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Biomedical subjects

F Verhey

Publications and source records attributed to F Verhey.

16 recordsLinked to original sources
PubMed2006

Checklist for cognitive and emotional consequences following stroke (CLCE-24): development, usability and quality of the self-report version.

OBJECTIVE: In this paper a new checklist (CLCE-24) for identification of cognitive and emotional problems after stroke is presented. The CLCE-24 is intended to support a clinical interview by health care professionals other than the trained (neuro)psychologist. METHODS: Patients were interviewed with the CLCE-24, 6 months post stroke. Usability was determined by interviews. Quality of the self-report version was determined using reference instruments (MMSE, CAMCOG). RESULTS: Sixty-nine patients participated in the study (37 men; mean age 66 years). Both patients and assessors were positive about the use of the CLCE-24. Eighty percent of the patients had cognitive and/or emotional problems (73% cognitive; 51% emotional problems). Patients with complaints on the CLCE-24 also showed problems on the MMSE and the CAMCOG (p<0.05). The CLCE-24 was a predictor of the MMSE and CAMCOG (Adj. R(2)=0.13 and 0.16, respectively) at 12 months post stroke. Internal consistency of the CLCE-24 was good (alpha of 0.81). CONCLUSIONS: The CLCE-24 is a usable and valid instrument for cognitive screening by health care professionals in the stroke service in the chronic phase after stroke.

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PubMed2006

3-year study of donepezil therapy in Alzheimer's disease: effects of early and continuous therapy.

Delays in the diagnosis of Alzheimer's disease, and, therefore, delays in treatment, may have a detrimental effect on a patient's long-term well-being. This study assessed the effects of postponing donepezil treatment for 1 year by comparing patients treated continuously for 3 years with those who received placebo for 1 year followed by open-label donepezil for 2 years. Patients (n = 286) with possible or probable Alzheimer's disease (according to DSM-IV, NINCDS-ADRDA, and Mini-Mental State Examination criteria; see text) were randomized to receive donepezil (5 mg/day for 4 weeks, 10 mg/day thereafter) or placebo (delayed-start group) for 1 year. Of the 192 completers, 157 began a 2-year, open-label phase of donepezil treatment. Outcome measures were the Gottfries-Bråne-Steen scale, the Mini-Mental State Examination, the Global Deterioration Scale, the Progressive Deterioration Scale, the Neuropsychiatric Inventory, and safety (adverse events). Mixed regression analysis was used to compare changes between the groups over 3 years on the efficacy measures. There was a trend for patients receiving continuous therapy to have less global deterioration (Gottfries-Bråne-Steen scale) than those who had delayed treatment (p = 0.056). Small but statistically significant differences between the groups were observed for the secondary measures of cognitive function (Mini-Mental State Examination; p = 0.004) and cognitive and functional abilities (Global Deterioration Scale; p = 0.0231) in favor of continuous donepezil therapy. Over 90% of the patients in both cohorts experienced one treatment-emergent adverse event; most were considered mild or moderate. In conclusion, patients in whom the start of treatment is delayed may demonstrate slightly reduced benefits as compared with those seen in patients starting donepezil therapy early in the course of Alzheimer's disease. These data support the long-term efficacy and safety of donepezil.

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PubMed2006

Focal or generalized vascular brain damage and vulnerability to depression after stroke: a 1-year prospective follow-up study.

BACKGROUND: Both the lesion location hypothesis and the vascular depression hypothesis have been proposed to explain the high incidence of depression in stroke patients. However, research studying both hypotheses in a single cohort is, at present, scarce. OBJECTIVE: To test the independent effects of lesion location (left hemisphere, anterior region) and of co-occurring generalized vascular damage on the development of depression in the first year after ischemic stroke, while other risk factors for depression are controlled for. METHODS: One hundred and ninety consecutive patients with a first-ever, supratentorial infarct were followed up for one year. CT was performed in the acute phase of stroke, while in 75 patients an additional MRI scan was also available. Depression was assessed at 1, 3, 6, 9, and 12 months after stroke using self-rating scales as screening tools and the SCID-I to diagnose depression according to DSM-IV criteria. RESULTS: Separate analyses of the lesion location hypothesis and the vascular depression hypothesis failed to reveal significant support for either of these biological models of post-stroke depression. Similar negative results appeared from one overall, multivariate analysis including variables of both focal and generalized vascular brain damage, as well as other non-cerebral risk factors. In addition, level of handicap and neuroticism were independent predictors of depression in this cohort, as has been reported previously. CONCLUSION: This study supports neither the lesion location nor the vascular depression hypothesis of post-stroke depression. A biopsychosocial model including both premorbid (prior to stroke) vulnerability factors, such as neuroticism and (family) history of depression, as well as post-stroke stressors, such as level of handicap, may be more appropriate and deserves further study.

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PubMed2006

Depression after a cerebrovascular accident. The importance of the integration of neurobiological and psychosocial pathogenic models.

Stroke survivors frequently suffer from depression. Research has focused on the incidence, phenomenology, course and risk factors of poststroke depression (PSD). Special attention has been paid to biological explanatory models, such as the lesion location and vascular depression hypotheses. In addition to such biological approaches, the role of psychosocial factors should not be neglected. This review critically discusses the proceedings in PSD research emphasizing the need for a biopsychosocial approach.

Antidepressive Agents↗
PubMed2003

Combination of serum markers related to several mechanisms in Alzheimer's disease.

Alzheimer's disease (AD) probably involves several pathobiochemical mechanisms and this may be reflected by changes in different serum components. The present study investigated whether the combined analysis of serum molecules related to different mechanisms improves the discrimination of AD patients from healthy controls. Serum of patients with AD was analyzed for a broad spectrum of marker molecules, including 11 inflammatory proteins, 12 sterol intermediates and phytosterols, 2 brain-specific proteins and 4 constituents involved in homocysteine homeostasis. The serum molecule concentrations were combined in a logistic regression model, using a forward stepwise inclusion mode. The results showed that the combination of interleukin-6 (IL-6) receptor, protein alpha1 fraction, cysteine and cholesterol concentrations improved the discrimination between AD patients and healthy controls compared to the single markers. In conclusion, the results of this study have shown that the complex pathology in AD is reflected in a pattern of altered serum concentrations of several marker molecules related to several pathobiochemical mechanisms.

Adult↗
PubMed2003

A comparative study into the one year cumulative incidence of depression after stroke and myocardial infarction.

BACKGROUND: The high incidence of post-stroke depression has been claimed to reflect a specific, stroke related pathogenesis in which lesion location plays an important role. To substantiate this claim, post-stroke depression should occur more often than depression after another acute, life threatening, disabling disease that does not involve cerebrovascular damage. OBJECTIVES: To compare the cumulative one year incidence of depression after stroke and after myocardial infarction, taking into consideration differences in age, sex, and the level of handicap. METHODS: In a longitudinal design, 190 first ever stroke patients and 200 first ever myocardial infarction patients were followed up for one year. Depression self rating scales were used as a screening instrument to detect patients with depressive symptoms. Major and minor depression was assessed at one, three, six, nine, and 12 months after stroke or myocardial infarction according to DSM-IV criteria, using the structured clinical interview from DSM-IV. The severity of depressive symptoms was measured with the Hamilton depression rating scale. Level of disability and handicap was rated with the Rankin handicap scale. RESULTS: The cumulative one year incidence of major and minor depression was 37.8% in stroke patients and 25% in patients with myocardial infarction (hazard ratio 1.6; p = 0.06). This difference disappeared after controlling for sex, age, and level of handicap. In addition, no differences were found in the severity of depressive symptoms or in the time of onset of the depressive episode after stroke or myocardial infarction. CONCLUSIONS: Depression occurs equally often during the first year after stroke and after myocardial infarction when non-specific factors such as sex, age, and level of handicap are taken into account. Thus the relatively high incidence of post-stroke depression seems not to reflect a specific pathogenic mechanism. Further research is needed to investigate whether vascular factors play a common role in the development of depression after stroke and myocardial infarction.

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PubMed2001

A comparative study of the effects of carbamazepine and the NMDA receptor antagonist remacemide on road tracking and car-following performance in actual traffic.

RATIONALE: Antiepileptic drugs are known to produce side effects which may impair driving performance. Performance effects, however, may differ substantially between individual antiepileptic drugs. OBJECTIVE: To compare the effects of carbamazepine, remacemide, and placebo on actual driving performance during a 12-day incremental dosing regimen. METHODS: Twenty-two healthy volunteers participated in a three-way, double-blind, cross-over driving study. Treatment effects were assessed in two actual driving tests carried out on days 8, 10, and 12 of each treatment period. The Road Tracking Test involved driving an instrumented vehicle at a constant speed and steady lateral position between the delineated lane boundaries. Standard deviation of lateral position (SDLP) was measured to indicate precision of road tracking control. The Car-Following Test involved driving the same vehicle behind a leading car and maintaining that distance while the latter executed a series of deceleration/acceleration maneuvers. Time to speed adaptation (TSA) and brake reaction time were the primary measures. RESULTS: Remacemide did not affect the subjects' driving performance. Carbamazepine increased SDLP throughout treatment and lengthened TSA on day 8. Changes in SDLP relative to placebo were comparable to those previously seen in drivers conducting the same test with blood alcohol concentrations of 0.05 g/dl. CONCLUSION: Remacemide, at the given dose regimen, does not affect driving performance. Carbamazepine, at the given dose regimen, can produce mild but sufficient impairment to put epileptic patients at risk when driving, at least during initiation therapy.

Acetamides↗
PubMed2001

A 1-year, randomized, placebo-controlled study of donepezil in patients with mild to moderate AD.

OBJECTIVE: To evaluate the long-term clinical efficacy and safety of donepezil versus placebo over 1 year in patients with mild to moderate AD. METHODS: Patients (n = 286; mean age, 72.5 years) with possible or probable AD from five Northern European countries were randomized to receive either donepezil (n = 142; 5 mg/day for 28 days, followed by 10 mg/day) or placebo (n = 144) for 1 year. RESULTS: The study was completed by 66.9% of the donepezil- and 67.4% of the placebo-treated patients. The benefit of donepezil over placebo was demonstrated by the Gottfries-Bråne-Steen (a global assessment for rating dementia symptoms) total score at weeks 24, 36, and 52 (p < 0.05) and at the study end point (week 52, last observation carried forward; p = 0.054). Advantages of donepezil over placebo were also observed in cognition and activities of daily living (ADL) assessed by the Mini-Mental State Examination at weeks 24, 36, and 52, and the end point (p < 0.02) and by the Progressive Deterioration Scale at week 52 and the end point (p < 0.05). Adverse events (AE) were recorded for 81.7% of donepezil- and 75.7% of placebo-treated patients, with 7% of donepezil- and 6.3% of placebo-treated patients discontinuing because of AE. Treatment response to donepezil was not predicted by APOE genotype or sex in this population. CONCLUSION: As the first 1-year, multinational, double-blinded, placebo-controlled study of a cholinesterase inhibitor in AD, these data support donepezil as a well tolerated and effective long-term treatment for patients with AD, with benefits over placebo on global assessment, cognition, and ADL.

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PubMed2001

Stroke and mental health care: a record linkage study.

BACKGROUND: Stroke is associated with psychiatric morbidity but little is known about mental health care use in stroke patients. METHOD: A probability record linkage study was conducted linking stroke cases admitted to a teaching hospital serving a catchment area between 1987 and 1995 with records from a psychiatric case register covering the same area. RESULTS: Stroke patients had a more than twofold increased risk of contact with mental health care than individuals in the general population (yearly prevalences of respectively 88 and 39 per 1000; risk ratio 2.24; 95 % CI 2.04-2.45). One-third of all stroke admissions had had mental health care before and more than half had had mental health care after the stroke. In the year of admission for stroke, the probability of receiving mental health care was highest, while in the more remote years the risk was lower. CONCLUSION: Stroke is associated with an increased probability of contact with mental health services. The pattern of mental health care of a stroke patient is different from that of other mental health patients: more episodic and concentrated around the time of admission for stroke.

Adult↗
PubMed2001

Research into the specificity of depression after stroke: a review on an unresolved issue.

Iwo decades of research have failed to generate consistent insight into the specificity of poststroke depression (PSD). This is, at least in part, caused by methodological difficulties. Differences in symptom profile between PSD and depression with no or another medical cause were described, but no specific and unequivocal clinical picture has been established so far. Prevalence rates of PSD varied largely between studies. In community based studies using standardised diagnostic instruments for depression, relatively low prevalence rates were reported compared to inpatient or rehabilitation studies. PSD occurs most frequently in the first few months after stroke, while a new incidence peak may occur 2-3 years after stroke. Two systematic reviews on the relation between lesion location and depression did not support the claim that left hemisphere lesions are a risk factor for PSD. A new concept of vascular depression has been proposed, which relates depression in the elderly to acute or chronic damage to the cerebral vascular system. Future efforts should aim at increasing the uniformity of study designs, assessment tools should be further improved for use in cognitively impaired patients and appropriate control groups should be defined to study the characteristic features of PSD.

Depressive Disorder↗
PubMed2000

Normal cognitive performance in patients with chronic alcoholism in contrast to patients with Korsakoff's syndrome.

This study investigated which cognitive deficits are associated with chronic alcoholism. Neuropsychological profiles and MRI brain structure volumes of 14 patients with Korsakoff's syndrome, 15 patients with chronic alcoholism, and 16 healthy control subjects were compared. The patients with alcoholism had a normal cognitive performance and normal brain structure volumes. The patients with Korsakoff's syndrome had performance deficits on tests of memory, visuoperceptual, and executive functions, as well as reduced brain structure volumes. The results suggest that the cognitive deficits cannot be ascribed to mere chronic consumption of alcohol. If cognitive deficits are present in patients with chronic alcoholism, this may point to an underlying brain disorder.

Adult↗
PubMed1995

Caffeine attenuates scopolamine-induced memory impairment in humans.

Caffeine consumption can be beneficial for cognitive functioning. Although caffeine is widely recognized as a mild CNS stimulant drug, the most important consequence of its adenosine antagonism is cholinergic stimulation, which might lead to improvement of higher cognitive functions, particularly memory. In this study, the scopolamine model of amnesia was used to test the cholinergic effects of caffeine, administered as three cups of coffee. Subjects were 16 healthy volunteers who received 250 mg caffeine and 2 mg nicotine separately, in a placebo-controlled double-blind cross-over design. Compared to placebo, nicotine attenuated the scopolamine-induced impairment of storage in short-term memory and attenuated the scopolamine-induced slowing of speed of short-term memory scanning. Nicotine also attenuated the scopolamine-induced slowing of reaction time in a response competition task. Caffeine attenuated the scopolamine-induced impairment of free recall from short- and long-term memory, quality and speed of retrieval from long-term memory in a word learning task, and other cognitive and non-cognitive measures, such as perceptual sensitivity in visual search, reading speed, and rate of finger-tapping. On the basis of these results it was concluded that caffeine possesses cholinergic cognition enhancing properties. Caffeine could be used as a control drug in studies using the scopolamine paradigm and possibly also in other experimental studies of cognitive enhancers, as the effects of a newly developed cognition enhancing drug should at least be superior to the effects of three cups of coffee.

Adult↗
PubMed1985

[Contribution of contingent negative variation (CNV) to the study of schizophrenia].

The authors first review neurobiological and psychopathological data supporting the use of Contingent Negative Variation (CNV) for the study of Schizophrenia. Next, results obtained with the method are presented (i.e. with S1-S2 interval = 1 sec, and recording leads = Cz and Fz) comparing 34 control subjects with 29 schizophrenic patients, all diagnosed with the "Present State Examination" test or PSE (Wing and Sartorius). In patients, reduced CNV amplitude (p less than 0.0001), together with reduced CNV resolution (p less than 0.02) and less differentiated topographical spreading (p less than 0.02) were observed relatively to controls. There is also a slower reaction time (p less than 0.02). Such abnormalities are sufficiently frequent as to allow CNV as a helping diagnostic tool, with a sensitivity rate of 83% and a specificity rate of 85%. These results are discussed with respect to the psychopathological and neurobiological problems in relation with schizophrenia.

Contingent Negative Variation↗
PubMedDate not supplied

Recommendations concerning neuropsychiatric symptoms assessment.

In the last decades, there has been an increased awareness of the importance of neuropsychiatric symptoms in dementia, as they are highly frequent, put a large burden on the caregiver, and often may lead to early institutionalization. Whereas dementia is still principally defined as a cognitive disorders, neuropsychiatric symptoms are now regarded as an intrinsic aspect of dementia and neurodegenerative processes. The question to be addressed here is what neuropsychiatric assessments should be used in long term trials adhering a disease modifying approach to Alzheimer's Disease (AD). An ideal marker should be valid, be measured reliably, be highly sensitive to change, have a clear correlation with the progression of disease, and have a clear relationship with the neuropathological substrate. In addition, the marker should address particularly the early stages of AD, preferably the prodromal predementia stages.

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