[Rheopolyglucine treatment of patients with brain infarct in the acute period].
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Multiple infarcts were produced in cerebral hemispheres of rats by injecting calibrated 50-micron microspheres into the left internal carotid artery, and alterations in lipid and energy metabolism were evaluated 24 hours later in the embolized hemisphere. Total phospholipid content was decreased by 26%, but the different classes of phospholipids were not equally affected. Phosphatidylinositol and phosphatidylserine levels were decreased by about 40% and phosphatidylcholine and phosphatidylethanolamine by 25%, while sphingomyelin level remained unchanged. There was a 3.2-fold increase in total free fatty acid content with a relatively larger rise in polyunsaturated free fatty acids 20:4 and 22:6 (20-fold increase). Determination of enzyme activities showed decreases in Na+,K+-ATPase (-21%) and hexokinase (-14%) but no changes in phosphofructokinase and pyruvate kinase. Study of energy metabolism using the closed system method of Lowry et al showed a significant depression (-36%) of the cerebral metabolic rate. Taken together, these data suggest a relation between lipid alterations and dysfunction of energy metabolism. Phospholipid degradation with subsequent free fatty acid release and alteration in membrane-bound enzymes may have a direct effect on metabolic machinery and may slow cerebral metabolic rate.
BACKGROUND AND OBJECTIVE: The presence of patent foramen ovale (PFO) and atrioseptal aneurysm (ASA)has been described as a risk factor in cryptogenetic stroke. Patients with unknown origin stroke and PFO have less severe symptoms compared to the rest of cryptogenetic stroke patients. We evaluated the clinical situation in stroke patients with PFO and describe the factors predictive of a better outcome after a year. PATIENTS AND METHOD: 1118 patients between 18 and 70 years old were evaluated, and 223 were classified as having cryptogenetic stroke. Our protocol Included transcranial Doppler, a transesophageal echocardiography (TEE) and a cranial RM. We used the NIH Stroke Scale (NIHSS) to evaluate the clinical situation, and the modified Ranking Scale for the functional outcome. RESULTS: A total of 117 patients had all inclusion criteria. 66 (56.4%) showed a PFO. We observed a younger age, a higher percentage of females (48.4% in PFO vs. 25.5% in no-PFO) and less risk factors in PFO patients, except for migraine (24.6% in PFO vs. 5.9% in no-PFO; p = 0.01). PFO patients had less severe strokes (NIHSS: 3--median--in PFO vs. 5 in no-PFO; p = 0.010) and a lower grade of sequelae (p 0.024). Worse outcome was related to male, initial neurological evaluation (NIHSS) and presence of ASA. After a logistic regression, only the initial clinical situation (NIHSS) and the presence of ASA were associated with sequelae. CONCLUSIONS: PFO patients showed a less severe stroke and better functional outcome. The initial neurological involvement and the presence of ASA are predictive of the clinical situation after a year.
PURPOSE: To investigate the development of ischemic brain lesions, as present in the acute stroke phase, by diffusion-weighted magnetic resonance imaging (DWI), and in the subacute and chronic phases until up to four months after stroke, in fluid-attenuated inversion recovery (FLAIR)- and T2-weighted (T2W) magnetic resonance (MR) images. MATERIALS AND METHODS: Twelve consecutive patients with their first middle cerebral artery (MCA) infarction were included. Lesion volumes were assessed on T2W images recorded with a turbo spin echo (TSE) and on images recorded with the FLAIR sequence on average on day 8 and after about four months. They were compared with acute lesion volumes in perfusion and DWI images taken within 24 hours of stroke onset. RESULTS: On day 8, lesion volumes in images obtained with FLAIR exceeded the acute infarct volumes in DWI. The chronic lesion volumes were almost identical in T2W and FLAIR images but significantly reduced compared with the acute DWI lesions. The lesion volumes assessed on DWI images correlated highly with the lesions in the images obtained with TSE or FLAIR, as did the lesions in the images obtained with FLAIR and TSE. The secondary lesion shrinkage was accompanied by ventricular enlargement and perilesional sulcal widening, as most clearly visible in the images obtained with FLAIR. CONCLUSION: Our results show that the acute DWI lesions are highly predictive for the infarct lesion in the chronic stage after stroke despite a dynamic lesion evolution most evident in MR images obtained with FLAIR.
BACKGROUND: Cerebrovascular disease is a major factor related to cognitive impairment. However, behavioral correlates of ischemic brain lesions are insufficiently characterized. OBJECTIVE: To examine magnetic resonance imaging correlates of dementia in a large, well-defined series of patients with ischemic stroke. METHODS: Detailed medical, neurological, and neuropsychological examinations were conducted 3 months after ischemic stroke for 337 of 486 consecutive patients aged 55 to 85 years. Infarcts (type, site, side, number, and volume), extent of white matter lesions (WMLs), and degree of atrophy were categorized according to magnetic resonance images of the head. The definition for dementia of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III) was used. RESULTS: Dementia was diagnosed in 107 (31.8%) of the patients and stroke-related dementia in 87 (25.8%). Volumes, numbers, distinct sites of infarcts, extent of WMLs, and degree of atrophy were different for the demented and nondemented subjects. Particularly, volumes of infarcts in any (right- or left-sided) superior middle cerebral artery territory (27.3 vs 13.7 cm(3), P =. 002) and left thalamocortical connection (14.8 vs 4.0 cm(3), P =. 002) differentiated the 2 groups. Logistic regression analysis showed that the correlates of any dementia included the combination of infarct features (volume of infarcts in any superior middle cerebral artery: odds ratio [OR], 1.11; frequency of left-sided infarcts: OR, 1.21), extent of WMLs (OR, 1.3), medial temporal lobe atrophy (OR, 2.1), and host factors (education; OR, 0.91). In the patients with stroke-related dementia, the main correlate was volume of infarcts in the left anterior corona radiata (OR, 1.68). CONCLUSION: Correlates of poststroke dementia do not include merely 1 feature but a combination of infarct features, extent of WMLs, medial temporal lobe atrophy, and host features.
A 58-year-old woman suddenly noticed that soccer players disappeared and emerged in right inferior portion of her vision while she was watching soccer game on TV. She was admitted in our hospital on the day 9. Goldman perimeter revealed strange formed hemianopic soctomas which located at right side of her both visual fields. Brain MRI scan showed a tiny infarction in left lateral geniculate body. No abnormalities were found on cerebral angiography and 24 hours holter ECG study. Transesophageal echocardiography and transcranial Doppler study showed the presence of intracardiac right-to-left shunting via atrial septum defect. Paradoxical embolism was considered and oral anticoagulation therapy was started. Her visual defect disappeared by the day 79. Strange formed homonymous hemianopic scotomas were attributable to highly localized small lesion in left anterior choroidal artery territory of lateral geniculate body.
In recent years medical imaging is directed towards functional evaluation of tissues. Perfusion CT is an established functional method providing information on brain perfusion, enlightening the differentiation between irreversibly injured tissue and reversibly impaired "tissue at risk". With the new generation of multislice CT scanners, the performance of three examinations in a very short time is now feasible: Non-enhanced CT, CT angiography (CTA) and perfusion CT. Since these technologies are available in most hospitals 24 hours daily, comprehensive evaluation of the extent of ischemic event is now possible even in the emergency room. This information allows intravenous tissue plasminogen activator therapy within 3 hours of stroke onset in cases of acute ischemic stroke. We present the technique of CT perfusion and discuss its advantages and limitations as well as future applications.
The effects of hypercapnia on enhancement of reduced cerebral perfusion were re-evaluated in areas of ischemia produced by occlusion of the canine middle cerebral artery. Perfusion was measured by 85Kr (beta-ray) and 133Xe (gamma-ray) clearances, fluorescein angiography and diameter measurement of arteries. Between 45 and 55 mm Hg of PaCO2 rCBF measured with both isotopes increased significantly. When PaCO2 was elevated above 55 mm Hg, there was a remarkable dissociation in the rCBF measured by both isotopes. Cortical blood flow measured by 85Kr clearance decreased and, conversely, rCBF measured by 133Xe continued to increase. Arteries of less than 50 mu in diameter in areas of ischemia dilated significantly during hypercapnia. At PaCO2 above 65 mm Hg, progressive sub-pial hemorrhage and extravasation of dye were observed as side effects of hypercapnia. The use of mannitol combined with hypercapnia appeared to be harmful. A PaCO2 level between 45 and 55 mm Hg increases perfusion in areas of mildly reduced rCBF.
A combined measurement of regional cerebral blood flow (r CBF) and volume (r CBV) by SPECT was performed in 15 patients with ischaemic cerebral infarction. For measurement of r CBF 99mTc-HMPAO was used, and for r CBV 99mTc-labelled red blood cells. Patients with acute or subacute cerebral infarction (n = 10) showed elevation of r CBV whereas r CBF was either reduced or elevated. Patients with chronic cerebral infarction (n = 5) showed reduction of both r CBF and r CBV. The combined measurement of both r CBF and r CBV by SPECT allows imaging and semiquantitative evaluation of haemodynamic changes in ischaemic cerebral infarction at various stages. The resulting data may be helpful in describing the pathophysiologic compensatory mechanisms.
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Ten patients were treated with systemic administration of mannitol followed by blood substitute (perfluorochemicals) in the acute period of cerebral infarction in order to suppress the development of infarction and progressive deterioration. This chemotherapy was followed by reconstructive vascular surgery. There were 8 patients with cerebral infarction and 2 others in whom cerebral vascular occlusion occurred during an operation. Due to this treatment, there was no case in which the patient's condition was aggravated or in which death occurred. At examination two months later, 8 of the 10 patients had returned to productive lives. We consequently believe that this therapeutic method may prove to be an effective means of treating cerebral infarction in the acute stage. It is also thought that this method is applicable in surgical cases in which long-term vascular occlusion is required.
On the basis of a clinico-anatomical comparison in 70 cases of complicated infarctions and 77 observations of white infarctions the author elaborated computing tables. It was established that the following signs have certain diagnostic significance: the degree of changed consciousness, meningeal symptoms, symptoms indicating a secondary lesion of the brain stem and symptoms characterizing the degree of focal neurological disturbances. Among the supplementary methods of special significance is CSF analysis.
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In the experimental ischemia induced by occlusion of the rat middle cerebral artery, axons of both cortical and thalamic neurons were affected. However, cortical neurons survived thereafter and thalamic neurons died because of retrograde degeneration. The fate in these two groups of neurons was remarkably different and may be related to neurotrophic activity induced by ischemia. To detect ischemia-induced neurotrophic activity, fetal cortical neuron was cultured and neurotrophic activity was detected by applying tissue extract to the culture system. Fetal neurons obtained from 17 days rat embryo were cultured for 24 hours at 3.75 x 10(4) cells per 15 mm well in modified Eagle's minimum essential (MEM) supplemented by 10% fetal bovine serum (FBS), then for next 3 to 7 days with Dulbecco's modified Eagle's medium/Ham's nutrient mixture F-12 (DME/F-12) supplemented with insulin 5 mg/l, transferrin 10 mg/l, progesterone 6.3 micrograms/l, Na2SeO3 5.2 micrograms/l. The tissue extract was obtained from the rat subjected to ischemia and homogenized with DME/F-12. The homogenate was centrifuged at 100,000 g for 90 minutes and the supernatant was obtained. Application of peri-ischemic cortical extract improved neurons' survival by 50% as compared to extract of the contralateral side. However, the thalamic extract of the ischemic side had no neurotrophic activity as compared to the contralateral side. The activity was detected in the extract obtained at 8 days after ischemia but not detected in the extract obtained at 4 days after ischemia. The neurotrophic activity was disappeared by heating the extract at 90 degrees C for 10 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)
The diagnostic value of positron emission tomography (PET) was evaluated in 41 examinations of 40 patients. 68Ga-EDTA was used as a positron source. The findings were correlated with those of conventional of CT scanning. A clearly pathologic accumulation of 68Ga-EDTA was detected in 29 of 41 PET scans. The precontrast CT scans were negative in 11 and non-conclusive in one patient. CT after administration of contrast medium was performed in 29 patients. Of these, 21 had a clearly pathologic PET scan and 14 had visible contrast enhancement on CT examination. The injury of the blood-brain barrier thus was better demonstrated with PET than with CT. The topologic diagnosis was, however, better demonstrated at CT. It seems that CT and PET are supplementary examinations and that PET is superior to CT in the detection of injury of or absence of the blood-brain barrier.
EEGs from 16 patients with stroke in three different stages of evolution were recorded. EEG sources were calculated every 0.39 Hz by frequency domain VARETA. The main source was within the delta band in 2 out of 4 chronic patients, and in 67% of the patients in the acute or subacute stages when edema (cytotoxic or vasogenic) was present. Moreover, all patients showed abnormal activity in the theta band. Sources of abnormal activity in cortical or corticosubcortical infarcts were located in the cortex, surrounding the lesion. At the site of the infarct, a decrease of EEG power was observed. Sources of abnormal theta power coincided with edema and/or ischemic penumbra.
HISTORY AND ADMISSION FINDINGS: Over the period of one year three long-distance airline passengers (aged 21, 63, and 64 years) were admitted to our department because of a first-time acute neurological deficit having occurred during their long-distance flights. INVESTIGATIONS: In all three cases acute stroke MRI showed embolic cerebral ischemia, and transesophageal echocardiography revealed a persistent foramen ovale (PFO). Venous duplex and compression ultrasonography of the legs showed no signs of thrombosis. Extra- and transcranial Doppler, Holter ECG recording, routine blood analysis and additional tests for thrombophilia (incl. lupus anticoagulans, APC resistance, protein C, S, and AT III) revealed no signs of cardiovascular disease or other stroke causes. Only in case 3 the prothrombin gene G 20210A was found. DIAGNOSIS, TREATMENT AND COURSE: Ischemic stroke due to paradoxical embolism through a PFO was diagnosed in all three patients. One patient recovered fully within 2 days, one was discharged with a persistent motor deficit and the third patient died subsequently as a result of multiple cerebral infarctions accompanied by massive pulmonary embolism. CONCLUSION: These three cases illustrate that paradoxical embolic stroke is a possible severe complication of long-distance air travel in passengers with a PFO and this should be taken into account when deciding upon individual risk-adjusted prophylactic measures.
"Lacunar stroke" is described and 4 characteristic lacunar syndromes are presented. These small infarcts frequently occur in patients with essential hypertension. At their peak they cause a relatively minor neurologic deficit and are followed by almost complete recovery. Arterigraphic examination is not indicated as only the small arteries are involved. Treatment consists exclusively of control of hypertension. The prognosis is usually good. The small infarcts arise from pathologic changes and occlusions of penetrating arteries. Localization of the pale softenings which produce the typical lacunar syndromes is briefly discussed.