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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To compare the psychometric properties of the Hamilton Rating Scale for Depression (Ham-D) in patients with stroke, Alzheimer's dementia (AD), and Parkinson's disease (PD), receiver operating characteristic curves were plotted for each group. The concurrent validity of the Ham-D with the DSM-IV criteria for major depressive disorder was high in each of these groups. However, optimal performance of the Ham-D requires the application of disease-specific cutoff scores for screening, diagnostic, and dichotomization purposes. These disease-specific cutoff scores were highest in PD, lower in AD, and lowest in stroke patients.
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PMID:Disease-specific properties of the Rating Scale for Depression in patients with stroke, Alzheimer's dementia, and Parkinson's disease. 1215 58

The goal of treatment of major depression should be full remission. Many patients, however, fail to achieve or maintain symptom-free status. Residual depressive symptoms are common, even where there has been a robust response to antidepressant therapy. In clinical studies, approximately one-third of patients achieve a full remission, one-third experience a response and one-third are nonresponders. Partial remission is characterized by the presence of poorly defined residual symptoms. These symptoms typically include depressed mood, psychic anxiety, sleep disturbance, fatigue and diminished interest or pleasure. It is currently unclear which factors predict partial remission. However, it is clear that residual symptoms are powerful predictors of relapse, with relapse rates 3-6 times higher in patients with residual symptoms than in those who experience full remission. Residual symptoms are also associated with more medical and psychiatric visits, increased public assistance, disability benefits, thoughts of and attempts at suicide and chronicity. The risk of stroke and coronary events is also higher in patients with residual depressive symptoms. The substantial proportion of patients who achieve only partial remission has traditionally been neglected in antidepressant trials. Given that residual symptoms may relate, in part, to an incompatibility between patient and treatment, further research is needed to predict a better match. These symptoms are a clinically relevant state of illness, and the correct choice of initial antidepressant treatment should offer the greatest chance of achieving full remission.
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PMID:Prevalence and outcome of partial remission in depression. 1217 33

Several studies have reported an association between cognitive impairment and major depression following stroke but failed to find a similar association among patients with traumatic brain injury (TBI). This study examined the hypothesis that age differences between stroke and TBI patients would account for the differences in the effect of major depression on cognitive function. We examined subjects' cognitive function using the Mini-Mental State Examination and compared findings among patients with stroke or TBI. Results indicated that stroke patients with major depression (N = 73) were significantly older and more cognitively impaired than similar TBI patients (N = 35), even after matching patients for lesion volume and years of education. After matching for age, however, there was no association of major depression with cognitive impairment in this relatively young stroke population. These findings support the hypothesis that age, presumably related to physiological response to brain injury, accounts for differences in the effect of major depression on cognitive function between stroke and TBI patients.
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PMID:Comparison of cognitive impairment associated with major depression following stroke versus traumatic brain injury. 1218 55

Normal ageing and Alzheimer's disease (AD) have many features in common and, in many respects, both conditions only differ by quantitative criteria. A variety of genetic, medical and environmental factors modulate the ageing-related processes leading the brain into the devastation of AD. In accordance with the concept that AD is a metabolic disease, these risk factors deteriorate the homeostasis of the Ca(2+)-energy-redox triangle and disrupt the cerebral reserve capacity under metabolic stress. The major genetic risk factors (APP and presenilin mutations, Down's syndrome, apolipoprotein E4) are associated with a compromise of the homeostatic triangle. The pathophysiological processes leading to this vulnerability remain elusive at present, while mitochondrial mutations can be plausibly integrated into the metabolic scenario. The metabolic leitmotif is particularly evident with medical risk factors which are associated with an impaired cerebral perfusion, such as cerebrovascular diseases including stroke, cardiovascular diseases, hypo- and hypertension. Traumatic brain injury represents another example due to the persistent metabolic stress following the acute event. Thyroid diseases have detrimental sequela for cerebral metabolism as well. Furthermore, major depression and presumably chronic stress endanger susceptible brain areas mediated by a host of hormonal imbalances, particularly the HPA-axis dysregulation. Sociocultural and lifestyle factors like education, physical activity, diet and smoking may also modulate the individual risk affecting both reserve capacity and vulnerability. The pathophysiological relevance of trace metals, including aluminum and iron, is highly controversial; at any rate, they may adversely affect cellular defences, antioxidant competence in particular. The relative contribution of these factors, however, is as individual as the pattern of the factors. In familial AD, the genetic factors clearly drive the sequence of events. A strong interaction of fat metabolism and apoE polymorphism is suggested by intercultural epidemiological findings. In cultures, less plagued by the 'blessings' of the 'cafeteria diet-sedentary' Western lifestyle, apoE4 appears to be not a risk factor for AD. This intriguing evidence suggests that, analogous to cardiovascular diseases, apoE4 requires a hyperlipidaemic lifestyle to manifest as AD risk factor. Overall, the etiology of AD is a key paradigm for a gene-environment interaction. Copyright 2000 John Wiley & Sons, Ltd.
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PMID:A unifying hypothesis of Alzheimer's disease. III. Risk factors. 1240 43

Causes of cognitive impairment after stroke are not yet clear because a large number of sociodemographic and clinical variables complicate the understanding of the phenomenon. We aim to evaluate sociodemographic and clinical predictors of cognitive level and depression in subjects with different lesion laterality. We assessed 153 right (n = 87) and left (n = 66) unilateral first-ever stroke patients within the first year of illness with the Structured Clinical Interview for DSM-IV-Patient Edition, the Hamilton Depression Rating Scale, the Hamilton Anxiety Rating Scale, the State Trait Anger Expression Inventory, the Barthel Index, and the Mini Mental State Examination (MMSE). Sociodemographic variables were also measured. Sixty-two (41 %) patients suffered from Major Depression (MDD), and 26 (17 %) suffered from Minor Depression (MIND). An univariate analysis of variance showed that MMSE scores were different throughout the groups of left and right stroke patients with MDD, MIND and without depression. Left stroke patients with MDD were more cognitively impaired than all the other groups. This result was valid after controlling for the effect of lesion location on cognitive level difference between the groups. A series of stepwise multiple regression analyses indicated that depression severity was a predictor of cognitive level and vice-versa in left hemispheric stroke patients only. Moreover, educational level in right hemispheric stroke patients and state-anger and number of regions affected in left hemispheric stroke patients were other predictors of cognitive level. The study confirms the hypothesis that predictors of cognitive level and depression severity are different in subjects with different laterality of lesion and that MDD is associated with cognitive impairment in left stroke patients.
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PMID:Predictors of cognitive level and depression severity are different in patients with left and right hemispheric stroke within the first year of illness. 1242 95

The objective of the study was to detect changes of depression and cognitive level associated with right and left brain damage during SSRI treatment in subjects with post-stroke Major Depressive Disorder (MDD). After the baseline evaluation, the 45 patients included received a single oral dose of 20-40 mg of fluoxetine or 50-100 mg of sertraline. At day 0, 7, 14, 28, 42, and 56 a psychometric test battery comprising the Hamilton Depression Rating Scale (HDRS) and the Mini Mental State Examination (MMSE) was administered. In the whole group repeated measures ANOVAs revealed a highly significant (p < 0.0001) time effect for HDRS and MMSE scores. However, depression improved much more in right stroke subjects in comparison with left stroke subjects (p < 0.001 for the HDRS by laterality interaction). Moreover, there is a suggestion of a possible selective serotonin reuptake inhibitor (SSRI) efficacy in cognitive impairment associated to post-stroke MDD but in treatment-responders only. At the endpoint, chi-square analysis showed that there was a different prevalence rate of MDD between left (n = 10; 50 %) and right (n = 4; 16 %) stroke patients, whereas the prevalence rate of Minor Depression was identical (25 %). The SSRIs fluoxetine and sertraline could be efficacious treatments for post-stroke MDD but these findings suggest that left stroke could be a predictor of treatment resistance.
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PMID:Is left stroke a risk-factor for selective serotonin reuptake inhibitor antidepressant treatment resistance? 1270 Sep 11

The aim of this study was to determine the effect of mood disorders, including psychological distress and depression, on stroke outcome. Male Fischer rats were exposed to immobilisation stress, an animal paradigm of psychological stress, major depression and post-traumatic stress disorder. Either a subacute (1 h for 7 days) or a chronic (6 h for 21 days) exposure to stress was applied 24 h before permanent middle cerebral artery occlusion (MCAO). Stroke outcome was assessed by measurement of infarct size and behavioural characterisation. Serum glutamate and brain ATP levels as well as brain glutamate transporter function and expression were studied in the search for the molecular mechanisms involved. Subacute stress exposure increased infarct size and decreased behavioural scores after stroke. On the contrary, chronic stress exposure decreased infarct size. Peak serum glutamate levels correlated with infarct size after MCAO. Expression of glutamate transporters was decreased by subacute stress, whereas the expression of EAAT1, a glial glutamate carrier, was increased after the chronic stress protocol. Our results indicate that distinct patterns of stress determine different stroke outcomes, and that expressional changes of brain glutamate transporters, able to affect glutamate release after stroke, are involved.
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PMID:Effect of subacute and chronic immobilisation stress on the outcome of permanent focal cerebral ischaemia in rats. 1285 May 80

In recent years, poststroke depression has attracted worldwide interest. This review focuses on the major research themes that have emerged. Pooled data from studies conducted throughout the world have found prevalence rates for major depression of 19.3% among hospitalized patients and 23.3% among outpatient samples. The diagnosis of poststroke depression is most appropriately based on a structured mental state exam and DSM-IV criteria for depression due to stroke with major depressive-like episode or depressive features. Rarely, poststroke patients may also develop bipolar mood disorder. The treatment of poststroke depression has been examined in several placebo-controlled randomized clinical trials with both nortriptyline and citalopram showing efficacy. The progression of recovery following stroke can be altered by treating depression, which has been shown to improve recovery in activities of daily living and cognitive impairment and to decrease mortality. In addition, two studies have demonstrated that poststroke depression can be prevented using antidepressant medication, which also decreases the frequency of associated physical illness. Furthermore, two studies have shown that premorbid depression can significantly increase the risk of stroke over the subsequent 10-15 years. The mechanisms underlying the association of cerebrovascular diseases and mood disorder are important areas for future investigation.
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PMID:Poststroke depression: prevalence, diagnosis, treatment, and disease progression. 1289 12

Impairments in activities of daily living (ADL) are common after stroke and may be related to poststroke depression. We have demonstrated that remission of poststroke major depression was associated with improvement in ADL. The administration of antidepressants within the first 3 months after stroke has been shown to prevent poststroke depression, early administration might also improve recovery of ADL among patients with stroke. This study examines the effect of early versus late treatment with antidepressants on recovery in ADL. Among 62 patients after stroke, the therapeutic effect of a 3-month course of antidepressants begun during the first month after stroke was compared with the effect of treatment begun after 1 month. The severity of impairment was measured using the Functional Independence Measure (FIM) and post-treatment outcome was assessed over the following 21 months. Although both the early and late treatment groups showed improvements in FIM scores during the 3 months of treatment, the early treatment group improved significantly more than the late treatment group. After the treatment, the early treatment group maintained this improvement over 2 years while the late treatment group deteriorated over time. There were no significant differences in the 2 groups that would explain the findings. Recovery in ADL impairment after stroke appeared to be enhanced by the use of antidepressant medication if treatment was started within the first month after stroke. These findings are consistent with the hypothesis that there may be a time-related therapeutic window in the treatment of physical impairment associated with poststroke depression.
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PMID:The effect of early versus late antidepressant treatment on physical impairment associated with poststroke depression: is there a time-related therapeutic window? 1455 66

Depression is the most frequent psychiatric complication among stroke survivors. Several aspects have been indicated as risk factors for its occurrence. This review investigates the risk factors and the state of the art of the treatment for poststroke depression, in order to stimulate its detection and adequate treatment by the physician. The point prevalence of Major Depression after stroke varies from 10% to 34%, varying according to differences among the research methods. The length of poststroke period, characteristics of the sample, type of treatment received by patients and diagnostic criteria used can influence the reported prevalence of poststroke depression. The risk factors that have been associated with the occurrence of poststroke depression, are: functional and cognitive impairment, previous history of depression and stroke, sex, age, hypercortisolism, poor social support and stroke neuroanatomic correlates. This one has supported the formulation of a pathophysiological mechanism for poststroke depression related with prefrontosubcortical circuits and neurotransmission of biogenic amines. The depression has a harmful impact on stroke prognosis. It can cause a more severe functional impairment, retardation of the rehabilitation process, outcome complications, and a higher mortality risk. In addition, poststroke depression has not been accurately diagnosed and treated. With the advantage of the magnetic resonance, researchers should focus investigations on the association of specific cerebral regions with the depressive manifestation and treatment response. Methodological issues such as previous history of depression and the type of the depressive manifestation should be considered for analysis.
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PMID:[Poststroke depression: risk factors and antidepressant treatment]. 1496 1


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