Evolution Of Cerebral Infarction Research Articles

Neuroimaging for the Clinician

Modern neuroimaging has revolutionized the practice of neurology by allowing visualization and monitoring of evolving pathophysiologic processes. High-resolution magnetic resonance imaging (MRI) can now resolve structural abnormalities on a near-cellular level. Advances in functional imaging can assess the in vivo metabolic, vascular, and functional states of neuronal and glial populations in real time. Given the high density of data obtained from neuroimaging studies, it is essential for the clinician to take an active role in understanding the nature and significance of imaging abnormalities. This chapter reviews computed tomography and MRI techniques (including angiography and advanced sequences), specialized protocols for investigating specific diagnoses, risks associated with imaging, disease-specific imaging findings with general strategies for interpretation, and incidental findings and artifacts. Figures include computed tomography, T1- and T2-weighted signal intensity, diffusion-weighted magnetic resonance imaging, magnetic resonance spectroscopy, imaging in epilepsy and dementia, extra-axial versus intra-axial lesions, typical lesions of multiple sclerosis, spinal imaging, spinal pathology, vascular pathology, intracranial hemorrhage, and common imaging artifacts. Tables list Hounsfield units, patterns of enhancement from imaging, advanced techniques in imaging, magnetic resonance imaging sequences, and the evolution of cerebral infarction and intraparenchymal hemorrhage on magnetic resonance imaging. This chapter contains 213 references.

Neuroimaging for the Clinician

Modern neuroimaging has revolutionized the practice of neurology by allowing visualization and monitoring of evolving pathophysiologic processes. High-resolution magnetic resonance imaging (MRI) can now resolve structural abnormalities on a near-cellular level. Advances in functional imaging can assess the in vivo metabolic, vascular, and functional states of neuronal and glial populations in real time. Given the high density of data obtained from neuroimaging studies, it is essential for the clinician to take an active role in understanding the nature and significance of imaging abnormalities. This chapter reviews computed tomography and MRI techniques (including angiography and advanced sequences), specialized protocols for investigating specific diagnoses, risks associated with imaging, disease-specific imaging findings with general strategies for interpretation, and incidental findings and artifacts. Figures include computed tomography, T1- and T2-weighted signal intensity, diffusion-weighted magnetic resonance imaging, magnetic resonance spectroscopy, imaging in epilepsy and dementia, extra-axial versus intra-axial lesions, typical lesions of multiple sclerosis, spinal imaging, spinal pathology, vascular pathology, intracranial hemorrhage, and common imaging artifacts. Tables list Hounsfield units, patterns of enhancement from imaging, advanced techniques in imaging, magnetic resonance imaging sequences, and the evolution of cerebral infarction and intraparenchymal hemorrhage on magnetic resonance imaging. This review contains 12 figures, 6 tables, and 213 references.

Neuroimaging for the Clinician

Modern neuroimaging has revolutionized the practice of neurology by allowing visualization and monitoring of evolving pathophysiologic processes. High-resolution magnetic resonance imaging (MRI) can now resolve structural abnormalities on a near-cellular level. Advances in functional imaging can assess the in vivo metabolic, vascular, and functional states of neuronal and glial populations in real time. Given the high density of data obtained from neuroimaging studies, it is essential for the clinician to take an active role in understanding the nature and significance of imaging abnormalities. This chapter reviews computed tomography and MRI techniques (including angiography and advanced sequences), specialized protocols for investigating specific diagnoses, risks associated with imaging, disease-specific imaging findings with general strategies for interpretation, and incidental findings and artifacts. Figures include computed tomography, T1- and T2-weighted signal intensity, diffusion-weighted magnetic resonance imaging, magnetic resonance spectroscopy, imaging in epilepsy and dementia, extra-axial versus intra-axial lesions, typical lesions of multiple sclerosis, spinal imaging, spinal pathology, vascular pathology, intracranial hemorrhage, and common imaging artifacts. Tables list Hounsfield units, patterns of enhancement from imaging, advanced techniques in imaging, magnetic resonance imaging sequences, and the evolution of cerebral infarction and intraparenchymal hemorrhage on magnetic resonance imaging. This chapter contains 213 references.

Neuroimaging for the Clinician

Modern neuroimaging has revolutionized the practice of neurology by allowing visualization and monitoring of evolving pathophysiologic processes. High-resolution magnetic resonance imaging (MRI) can now resolve structural abnormalities on a near-cellular level. Advances in functional imaging can assess the in vivo metabolic, vascular, and functional states of neuronal and glial populations in real time. Given the high density of data obtained from neuroimaging studies, it is essential for the clinician to take an active role in understanding the nature and significance of imaging abnormalities. This chapter reviews computed tomography and MRI techniques (including angiography and advanced sequences), specialized protocols for investigating specific diagnoses, risks associated with imaging, disease-specific imaging findings with general strategies for interpretation, and incidental findings and artifacts. Figures include computed tomography, T1- and T2-weighted signal intensity, diffusion-weighted magnetic resonance imaging, magnetic resonance spectroscopy, imaging in epilepsy and dementia, extra-axial versus intra-axial lesions, typical lesions of multiple sclerosis, spinal imaging, spinal pathology, vascular pathology, intracranial hemorrhage, and common imaging artifacts. Tables list Hounsfield units, patterns of enhancement from imaging, advanced techniques in imaging, magnetic resonance imaging sequences, and the evolution of cerebral infarction and intraparenchymal hemorrhage on magnetic resonance imaging. This review contains 12 figures, 6 tables, and 213 references.

Morphometrical evaluation of triflusal in brain infarction.

MCA occlusion in animals is a common model for experimental stroke. In previous studies we have shown that one of the factors, which influence evolution of an infarct is microthrombosis in the area of infarction and in the surrounding brain tissue. The present study was undertaken for assessment of the number of microthrombi and of the size of brain infarcting in rats treated with the antiaggregatory substance Triflusal. 7 groups of Sprague-Dawley rats, each group consisting of 6 animals, underwent transsphenoidal MCA occlusion. The animals received Triflusal in various amounts from day 2 till day 6. At day 7 animals were decapitated and the brains were fixed in formaldehyde. The brain was dissected at the level of the optic chiasm and embedded in paraffin. Fresh microthrombi were detected py PTAH (Phosphotungstic acid hematoxylin) staining. In each animal the hemisphere with the ischemic lesion as well as the contralateral hemisphere were examined. The area of both hemispheres was calculated by subtraction of the ventricle area from the total brain area of a section. Infarct was defined as the region of necrosis which was sharply demarcated from normal brain. The infarcted area was planimetrically measured to obtain a ratio of infarcted to normal brain. A correlation between the effect of Triflusal, number of microthrombi and size of the infarcted area could be demonstrated. The pathogenetic role of the microthrombi in the evolution of cerebral infarction as well as the effect of Triflusal in different dosages on the number of microthrombi could be clearly assessed by quantitative morphometry.

Evolution of cerebral infarction: MRI appearance with pathophysiological correlation

Craniopharyngiomas represent one of the major challenges of neurosurgery. Surgical management of craniopharyngiomas classically required various transcranial approaches with the transsphenoidal route reserved for very selected cases. With the widespread use of endoscopes in endonasal surgery in the past decade, the extended endoscopic endonasal transtuberculum and transplanum approaches have been proposed as an alternative surgical route for removal of different types of suprasellar tumors, including solid craniopharyngiomas in patients with normal pituitary function and small sella.A detailed report is presented of the technique used by the authors for the endoscopic endonasal approach for the resection of craniopharyngiomas. For each type of craniopharyngioma, hints and anatomic “main landmarks” are provided throughout each step of the procedure.The endoscopic endonasal approach offers advantages in the management of craniopharyngiomas that historically have been approached via the transsphenoidal route (i.e., purely intrasellar or intra-suprasellar infradiaphragmatic, preferably cystic lesions in patients with panhypopituitarism). Use of the “extended” endoscopic endonasal approach overcomes the limits of the transsphenoidal route to the sella enabling the management of different purely suprasellar and retrosellar cystic/solid craniopharyngiomas, regardless of the sellar size or pituitary function.

Modification of focal cerebral ischemia by prostacyclin and indomethacin.

✓ The object of this investigation was to study the effects of prostacyclin (PGI2), with and without indomethacin, upon the evolution of cerebral infarction in the cat. Thirty-five fasted adult cats, lightly anesthetized with nitrous oxide, underwent right middle cerebral artery (MCA) occlusion. Eleven cats received an intracarotid infusion of 10 mg/ml PGI2 in buffered saline, pH 10.5, at a rate of 0.01 ml/kg/min (100 ng/kg/min), 10 cats received the same infusion plus a single dose of intravenous indomethacin (4 mg/kg) in buffered saline, and 11 cats received intracarotid buffered saline, pH 10.5, at a rate of 0.01 ml/kg/min, without therapeutic agents. Treatment with PGI2 was started upon MCA occlusion and continued for 6 hours, whereas indomethacin was given immediately prior to occlusion. Thirty minutes before perfusion, the animals were given fluorescein and Evans blue by intravenous injection. The cats were perfusion-fixed in vivo with carbon and buffered formalin 6 hours after MCA occlusion. Another five cats received tritium-labeled PGI2, and peripheral venous samples were collected and assayed for PGI2 and its alpha-keto metabolite. Mean arterial pressure was stable in treated animals during 6 hours of MCA occlusion, while untreated cats had significant (α = 0.05) progressive hypertension during that period. The regional cerebral blood flow (rCBF), measured by the intracarotid xenon-133 clearance method, decreased markedly in all animals immediately upon MCA occlusion. Untreated animals had a significant progressive improvement in rCBF during the occlusion period (α = 0.005), while treated animals had no such improvement. Quantitative electroencephalographic changes, gross edema, areas of fluorescein extravasation, and microscopic morphology (edema and infarct size) were not significantly different in the three groups. Prostacyclin appeared to reduce the extravasation of Evans blue dye. Systemic PGI2 levels were significant despite intracarotid administration. The authors conclude that 1) intracarotid PGI2 has a protective effect against the breakdown of the blood-brain barrier to protein-bound dyes seen in ischemic edema; 2) the systemic hemodynamic influence of PGI2, in the presence of impaired autoregulation, may compromise rCBF in the ischemic zone and offset any direct beneficial effects; and 3) indomethacin fails to modify the effects of PGI2.

Treatment of acute focal cerebral ischemia with dimethyl sulfoxide.

The object of this investigation was to study the effects of dimethyl sulfoxide (DMSO) upon the evolution of cerebral infarction. Twenty adult cats anesthetized lightly with ketamine hydrochloride underwent right middle cerebral artery occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. Regional cerebral blood flow (rCBF) changes in the right sylvian region were similar in the untreated and treated groups. The mean rCBF before occlusion was 46 +/- 10 ml/100 g/minute in the untreated group and 45 +/- 10 ml/100 g/minute in the treated group. Eight cats in both groups had rCBF measurements consistently below 18 ml/100 g/minute during the 6-hour period after occlusion. An index of erythrocyte flow was determined by measuring the transit of technetium-99 (99Tc)-labeled erythrocytes in the right sylvian region. The period of erythrocyte transit before occlusion was 10 +/- 1 seconds in the untreated group and 10 +/- 2 seconds in the treated group. After 6 hours of occlusion, the erythrocyte transit time was 18 +/- 3 seconds in the untreated group and 19 +/- 3 seconds in the treated group. Increasing delay in erythrocyte transit during the 6-hour occlusion period was seen in 5 untreated cats and 6 treated cats and was thought to represent a progressive increase in microvascular resistance. The complete washout of erythrocytes indicated the absence of microcirculatory obstruction. Electroencephalography (EEG) showed a reduced amplitude of activity in the right cerebral hemisphere after occlusion in cats with an rCBF consistently below 18 ml/100 g/minute. No significant EEG differences were found between the untreated and treated groups. Treatment with DMSO failed to modify the developing ischemia edema, neuronal alterations, or the changes in blood-brain barrier permeability to Evans blue dye and fluorescein. In this study DMSO was ineffective in preventing ischemic damage or acted when irreversible injury had already taken place.