| 1. |
- Grabowski, Martin, et al.
(författare)
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Paw-reaching, sensorimotor, and rotational behavior after brain infarction in rats
- 1993
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Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 24:6, s. 889-895
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: Functional tests that are stable and consistent over time are an advantage for long-term evaluation of treatment in experimental stroke research. Because little information on this subject is available in rodents with focal cerebral ischemia, we investigated the outcome of three behavioral tests for a period of 3 months after the insult. METHODS: Spontaneously hypertensive rats were sham-operated (n = 27) or underwent an occlusion (n = 36) of the right middle cerebral artery. Before surgery all rats were tested for amphetamine-induced rotational behavior, and half of the rats were trained in a paw-reaching task. One, 2, and 3 months after surgery the tests were repeated, together with a test for sensorimotor function. Infarct size was measured morphometrically. RESULTS: In the lesion group, total hemisphere area was reduced by 22%, caudate putamen by 47%, and the thalamus by 24%. Contralateral to the lesion, paw-reaching was highly impaired, regardless of whether or not the rats had been pretrained, and lesion size correlated significantly to paw-reach performance. Ipsilateral rotation increased and sensorimotor function recovered with time in infarcted rats. CONCLUSIONS: In contrast to amphetamine-induced rotation and sensorimotor behavior, the paw-reaching test provides a stable behavioral parameter after a middle cerebral artery occlusion. Moreover, the lesion-induced deficit in paw-reaching is highly correlated to the extent of the infarct, suggesting that this test is useful in evaluating treatment effects for a longer period of time.
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| 2. |
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| 3. |
- Johansson, Barbro
(författare)
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Brain plasticity and stroke rehabilitation. The Willis lecture
- 2000
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Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 31:1, s. 223-230
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Tidskriftsartikel (refereegranskat)abstract
- Neuronal connections and cortical maps are continuously remodeled by our experience. Knowledge of the potential capabilityof the brain to compensate for lesions is a prerequisite for optimal stroke rehabilitation strategies. Experimental focal cortical lesions induce changes in adjacent cortex and in the contralateral hemisphere. Neuroimaging studies in stroke patients indicate altered poststroke activation patterns, which suggest some functional reorganization. To what extent functional imaging data correspond to outcome data needs to be evaluated. Reorganization may be the principle process responsible for recovery of function after stroke, but what are the limits, and to what extent can postischemic intervention facilitate such changes? Postoperative housing of animals in an enriched environment can significantly enhance functional outcome and can also interact with other interventions, including neocortical grafting. What role will neuronal progenitor cells play in future rehabilitation-stimulated in situ or as neural replacement? And what is the future for blocking neural growth inhibitory factors? Better knowledge of postischemic molecular and neurophysiological events, and close interaction between basic and applied research, will hopefully enable us to design rehabilitation strategies based on neurobiological principles in a not-too-distant future.
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| 4. |
- Johansson, Barbro
(författare)
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Functional outcome in rats transferred to an enriched environment 15 days after focal brain ischemia
- 1996
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Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 27:2, s. 324-326
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: The aim was to determine whether a delayed transfer to an enriched environment improves outcome after focal brain ischemia. METHODS: Performance on a rotating pole, prehensile traction, limb placement, and postural reflexes were tested in 15 spontaneously hypertensive rats housed in standard laboratory cages for 2 weeks after middle cerebral artery ligation. Seven of the 15 rats were then transferred to an enriched environment, and the two groups were tested 1, 3, and 5 weeks later. RESULTS: The enriched environment significantly improved pole performance, prehensile traction, and limb placement. CONCLUSIONS: Delayed postoperative environmental enrichment improves outcome in experimental stroke.
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| 5. |
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| 6. |
- Lindgren, Arne, et al.
(författare)
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Carotid artery and heart disease in subtypes of cerebral infarction
- 1994
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Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 25:12, s. 2356-2362
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: The aim of the study was to determine the prevalences of carotid artery disease and major and minor potential cardioembolic sources (1) in patients with cerebral infarction and age-matched control subjects and (2) in different clinical subtypes of cerebral infarction. METHODS: A series of 166 consecutive patients with cerebral infarction and 59 control subjects was examined. The study protocol included clinical subtyping of the cerebral infarctions, ultrasonography of the carotid arteries, transthoracic echocardiography (TTE), transesophageal echocardiography (TEE), ECG, and examination of the brain with computed tomography, magnetic resonance imaging, or autopsy. RESULTS: Carotid artery stenosis > or = 80% or occlusion was present in 35 (21%) patients but in no control subjects (P < .001; chi 2 test). A major potential cardioembolic source was detected in 65 (39%) patients and 3 (5%) control subjects. Atrial fibrillation was present in 35 (21%) patients and 3 (5%) control subjects at initial ECG (P < .01) and in 47 (28%) patients at repeat examination; 17 patients had paroxysmal atrial fibrillation. Sinus rhythm and a major potential cardioembolic source were detected in 18 (11%) patients but in no control subjects (P < .01) at TTE (all patients and control subjects examined) or TEE (118 patients and 52 control subjects examined). The frequency of a minor potential cardioembolic source detectable at TTE or TEE was similar in the patient and control groups (51% and 53%, respectively [NS]) and increased significantly with age. A finding of carotid artery stenosis > or = 80% or occlusion, atrial fibrillation, or a major cardioembolic source detected at TTE or TEE was more frequent among patients with cortical symptoms from anterior or middle cerebral artery territories than among those with lacunar syndromes (66% versus 22%, respectively). The probable source of cerebral infarction was identified in most of the 166 patients: cardiac embolism in 28% of cases (n = 46), carotid artery disease in 8% (n = 14), both cardiac embolism and carotid artery disease in 7% (n = 11), and lacunar infarction in 23% (n = 38). In 57 (34%) of the patients no unequivocal cause of the cerebral infarction was found. CONCLUSIONS: The prevalences of carotid artery and heart disease differ significantly between clinical subtypes of cerebral infarction. The cause of cerebral infarction remains uncertain in one third of patients. Because a minor potential cardioembolic source occurs in about 50% of both patients and control subjects, this finding is of questionable value as a risk factor for stroke in the elderly.
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| 7. |
- Lindgren, Arne, et al.
(författare)
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Cerebral lesions on magnetic resonance imaging, heart disease, and vascular risk factors in subjects without stroke. A population-based study
- 1994
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Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 25:5, s. 929-934
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: To assess the prevalence of asymptomatic abnormalities on magnetic resonance imaging of the brain and their possible relation to hypertension, heart disease, and carotid artery disease, we studied 77 randomly selected subjects (mean age, 65.1 years; range, 36 to 95 years) with no history of focal brain lesions. METHODS: The study protocol included magnetic resonance imaging of the brain, transthoracic and transesophageal echocardiography, ultrasonography of the carotid arteries, and electrocardiographic recording. Deep and periventricular white matter hyperintensities on magnetic resonance imaging were assessed both separately and together. RESULTS: On magnetic resonance imaging of the brain 62.3% (95% confidence interval [CI], 51.5% to 73.2%) of the subjects had white matter hyperintensities. These abnormalities increased significantly with age (chi 2 test; P = .0001), from 13.6% (95% CI, 0% to 28.0%) of subjects aged younger than 55 years to 85.2% (95% CI, 71.8% to 98.6%) of subjects aged 75 years or older. Six subjects had deep gray matter hyperintensities localized in the basal ganglia, and one had a cerebellar infarction. Stepwise logistic regression analysis identified age and a history of heart disease (but not echocardiographic findings) to be independently associated with deep and periventricular white matter hyperintensities. Hypertension was only independently associated with periventricular white matter hyperintensities. Of the 68 subjects examined with both transthoracic and transesophageal echocardiography, potential cardioembolic sources were detected in 38.2% (95% CI, 26.7% to 49.8%) of the subjects with transthoracic echocardiography and in 47.1% (95% CI, 35.2% to 58.9%) of those with transthoracic and transesophageal echocardiography combined. In subjects aged 75 years or older, a possible cardiac embolic source was detected in 64.0% on transthoracic echocardiography and in 72.0% on transthoracic and transesophageal echocardiography combined, compared with 5.3% and 15.8%, respectively, in subjects aged younger than 55 years. CONCLUSIONS: White matter hyperintensities and potential cardioembolic sources are frequently present in asymptomatic individuals, stressing the need for age-matched control subjects in studies of patients with stroke or dementia.
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| 8. |
- Lindgren, Arne, et al.
(författare)
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Comparison of clinical and neuroradiological findings in first-ever stroke. A population-based study
- 1994
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Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 25:7, s. 1371-1377
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: To determine how a recently proposed clinical stroke subclassification corresponds to specific findings on computed tomography (CT) and magnetic resonance imaging (MRI) of the brain. METHODS: Two hundred twenty-eight patients with first-ever stroke were divided into four clinical subgroups: (1) total anterior circulation syndrome: both cortical and subcortical symptoms from anterior and middle cerebral artery territory; (2) partial anterior circulation syndrome: more restricted and predominantly cortical symptoms from the same arterial territories; (3) lacunar syndrome; and (4) posterior circulation syndrome: vertebrobasilar or posterior cerebral artery symptoms. The imaging protocol included CT of the brain on day 0 through 15 and a second CT and an MRI of the brain on day 16 through 180 after acute stroke onset. RESULTS: There were 200 patients with cerebral infarction and 28 patients with intracerebral hemorrhage. Intracerebral hemorrhage was found in 19% of patients with total anterior circulation syndrome and in no patients with lacunar syndrome (chi 2 test; P < .01 for the difference between the four clinical subgroups). Of the 200 patients with cerebral infarction, 27% had total anterior circulation, 30% partial anterior circulation, 26% lacunar, and 16% posterior circulation syndromes. CT within 2 days revealed a visible lesion in about two thirds of patients with infarctions of total or partial anterior circulation syndrome type, compared with only 22% of patients with lacunar infarction (chi 2 test; P = .02 for the difference between the four subgroups). The mean volume of the symptomatic infarction on CT within 15 days was 95 mL for total anterior circulation, 20 mL for partial anterior circulation, and 2.5 mL for lacunar syndrome (one-factor ANOVA; P = .0001). A cortical involvement of the infarction on CT day 16 through 180 was seen in 81% of patients with total anterior circulation syndrome and 58% of those with partial anterior circulation syndrome, compared with only 8% of patients with lacunar syndrome (chi 2 test; P = .0001). MRI more often than CT showed a cortical involvement of lacunar infarctions and also revealed more silent lesions. CONCLUSIONS: The described clinical subgroups significantly differed in frequencies of intracerebral hemorrhage, cortical involvement, and lesion volume on CT and MRI.
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| 9. |
- Lindgren, Arne, et al.
(författare)
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Plasma homocysteine in the acute and convalescent phases after stroke
- 1995
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Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 26:5, s. 795-800
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: Stroke patients frequently manifest moderate hyperhomocysteinemia. In most published studies, plasma homocysteine was measured at least 1 month after stroke (or the interval was not reported). To determine whether plasma homocysteine concentrations change in the acute phase, we compared acute-phase values with both convalescent-phase and control values. METHODS: Plasma homocysteine concentrations were measured in the acute phase (mean, 2 days after stroke onset) in 162 first-ever stroke patients aged 50 years or more (median, 75 years) and again at a median interval of 583 days (range, 460 to 645 days) after stroke onset in a subgroup of 17 patients, with values for 60 age-matched subjects serving as controls. Twenty of the control subjects were reexamined 2 to 3 years after their initial examination. RESULTS: The median plasma homocysteine concentration was 13.4 mumol/L in the patient group compared with 13.8 mumol/L for control subjects (NS, Mann-Whitney U test) and increased from 11.4 mumol/L in the acute phase to 14.5 mumol/L in the convalescent phase in the subgroup of patients examined twice (P < .01, Wilcoxon signed rank test). In the 20 reexamined control subjects, no significant change over time in plasma homocysteine concentration was found. CONCLUSIONS: The post-acute-phase increase in plasma homocysteine may explain why higher values were obtained for stroke patients than for control subjects in previous studies. Possible reasons for the variation in plasma homocysteine concentrations over time are (1) an acute-phase reduction secondary to a decrease in plasma albumin and (2) an increase in plasma homocysteine during the convalescent phase due to modified vitamin intake and/or lifestyle. The timing of plasma homocysteine measurements relative to stroke onset is a factor to be considered in the interpretation of results.
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| 10. |
- Lindgren, Arne, et al.
(författare)
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Tissue plasminogen activator and plasminogen activator inhibitor-1 in stroke patients
- 1996
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Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 27:6, s. 1066-1071
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: Abnormal endogenous fibrinolytic activity may be a risk factor for stroke. Since the possible variation of tissue-type plasminogen activator (TPA) antigen and plasminogen activator inhibitor-1 (PAI-1) antigen concentrations over time after stroke has been rarely studied, it was examined in plasma from stroke patients in the acute and convalescent phases of the disease and in a control group. METHODS: Plasma concentrations of TPA and PAI-1 were determined in 135 stroke patients and in 77 control subjects. All but 4 patients were examined within 7 days after stroke onset, and 32 patients and 18 control subjects were reexamined 2 to 4 years later. RESULTS: In the acute phase, stroke patients had significantly higher TPA (median, 10 micrograms/L) and PAI-1 (median, 14 micrograms/L) antigen concentrations, compared with control subjects (median values, 6 micrograms/L [P = .0001] and 8 micrograms/L [P < .01], respectively); TPA levels were higher in both the cerebral infarction (n = 122) and cerebral hemorrhage (n = 12) subgroups, whereas PAI-1 levels were higher in the cerebral infarction subgroup only. Stepwise logistic regression analysis (with correction for age, sex, history of hypertension, diabetes mellitus, and heart disease) showed TPA antigen level to be an independent discriminator between the cerebral infarction subgroup and control subjects (P = .0001), whereas the corresponding difference for PAI-1 antigen levels just failed to reach significance (P = .05). TPA antigen levels were correlated with concentrations of serum cholesterol (Spearman's rho = 0.15; P < .05), serum triglyceride (rho = 0.33; P = .0001), and plasma homocysteine (rho = 0.19; P < .01). PAI-1 antigen levels were correlated with serum triglyceride levels only (rho = 0.41; P = .0001). At reexamination after 2 to 4 years, neither TPA nor PAI-1 levels had changed significantly from the baseline values. CONCLUSIONS: In stroke patients, high TPA antigen concentrations may indicate an activation of the fibrinolytic system or may be due to a delayed clearance of TPA complexed with inhibitors. High PAI-1 antigen concentrations in patients with cerebral infarction represent increased fibrinolytic inhibition. The findings in this longitudinal study suggest that TPA and PAI-1 antigen concentrations both differ little between the acute and convalescent phases after stroke.
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