous transient ischaemic attacks had no influence on mortality. The cause of decline in the incidence of cerebral hemorrhage might be improved care of hypertension: the decline in the incidence of subarachnoid hemorrhage however remains unclear.

A double blind trial of naloxone in the treatment of acute stroke.

Abstract: Naloxone has been reported to have potential benefit in the treatment of stroke. We evaluated the effect of naloxone in a double-blind trial conducted with 15 stroke patients whose deficits ranged from 8 to 60 hours in duration. All but one patient sustained a cerebral infarction. Neurologic function was assessed before and five minutes after each of two injections given to each patient in a double-blind fashion. The injections consisted of naloxone (0.4 mg in 3 patients and 4.0 mg in 12 patients) and saline. Prior to the trial, samples of plasma were obtained for determination of immunoreactive beta-endorphin for each patient. Four patients showed minimal improvement following injection of naloxone, while five patients exhibited a slightly greater improvement following saline injection. There were no significant elevations of plasma beta-endorphin among stroke patients. We conclude that naloxone may not have a significant therapeutic role for stroke in the clinical setting.

Anticoagulant-related hemorrhage in acute cerebral embolism.

Abstract: Five patients with nonseptic cerebral embolism of cardiac origin are reported in whom early anticoagulant therapy resulted in clinical deterioration or death from frank hemorrhage into the acute infarct. In each patient an initial CT scan excluded the presence of intracerebral hemorrhage and a second CT scan, after clinical deterioration had occurred, documented frank hemorrhage into the infarcted zone. All five patients had large infarctions in the right middle cerebral artery territory and three patients were mildly hypertensive. Four patients received heparin within 36 hours of their stroke and one was on warfarin at time of the embolism. Clinical deterioration occurred after intervals of several hours (2 cases), 5-6 days (2 cases) and 30 days (1 case). In only 2 patients was anticoagulant activity excessive at time of clinical deterioration. This report illustrates the danger of early anticoagulant therapy of acute nonseptic cerebral embolism, particularly in the setting of large infarction.

Cerebrovascular diseases in a fixed population of Hiroshima and Nagasaki, with special reference to relationship between type and risk factors.

Abstract: A study was made of the incidence of cerebrovascular disease, the chronological trends, and the relationship between the disease types and risk factors in 16,491 citizens of Hiroshima and Nagasaki. The subjects underwent medical examination at least once between 1958-74, and were free of cerebrovascular disease at the initial examination. During the 16-year period, 1.162 cases of cerebrovascular disease developed in the study population, with diagnosis definite in 621. By type, there were 108 cases of cerebral hemorrhage, 469 cases of cerebral infarction, 33 cases of subarachnoid hemorrhage, and 11 cases of other unclassifiable types. As a risk factor of cerebral hemorrhage, elevation of systolic and diastolic blood pressure was the most closely related to onset, and left ventricular hypertrophy on electrocardiogram (ECG), and proteinuria were also related. However, a tendency was seen for the risk to be higher when the levels of serum cholesterol were lower. In cerebral infarction, aging like systolic blood pressure, was a most important risk factor. Left ventricular hypertrophy on ECG, proteinuria, and diabetes could also be risk factors. However, the relation to blood pressure, especially diastolic blood pressure, was not so great as in the case of cerebral hemorrhage.

A dynamic concept of middle cerebral artery occlusion and cerebral infarction in the acute state based on interpreting severe hyperemia as a sign of embolic migration.

Abstract: The present study investigates the pathogenesis of focal cerebral hyperemia, its effect on brain tissue and discusses its pathophysiological and therapeutic importance in the light of interpreting severe hyperemia as a sign of arterial reopening probably due to embolic migration Cerebral angiography, serial CT-scans and serial TC99 -scans were performed in a consecutive group of 73 patients with completed stroke all admitted to hospital within 3 days after stroke onset When possible the regional cerebral blood flow (rCBF) was studied with the intracarotid Xe 133 injection method Twenty-nine patients had evidence of middle cerebral artery (MCA) occlusion; rCBF was investigated in 24 Fourteen patients had either occlusion or severe internal carotid artery (ICA) stenosis; rCBF was not measured in these patients Thirty patients had no angiographical evidence of MCA occlusion, ICA occlusion or severe ICA stenosis; rCBF was investigated in 24 Focal hyperemia was observed in 21 patients but exclusively in the group with evidence of MCA occlusion Hence, these 21 patients are typical and representative for the group of patients with evidence of MCA occlusion Hyperemia was found in infarcted as well as in non-infarcted tissue Apparently, it is the severity of the initial ischemic episode and not the hyperemia that determines whether or not tissue necrosis develops Interpreting severe hyperemia as a sign of arterial reopening and embolic migration (evidenced by partial reopening affecting only some MCA branches) reopening had occurred in about 1/3 of the patients with MCA occlusion before they were examined 1 to 4 days after stroke onset Autopsy studies performed in 8 of the patients with MCA occlusion indicate that arterial reopening also takes place in many patients later on (7 of 8) According to this interpretation, hypothetical as it is, the changing position of the embolus is associated with partial or complete reperfusion leading to hyperemia in the initially ischemic brain tissue The hemodynamic basis for appropriate therapy therefore may change from one day to the next in the acute state of stroke due to MCA occlusion

Cerebral blood volume, blood flow, and oxygen metabolism in cerebral ischaemia and subarachnoid haemorrhage: An in-vivo study using positron emission tomography

Abstract: A characteristic sequence of metabolic and haemodynamic changes has been shown to occur in the brain as cerebral perfusion pressure is reduced in experimental animals. Increased cerebral blood volume (CBV) occurs initially, followed by a fall in blood flow (CBF) and, finally, a fall in oxygen metabolism (CMRO2). By measuring CBV, CBF, and CMRO2 with positron emission tomography in patients with vasospasm associated with subarachnoid haemorrhage and in patients with arteriosclerotic occlusion or stenosis of extraparenchymal cerebral arteries, we have demonstrated the presence of similar changes distal to such lesions in man. These findings suggest the presence of a local decrease in perfusion pressure. This study demonstrates the utility of positron emission tomography in the assessment of cerebral circulation and metabolism in man. Measurements of regional CBV must be included for a complete assessment of the dynamics of the cerebral circulation.

Correlation of CT cerebral vascular territories with function: 3. Middle cerebral artery

Abstract: Schematic displays are presented of the cerebral territories supplied by branches of the middle cerebral artery as they would appear on axial and coronal computed tomographic (CT) scan sections. Companion diagrams of regional cortical function and a discussion of the fiber tracts are provided to simplify correlation of clinical deficits with coronal and axial CT abnormalities.

Evidence of vascular disease from CT scanning in late onset epilepsy.

Abstract: The CT scans of 74 patients presenting with late-onset epilepsy not due to cerebral tumour were compared with those of an age and sex-matched control group for evidence of cerebral vascular disease. Changes in the scan indicative of cerebral atrophy (enlarged ventricles and cortical sulci) were seen in similar numbers in both patients and controls. However, the scans revealed a highly significant excess of ischaemic lesions in the epileptic patients, in the form of discrete areas of infarction and low attenuation of the periventricular white matter. These changes, which were only seen in two of the controls, were present in 13 of the epileptic patients. The median age at the onset of epilepsy in the 13 patients with ischaemic lesions was 62 years, and they showed an increased incidence of systemic vascular disease and of abnormal neurological signs. In six of the 13 cases, however, clinical examination was normal and CT scanning provided the only evidence of underlying vascular disease.

Clinical-CT correlations in TIA, RIND, and strokes with minimum residuum.

Abstract: An approach to the controversy of the physiopathology and classification of ischemic stroke is attempted in this study. The computed tomographies (CT) of 88 patients with transient ischemic attacks (TIA), 46 with reversible ischemic neurologic deficits (RIND) and 70 with ischemic strokes with minimum residuum (SMR) are analysed. The incidence of focal ischemic lesions on CT is 25% in TIA and RIND and 35% in SMR, when the study was performed after the first 24 hours. The incidence of cerebral infarction was much lower when the CT was performed within the first 24 hours after the clinical event. No significant differences in size or location of the infarction were found between the different groups. Deep infarctions were smaller than superficial ones. TIA duration correlated neither with the incidence of CT abnormalities nor with the size of the lesions. No correlation was found between doppler or oculoplethysmography abnormalities, clinical groups and CT findings. In reference to the structural lesions that underlie the clinical syndromes, TIA, RIND and SMR should not be considered as different groups.

Determination of Regional Cerebral Blood Flow in Patients With Cerebral Infarction: Use of Fluoromethane Labeled With Fluorine 18 and Positron Emission Tomography

Abstract: • Regional cerebral blood flow (rCBF) was determined using the tissue kinetic of fluoromethane labeled with fluorine 18 and positron emission tomography (PET) in 13 normal subjects and 21 patients with cerebrovascular diseases. The mean brain rCBF was 42.9 ± 4.3 mL/100 g/ min during the resting state. The highest rCBF (60 ± 8 mL/100 g/min) was noted in the mesial occipital region corresponding to cortical area 17. All 17 cases of cerebral ischemic infarcts had depressed rCBF in the hemisphere ipsilateral to the infarct. Every area of decreased density shown in the conventional computed tomograms (CT) was detected on the PET as an area of decreased rCBF (mean rCBF of infarcted area, 14.3 ± 6 mL/100 g/ min). The PET images showed a wider area of depressed rCBF than the region of the anatomic infarct. Five types of remote effects were noted in areas without structural damage: (1) decreased flow in the thalamus and caudate ipsilateral to the infarct; (2) decreased flow in the hemisphere contralateral to the cerebral infarct; (3) decreased flow in the cerebellar hemisphere contralateral to the cerebral infarct; (4) decreased flow in the visual cortex distal to the optic radiation lesion; and (5) decreased flow in the frontal cortex ipsilateral to the infarct. The effects in the contralateral hemisphere and the cerebellum were present only in the acute postictal phase. In four cases of transient ischemic attacks, rCBF was normal. It is concluded that this technique of measuring rCBF is a reliable method of identifying cerebral ischemia and that the determination of the extent of impaired rCBF provides a more accurate assessment of the region of brain dysfunction than CTs.

Brain and plasma proteins in spinal fluid as markers for brain damage and severity of stroke.

Abstract: Forty well-defined acute stroke patients were investigated for some cerebro-spinal fluid (CSF) markers of cerebral damage Myelin-basic protein (MBP), tau-fraction, albumin, IgG and transferrin were analyzed on two early occasions after onset of clinical symptoms Patients with transitory ischaemic attack (TIA) had normal values for MBP both at first and second lumbar puncture Patients with cerebral infarction and haemorrhage had mean MBP concentrations higher than normal at both lumbar punctures In cerebral infarction there was a significant increase in MBP from the first to the second lumbar puncture Patients with intracerebral haemorrhage showed the highest mean MBP values and MBP was markedly elevated already at the first lumbar puncture, suggesting different mechanisms of destruction of nervous tissue in cerebral infarction and bleeding The amount of MBP was also significantly correlated to the visibility of the cerebral lesion at CT-scan and to the short-term outcome of the patients The tau-fraction, indicating damage to grey matter, was higher than normal in the majority of patients with cerebral infarction and TIA The concentration of MBP increases with the extent of brain lesion and a high value indicates a poor short-term prognosis for the patient This study shows that the brain specific MBP in CSF is a useful marker of cerebral damage in acute cerebrovascular disease

Late seizures in patients with internal carotid and middle cerebral artery occlusive disease following ischaemic events.

Abstract: The occurrence of post-infarction epilepsy was investigated in 68 patients with angiographically proven internal carotid artery occlusion and in 56 patients with middle cerebral artery occlusion. Epileptic seizures occurred during follow-up in 9% of the carotid artery group and in 21.4% of the middle cerebral artery group. The different incidence of seizures in the two groups was statistically significant. The physiopathological mechanism of the late post-infarction epilepsy is discussed.