Showing papers on "Cerebral infarction published in 1987"
TL;DR: In stroke patients, the S-100 and neuron-specific enolase concentrations may reflect the extent of brain damage and could be useful in selecting patients with major stroke for more aggressive treatment during the acute phase.
Abstract: The development of a radioimmunoassay for S-100 protein is described. This method was used in combination with a recently developed radioimmunoassay for neuron-specific enolase in cerebrospinal fluid and serum from 47 patients with cerebral infarction, transient ischemic attack, intracerebral hemorrhage, subarachnoid hemorrhage, and head injury. In cerebrospinal fluid, increased concentrations of both S-100 and neuron-specific enolase were found after large infarcts, whereas after small infarcts and transient ischemic attacks, only neuron-specific enolase increased. The increased concentrations of S-100 and/or neuron-specific enolase were noted 18 hours to 4 days after cerebral infarction and transient ischemic attacks. Cerebrospinal fluid concentrations of these proteins also reflected the severity of the disease in patients with intracerebral hematoma, subarachnoid hemorrhage, or head injury. Temporal changes in serum S-100 and neuron-specific enolase concentrations reflected the clinical course in 4 patients. In stroke patients, the S-100 and neuron-specific enolase concentrations may reflect the extent of brain damage and could be useful in selecting patients with major stroke for more aggressive treatment during the acute phase.
491 citations
TL;DR: A significant relationship was found between the PET measurements of cerebral hemodynamics and the arteriographic circulation pattern and the role of hemodynamic factors in the pathogenesis and treatment of cerebrovascular disease cannot be determined from the severity of carotid artery disease alone.
Abstract: Although the presence of a hemodynamically significant carotid artery lesion is commonly used as an indicator of impaired cerebral circulation, the effect of such lesions on cerebral perfusion pressure and cerebral blood flow has never been determined accurately. We used positron emission tomography (PET) to study 19 patients with unilateral hemodynamically significant carotid artery disease (greater than 66% diameter reduction) and no evidence of cerebral infarction. According to PET measurements in the cerebral hemisphere distal to the lesion, 7 patients had normal cerebral hemodynamics, 8 had reduced perfusion pressure with normal blood flow, and 4 had reduced blood flow. Neither the percent stenosis nor the residual lumen diameter in the carotid artery was a reliable indicator of the hemodynamic status of the cerebral circulation. However, a significant relationship was found between the PET measurements of cerebral hemodynamics and the arteriographic circulation pattern (p = 0.006). The role of hemodynamic factors in the pathogenesis and treatment of cerebrovascular disease cannot be determined from the severity of carotid artery disease alone.
453 citations
TL;DR: In a consecutive series of 515 first-ever strokes in a community-based study of stroke that combined prompt clinical assessment by a study neurologist with a high rate of confirmed pathologic diagnosis, 108 cases (21%) had a lacunar syndrome.
Abstract: In a consecutive series of 515 first-ever strokes in a community-based study of stroke that combined prompt clinical assessment by a study neurologist with a high rate of confirmed pathologic diagnosis, 108 cases (21%) had a lacunar syndrome. A computed tomography (CT) scan was performed in 104 (96%) of these cases. Only 3 cases had primary intracerebral hemorrhage, and another 3 had "inappropriate" areas of infarcts were seen in 34 of the remaining 98 (35%) CT scans. The crude annual incidence of lacunar infarction was 0.33/1,000. There was no excess risk among men. The case fatality rates were 1% at 1 month and 9.8% at 1 year. The rate of recurrent strokes was 11.8% in the first year. Among patients surviving 1 year, 66% were capable of independent existence.
428 citations
TL;DR: Thirty (2.5%) of 1200 consecutive patients with a first stroke had a spontaneous dissection with occlusion of the cervical internal carotid artery (ICA), and during follow-up, 12 survivors had a good recovery and early reopening of the occluded ICA, and 11 had a poor recovery usually without reopens of the ICA.
Abstract: • Thirty (2.5%) of 1200 consecutive patients with a first stroke had a spontaneous dissection with occlusion of the cervical internal carotid artery (ICA). A suggestive picture with ipsilateral headache and oculosympathetic paresis was uncommon (17%), so that diagnosis was uncertain before angiography. Seven patients died within one week. During follow-up (mean, 3.2 years) with sequential Doppler ultrasonographic testing, 12 survivors had a good recovery and early reopening of the occluded ICA, and 11 had a poor recovery usually without reopening of the ICA. Recurrence of a dissection occurred in only one patient. Large infarcts causing death or a severe disability were associated with an ICA thrombus and distal emboli; the organization of this intraluminal thrombosis may explain the absence of reopening in these cases while resorption of the intramural hematoma developed. Early heparin sodium therapy may help prevent intraluminal clotting without carrying an important risk of extending the dissection, but its clinical benefit remains unproven. Contrary to current opinions, ICA dissection with occlusion causing cerebral infarction may often carry a severe prognosis.
311 citations
TL;DR: The volumetric assessment allows an objective assessment of drug therapy and management strategies in the treatment of cerebral infarction and can readily detect the increase in amount of structural damage in cerebral cortex following a transient episode of hypotension.
Abstract: A method for the volumetric assessment of early cerebral infarction, together with its statistical and biological validation, is described. In halothane anaesthetised rats the stem of the right middle cerebral artery was occluded and 3 hours later (with full monitoring of respiratory and cardiovascular status) the animals were killed by perfusion fixation. In normotensive normocapnic animals the volume of infarction was 52 +/- 4 mm3 in the cerebral cortex and 21 +/- 1 mm3 in the corpus striatum. The reproducibility of the volumetric assessment was found to be excellent (coefficient of correlation 0.995 on 18 replicate measurements). The minimum number of stereotactic levels which must be assessed to yield accurate volumetric measurements of infarction is 8. The method is sensitive at detecting alterations in the amount of infarction. For example, it can readily detect the increase in amount of structural damage in cerebral cortex following a transient episode of hypotension. This approach allows an objective assessment of drug therapy and management strategies in the treatment of cerebral infarction.
310 citations
TL;DR: The major determinants for long-term mortality in patients with acute stroke followed for 2 to 8 years were low level of activity at hospital discharge, advanced age, male sex, heart disease, and hypertension.
Abstract: We evaluated factors affecting mortality and quality of life in 1,013 patients with acute stroke followed for 2 to 8 years. In cerebral infarction, the major determinants for short-term mortality were impaired consciousness, leg weakness, and increasing age. The major determinants for long-term mortality were low level of activity at hospital discharge, advanced age, male sex, heart disease, and hypertension.
243 citations
TL;DR: It is concluded that these lesions are present in AF patients without history of cerebrovascular events and occur more frequently than in controls without atrial fibrillation.
Abstract: Atrial fibrillation (AF) is associated with an increased risk of stroke. In AF patients with acute stroke, cerebral computed tomography (CT) often reveals old asymptomatic infarcts. To investigate the frequency of such lesions, 29 AF patients and 29 controls in sinus rhythm without history of cerebrovascular disease were CT scanned. Fourteen patients with AF (48%) had abnormal CT scans with areas of low density with sharp demarcation from surrounding tissue compared with 8 patients in sinus rhythm (28%) (p greater than 0.10). However, the number of abnormal areas with apparent tissue loss was significantly higher in the AF group (39 lesions) compared with the control group (16 lesions) (p = 0.033). The lesions were mainly located in the cortex with no significant difference in lesion size between AF patients and controls. The abnormal areas probably reflected small, clinically silent infarcts. We conclude that these lesions are present in AF patients without history of cerebrovascular events and occur more frequently than in controls without atrial fibrillation.
184 citations
TL;DR: A small but definite beneficial effect of hyperglycemia in this end-arteriolar thrombotic infarction model is possibly attributable to improved local energy metabolism at the periphery of the lesion during the early period of lesion expansion.
Abstract: Although hyperglycemia is known to exacerbate neuronal injury in the setting of reversible brain ischemia, its effect on irreversible thrombotic infarction is less well understood. In this study, unilateral thrombotic infarction was induced photochemically in the parietal cortex of Wistar rats. Seven days later, brains were perfusion-fixed for light microscopy. Infarct areas were measured by computer-assisted planimetry on multiple coronal sections at 250-micron intervals; these data were integrated to yield infarct volumes. Fasted, normoglycemic rats were compared with hyperglycemic rats that had received 1.2-1.5 ml of 50% dextrose i.p. 15 minutes prior to the induction of infarction. Infarct volume averaged 12.5 +/- 4.0 mm3 (mean +/- SD) in rats (n = 14) with plasma glucose levels of 72-184 mg/dl; this differed statistically from the average volume of 9.3 +/- 3.3 mm3 observed in rats (n = 13) with elevated plasma glucose (range 264-607 mg/dl). Spearman rank correlation analysis confirmed a significant correlation of larger infarct volumes with lower plasma glucose levels. In contrast, rats receiving mannitol i.p. to produce an osmotic load comparable with that of the dextrose-pretreated animals showed larger infarct volumes than saline-treated controls. The small but definite beneficial effect of hyperglycemia in this end-arteriolar thrombotic infarction model is possibly attributable to improved local energy metabolism at the periphery of the lesion during the early period of lesion expansion.
176 citations
TL;DR: The clinical and pathologic findings in 42 autopsy proved cases of cerebral infarction from cancer-associated non-bacterial thrombotic endocarditis were reviewed, and early diagnosis and vigorous treatment of non-Bacterial end Carditis may prevent severe neurologic disability.
174 citations
TL;DR: The findings show that hyperglycemia increases brain damage during transient ischemia by conversion of selective neuronal injury into cerebral infarction.
164 citations
TL;DR: In the present study there was no prophylactic effect of high-dose ASA after cerebral infarction and the risk of transient ischemic attack and myocardial infarctions was not reduced in the ASA group.
Abstract: Within 3 weeks of the event, 505 patients with cerebral infarction, minor or major stroke, were randomly assigned to treatment with acetylsalicylic acid (ASA) 1.5 g/day or placebo in a double-blind clinical trial with a follow-up of 2 years in all patients. Primary events were considered to be recurrent stroke or death; secondary events, myocardial infarction and transient ischemic attack. There was no difference in stroke recurrence rate in the ASA and placebo groups (12 and 13%, respectively), nor was there any significant difference in the rate of recurrent stroke or death, first event counted (23% in the ASA and 22% in the placebo group). The risk of transient ischemic attack and myocardial infarction was not reduced in the ASA group. In the present study there was no prophylactic effect of high-dose ASA after cerebral infarction. A compilation of the major trials of ASA after transient ischemic attack and cerebral infarction is presented.
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TL;DR: The findings are preliminary and will require further large-scale clinical and epidemiological analyses to substantiate their roles as causal factors or potentiators of stroke.
Abstract: Alcohol might contribute to stroke in several ways: induction of cardiac arrhythmias and cardiac wall motion abnormalities which predispose to cerebral embolism, induction of hypertension, enhancement of platelet aggregation and activation of the clotting cascade, and reduction of cerebral blood flow by stimulation of cerebral vascular smooth muscle contraction or by altering cerebral metabolism While these pathophysiological mechanisms have gained enthusiastic experimental and theoretical support, the findings are preliminary and will require further large-scale clinical and epidemiological analyses to substantiate their roles as causal factors or potentiators of stroke Documentation of measurable platelet and coagulation cascade abnormalities reported in healthy volunteers who have ingested alcohol will need to be confirmed on a broader scale in stroke patients with recent ethanol consumption The risk of stroke in those with alcohol-induced atrial fibrillation and cardiomyopathy must be ascertained for the general population While the experimental evidence is exciting and provocative, epidemiological evidence also suggests a link between alcohol consumption and stroke Regular alcohol ingestion is associated with hypertension, fatal and nonfatal intracranial hemorrhage, cerebral infarction, and increased risk of death from stroke Recent, less stringently controlled studies suggest that alcohol consumption is a risk factor for cerebral infarction in young adults with occasional ethanol intoxication and middle-aged women and young men with occasional alcohol intoxication and regular heavy drinking Alcohol may also be a risk factor for subarachnoid hemorrhage
TL;DR: In 242 neurologically symptomless patients with at least one non-occlusive carotid stenosis on ultrasonography (continuous wave doppler and echotomography-B mode imaging), stenoses of greater than 50% were associated with more ischaemic events than were lesser degrees of narrowing.
TL;DR: In this paper, four patients with recurrent stroke and multi-infarct dementia were presented in whom the dementia was progressive and severe, and three of the patients developed the dementia during the course of an illness which was punctuated by repeated episodes of cerebral infarction demonstrated by computed tomographic (CT) scans.
Abstract: Four patients with recurrent stroke and multi-infarct dementia are presented in whom the dementia was progressive and severe. Three of the patients developed the dementia during the course of an illness which was punctuated by repeated episodes of cerebral infarction demonstrated by computed tomographic (CT) scans. The fourth patient presented with an illness dominated by progressive and deteriorating higher mental functions, which culminated in a major stroke 18 months later. Three patients fulfilled the American Rheumatism Association (ARA) criteria for the classification of systemic lupus erythematosus, the fourth had a 'lupus-like' disease. All had livedo reticularis, severe migraines, and also demonstrated antibodies to phospholipids. All four patients suffered deep vein thromboses.
TL;DR: Patients who had no areas of infarction on serial CT scans typically had a CMRO2 and CMRL, which can be obtained at the bedside and can indicate the presence of an evolving ischemic infarct after head injury.
Abstract: Cerebral ischemia is a common mechanism of secondary brain injury following severe head injury. The cerebral metabolic rate of oxygen (CMRO2) and of lactate (CMRL), as well as cerebral blood flow (CBF) were measured daily for 5 days after head injury in 44 comatose head-injured patients to determine if metabolic changes could identify the patients who would develop cerebral infarction. Of 41 patients whose CBF remained at levels regarded as adequate to prevent infarction (CBF greater than or equal to 0.2 ml/gm/min), the six who showed a cerebral infarction on computerized tomography (CT) scans exhibited characteristic cerebral metabolic patterns: a CMRO2 of less than 0.6 mumol/gm/min on one or more of the days monitored, and markedly elevated cerebral lactate production (CMRL less than -0.06 mumol/gm/min) on Days 1 and/or 2 after injury. Patients who had no areas of infarction on serial CT scans typically had a CMRO2 and CMRL can be obtained at the bedside and can indicate the presence of an evolving ischemic infarct after head injury.
TL;DR: Stroke in the posterior cerebral artery territory was found in a heterogeneous group of patients, although embolism was the most common stroke mechanism, and six patients died.
Abstract: To clarify the clinical features and mechanism of infarction in the posterior cerebral artery territory, we investigated 35 consecutive patients who presented with homonymous visual field defects and occipital infarction documented by computed tomography. Cerebral angiographic findings in 23 patients, and the clinical features of rare transient ischemic attacks and maximal deficit occurring at stroke onset, were consistent with embolism of the posterior cerebral artery. Visual field defects were the only neurological abnormality in 17 patients; the remainder had additional findings. Three patients had a major brainstem stroke. Stroke in the posterior cerebral artery territory was found in a heterogeneous group of patients, although embolism was the most common stroke mechanism. Several distinct patient groups were identified: cardiac source embolism (10 patients), vertebrobasilar atheroma with local embolism (6), migraine (5), systemic illness with presumed coagulopathy (3), and "unknown source embolism" after negative cardiac investigation (11 patients). During follow-up, 26 patients had no further neurological events (the majority on anticoagulation or antiplatelet treatment), 3 suffered new strokes, and 6 died.
TL;DR: In four preterm infant brains, four contained early intraparenchymal haemorrhage supero‐lateral to the angles of the lateral ventricles which were associated with large germinal layer and intraventricular haem orrhage, the anatomical distribution and histological features suggested that they resulted from venous infarction.
Abstract: Haemorrhage into cerebral parenchymal tissue supero-lateral to the angles of the lateral ventricles is a major cause of death and disability in preterm infants. It is frequently associated with germinal layer and intraventricular haemorrhage but the mechanism by which parenchymal haemorrhage occurs is uncertain. Recent studies have suggested that it is due to bleeding into tissue previously damaged by ischaemia following cerebral hypoperfusion. We have studied 68 preterm infant brains, of which four contained early intraparenchymal haemorrhage supero-lateral to the angles of the lateral ventricles which were associated with large germinal layer and intraventricular haemorrhages. The anatomical distribution and histological features of these haemorrhages suggested that they resulted from venous infarction and that the venous drainage of the periventricular tissues had been obstructed by the germinal layer haemorrhages. In these four infants, bleeding into parenchymal tissues could be regarded as a complication of germinal layer and intraventricular haemorrhage rather than of cerebral hypoperfusion.
TL;DR: The data suggest that, within 48 hours of the clinical onset of stroke, the ischemic cortex is already reperfused in one third of patients and, despite evidence of an increased CMRGlc/CMRo2 ratio, acidosis is not evident in the reperfuse regions.
Abstract: Twelve patients were studied within 48 hours of stroke using positron emission tomography to determine cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction, cerebral blood volume, cerebral pH (CpH), and cerebral metabolic rate for glucose (CMRGlc), the last calculated using published normal rate constants (CMRGlc[N]) and those for severe ischemia. In these studies, a cortical region of severe ischemia (I) was outlined, its metabolic and perfusion properties evaluated, and its length measured. The contralateral uninvolved cortical rim (C) in these patients and the cortical rim in 5 older normal patients were used for comparison. The length of region I correlated with the neurological deficit measured independently by a clinical scoring method. The 12 patients fell into two groups: Group I (8 patients), whose CBF in I was 9.3 +/- 2.5 ml/100 gm/min (mean +/- SEM) and was in every patient lower than that in C (33.1 +/- 2.2), and Group 2 (4 patients), whose CBF in I was 42.1 +/- 8.5 ml/100 gm/min and was in every case higher than that in C (28.2 +/- 1.5). In Group I, region I showed a CMRGlc(N)/CMRO2 ratio of 0.22 +/- 0.06 and a CpH of 6.83 +/- 0.06. In Group 2, the same ratio in the region I was 0.58 +/- 0.09 and the CpH was 7.12 +/- 0.05. The CMRGlc (N)/CMRO2 ratio for the contralateral hemisphere was comparable in the two groups. Our data suggest that, within 48 hours of the clinical onset of stroke, the ischemic cortex is already reperfused in one third of patients. Those ischemic regions with persistent hypoperfusion appear acidotic, whereas in the reperfused regions, despite evidence of an increased CMRGlc/CMRO2 ratio, acidosis is not evident. The implications of these findings for therapies proposed in acute human cerebral ischemia are discussed.
TL;DR: An analysis was performed of 2,168 consecutive stroke patients who were examined by computed tomography and entered into a hospital-based stroke registry in Akita Prefecture, Japan, finding that total strokes increased in the winter; this seasonal difference was confined to cerebral hemorrhage.
Abstract: An analysis was performed of 2,168 consecutive stroke patients who were examined by computed tomography and entered into a hospital-based stroke registry in Akita Prefecture, Japan. The occurrence of cerebral hemorrhage, cerebral infarction, and subarachnoid hemorrhage was 30, 55, and 14%, respectively. Age-specific rates of subarachnoid hemorrhage were higher in women than men; other types of stroke showed a preponderance in men. Total strokes increased in the winter; this seasonal difference was confined to cerebral hemorrhage. Putaminal hemorrhages predominated in the younger age groups; thalamic hemorrhage and cerebellar hemorrhage were predominant in the older age groups. The increased accuracy of the diagnosis of stroke subtypes by the use of computed tomography in this study is in contrast to other community-based epidemiologic studies that have relied solely on clinical diagnosis. This increased accuracy is seen to be the reason that new ratios of stroke subtype incidence have been identified.
TL;DR: The latency of wave V of the auditory brain-stem response was within normal limits in the majority of the patients studied regardless of the site of their cortical lesion, and no MLR asymmetries were demonstrated.
TL;DR: Investigation of acute confusional state and acute agitated delirium after infarction in the right middle cerebral artery territory found that cognitive and integrative functions become defective, reflecting disturbance of global attention, and is closely correlated with other right hemispheric global and directed attentional disorders.
Abstract: • Acute confusional state (ACS) and acute agitated delirium (AAD) after infarction in the right middle cerebral artery territory were investigated in 41 consecutive patients. Acute confusional state was diagnosed on the basis of the results of the Mini-Mental State Examination, and AAD was distinguished from ACS by the characteristic behavioral abnormality. Of these patients, 25 presented with ACS, and six with AAD. Acute confusional state and AAD are common syndromes after infarction of the right middle cerebral artery, and infarction in this territory, therefore, has an important clinical implication as a cause of these syndromes. Acute confusional state is a disorder in which cognitive and integrative functions become defective, reflecting disturbance of global attention, and is closely correlated with other right hemispheric global and directed attentional disorders. It is linked to damage to the right frontostriatal region and is associated with lesion volume. In comparison, AAD is a disorder in which emotional and affective components are predominantly altered. None of the right hemispheric behavioral syndromes correlated with AAD. It may be related to damage to the right middle temporal gyrus.
TL;DR: The records of 4874 patients, aged 50 years and younger, who were seen at the Mayo Clinic, Rochester, Minn, from 1976 to 1980, and had received a diagnosis of migraine, migraine equivalent, or vascular headache are reviewed; 25% of all incidence cases of cerebral infarction were migraine associated.
Abstract: • We reviewed the records of 4874 patients, aged 50 years and younger, who were seen at the Mayo Clinic, Rochester, Minn, from 1976 to 1980, and had received a diagnosis of migraine, migraine equivalent, or vascular headache. Twenty patients (16 females and four males) who had migraine-associated brain infarctions are described. The areas of infarction and corresponding angiographic abnormalities were most frequently in the distribution of the posterior cerebral artery. During a mean follow-up period of seven years, two patients had a second brain infarction. At last follow-up examination, 18 of the 20 patients had minimal or no functional impairment. For the period 1976 to 1979, we reviewed the available data on cerebral infarction for the Rochester, Minn, population aged 50 years or younger; 25% of all incidence cases of cerebral infarction were migraine associated.
TL;DR: MRI is useful in following the evolution of strokes and distinguishing acute and chronic infarcts without contrast agents, and CT is the method of choice to rule out intracerebral bleeding, but MRI is more specific in later stages of hemorrhage.
Abstract: We compared MRI and CT in a study of 175 patients; 87 infarcts within a week, 40 from 1 to 40 weeks, 25 a year after onset, and 23 hemorrhages, 18 within 2 weeks and 5 in 4 to 8 weeks. Fifty-nine infarcts and eight hemorrhages had sequential scanning. MRI is more sensitive than CT in the early detection of cerebral infarcts. CT is the method of choice to rule out intracerebral bleeding, but MRI is more specific in later stages of hemorrhage. Periventricular hyperintensity is seen more frequently with diabetes than without. Hyperintense white matter patches are often unrelated to clinical events. MRI is useful in following the evolution of strokes and distinguishing acute and chronic infarcts without contrast agents.
TL;DR: The occurrence of anticardiolipin antibodies in patients with multiple cerebral infarctions who do not have evidence of a systemic vasculitis or inflammatory condition suggests that this association may be more common than previously recognized.
Abstract: Antibodies to negatively charged phospholipids including cardiolipin have been recognized in the sera of patients with systemic lupus erythematosus and other disorders. We report 4 patients who experienced cerebral infarctions and dementia in association with anticardiolipin antibodies. These patients did not have the characteristic lupus anticoagulant or systemic lupus erythematosus. The occurrence of anticardiolipin antibodies in patients with multiple cerebral infarctions who do not have evidence of a systemic vasculitis or inflammatory condition suggests that this association may be more common than previously recognized. It may be useful to test for the presence of anticardiolipin antibodies in patients who have unexplained cerebral infarctions.
TL;DR: This survey will briefly review these studies in the context of current therapy for the following: prevention of stroke after transient ischemic attack or stroke, acute cerebral infarction and progressing stroke, cardiogenic embolism to the brain, cerebral arteritis, intracerebral hematoma, arteriovenous malformation.
Abstract: THE past several years have witnessed a flurry of prospective clinical trials of new treatments for transient ischemic attack, cerebral infarction, and cerebral hemorrhage, and the results have markedly altered our management of these conditions (Table 1). Furthermore, another generation of Phase II and controlled prospective studies (based on pilot studies) are planned or under way (Table 2). This survey will briefly review these studies in the context of current therapy for the following: prevention of stroke after transient ischemic attack or stroke, acute cerebral infarction and progressing stroke, cardiogenic embolism to the brain, cerebral arteritis, intracerebral hematoma, arteriovenous malformation, . . .
TL;DR: In this rat model, TPA increases blood flow with subsequent improvement in the EEG recording after thromboembolic stroke without evidence of systemic fibrinolysis, suggesting that Intravenous TPA may be useful in the treatment of acute stroke in man.
Abstract: ✓ Systemic fibrinolytic therapy for acute stroke is no longer recommended because of resulting systemic fibrinolysis and the risk of intracerebral hemorrhage. Human tissue-type plasminogen activator (TPA) is a native enzyme that converts plasminogen to plasmin with subsequent clot lysis. The affinity for plasminogen is increased several-fold when the substrate is bound to fibrin. At appropriate dosage, “clot-specific” throm-bolysis may be achieved at the surface of the thrombus without creating systemic fibrinolysis. The authors designed a study to evaluate the effect of intravenous TPA administered 2 hours after acute thromboembolic stroke in rats. This time course was chosen to simulate an analogous clinical situation. Middle cerebral artery embolic stroke was caused by intracarotid injection of 0.025 cc of human blood clot in 16 rats. Regional cerebral blood flow, measured by the hydfogen clearance technique, and electroencephalographic (EEG) recordings were obtained every 30 minutes for 5 hours after ...
TL;DR: In premature neonates with very water, low-intensity white matter on T1-weighted images, ultrasound was better than both computed tomography and magnetic resonance (MR) imaging in depicting parenchymal changes of infarction or edema, but after 37 weeks gestation, MR imaging was superior.
Abstract: Eighty-five infants, 82 of whom were 29-44 weeks postconceptional age, were imaged with a 0.6-T magnet. Eight infants had cerebral infarction. In premature neonates with very water, low-intensity white matter on T1-weighted images, ultrasound was better than both computed tomography and magnetic resonance (MR) imaging in depicting parenchymal changes of infarction or edema. However, after 37 weeks gestation, MR imaging was superior. Cerebral atrophy, present in seven infants, was consistent with subarachnoid space widths of 7 mm or more, or subarachnoid space widths of 5-6 mm with ventricular/brain ratios of 0.36 or greater. Delayed myelination was seen in a total of 18 infants with histories of hypoxic-ischemic insult. MR imaging shows promise in the neonatal period. It facilitates recognition of infarcts in full-term infants and may be used to predict abnormal neurologic outcome in infants who have initial delayed myelination.
TL;DR: Reduced uptake was observed in the left cerebral hemisphere contralateral to the cerebellar infarction with the most marked reduction in theleft premotor region, which might be explained by the functional depression of cerebello-ponto-thalamo-cerebral pathways.
TL;DR: The features of strokes caused by embolism from the vertebral artery (VA) to the posterior cerebral artery (PCA) are reported in 12 patients (“local” or “artery-to-artery embolisms”).
Abstract: The features of strokes caused by embolism from the vertebral artery (VA) to the posterior cerebral artery (PCA) are reported in 12 patients ("local" or "artery-to-artery embolism"). Occipital infarction occurred with prominent, fluctuating brainstem ischemic symptoms in six; with minor, transient brainstem symptoms in five; and with basilar artery occlusion in one. Visual field abnormalities were found on initial examination in eight and several days after the onset of brainstem symptoms in four. Radiographic studies in 11 identified extracranial (5 patients) or intracranial (3 patients) VA disease, or occlusion of both segments (3 patients) as sources of emboli to the PCA. Mural thrombus in the VA or embolic occlusion of distal branches of the PCA was visualized in five.
TL;DR: It is suggested that monocytes may affect the endothelium, perhaps disturbing the so-called blood-brain barrier to proteins, in stroke-prone spontaneously hypertensive rats.
Abstract: We studied ultrastructurally cerebral perforating arteries in 60 stroke-prone spontaneously hypertensive rats (SHRSP), which were sequentially killed at 4-52 weeks of age before showing symptoms of stroke. Another 24 SHRSP were killed soon after they showed symptoms of cerebral infarction. The initial vascular lesions observed in the asymptomatic group included focal cytoplasmic necrosis in the outer layers of the media. This change progressed to widespread medial necrosis with time. In the infarction group, numerous monocytes were seen adhering to the endothelium of the arteries having advanced medial damage. Following the adherence of monocytes to the endothelium, large amounts of plasma components were visible in the arterial wall. The accumulation of the plasma components (especially fibrin) thickened the wall, narrowed the lumen, and resulted in occlusion. These results suggest that monocytes may affect the endothelium, perhaps disturbing the so-called blood-brain barrier to proteins. The monocytes may therefore be closely related to the occurrence of arterial occlusion with resultant cerebral infarction.