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Importance: Prevention is more effective than treatment to decrease the burden of significant medical conditions such as depressive disorders, a major cause of disability worldwide. Traumatic brain injury (TBI) is a candidate for selective strategies to prevent depression given the incidence, prevalence, and functional effect of depression that occurs after TBI.Objective: To assess the efficacy of sertraline treatment in preventing depressive disorders following TBI.Design, Setting, and Participants: A double-blind, placebo-controlled, parallel-group randomized clinical trial was conducted at a university hospital from July 3, 2008, to September 17, 2012, with 24 weeks of follow-up. A consecutive sample of 534 patients aged 18 to 85 years, hospitalized for mild, moderate, or severe TBI, was eligible for the study. Ninety-four patients consented to participate and were randomized (46 to placebo and 48 to sertraline), of whom 79 (84%) completed the study. Intention-to-treat data analysis was conducted from July 1, 2014, to December 31, 2015.Interventions: Placebo or sertraline, 100 mg/d, for 24 weeks or until development of a mood disorder.Main Outcomes and Measures: Time to onset of depressive disorders, as defined by the DSM-IV, associated with TBI.Results: Of the 94 patients in the study (38 female and 56 male; 92 white), the number needed to treat to prevent depression after TBI at 24 weeks was 5.9 (95% CI, 3.1-71.1; χ2 = 4.6; P = .03) for sertraline treatment vs placebo. The influence of sertraline in the course of neuropsychological variables was not detected. The intervention was well tolerated, and adverse effects were mild in both the sertraline and placebo groups.Conclusions and Relevance: Sertraline appears to be efficacious to prevent the onset of depressive disorders following TBI. Future studies should replicate these findings in a large sample of patients with TBI and depict their long-term physical, cognitive, behavioral, and functional outcomes.Trial Registration: clinicaltrials.gov Identifier: NCT00704379. [ABSTRACT FROM AUTHOR]

Poststroke depression (PSD) has been recognized by psychiatrists for more than 100 years, but controlled systematic studies did not begin until the 1970s. Meta-analyses addressing almost all major clinical issues in the field have emerged because of the relatively small number of patients included in some stroke studies. In order to build large databases, these meta-analyses have merged patients with rigorously assessed mood disorders with major depressive features with patients scoring above arbitrary cutoff points on depression rating scales, thus missing important findings such as cognitive impairment associated with major but not minor depression. Nevertheless, PSD occurs in a significant number of patients and constitutes an important complication of stroke, leading to greater disability as well as increased mortality. The most clinically important advances, however, have been in the treatment and prevention of PSD. Recent meta-analyses of randomized controlled trials for the treatment of PSD have demonstrated the efficacy of antidepressants. Similarly, randomized controlled trials for prevention of PSD have shown that antidepressants significantly decrease the incidence of PSD compared with placebo. Early antidepressant treatment of PSD appears to enhance both physical and cognitive recovery from stroke and might increase survival up to 10 years following stroke. There has also been progress in understanding the pathophysiology of PSD. Inflammatory processes might be associated with the onset of at least some depressive symptoms. In addition, genetic and epigenetic variations, white matter disease, cerebrovascular deregulation, altered neuroplasticity, and changes in glutamate neurotransmission might be relevant etiological factors. Further elucidation of the mechanism of PSD may ultimately lead to specific targeted treatments. [ABSTRACT FROM AUTHOR]

Late-life depression (LLD) is a frequent complication of the ageing process, occurring in up to 5% of community-dwelling elderly and in a higher proportion of subjects with coexistent medical illnesses. Its presence has been consistently associated with cognitive impairment, greater disability and increased mortality. Approximately half of patients with LLD have evidence of subcortical ischaemic damage in prefrontal circuits revealed by MRI. This might constitute the biological substrate of the cardinal symptoms of depression and of executive dysfunction. An important proportion of patients with LLD do not achieve remission of their depressive symptoms in spite of adequate pharmacological and psychotherapeutic treatment. In addition, a group of LLD patients progress to further impairment and disability in the form of a dementing disorder. There is an imperative need to develop new treatment strategies for LLD. Non-invasive brain stimulation techniques such as repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) are safe and efficacious interventions that might be used in combination with other therapeutic options to improve treatment outcomes. However, there are still questions regarding the optimal way in which rTMS and dTCS should be delivered as well as to the way in which we may identify the subjects who will benefit the most from these interventions. [ABSTRACT FROM AUTHOR]

Objective: To review the world's (English-language) publications related to depression following stroke. Method: The databases from MEDLINE and PubMed were reviewed for articles related to poststroke depression (PSD), depression and cerebral vascular accident, depression and cerebral vascular disease, and depression and cerebral infarction. Results: Most studies examined prevalence rates of depression and the clinical correlates of depression. Based on pooled data, the overall prevalence of major depression was 21.7% and minor depression was 19.5%. The strongest single correlate of depression was severity of impairment in activities of daily living. However, the existence of depression at baseline was found to be associated with greater impairment at follow-up, ranging from 6 weeks to 2 years in 83% of studies. Further, depression following acute stroke was also associated with greater cognitive impairment and increased mortality. PSD has been shown in 6 double-blind controlled studies to be effectively treated with antidepressants, and 1 study has recently shown that PSD can be effectively prevented. Conclusions: During the past 20 years, significant progress has been made in the identification and treatment of depression following stroke. In the future, antidepressant treatment will likely play an increasing role in the management of patients with acute stroke. Further research is needed to identify the mechanisms of depression and why antidepressants lead to improved physical and cognitive recovery and decreased mortality. [ABSTRACT FROM AUTHOR]

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The article describes a study aimed at determining the effectiveness of escitalopram and problem-solving therapy in preventing depression in acute-stroke patients. A total of 176 patients were randomly assigned to one of three groups--a placebo group, a group receiving escitalopram, and a group subject to problem-solving therapy. Treatment lasted for twelve months. Results indicated that both escitalopram and problem-solving therapy substantially reduced the incidence of depression relative to those who received a placebo.

The article focuses on the study that examines the efficacy and safety of repetitive transcranial magnetic stimulation (rTMS) in treating patients with vascular depression (VD). To test, 92 patients have been asked to stop the use of antidepressant therapy and instead recommend them to receive active or sham rTMS of the left dorsolateral prefrontal cortex. Other patients were also asked to undergo magnetic resonance imaging-defined VD as well as take a total cumulative dose (TCD) for further research. Results showed that the sham group has gained a 13.6 percent decrease in the 17-item Hamilton Depression Rating Scale scores compared to the TCD group. The efficacy of rTMS among geriatric patients with VD was then proven.

Background: Executive dysfunction is common after stroke and may impair long-term outcome. Remedies for this condition are limited.Aims: To examine the effect of antidepressants on executive function after stroke.Method: Forty-seven patients who had had a stroke during the prior 6 months received 12 weeks of antidepressant treatment in double-blind placebo-controlled fashion, followed by assessment of executive function at the end of treatment and after 2 years.Results: No significant group effect was found at the end of treatment. However, 21 months after the end of treatment the placebo group showed deterioration of executive function, whereas the active treatment group showed clear and significant improvement independent of depressive symptoms (F=12.1, d.f.=1,45, P= 0.001).Conclusions: Antidepressant treatment fosters long-term improvement of executive function following stroke. This phenomenon is consistent with a reorganisation of neuronal networks associated with prefrontal functions based on modulation of monoaminergic neurotransmission and the activity of neurotrophins. [ABSTRACT FROM AUTHOR]

Objective: This study examined the frequency of major and minor depression in Alzheimer's disease and determined whether these types of depression have a different functional and psychopathologi- cal impact and whether there is a change in the prevalence of major and minor de- pression throughout the stages of Alzhei- mer's disease. Method: A consecutive series of 670 pa- tients with probable Alzheimer's disease were assessed with the Structured Clinical Interview for DSM-IV; specific instruments to rate the presence and severity of depres- sion, anxiety, apathy, irritability, delusions, pathological affective crying, performance of activities of daily living, and social func- tioning; and a standardized neuropsycho- logical evaluation. Diagnoses of major and minor depression were generated from DSM-IV criteria. Results: Twenty-six percent of the pa- tients had major depression, 26% had minor depression, and 48% were not depressed. Major depression was signifi- cantly associated with sad mood in all three stages of the illness, although this as- sociation dropped significantly for minor depression in severe Alzheimer's disease. Both major and minor depression were significantly associated with more severe psychopathology, functional impairments, and social dysfunction. Depressive symp- toms that most strongly discriminated be- tween Alzheimer's disease patients with and without sad mood were guilty ide- ation, suicidal ideation, toss of energy, in- somnia, weight loss, psychomotor retarda- tion/agitation, poor concentration, and loss of interest. Conclusions: Our study demonstrates that DSM-IV criteria for major and minor depression identify clinically relevant syndromes of depression in Alzheimer's disease, mild levels of depression can pro- duce significant functional impairment, and the severity of psychopathological and neurological impairments increases with increasing severity of depression. [ABSTRACT FROM AUTHOR]

: BackgroundDepression has a significant impact on poststroke recovery and mortality. There are a proportion of patients with poststroke depression (PSD) who do not respond to antidepressants. Repetitive Transcranial Magnetic Stimulation (rTMS) might be a safe and effective alternative in these refractory cases.: MethodsWe conducted a randomized, parallel, double-blind study of active versus sham left prefrontal rTMS in patients with refractory PSD. After discontinuing antidepressants, patients were randomly assigned to receive 10 sessions of active (10 Hz, 110% of the motor threshold, 20 trains of 5 seconds duration) or sham left prefontal rTMS. Efficacy measures included HAM-D scores, response and remission rates. Patients completed a neuropsychological battery at baseline and after completing the protocol.: ResultsWhen compared with sham stimulation, 10 sessions of active rTMS of the left dorsolateral prefrontal cortex were associated with a significant reduction of depressive symptoms. This reduction was not influenced by patient’s age, type or location of stroke, volume of left frontal leukoaraiosis or by the distance of the stimulating coil to the prefrontal cortex. However, there was a significant positive correlation between the percentage of reduction of Ham-D scores and frontal gray and white matter volumes. There were no significant changes in cognitive functioning between the active and the sham stimulation groups. In addition, there were few and mild adverse effects that were equally distributed among groups.: ConclusionsTaken together, these preliminary findings suggest that rTMS may be an effective and safe treatment alternative for patients with refractory depression and stroke. [Copyright &y& Elsevier]

Se ha demostrado que la depresión postictal aumenta la mortalidad en más de 5 años después de un accidente vascular cerebral. Los autores evaluaron si el tratamiento antidepresivo reducía la mortalidad postictal a lo largo de 9 años de seguimiento. Método: Un total de 104 pacientes fueron asignados de forma aleatorizada a un tratamiento doble ciego de 12 semanas de duración con nortriptilina, fluoxetina o placebo al principio del período de recuperación de un accidente vascular cerebral. Se obtuvieron los índices de mortalidad de 104 pacientes a los 9 años de haber iniciado el estudio. A los 3, 6,9,12,18 y 24 meses del accidente vascular cerebral se recopilaron los datos demográficos y clínicos. Los datos de supervivencia señalizaron utilizando el método de Kaplan-Meier. Resultados: De los 104 pacientes, 50 (48,1 %) habían fallecido una vez transcurridos Ios 9 años del período de seguimiento. De los 53 pacientes a los que se habían administrado antidepresivos en dosis altas, 36 (67,9 %) seguían vivos en la evaluación de seguimiento frente a solo 10 (35,7 %} de los 28 pacientes tratados con placebo, una diferencia significativa. El análisis de regresión logística demostró que el efecto beneficioso de los antidepresivos seguía siendo significativo, tanto en los pacientes con depresión como en los que no presentaban depresión al incorporarse al estudio, una vez controlados los efectos de los demás factores relacionados con la mortalidad (edad, diabetes mellitus concomitante y depresión crónica recurrente]. No se observaron diferencias entre los grupos en cuanto a la gravedad del ictus, el deterioro de la capacidad cognitiva, las alteraciones de las actividades cotidianas y los demás fármacos recibidos. Conclusiones: Las 12 semanas de tratamiento con fluoxetina o nortriptilina durante los primeros 6 meses del período postictal aumentaron, significativamente, la supervivencia de los pacientes con depresión o sin ella. Este resultado indica que los procesos fisiopatológicos que determinan el mayor riesgo de mortalidad y acompañan a la depresión postictal perduran más tiempo que la depresión propiamente dicha y pueden ser modificados con los antidepresivos. [ABSTRACT FROM PUBLISHER]

Backgroud: Major depression is a frequent psychiatric complication among patients with traumatic brain injury (TBI). To our knowledge, however, the clinical correlates of major depression have not been extensively studied. Objective: To determine the clinical, neuropsychological, and structural neuroimaging correlates of major depression occurring after TBI. Design: Prospective, case-controlled, surveillance study conducted during the first year after the traumatic episode occurred. Settings: University hospital level I trauma center and a specialized rehabilitation unit. Methods: The study group consisted of 91 patients with TBI. In addition, 27 patients with multiple traumas but without evidence of central nervous system injury constituted the control group. The patients' conditions were evaluated at baseline and at 3, 6, and 12 months after the traumatic episode. Psychiatric diagnosis was made using a structured clinical interview and DSM-IV criteria. Neuropsychological testing and quantitative magnetic resonance imaging were performed at the 3-month follow-up visit. Results: Major depressive disorder was observed in 30 (33%) of 91 patients during the first year after sustaining a TBI. Major depressive disorder was significantly more frequent among patients with TBI than among the controls. Patients with TBI who had major depression were more likely to have a personal history of mood and anxiety disorders than patients who did not have major depression. Patients with major depression exhibited comorbid anxiety (76.7%) and aggressive behavior (56.7%). Patients with major depression had significantly greater impairment in executive functions than their nondepressed counterparts. Major depression was also associated with poorer social functioning at the 6-and 12-month follow-up, as well as significantly reduced left prefrontal gray matter volumes, particularly in the ventrolateral and dorsolateral regions. Conclusions: Major depression is a frequent complication of TBI that hinders a patient's recovery. It is associated with executive dysfunction, negative affect, and prominent anxiety symptoms. The neuropathological changes produced by TBI may lead to deactivation of lateral and dorsal prefrontal cortices and increased activation of ventral limbic and paralimbic structures including the amygdala. [ABSTRACT FROM AUTHOR]

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. [Copyright &y& Elsevier]

Objective: Cognitive impairment is common after stroke and may be caused by poststroke depression. Remission of poststroke major depression after treatment has been associated with improvement in cognitive function. The current study was designed to examine how long that cognitive improvement lasts and to compare depressed patients' cognitive status with that of nondepressed patients with comparable lesions. Method: Seventeen patients with poststroke depression and cognitive impairment who had early and sustained remission of their depression during a doubleblind treatment study were compared with 42 nondepressed stroke patients who remained nondepressed throughout the follow-up. Mood and cognitive function were followed-up over 2 years with the Hamilton Depression Rating Scale and Mini-Mental State Examination (MMSE). Results: In the patients with early and sustained remission of depression, there was rapid improvement of cognitive function, which was maintained over 2 years. Their initial MMSE score of 23.3 (SD=4.2) improved to 26.6 (SD=3.5) at 3 months and was 26.1 (SD=3.6) at 2 years. The nondepressed patients showed essentially no change in cognitive function over 2 years (initial MMSE score: mean=26.3, SD=3.1; score at 2-year follow-up: mean= 25.7, SD=4.1). Conclusions: Cognitive function, once improved after remission of poststroke depression, is likely to remain stable over the next 2 years in the absence of subsequent rein jury to the central nervous system. Cognitive impairment due to poststroke depression is reversible and can be quantified separately from cognitive impairment on the basis of the location and extent of ischemic brain damage. [ABSTRACT FROM AUTHOR]

Deals with a study which examined the available evidence regarding the prevalence of depressive disorders following traumatic brain injury (TBI). Prevalence of depressive disorders; Diagnosis of depression; Effect of depressive disorders on the outcome of TBI patients.

Presents a medical discussion regarding the case of an 82-year-old woman who suffered from mood changes following a thrombotic stroke. Prevalence of depression following stroke; Mechanisms of post-stroke depression; Differential diagnosis of mood change after stroke; Evaluation of patients to ascertain correct diagnosis; Treatment of post-stroke depression; Questions and discussion.

Objective: This study compared nortriptyline and fluoxetine with placebo in the treatment of depression and in recovery from physical and cognitive impairments after stroke. Method: A total of 104 patients with acute stroke enrolled between 1991 and 1997 entered a double-blind randomized study comparing nortriptyline, fluoxetine, and placebo over 12 weeks of treatment. The majority of patients were recruited from a rehabilitation hospital in Des Moines, Iowa, but other enrollment sites were also used. Both depressed and nondepressed patients were enrolled to determine whether improved recovery could be mediated by mechanisms unrelated to depression. Nortriptyline in doses of 25 mg/day gradually increased to 100 mg/day or fluoxetine in doses of 10 mg/day gradually increased to 40 mg/day or identical placebo were given over 12 weeks. Response to treatment of depression for individual patients was defined as a greater-than-50% reduction in scores on the Hamilton Rating Scale for Depression and no longer fulfilling diagnostic criteria for major or minor depression. Improved recovery for a treatment group was defined as a significantly higher mean score from baseline to end of the treatment trial, compared with patients treated with placebo, on measures of impairment in activities of daily living and levels of cognitive and social functioning. Results: Nortriptyline produced a significantly higher response rate than fluoxetine or placebo in treating poststroke depression, in improving anxiety symptoms, and in improving recovery of activities of daily living as measured by the Functional Independence Measure. There was no effect of nortriptyline or fluoxetine on recovery of cognitive or social functioning among depressed or nondepressed patients. Fluoxetine in increasing doses of 10-40 mg/day led to an average weight loss of 15. 1 pounds (8% of initial body weight) over 12 weeks of treatment that was not seen with nortriptyline or placebo. Conclusions: Given the doses of medication used in this study, nortriptyline was superior to fluoxetine in the treatment of poststroke depression. Demonstrating a benefit of antidepressant treatment in recovery from stroke may require the identification of specific subgroups of patients, alternative measurement scales, or the optimal time of treatment. [ABSTRACT FROM AUTHOR]

Cites a study which used 142 patients with acute stroke, to investigate the relationship between social impairment and depression. Information on the subjects used in the study; Details on the psychiatric and neurological evaluations of the patients; Assessment of patients' satisfaction with their closest social relationship; Finding of a weak correlation between social functioning score and severity of depression; In-depth look at the results of the study.

Depression is perhaps the most frequent emotional disorder to occur after a stroke. These depressions may be either major or minor in type and usually remit within the first year after the stroke. In addition to emotional suffering, poststroke depression has been associated with inhibited physical recovery, impaired cognitive functioning, and increased mortality. Determining whether these consequences of stroke may be improved by treatment of depression constitutes both a major challenge and an enormous opportunity for new approaches to poststroke pharmacotherapy. Previous controlled and uncontrolled treatment trials have provided partial support for the hypothesis that mood, cognitive, physical, and survival consequences of poststroke depression may be improved by antidepressant therapy. Depression and Anxiety, Volume 8, Supplement 1:85–90, 1998. © 1998 Wiley-Liss, Inc [ABSTRACT FROM AUTHOR]

Ninety-three patients with acute stroke lesions restricted to the right hemisphere were examined for the presence of mood changes. While 46 patients showed no mood changes, 19 were unduly cheerful, 17 had developed major depression, and 11 had developed minor depression. Although there were no significant between-groups differences in other demographic variables, neurological deficits, activities of daily living, cognitive impairment, or quality of social support, patients with major depression had a significantly higher frequency of familial history of psychiatric disorder and lesions of the parietal cortex than patients with either no mood change or major depression following left-hemisphere lesions. On the other hand, undue cheerfulness was significantly associated with lesions of the right frontal operculum. These findings suggest that major depression following right-hemisphere lesions may have a different aetiology and mechanism than major depression following left frontal or basal ganglia lesions. [ABSTRACT FROM AUTHOR]

Patients with ischaemic lesions of the left cerebral hemisphere were examined for depression and intellectual impairment: in non-depressed patients, the severity of impairment was related to both lesion volume and location, as assessed by CT scan analysis. Cognitive impairment in patients with major depression was greater than predicted by lesion volume alone, and when patients were matched for severity of impairment, depressed patients had smaller lesion volumes than the non-depressed. After six months, non-depressed patients had significantly less cognitive impairment than depressed patients who showed no improvement. Both depression and lesion volume were significantly and independently related to cognitive impairment. These findings suggest that post-stroke depression can produce a true dementia in its own right, and that treatment of post-stroke depression might benefit cognitive function. [ABSTRACT FROM AUTHOR]

We are conducting a two year longitudinal study of mood disorders in a group of 103 stroke patients. During the first six month period following the stroke the prevalence of symptoms of major depression increased from 23 per cent to 34 per cent while the frequency of symptoms of dysthymic depression increased from 20 per cent to 26 per cent. In addition, 10 of 13 patients who had major depressive symptoms during the initial evaluation continued to have these symptoms at six months follow-up and 4 of 9 patients who had minor depression in hospital developed major depression, while 5 of 9 continued to have minor depressive symptoms. Thus, the duration of depression following stroke is more than six months and the prevalence of major depressive symptoms increases steadily for the first half year after a cerebral hemorrhage or ischemic lesion. [ABSTRACT FROM AUTHOR]

Fifteen patients with bilateral hemisphere brain injury secondary to thromboembolic stroke or trauma were evaluated for depression, cognitive impairment, and functional physical impairment. Analysis of CT scans and standardized mood scales revealed that patients with left anterior brain injury were significantly more depressed than patients without such injury. Depression severity was directly and significantly correlated with left lesion proximity to the frontal pole. Left lesion age, lesion temporal sequence, right lesion location, cognitive impairment, and functional physical impairment did not significantly correlate with depression. Depressive symptomatology previously shown to be associated with single left frontal lobe lesions appeared to dominate post-brain injury psychopathology regardless of location or temporal sequence of other brain lesions. [ABSTRACT FROM AUTHOR]

Objective: Some investigators have suggested that major depression might be overdiagnosed in stroke patients because of changes in appetite, sleep, or sexual interest caused by their medical illness; others have suggested that depression may be underdiagnosed in stroke patients who deny symptoms of depression because of anosognosia, neglect, or aprosody. The authors' goal was to determine how frequently depressive symptoms occur in acute stroke patients with and without depressed mood to estimate how often diagnostic errors of inclusion or exclusion may be made. Method: They examined the rate of autonomic and psychological symptoms of depression in 205 patients who were consecutively hospitalized for acute stroke. Eighty-five (41%) of these patients had depressed mood, and 120 (59%) had no mood disturbance. Forty-six (54%) of the 85 patients with depressed mood (22% of all patients) were assigned the DSM-III diagnosis of major depression. Results: The 120 patients without mood disturbance had a mean of one autonomic symptom, but the 85 patients with depressed mood had a mean of almost four. Tightening the diagnostic criteria to account for one more nonspecific autonomic symptom decreased the number of patients with major depression by only three; adding two more criteria decreased the number by only five. Thus, the rate of DSM-III major depression was 1% higher than the rate with one extra nonspecific autonomic symptom and 2% higher than the rate with two extra criteria. Conversely, loosening diagnostic criteria to account for denial of depressive illness increased the rate of major depression by only 5%. Conclusions: Both autonomic and psychological depressive symptoms are strongly associated with depressed mood in acute stroke patients. [ABSTRACT FROM AUTHOR]

In a group of stroke patients with left-hemisphere lesions, those with major depression performed significantly below nondepressed patients on four of nine cognitive domains examined with a neuropsychological test battery. Among patients with right-hemisphere stroke, those with major depression did not perform below nondepressed patients on any of the nine cognitive domains. The differential effect of depression on cognitive performance between left- and right-hemisphere lesion groups could not be accounted for by demographic variables, neurological symptoms, lesion location, or lesion size. Poststroke major depression appeared to produce a decline in cognitive performance or dementia of depression that depended on the laterality of the lesion. [ABSTRACT FROM AUTHOR]

Patients with right-hemisphere strokes (N=9) more than 1 year after injury had greater cortical binding of (3-N-[11C]methyl)spiperone than a similar group of patients with left-hemisphere strokes (N=8) or normal control subjects (N= 17). The higher S2 serotonin receptor binding occurred in uninjured regions of the right parietal and temporal cortex. The ratio of binding in the ipsilateral to contralateral cortex showed a significant negative correlation with severity of depression scores in the left temporal cortex. These findings suggest that the biochemical response of the brain may be different depending on which hemisphere is injured and that some depressions may be a consequence of the failure to upregulate serotonin receptors after stroke. [ABSTRACT FROM AUTHOR]

Patients who developed secondary mania after brain injury (N=17) had a significantly greater frequency of injury to right hemisphere areas connected with the limbic system than poststroke patients with major depression (N=31), who had injury primarily in the left frontal cortex and basal ganglia. For patients without mood disturbance after brain injury (N=28), the location of the lesion was not significant. Secondary mania patients also had a significantly greater frequency of family history of affective disorder than did the other two groups. These results suggest that an interaction between injury to certain areas of the right hemisphere and genetic factors or other neuro pathological conditions produces secondary mania. [ABSTRACT FROM AUTHOR]

The article reflects on diagnosing depression in patients with stroke. It is said that the only symptom which has been found to be valid in the diagnosis of poststroke depression is a psychological symptom of depression, that is feelings of guilt. It is also said that poststroke depression is phenomenologically similar to depression without brain injury.

The article focuses on two clinical conditions that illustrate the link between psychiatry and neuroscience. The dementia syndrome of depression called pseudodementia syndrome is a cognitive disorder in which there is no apparent injury to the cerebral cortex although its function is impaired by unknown mechanisms. The other condition is depression following stroke. In this condition, the patient develops a depressed mood with sleep, appetite disturbance and hopelessness that can last for months after the stroke.

Preventive intervention for first-episode depression is an exciting, emerging field. Many questions remain, however. Should we target patients who have sub-syndromal symptom elevations (i.e. indicated intervention) or should we intervene in high-risk groups (i.e. selective intervention)? Furthermore, should primary outcomes be incident depressions or long-term decreases in morbidity or mortality? [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Escitalopram and Problem-solving Therapy for Prevention of Poststroke Depression: A Randomized Controlled Trial," by R.G. Robinson, R.E. Jorge, D.J. Moser, et al.

Discusses a study which examined the longitudinal course of mood disorders associated with brain injury among a sample of World War II veterans. Prevalence of major depression in men who had suffered a head injury during World War II; Assessment of patients with depressive disorders; Implications of traumatic brain injuries on the incidence of mood disorders.

Provides an overview of articles on the problem of depression or anxiety associated with physical illness, including the frequency of mood disorders in patients with HIV infections.

Abstract: Disorders of the basal ganglia (BG) alter perception and experience of emotions. Left hemisphere BG (LBG) stroke is also associated with depression. The interplay between depression and alterations in emotional processing following LBG stroke was examined. Evoked affective responses to emotion-laden pictorial stimuli were compared among LBG stroke and healthy participants and participants with stroke damage in brain regions not including the LBG selected to equate depression severity (measured using the Hamilton Depression Scale) with LBG damage participants. Brain activity {[O15]water positron emission tomography, PET} was measured in LBG stroke relative to healthy participants to identify changes in regions associated with emotion processing and depression. LBG stroke subjects reported less intense emotions compared with healthy, but not stroke comparison participants. Depression negatively correlated with emotional experience for positive and negative emotions. In response to positive stimuli, LBG subjects exhibited higher activity in amygdala, anterior cingulate, dorsal prefrontal cortex, and insula compared to healthy volunteers. In response to negative stimuli, LBG subjects demonstrated lower activity in right frontal-polar region and fusiform gyrus. Higher baseline activity in amygdala and ventral and mesial prefrontal cortex and lower activity in left dorsal lateral prefrontal cortex were associated with higher depression scores. LBG stroke led to blunted emotions, and brain activity alterations accounting for reduced affective experience, awareness and depression. Depression and fronto-limbic activity changes may contribute to emotional blunting following LBG stroke. [Copyright &y& Elsevier]