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Biomedical subjects

Markku Kaste

Publications and source records attributed to Markku Kaste.

52 records · Page 3Linked to original sources
PubMed2003

Complaints of poststroke insomnia and its treatment with mianserin.

We assessed the prevalence and associations of symptoms of insomnia in patients with acute ischemic stroke, and evaluated whether mianserin as a sedative antidepressant is beneficial in the treatment of poststroke insomnia. One hundred consecutively hospitalized patients were randomized to receive 60 mg/day of mianserin (n = 51) or placebo for 1 year in a double-blind trial with a 6-month follow-up after the therapy. Symptoms of insomnia were assessed with the three insomnia-related items of the Hamilton Depression Scale; patients were defined as insomniacs if any of these items was positive. Complaints of insomnia occurred in 68% of patients on admission, and in 49% at 18 months, and they were as frequent in all subgroups of patients. From 2 months, symptoms of insomnia were associated independently with depression. Living alone before stroke (at 0 and 2 months) and age (at 12 months) were other independent predictors of insomnia. The rate of recovery as evaluated by the insomnia score was more rapid in patients on mianserin than in those on placebo. At 2 months, the scores were significantly different favoring mianserin treatment (1.3 vs. 0.8, p = 0.02). We conclude that insomnia is a common complaint after ischemic stroke. Mianserin had a beneficial influence on the recovery from symptoms of insomnia, even though the intensity of poststroke depression was low.

Age Factors↗
PubMed2003

Generalized anxiety disorders three to four months after ischemic stroke.

BACKGROUND AND OBJECTIVE: The main objective of our study was to detail the frequency and clinical determinants of poststroke generalized anxiety disorders in a large, well-defined stroke cohort. METHODS: A total of 277 stroke patients aged 55-85 were subjected to a comprehensive psychiatric evaluation between 3 and 4 months after ischemic stroke. Primary generalized anxiety disorder or generalized anxiety disorder due to stroke were diagnosed according to DSM-IV symptom criteria. RESULTS: The frequency of any generalized anxiety disorder was 20.6% (n = 57). According to a logistic model, any generalized anxiety disorder was associated with a history of epilepsy, comorbid depressive disorder, severity of depression, severity of anxiety, and the use of anxiolytic drugs. A discriminant analysis identified four factors that distinguished the two diagnostic subgroups from one another: the level of psychosocial functioning (worse score in patients with generalized anxiety due to stroke), a history of migraine, anterior circulation stroke localization (more frequent in patients with generalized anxiety disorder due to stroke), and a history of insomnia (more frequent in patients with primary generalized anxiety disorder). CONCLUSIONS: Clinically significant anxiety is common in ischemic stroke patients and may hamper their rehabilitation.

Aged↗
PubMed2003

Poststroke depression: an 18-month follow-up.

BACKGROUND AND PURPOSE: This prospective study was designed to examine the course, associates, and predictors of depressive symptoms during the first 18 months after stroke. METHODS: A total of 100 patients were followed up for 18 months after stroke. Depressive symptoms were assessed at 2 weeks and 2, 6, 12, and 18 months after stroke with the Beck Depression Inventory and the Hamilton Rating Scale for Depression, and diagnoses were performed using criteria outlined in the Diagnostic and Statistical Manual of Mental Disorders, Third Edition-Revised. Stroke severity was assessed with the Scandinavian Stroke Scale and cognitive functions with a comprehensive neuropsychological battery. Patients participated in a randomized clinical trial of antidepressive medication. RESULTS: In all, 54% of patients felt at least mildly depressive at some time during the follow-up; 46% of those who were depressive during the first 2 months were also depressive at 12 and/or 18 months. Only 12% of patients were depressive for the first time at 12 or 18 months. The male sex was associated with a more negative change in depressive symptoms during the follow-up. Older age was associated with depressive symptoms during the first 2 months, stroke severity from 6 to 12 months, and the male sex at 18 months. Depressive symptoms were unrelated to the lesion location. CONCLUSIONS: Depressive symptoms are frequent and they often have a chronic course. Depression is associated with stroke severity and functional impairment, and with the male sex at 18 months. Attention should be focused on the long-term prognosis of mood disturbances and adaptation.

Antidepressive Agents, Second-Generation↗
PubMed2002

Fiblast (trafermin) in acute stroke: results of the European-Australian phase II/III safety and efficacy trial.

BACKGROUND: Trafermin (basic fibroblast growth factor) has been shown to reduce infarct volume in acute ischemic stroke models, and to promote functional recovery and new synapse formation when given to animals with completed cerebral infarction. A previous study in acute stroke patients suggested that trafermin was safe and well tolerated when given over a 3-hour period over a wide dose range. METHODS AND RESULTS: Double-blind, parallel group, placebo-controlled trial of a single 24-hour intravenous infusion of trafermin. Patients having onset of stroke symptoms within 6 h and a baseline score of >/=7 on the NIH Stroke Scale (>/=2 motor) were randomized to receive 5 or 10 mg of trafermin or placebo intravenously infused over 24 h. The primary efficacy outcome was a categorized combination of the Barthel and Rankin scales assessed at 90 days. A total of 286 patients had been enrolled at 55 sites in 11 countries when the sponsor directed that enrollment be stopped because an interim analysis of efficacy data predicted too small a chance of demonstrating a statistically significant benefit after recruitment of the planned 900 patients. The 5-mg group showed a slight but nonsignificant advantage over placebo (OR 1.2, 95% CI 0.72-2.00, p = 0.48); the 10-mg group showed a nonsignificant disadvantage (OR 0.74, 95% CI 0.44-1.22, p = 0.24). Mortality rates at 90 days were 17% in the 5-mg group, 24% in the 10-mg group and 18% in the placebo group. Treatment with trafermin was associated with an increased leukocytosis and a decrease in blood pressure: mean decrease in systolic blood pressure from baseline was 19 mm Hg in the 5-mg group, 22 mm Hg in the 10-mg group and 8 mm Hg in the placebo group. In a post hoc subgroup analysis, patients in the 5-mg group treated more than 5 h after the onset of symptoms showed an apparent advantage over placebo (OR 2.1, 95% CI 1.00-4.41, p = 0.044; after age adjustment: OR 1.9, 95% CI 0.91-4.13, p = 0.08). CONCLUSIONS: With the proper treatment regimen, trafermin can likely be given safely to stroke patients. The 5-mg dose showed a trend toward a treatment advantage. The ideal time window for this agent may exceed 5 h. This may open new avenues for acute stroke therapy, aiming at enhancing recovery mechanisms rather than immediate neuroprotection.

Dose-Response Relationship, Drug↗
PubMed2002

AMPA antagonist ZK200775 in patients with acute ischemic stroke: possible glial cell toxicity detected by monitoring of S-100B serum levels.

BACKGROUND AND PURPOSE: S-100B and neuron-specific enolase (NSE) serum concentrations can be used as peripheral markers of glial cell and neuronal damage, respectively. We investigated these markers in a clinical trial with the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) antagonist ZK200775 in acute ischemic stroke patients. METHODS: In a multicenter, double-blind, randomized, placebo-controlled phase 2 trial, 61 ischemic stroke patients were treated with either placebo or active drug in a dose-finding design. Twenty-five patients received placebo, 12 patients received a total dose of 262.5 mg in 48 hours (dose group 1), and 13 patients received a total dose of 525 mg in 48 hours (dose group 2). Eleven patients received a total dose of 105 mg over a period of 6 hours (dose group 3; reduction of total dose and infusion time because of adverse events in group 2). Serum concentrations of S-100B and NSE were analyzed with the use of a monoclonal sandwich immunoluminometric assay. Neurological outcome was assessed with the National Institutes of Health Stroke Scale (NIHSS). RESULTS: In group 2 there was a significant transient worsening in the mean NIHSS score 48 hours after the start of treatment. The mean increase was 11 points. This was due to reduction of consciousness (stupor and coma) in 8 of 13 patients. Neurological deterioration in group 2 was associated with a higher increase of S-100B concentrations, but not of NSE concentrations, than in the placebo group. The trial was stopped prematurely for safety reasons. CONCLUSIONS: The AMPA antagonist ZK200775 transiently worsened the neurological condition in patients with acute ischemic stroke. Our results suggest that in addition to neuronal dysfunction, glial cell toxicity may have occurred. It may be useful to introduce monitoring of serum markers of brain damage in phase 2 trials with glutamate receptor antagonists.

Acute Disease↗
PubMed2002

Leukoaraiosis, ischemic stroke, and normal white matter on diffusion-weighted MRI.

BACKGROUND AND PURPOSE: Leukoaraiosis is a radiological finding of uncertain pathogenesis with bilateral patchy or diffuse areas of hyperintensity of the cerebral white matter (WM) on T2-weighted MRI. Using diffusion-weighted MRI (DWI), we aimed to test (1) whether the average apparent diffusion coefficient (ADC(av)) values of the regions of leukoaraiosis vary according to the degree of the severity of leukoaraiosis and whether the regions of leukoaraiosis could be distinguished (2) from normal WM or (3) from ischemic strokes of various ages. METHODS: We compared 85 patients with leukoaraiosis, 22 healthy subjects with no leukoaraiosis on the conventional MR images, and 10 patients with ischemic strokes serially imaged <6 hours, 24 hours, 1 week, 1 month, and 3 months after stroke onset. All subjects were studied with DWI in 3 orthogonal directions with 2 b values (b=0 and b=1000 s/mm(2)) at 1.5 T. ADC(av) values were determined for the regions of leukoaraiosis, ischemic lesions, and normal WM. RESULTS: The more severe the leukoaraiosis was, the higher the ADC(av) values of the leukoaraiotic regions became. The ADC(av) values (in 10(-3) mm(2)/s) of the regions of leukoaraiosis (0.92 to 1.27) were significantly higher than that of the normal WM (0.69+/-0.04) and that of the ischemic strokes at 6 hours (0.38+/-0.07), 24 hours (0.36+/-0.10), and 1 week (0.51+/-0.09). One-month-old ischemic strokes (1.08+/-0.33) had ADC(av) values similar to those of leukoaraiotic regions, whereas 3-month-old infarcts (1.59+/-0.32) showed significantly higher ADC(av) values than the leukoaraiotic regions. CONCLUSIONS: The regions of leukoaraiosis show characteristic changes in ADC(av) values, and DWI can be used to differentiate acute and chronic ischemic stroke lesions from leukoaraiosis.

Acute Disease↗
PubMed2002

Diffusion-weighted MR imaging in normal human brains in various age groups.

BACKGROUND AND PURPOSE: Few studies have concerned the absolute apparent diffusion coefficient (ADC) values in the normal human brain and the effect of aging on diffusion. Therefore, our purpose was to determine whether the average ADC (ADC(av)) values in the various regions of the brain differ with age, sex, or hemisphere and to establish reference values of the absolute ADC(av) for further studies. METHODS: Subjects (40 men and 40 women) were chosen from a healthy population; age groups were 20-34, 35-49, and 50-64 years and 65 years or older (n = 20 each). All subjects were examined with MR imaging, including conventional and diffusion-weighted imaging in three orthogonal directions with two b values (0 and 1000 s/mm(2)) at 1.5 T. Bilateral ADC(av) values were determined in 36 regions of interest encompassing the entire brain. RESULTS: ADC(av) values were highest in the cortical gray matter ([0.89 +/- 0.04] x 10(-3) mm(2)/s; range, 0.78-1.09 x 10(-3)), lower in the deep gray matter ([0.75 +/- 0.03] x 10(-3) mm(2)/s; range, 0.64-0.83 x 10(-3)), and lowest in the white matter ([0.70 +/- 0.03] x 10(-3) mm(2)/s; range, 0.62-0.79 x 10(-3)). The ADC(av) values did not significantly change with aging, except for an increase in the lateral ventricles. No difference was observed between women and men or between the hemispheres. CONCLUSION: The data reported herein are representative, and the ADC(av) values can be used for reference in future studies and in clinical settings.

Adult↗
PubMedDate not supplied

Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial.

BACKGROUND: Clopidogrel was superior to aspirin in patients with previous manifestations of atherothrombotic disease in the CAPRIE study and its benefit was amplified in some high-risk subgroups of patients. We aimed to assess whether addition of aspirin to clopidogrel could have a greater benefit than clopidogrel alone in prevention of vascular events with potentially higher bleeding risk. METHODS: We did a randomised, double-blind, placebo-controlled trial to compare aspirin (75 mg/day) with placebo in 7599 high-risk patients with recent ischaemic stroke or transient ischaemic attack and at least one additional vascular risk factor who were already receiving clopidogrel 75 mg/day. Duration of treatment and follow-up was 18 months. The primary endpoint was a composite of ischaemic stroke, myocardial infarction, vascular death, or rehospitalisation for acute ischaemia (including rehospitalisation for transient ischaemic attack, angina pectoris, or worsening of peripheral arterial disease). Analysis was by intention to treat, using logrank test and a Cox's proportional-hazards model. FINDINGS: 596 (15.7%) patients reached the primary endpoint in the group receiving aspirin and clopidogrel compared with 636 (16.7%) in the clopidogrel alone group (relative risk reduction 6.4%, [95% CI -4.6 to 16.3]; absolute risk reduction 1% [-0.6 to 2.7]). Life-threatening bleedings were higher in the group receiving aspirin and clopidogrel versus clopidogrel alone (96 [2.6%] vs 49 [1.3%]; absolute risk increase 1.3% [95% CI 0.6 to 1.9]). Major bleedings were also increased in the group receiving aspirin and clopidogrel but no difference was recorded in mortality. INTERPRETATION: Adding aspirin to clopidogrel in high-risk patients with recent ischaemic stroke or transient ischaemic attack is associated with a non-significant difference in reducing major vascular events. However, the risk of life-threatening or major bleeding is increased by the addition of aspirin.

Aged↗
PubMedDate not supplied

Clinical features of MRI-defined subcortical vascular disease.

BACKGROUND AND PURPOSE: Vascular cognitive impairment and vascular dementia are now seen to extend much beyond the traditional multi-infarct dementia.A more homogeneous subtype is the subcortical ischemic vascular disease (SIVD). We applied magnetic resonance imaging (MRI) criteria based on research criteria for SIVD in a large cohort of patients with ischemic stroke. We compared clinical features of patients with SIVD and patients with other stroke type. SUBJECT AND METHODS: The study group comprised 337 of 486 consecutive patients aged 55 to 85 years who 3 months after ischemic stroke completed a comprehensive neuropsychological test battery and MRI, including structured medical, neurologic, and laboratory evaluations; clinical mental status examination; interview of a knowledgeable informant; detailed history of risk factors; and evaluation of stroke type, localization, and syndrome. RESULTS: Patients with SIVD (n = 86) more often had a history of progressive cognitive decline (22.8% vs. 6.9%, P = 0.0002), walking disorder before stroke (27.9% vs. 2.0%, P = 0.02), and urinary difficulties (12.8% vs. 5.6%, P = 0.028) in comparison with patients with other stroke type (n = 251). Of the study population, 107 (31.8%) had DSM-III dementia. The patients with SIVD more often had DSM-III dementia (40.7% vs. 28.7%, P = 0.04), had less severe stroke as measured by Scandinavian Stroke Scale (56.6 vs. 55.1, P = 0.03), were more dependent in activities of daily living (ADL) functions as measured by FAQ scale (8.9 vs. 5.4, P = 0.001), were more dependent in instrumental activities of daily living (IADL) functions as measured by the Lawton scale (5.5 vs. 6.3, P = 0.01), and were more depressed as measured by the Beck Depression Inventory (11.8 vs. 8.4, P = 0.0003) poststroke than the patients without SIVD. The main cognitive domain that differentiated the patients with SIVD from those without was executive dysfunction (51.2% vs. 38.7%, P = 0.04). According to multiple regression model, apractic-atactic gait disorder (odds ratio 2.82, 95% confidence interval 1.21-6.53), ADL functions (odds ratio 1.04, 95% confidence interval 1.01-1.08), and the Beck Depression Inventory (odds ratio 1.05, 95% confidence interval 1.02-1.09) related to SIVD. CONCLUSIONS: The most significant clinical features of MRI-defined SIVD were found to be apractic-atactic gait, impaired ADL functions, and depression.

Aged↗