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Poststroke Depression (poststroke + depression)
Selected AbstractsThe Effect of Poststroke Depression on Recovery from StrokePSYCHOGERIATRICS, Issue 2 2002Amane Tateno Background: Stroke is a major health problem and poststroke depression is known to be one of the frequent and severe psychiatric complications following stroke. Methods: Based on the results of structured psychiatric mental state exams and DSM diagnostic criteria, the prevalence of poststroke depression has been examined in numerous study populations throughout the world. Longitudinal examinations have documented the effect of poststroke depression on recovery from stroke. Results: The mean prevalence of poststroke major depression was 21.1 % and minor depression was 17.1% among hospitalized or outpatient samples. Community samples showed a slightly lower rate of 14.1% and 9.1%, respectively. Furthermore, the existence of poststroke depression leads to poorer physical recovery, greater cognitive impairment, and worse recovery in activities of daily living compared with non-depressed patients. Several studies have also found that poststroke depression is associated with increased mortality compared with non-depressed patients who had comparable strokes and similar premorbid risk factors. Finally, several studies have found that successful treatment of poststroke depression improves both cognitive and physical recovery and decreases mortality. Conclusion: The current review documents the beneficial effect of identifying and treating poststroke depression on both recovery and survival following stroke. [source] Little evidence for different phenomenology in poststroke depressionACTA PSYCHIATRICA SCANDINAVICA, Issue 6 2010T. B. Cumming Cumming TB, Churilov L, Skoog I, Blomstrand C, Linden T. Little evidence for different phenomenology in poststroke depression. Objective:, It remains unclear whether mood depressive disorders after stroke have a distinct phenomenology. We evaluated the symptom profile of poststroke depression (PSD) and assessed whether somatic symptoms were reported disproportionately by stroke patients. Method:, The sample was 149 stroke patients at 18 months poststroke and 745 age- and sex-matched general population controls. A comprehensive psychiatric interview was undertaken and depression was diagnosed according to DSM-III-R criteria. Results:, Depressed controls reported more ,inability to feel' (P = 0.002) and ,disturbed sleep' (P = 0.008) than depressed stroke patients. Factor analysis of the 10 depressive symptoms identified two main factors, which appeared to represent somatic and psychological symptoms. There was no difference in scores on these two factors between stroke patients and controls. Conclusion:, Phenomenology of depression at 18 months poststroke is broadly similar but not the same as that described by controls. Somatic symptoms of depression were not over-reported by stroke patients. [source] The Effect of Poststroke Depression on Recovery from StrokePSYCHOGERIATRICS, Issue 2 2002Amane Tateno Background: Stroke is a major health problem and poststroke depression is known to be one of the frequent and severe psychiatric complications following stroke. Methods: Based on the results of structured psychiatric mental state exams and DSM diagnostic criteria, the prevalence of poststroke depression has been examined in numerous study populations throughout the world. Longitudinal examinations have documented the effect of poststroke depression on recovery from stroke. Results: The mean prevalence of poststroke major depression was 21.1 % and minor depression was 17.1% among hospitalized or outpatient samples. Community samples showed a slightly lower rate of 14.1% and 9.1%, respectively. Furthermore, the existence of poststroke depression leads to poorer physical recovery, greater cognitive impairment, and worse recovery in activities of daily living compared with non-depressed patients. Several studies have also found that poststroke depression is associated with increased mortality compared with non-depressed patients who had comparable strokes and similar premorbid risk factors. Finally, several studies have found that successful treatment of poststroke depression improves both cognitive and physical recovery and decreases mortality. Conclusion: The current review documents the beneficial effect of identifying and treating poststroke depression on both recovery and survival following stroke. [source] Protective Effect of Total Flavones of Abelmoschus manihot L. Medic Against Poststroke Depression Injury in Mice and Its Action MechanismTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 3 2009Mei Liu Abstract Total flavones of Abelmoschus manihot L. Medic (TFA) is the major active component isolated from the traditional Chinese herb Abelmoschus manihot L. Medic. We investigated the protective effect of TFA against poststroke depression (PSD) injury in mice and its action mechanism. A mouse model of PSD was induced by middle cerebral artery occlusion (MACO) 30 min/reperfusion, followed by isolation feeding and chronic unpredictable mild stress for 2 weeks. Treatment groups received TFA at three different doses (160, 80, and 40 mg/kg, p.o.) or fluoxetine (Flu, 2.5 mg/kg, p.o.) daily for 24 days. Change in behavior, brain tissue malondialdehyde (MDA) levels, and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured. The expression of brain-derived neurotrophic factor (BDNF) was detected by immunohistochemistry, and mRNA expression of BDNF and cAMP response element-binding protein (CREB) analyzed by reverse transcription-polymerase chain reaction (RT-PCR). Treatment with TFA (160, 80, and 40 mg/kg) significantly ameliorated mice escape-directed behavioral impairment induced by PSD, markedly reduced MDA levels, and increased the activity of SOD, GSH-Px close to normal levels. TFA administration also attenuated PSD-induced neuronal death/losses, upregulated expression of BDNF both at mRNA and protein levels, as well as CREB mRNA levels. TFA had a protective effect against PSD injury in mice. Cardioprotection involves the inhibition of lipid peroxidation and upregulation of BDNF-CREB levels in the hippocampus, which may also be important mechanism of its antidepressants. This potential protection makes TFA a promising therapeutic agent for the PSD. Anat Rec, 292:412,422, 2009. © 2009 Wiley-Liss, Inc. [source] Mirtazapine: only for depression?ACTA NEUROPSYCHIATRICA, Issue 3-4 2006Luis San Background:, Mirtazapine is an antidepressant first approved in the Netherlands in 1994 for the treatment of major depressive disorder. However, evidence suggests its effectiveness in a variety of other psychiatric disorders and non-psychiatric medical conditions. Objective:, The present paper reviews the published literature on the off-label indications of Mirtazapine. Methods:, A search of the relevant literature from MEDLINE, PsycLIT and EMBASE databases, included in the Science Citation Index and available up to March 2006, was conducted using the terms mirtazapine, case-reports, open-label trials and randomized controlled trials. Only articles referring to conditions other than major depression were included in this present review. Results:, Off-label use of mirtazapine has been reported in panic disorder, post-traumatic stress disorder, generalized anxiety disorder, social phobia, obsessive-compulsive disorder, dysthymia, menopausal depression, poststroke depression, depression as a result of infection with human immunodeficiency virus, elderly depression, Methylenedioxymethamphetamine (MDMA)-induced depression, hot flashes, alcohol and other substance use disorders, sleep disorders, sexual disorders, tension-type headaches, cancer pain, fibromyalgia, schizophrenia and other less frequent conditions. Conclusions:, So far, data on the off-label usefulness of mirtazapine are limited and mainly based on observations from case reports or open-label studies. However, positive cues suggest that confirmation of these preliminary data with randomized controlled trials may give sufficient evidence to warrant the use of mirtazapine in a broad range of disorders. [source] |