PubMed Health⌕ Search

Biomedical subjects

M Viitanen

Publications and source records attributed to M Viitanen.

At least 37 records · Page 2Linked to original sources
PubMed2001

Can the site of brain lesion predict improved motor function after low-TENS treatment on the post-stroke paretic arm?

OBJECTIVES: Previous reports suggest that afferent stimulation improves arm motor function in patients suffering from stroke. The aim of this pilot study was to test the hypothesis that the brain lesion location determines the response to low-frequency (1.7 Hz) transcutaneous electric nerve stimulation (Low-TENS) therapy. DESIGN: Magnetic resonance imaging (MRI) was performed on 14 patients who had previously received Low-TENS on the paretic arm after stroke. METHODS: MR images were classified with two different methods. First, lesions in the cortical and the subcortical areas were registered. Secondly, any change in a described periventricular white matter (PVWM) area was recorded. Interactions between the lesion site, as detected by MRI, and response to Low-TENS treatment were analysed. RESULTS: Arm motor function after Low-TENS treatment in relation to lesion in different brain areas showed that absence of lesions in the PVWM area increased the possibility for improved motor capacity after afferent stimulation. CONCLUSIONS: The site of lesion may play a role in prognosis/outcome after Low-TENS treatment but this hypothesis should be further tested in a larger prospective study.

Aged↗
PubMed2000

Incidence of stroke in relation to cognitive function and dementia in the Kungsholmen Project.

OBJECTIVE: To investigate whether cognitive function is related to incidence of stroke. METHODS: A population-based cohort of 1551 subjects with no clinical history or signs of stroke, age 75 years and over at baseline, were followed up for 3 years. Individuals with a first-ever stroke event that was recorded in the Stockholm inpatient register after the date of baseline interview were considered as incident stroke patients. Diagnosis of stroke followed the International Classification of Disease, 9th Revision (ICD-9). Diagnosis of dementia was made according to the Diagnostic and Statistical Manual of Mental Disorders, 3rd ed., revised (DSM-III-R). Cognitive functioning was assessed with the Mini-Mental State Examination. RESULTS: During the 4102 person-years of follow-up, 110 events were recorded, giving an overall incidence of stroke of 26.8 per 1000 person-years. Subjects with mild dementia had a relative risk of 2.6 (95% CI, 1.2 to 5.7) of developing stroke after controlling for the potential confounders. The corresponding figure for subjects with cognitive impairment was 2.0 (95% CI, 1.0 to 3.8; p = 0.05). There was a tendency for subjects who developed stroke to be more likely to have vascular factors (systolic blood pressure >180 mm Hg, heart disease, or diabetes mellitus) than those who did not. CONCLUSIONS: Mild dementia and cognitive impairment are associated with an increased incidence of stroke among subjects age 75 years old and over. Because stroke increases risk of dementia and prior stroke increases risk of a subsequent stroke, mild dementia and cognitive impairment may be a manifestation of clinically unrecognized stroke.

Aged↗
PubMed2000

Interaction between estrogen receptor 1 and the epsilon4 allele of apolipoprotein E increases the risk of familial Alzheimer's disease in women.

Estrogens may be implicated in the development of Alzheimer's disease (AD). Most of their effects are mediated via receptors whose function and expression may be modified by DNA polymorphisms. Here the estrogen receptor 1 gene (ESR1) polymorphisms XbaI and PvuII were analyzed in 214 AD patients and 290 controls. In logistic regression analysis, a significantly increased risk of familial AD due to interaction between the ESR1 xx genotype and the apolipoprotein E epsilon4 allele was observed in women in a Swedish clinic-based sample, taking subjects who had neither the xx genotype nor epsilon4 as reference (OR 11.3, 95% CI 2.9-43.8). The risk of AD was more pronounced in early-onset (OR 22.0, 95% CI 3. 7-132.7) than in late-onset (OR 6.0, 95% CI 1.2-29.7) female patients. For women carrying the pp genotype together with epsilon4 the risk of AD was similarly elevated. Likewise in a Swedish community-based set of women, an increased risk of familial AD was observed in subjects who had either the ESR1 xx or pp genotype together with epsilon4. Furthermore, the Pp genotype frequency was found to be significantly increased in Finnish women with sporadic AD. We, thus, conclude that the ESR1 gene may have a role in the development of AD in females.

Age of Onset↗
PubMed2000

Variant Alzheimer's disease with spastic paraparesis: clinical characterization.

OBJECTIVE: To present the clinical, neuroimaging, and electrophysiologic characteristics of a variant AD phenotype. BACKGROUND: The authors have identified a large Finnish kindred with presenile dementia and spastic paraparesis due to deletion of exon 9 of presenilin 1. Neuropathologic analysis showed unusual cortical "cotton wool" plaques, immunoreactive for the beta-amyloid peptide but lacking congophilic cores. PATIENTS AND METHODS: Twenty-two affected individuals (16 men and 6 women) were identified in four successive generations. All surviving five patients were examined and subjected to molecular genetic analysis. In addition, the neurologic records of nine deceased patients were evaluated. Electrophysiologic investigations were available in eight cases. CT or MRI of the head had been performed on 11 patients and PET was performed on three patients. RESULT: The mean age at onset (+/-SD) was 50.9 +/- 5.2 years (range 40 to 61 years). Memory impairment was present in all patients. Memory impairment appeared simultaneously with or was preceded by walking difficulty due to spasticity of the lower extremities (10/14). Impaired fine coordination of hands (9/14) and dysarthria (6/14) in some patients suggested cerebellar involvement. EEG showed intermittent generalized delta-theta activity. Head MRI showed temporal and hippocampal atrophy; PET showed bilateral temporo-parietal hypometabolism. CONCLUSION: Spastic paraparesis or brisk stretch reflexes of lower extremities or clumsiness of hands combined with dementia suggests this variant of AD.

Age of Onset↗
PubMed2000

The course of cognitive impairment in preclinical Alzheimer disease: three- and 6-year follow-up of a population-based sample.

OBJECTIVES: To examine the ability of the total score and individual items from the Mini-Mental State Examination in predicting the development of Alzheimer disease (AD) across a 3- and 6-year period in a population-based sample, and to describe the longitudinal changes in these measures across the same follow-up periods. DESIGN: Prospective follow-up of a community-based cohort, with 3 times of testing across a 6-year period. At each time of measurement, participants were clinically examined by physicians to identify demented and nondemented participants according to Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition, criteria. PARTICIPANTS: The study population consisted of all participants who were nondemented at the first follow-up and participated in the second follow-up examination. Among those, 459 remained nondemented and 73 developed AD during the second follow-up period. RESULTS: Baseline differences in the total Mini-Mental State Examination score and the delayed memory item were seen 6 years before eventual dementia diagnosis (P<.01). Analysis of the longitudinal changes showed no differences in the rate of decline for the incident AD or nondemented group between time 1 and time 2 (P>.10). However, the incident AD group exhibited precipitous declines in 8 of the 10 subscales between time 2 and time 3, the point at which they were clinically diagnosed (P<.01). Logistic regression analyses showed that only the delayed memory item was a significant predictor of who would develop AD, independent of age, sex, and years of education, at both of the first 2 times of measurement (P<.001). CONCLUSIONS: The diagnosis of AD is preceded by a long preclinical phase in which deficits in memory performance are most common. These deficits remain relatively stable up until the time that a dementia diagnosis can be rendered. Arch Neurol. 2000.

Aged↗
PubMed2000

Differences in the concentration of various synovial fluid constituents between the distal interphalangeal joint, the metacarpophalangeal joint and the navicular bursa in normal horses.

As a prerequisite for the identification of navicular disease markers, the concentrations of cartilage oligomeric matrix protein (COMP), total glycosaminoglycans (GAG), hyaluronan, metalloproteinases (MMP) 2 and 9 and total protein were measured in synovial fluid samples obtained from the distal interphalangeal joint (DIP), the metacarpophalangeal joint (MCP) and the navicular bursa of 24 horses. Mean GAG, COMP and total protein levels were significantly higher in the DIP joint and in the navicular bursa compared to the MCP joint. Hyaluronan content was lower. MMP -2 activity was present in all fluids measured and had similar levels in different joints. MMP -9 was present in 42 per cent of MCP joint samples and 58 per cent of DIP joint samples and of navicular bursal samples. In relation to the constituents measured, the composition of navicular bursal fluid was similar to the articular synovial fluids, in particular that obtained from the DIP joint. Correlation between the constituents of DIP joint fluid and navicular bursal fluid obtained from the same legs was statistically significant for all the parameters measured.

Animals↗
PubMed2000

Plasma beta-endorphin concentrations are increased in chronic obstructive pulmonary disease patients.

The present study is concerned with plasma beta-endorphin and glucose tolerance in patients with chronic obstructive pulmonary disease (COPD). Plasma beta-endorphin, glucagon and insulin concentrations were measured during an oral glucose tolerance test in 20 COPD patients and in 18 age-matched healthy controls (mean age 62 years). Seven patients had a moderate COPD (group I) and seven a severe COPD (group II). The remaining six severe COPD patients received long-term oxygen therapy (group III). We found that fasting levels of beta-endorphin were significantly increased in all patient groups compared to healthy controls (p < 0.01, 0.05 and 0.005, respectively). Six of the 13 severely diseased COPD patients had impaired glucose tolerance. Plasma beta-endorphin levels decreased significantly during OGTT in the COPD patients (p < 0.05). Fasting beta-endorphin levels were higher in patients with impaired glucose tolerance than in those patients with normal OGTT (42.0 pmol/L +/- 11.4 SD versus 34.8 +/- 10.2). However, this difference was not statistically significant. In conclusion, this study showed that beta-endorphin concentrations are increased in COPD patients whether or not they receive oxygen therapy.

Blood Glucose↗
PubMed2000

Mild cognitive impairment in the population and physical health: data on 1,435 individuals aged 75 to 95.

BACKGROUND: The physical health correlates of mild cognitive impairment (MCI) in the older individual are poorly known. The aim of this study was to investigate the relationship between physical health and MCI with population data. METHODS: Subjects were 1,435 nondemented 75- to 95-year-old subjects. MCI was defined as scoring one standard deviation below age- and education-specific means on the Mini-Mental State Examination. MCI was consistently associated with indicators of poorer health in logistic regression models with adjustment for potential confounders. RESULTS: The adjusted odds ratios for those with two, three, four, or more somatic symptoms compared with those with one or no symptoms were 1.3 (95% confidence intervals 1.0 to 1.9) and 2.1 (1.2 to 4.5; p for trend =.004); for those with poor self-rated health the odds ratio was 1.9 (1.4 to 2.6); for those with one, two, or more chronic diseases compared with those with no chronic diseases, the odds ratios were 1.3 (0.9 to 1.9) and 3.0 (1.2 to 7.6; p for trend =.02); and for those dying during the 3-year follow-up period the odds ratio was 1.5 (1.1 to 2.2). CONCLUSIONS: MCI is associated with poor physical health, leading to the hypothesis of a causal relationship between physical diseases and MCI in older populations.

Aged↗
PubMed2000

Morbidity and comorbidity in relation to functional status: a community-based study of the oldest old (90+ years).

OBJECTIVES: To describe health and functional status in the oldest old; to explore the relationships of morbidity and functional status; and to verify whether this relationship was modified by gender. DESIGN AND SETTING: A community-based survey including all inhabitants aged > or = 90 living in central Stockholm, Sweden. All participants were clinically examined by physicians, cognitively assessed by psychologists, and interviewed by nurses. Diagnoses were made according to the International Classification of Diseases-Ninth Revision (ICD-9), the DSM-III-R criteria for dementia, and Katz index of activities of daily living. PARTICIPANTS: Of the 698 subjects in the study population, 99 (14%) had died and 29 (4%) moved before examination. Of the remaining subjects, 502 (88.1%) were examined, and the refusal rate was 11.9%. MEASUREMENTS: Age- and gender-specific prevalence figures, and age-, gender- and education-adjusted odds ratios (OR) were used. RESULTS: Of 502 examined subjects, 19% had no disease and 73% were functionally independent. Dementia was the most prevalent disease among women (42.2%), and cardio- and cerebrovascular diseases were the most frequent among men (42.4%). Women had higher prevalences of dementia (adjusted OR = 2.1, 95% confidence interval (CI) 1.2-3.7) and fractures and musculoskeletal diseases (adjusted OR = 2.8, 95% CI 1.1-7.3), whereas men had a higher prevalence of malignancy (OR = 0.2, 95% CI 0.1-0.7). Women were more disabled than men independent of age, education, and number of diseases (adjusted OR = 2.2, 95% CI 1.1-4.3). CONCLUSIONS: A great proportion of nonagenarians were functionally independent despite their advanced age. Further studies are needed to clarify the excess of disability among very old women.

Activities of Daily Living↗
PubMed2000

CADASIL: hereditary arteriopathy leading to multiple brain infarcts and dementia.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) often begins with migraine with aura. Recurrent strokes usually appear between 30 and 50 years of age. The arteriopathy develops slowly, resulting in destruction of smooth muscle cells and thickening and fibrosis of the walls of small and medium-sized penetrating arteries with consequent narrowing of the lumen. This impairs cerebral blood flow, visible in PET, and produces characteristic white-matter hyperintensities in T2-weighted MRI on the basis of which CADASIL may be diagnosed well before the first stroke. Multiple lacunar infarcts, mainly in the frontal white matter and basal ganglia, lead to progressive permanent brain damage manifested as cognitive decline and finally as dementia. At present, no specific therapy is available. Infarcts result from thickening and fibrosis of the walls of small and medium-sized penetrating arteries with consequent obliteration and/or thrombosis. Although the symptoms are almost exclusively neurological, the arteriopathy is generalized and diagnosis can be made on the basis of accumulation of pathognomonic basophilic, PAS-positive and in electron microscopy osmiophilic material between degenerating smooth muscle cells in dermal arteries. CADASIL is caused by missense point mutations in the Notch3 gene, which encodes a transmembrane receptor protein with an important signaling function during development. The gene defects lead to either a gain or loss of a cysteine residue in the extracellular N-terminal part of the molecule, most probably causing a conformational and functional alteration. The function of Notch3 in adults and the definite pathogenesis of CADASIL are still unknown, but interestingly its intramembranous proteolytic cleavage may be regulated or implemented by presenilin similarly as cleavage of amyloid precursor protein in Alzheimer's disease.

Adult↗
PubMed2000

Incidence of dementia in relation to stroke and the apolipoprotein E epsilon4 allele in the very old. Findings from a population-based longitudinal study.

BACKGROUND AND PURPOSE: Both stroke and the apolipoprotein E (APOE) epsilon4 allele increase the risk of dementia. However, the interaction between stroke and APOE on dementia is still unclear. We addressed this topic by using a longitudinal design. METHODS: We followed up a community cohort of 1301 subjects aged >/=75 years, who did not have dementia at baseline. Among them, 92 subjects had a history of stroke (from 3 months to 16 years before baseline interview). After the 3-year follow-up, 224 dementia cases had been diagnosed. During the period of follow-up, 91 subjects had a first occurrence of stroke (incident stroke). The APOE genotype was known for 985 subjects. Cox proportional hazards regression models were constructed to estimate the risk for dementia in terms of relative risks (RRs) for stroke and the APOE epsilon4 allele, with adjustment for age, sex, education, systolic blood pressure, antihypertensive medication use, and heart disease. RESULTS: In the entire study population, RRs for dementia related to history of stroke and incident stroke were 1.7 (95% CI, 1.1 to 2.6) and 2.4 (95% CI, 1.6 to 3.5), respectively, after adjustment for all potential confounders. Subjects with stroke that occurred within 3 years before baseline had RR of 2.4 (95% CI, 1.4 to 4.2), whereas those with stroke occurring >3 years before baseline had RR of dementia of 1.1 (95% CI, 0.6 to 2.3). Among those with APOE information, individuals with only history of stroke (that occurred within 3 years before baseline) had RR of 3.1 (95% CI, 1.4 to 6.6), individuals with only the APOE epsilon4 allele had RR of 1.7 (95% CI, 1.1 to 2.5), and individuals with both factors had RR of 5.3 (95% CI, 2.1 to 13.4). The corresponding figures when incident stroke was examined instead of history of stroke were 2.3 (95% CI, 1.3 to 4.1), 1.7 (95% CI, 1.1 to 2.4), and 4.6 (95% CI, 2.0 to 10.6), respectively. The RR of interaction term for history of stroke and APOE epsilon4 was 1.1 (95% CI, 0.3 to 3.8; P=0.8). The corresponding figure was 1.2 (95% CI, 0.4 to 4.4; P=0.7) for incident stroke and APOE epsilon4. Furthermore, the RRs of dementia without any stroke and dementia with stroke in relation to APOE epsilon4 were 1.6 (95% CI, 1.1 to 2.3) and 1.2 (95% CI, 0.6 to 2.4), respectively. In addition, the APOE epsilon4 allele was not significantly related to the occurrence of stroke (RR=0.8; 95% CI, 0.5 to 1.5). CONCLUSIONS: A relatively fresh stroke is a risk factor for dementia. APOE epsilon4 increases the risk of dementia without stroke but not dementia with stroke. Our data do not support a multiplicative effect of stroke and the APOE epsilon4 allele on the risk of dementia. However, both factors seem to have an additive effect on the risk of dementia. The APOE epsilon4 allele does not increase the risk of stroke in this Swedish elderly population.

Aged↗
PubMed2000

Validity of self-reported stroke : The Tromso Study.

BACKGROUND AND PURPOSE: The aim of this study was to validate the diagnosis of self-reported stroke. METHODS: During 1994-1995, 27 159 people attended a population health survey in the community of Tromso, Norway, a response rate of 77%. A total of 418 attenders reported a history of stroke. In 1997, all individuals with a self-reported stroke who were still living in the community (n=362) were invited to a clinical reexamination. For each of the 269 people who were reexamined, a person who reported no history of stroke was selected and was reexamined in the same way. RESULTS: On the basis of the reexamination, 213 (79.2%) of the self-reported strokes were confirmed. Thirteen individuals (4.8%) had a possible stroke. The remaining 43 individuals had either transient ischemic attack (TIA; n=18), traumatic head injuries (n=16), or perinatal cerebral damage, complicated migraine, syncope, possible TIA, or cerebral aneurysm without bleeding (n=9). Among the confirmed strokes, 30 (14.1%) were hemorrhagic and 118 (55.4%) were thromboembolic. Of the 30 hemorrhages, 16 were subarachnoidal bleedings, 10 due to ruptured aneurysms. The histories of stroke, including both the symptoms and the signs, often had a paucity of details and precision, making it impossible to classify 65 stroke victims (30.5%) into stroke subtypes. The positive predictive value (PPV) of a self-reported stroke was 0.79. The PPV was significantly (P=0.016) greater in men (0.88) than in women (0.73). Individuals older than 60 years had a significantly greater PPV than those younger than 60 years (PPV 0.83 and 0.73, respectively; P=0.05). Hypertension was associated with a greater PPV, whereas a history of either ischemic heart disease, diabetes mellitus, lung disease, or depression had no impact on the PPV. The estimated sensitivity of self-reported stroke in the survey population was approximately 80% and the specificity was 99%. CONCLUSIONS: We conclude that a self-administered questionnaire can be used to assess the prevalence of stroke in epidemiological research.

Adult↗
PubMed2000

Low TENS treatment on post-stroke paretic arm: a three-year follow-up.

OBJECTIVE: To determine whether stroke patients with initial increases in arm motor recovery following low-frequency transcutaneous electrical nerve stimulation (low TENS) treatment go on to show long-term benefits. Also whether the same therapy results in long-term improvements in motor function, spasticity or activities of daily living (ADL). DESIGN: A three-year follow-up study. SUBJECTS: Twenty-eight stroke patients, who had participated in a randomized trial of daily treatment with low-frequency (1.7 Hz) transcutaneous electrical nerve stimulation (low TENS) on the paretic arm for three months starting 6-12 months after stroke. OUTCOMES: Fugl-Meyer Motor Performance Scale for evaluation of changes in arm motor function. A 6-point Ashworth Scale to measure spasticity. Barthel Index to evaluate performance in ADL. RESULTS: Motor function of the paretic arm had deteriorated in both treatment and control groups. Increased spasticity was seen in both groups. ADL score remained at a similar level in the low TENS group, whereas the control group had deteriorated during the same time period. CONCLUSIONS: Low TENS stimulation started 6-12 months after stroke may not have a specific effect on arm motor function years after completion of treatment.

Activities of Daily Living↗
PubMed2000

An in vitro study to compare 5 different techniques for injection of the navicular bursa in the horse.

Numerous different techniques for injection of the navicular bursa have been described but there is little conformity between these descriptions. A literature review was performed and techniques for injection of the navicular bursa were categorised into 5 approaches. This study was performed to evaluate the reproducibility of each technique and to assess which technique was consistently most successful. Five inexperienced operators performed each technique on 5 cadaver forelimbs. Once a needle had been placed, a radiograph was taken to confirm placement was in accordance with the description of the technique. Contrast agent was then injected and another radiograph taken to determine whether the navicular bursa had been injected successfully. The position of the navicular bone was highly predictable as a point 1 cm distal to the coronary band and halfway between the most dorsal and most palmar aspect of the coronary band. The use of this point as a landmark for injection of the navicular bursa allowed a high degree of accuracy and reliability of needle placement, irrespective of foot conformation.

Animals↗
PubMed1999

Tau gene polymorphisms and apolipoprotein E epsilon4 may interact to increase risk for Alzheimer's disease.

In an effort to analyze the genetic role of tau in Alzheimer's disease (AD), 17 polymorphisms were identified. Eleven of these polymorphisms were in complete linkage disequilibrium and segregated as two haplotypes, A and B. The A and B haplotypes were investigated in 269 AD cases and 238 controls from two different sources, a clinic-based group (mean age of onset 65+/-9 years), and a population-based group (mean age of onset 80+/-5 years). A synergistic effect between the common tau genotype AA and apolipoprotein E (APOE epsilon4) was found in the clinic-based AD group. Our study suggests that the common tau genotype AA may interact with APOE epsilon4 in increasing the risk of AD in a subgroup of the AD population.

Aged↗
PubMed1999

Mortality in nondemented subjects with cognitive impairment: the influence of health-related factors.

Nondemented older subjects with cognitive impairment are at higher risk of death than are mentally intact persons. It is unknown whether the effect of cognitive impairment on mortality is independent or mediated by poorer health or other factors. To address this issue, the authors used a prospective population-based cohort study with 8 years of follow-up started in 1987 in the urban district of Kungsholmen, Stockholm, Sweden. Subjects were all 75- to 95-year-old subjects nondemented at baseline (n = 1,435). Data on cognition, health (mental and subjective health, physical diseases and comorbidity, nutritional status, and disability), and apolipoprotein E genotype were collected at baseline as was time of death at follow-up. Cognitive impairment was defined on the basis of age- and education-specific cutoffs on the Mini-Mental State Examination. When compared with cognitively unimpaired subjects (n = 1,210), those cognitively impaired (n = 225) had poorer health conditions, were more frequently apolipoprotein E epsilon4 carriers, and had greater mortality risk (hazard ratio = 1.7; 95% confidence interval: 1.5, 2.1). Neither health nor apolipoprotein E genotype accounted for the association of cognitive impairment with mortality (adjusted hazard ratio = 1.6; 95% confidence interval: 1.3, 1.9). The functional and behavioral consequences associated with the progression of cognitive impairment may mediate the increased mortality risk.

Aged↗
PubMed1999

Smoking and the occurrence of Alzheimer's disease: cross-sectional and longitudinal data in a population-based study.

The authors tested the hypothesis that smoking exerts a protective effect on Alzheimer's disease or dementia in a population-based cohort of 668 people aged 75-101 years (Sweden). Smoking was negatively associated with prevalent Alzheimer's disease (adjusted odds ratio = 0.6, 95% confidence interval 0.4-1.1) and dementia (adjusted odds ratio = 0.6, 95% confidence interval 0.4-1.0). Over 3-year follow-up (1989-1992), the hazard ratios of incident Alzheimer's disease and dementia due to smoking were 1.1 (95% confidence interval 0.5-2.4) and 1.4 (95% confidence interval 0.8-2.7). Mortality over 5-year follow-up was greater among smokers in demented (hazard ratio = 3.4) than nondemented (hazard ratio = 0.8) subjects. Smoking does not seem protective against Alzheimer's disease or dementia, and the cross-sectional association might be due to differential mortality.

Aged↗