Non-depressed Stroke Patients Research Articles

Abnormal intrinsic functional hubs and connectivity in patients with post-stroke depression.

The present study aimed to investigate the specific alterations of brain networks in patients with post-stroke depression (PSD), and further assist in elucidating the brain mechanisms underlying the PSD which would provide supporting evidence for early diagnosis and interventions for the disease. Resting-state functional magnetic resonace imaging data were acquired from 82 nondepressed stroke patients (Stroke), 39 PSD patients, and 74 healthy controls (HC). Voxel-wise degree centrality (DC) conjoined with seed-based functional connectivity (FC) analyses were performed to investigate the PSD-related connectivity alterations. The relationship between these alterations and depression severity was further examined in PSD patients. Relative to both Stroke and HC groups, (1) PSD showed increased centrality in regions within the default mode network (DMN), including contralesional angular gyrus (ANG), posterior cingulate cortex (PCC), and hippocampus (HIP). DC values in contralesional ANG positively correlated with the Patient Health Questionnaire-9 (PHQ-9) scores in PSD group. (2) PSD exhibited increased connectivity between these three seeds showing altered DC and regions within the DMN: bilateral medial prefrontal cortex and middle temporal gyrus and ipsilesional superior parietal gyrus, and regions outside the DMN: bilateral calcarine, ipsilesional inferior occipital gyrus and contralesional lingual gyrus, while decreased connectivity between contralesional ANG and contralesional supramarginal gyrus. Moreover, these FC alterations could predict PHQ-9 scores in PSD group. These findings highlight that PSD was related with increased functional connectivity strength in some areas within the DMN, which might be attribute to the specific alterations of connectivity between within DMN and outside DMN regions in PSD.

Depression circuit adaptation in post-stroke depression

BackgroundLesion locations of post-stroke depression (PSD) mapped to a depression circuit which centered by the left dorsolateral prefrontal cortex (DLPFC). However, it remains unknown whether the compensatory adaptations that may occur in this depression circuit due to the lesions in PSD. MethodsRs-fMRI data were collected from 82 non-depressed stroke patients (Stroke), 39 PSD patients and 74 healthy controls (HC). We tested the existence of depression circuit, examined PSD-related alterations of DLPFC-seeded connectivity and their associations with depression severity, and analyzed the connectivity between each repetitive transcranial magnetic stimulation (rTMS) target and DLPFC to find the best treatment target for PSD. ResultsWe found that: 1) the left DLPFC showed significantly stronger connectivity to lesions of PSD than Stroke group; 2) in comparison to both Stroke and HC groups, PSD exhibited increased connectivity with DLPFC in bilateral lingual gyrus, contralesional superior frontal gyrus, precuneus, and middle frontal gyrus (MFG); 3) the connectivity between DLPFC and the contralesional lingual gyrus positively correlated with depression severity; 4) the rTMS target in center of MFG showed largest between-group difference in connectivity with DLPFC, and also reported the highest predicted clinical efficacy. LimitationsLongitudinal studies are required to explore the alterations of depression circuit in PSD as the disease progress. ConclusionPSD underwent specific alterations in depression circuit, which may help to establish objective imaging markers for early diagnosis and interventions of the disease.

Elevated plasma intestinal fatty acid binding protein and aberrant lipid metabolism predict post-stroke depression

Post-stroke depression (PSD) is the most common mood disorder caused by stroke. Stroke might bring about increased intestinal permeability accompanied by gut microbiota changes. According to the “gut-brain” axis hypothesis, increased intestinal permeability may contribute to PSD. Therefore, we investigated the association between increased intestinal permeability and the occurrence of PSD. Intestinal fatty acid binding protein (iFABP) is responsible for intestinal fatty acid absorption and transport and is often considered a biomarker of gut hyperpermeability, also known as leaky gut. We enrolled 48 healthy controls (HCs), 48 stroke patients without depression, and 48 PSD patients in this study. Plasma iFABP was measured in the three groups. CRP, LBP, and sCD14 were quantified for bacterial infection assessment. In addition, clinical laboratory indicators of lipid metabolism were assessed. The PSD patients exhibited higher iFABP levels compared with HCs and non-depressed stroke patients. Using OPLS discriminant analysis, four proteins (ApoA1, HDL-C, iFABP, and Lp(a)) were identified as potential biomarkers for distinguishing PSD patients from non-depression stroke patients. Our study discovered that elevated plasma iFABP levels in PSD patients correlated with the degree of depression, along with disturbed lipid metabolism. These findings also suggested the need to consider the role of a leaky gut in depression after stroke.

Update on the EFFECTS study of fluoxetine for stroke recovery: a randomised controlled trial in Sweden

Studies have suggested that fluoxetine might improve neurological recovery after stroke, but the results remain inconclusive. The EFFECTS (Efficacy oF Fluoxetine – a randomisEd Controlled Trial in Stroke) reached its recruitment target of 1500 patients in June 2019. The purpose of this article is to present all amendments to the protocol and describe how we formed the EFFECTS trial collaboration in Sweden.MethodsIn this investigator-led, multicentre, parallel-group, randomised, placebo-controlled trial, we enrolled non-depressed stroke patients aged 18 years or older between 2 and 15 days after stroke onset. The patients had a clinical diagnosis of stroke (ischaemic or intracerebral haemorrhage) with persisting focal neurological deficits. Patients were randomised to fluoxetine 20 mg or matching placebo capsules once daily for 6 months.ResultsSeven amendments were made and included clarification of drug interaction between fluoxetine and metoprolol and the use of metoprolol for severe heart failure as an exclusion criterion, inclusion of data from central Swedish registries and the Swedish Stroke Register, changes in informed consent from patients, and clarification of design of some sub-studies.EFFECTS recruited 1500 patients at 35 centres in Sweden between 20 October 2014 and 28 June 2019. We plan to unblind the data in January 2020 and report the primary outcome in May 2020.ConclusionEFFECTS will provide data on the safety and efficacy of 6 months of treatment with fluoxetine after stroke in a Swedish health system setting. The data from EFFECTS will also contribute to an individual patient data meta-analysis.Trial registrationEudraCT 2011-006130-16. Registered on 8 August 2014.ISRCTN, ISRCTN13020412. Registered on 19 December 2014.ClinicalTrials.gov: NCT02683213. Retrospectively registered on 2 February 2016.

Post-stroke Depression: Epidemiology, Diagnosis, Risk Factors, and Management

Post-stroke depression (PSD) is a widely encountered complexity of stroke, which is of notable importance. PSD ismultifactorial in origin; however, depression after stroke is unrecognized, infrequently diagnosed, and undertreated. Thisreview presents epidemiology, diagnosis and diagnostic tools, risk factors, and management of PSD. About one-third ofpatients experience depression after stroke. It is important to reliably screen and diagnose post-stroke depression aswell as measure its severity. PSD is associated with various risk factors and stroke characteristics. If left untreated, PSDcan worsen several other common post-stroke conditions. There is strong evidence that early initiation of antidepressanttherapy in non-depressed stroke patients is associated with reduced risk for the development and effective preventionof post-stroke depression. PSD needs special attention, and consensus should be reached regarding the diagnosis andmanagement of PSD.

Benefits of antidepressant treatment after a stroke

IntroductionStroke is an important cause of morbidity and is responsible for 9% of all deaths worldwide. The most frequent neuropsychiatric consequence of stroke is post-stroke depression (PSD). It has been shown to be associated with both impaired recovery and increased mortality. The aim of our study is to determine the benefits of antidepressant prescription after a stroke.MethodThe databases from Medline and PubMed were reviewed for articles related to post-stroke depression (PSD), antidepressant treatment and stroke, post-stroke depression and functional recovery, stroke related impairment.ResultsAntidepressant drugs have been shown to be effective in treating PSD in six double blind randomized studies. Patients treated with antidepressants had better recovery from disability than patients who did not receive antidepressant therapy: it was proved that antidepressant drugs cause an improvement in cognitive skills and functional recovery in PSD patients. In patients with ischemic stroke and moderate to severe motor deficit, the early prescription of fluoxetine with physiotherapy enhanced motor recovery after 3 months. Some studies showed that PSD can be effectively prevented: nortriptyline, fluoxetine, milnacipran and sertraline appeared to be efficacious in preventing depression after stroke and are to use without significant adverse effects in stroke patients.ConclusionAntidepressant treatment plays an increasing role in the management of patients with acute stroke. Therefore, early initiation of antidepressant therapy, in non-depressed stroke patients, may reduce the odds for development of PSD, and improve cognitive and functional recovery.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Efficacy of antidepressants in animal models of ischemic stroke: a systematic review and meta-analysis.

Poststroke depression is a prevalent complication of stroke with unclear pathogenesis. The benefits of antidepressants in this context and their effects on stroke recovery other than effects on mood are not clearly defined, with some studies suggesting efficacy in improving functional outcome in both depressed and nondepressed stroke patients. We have analyzed the preclinical animal data on antidepressant treatment in focal cerebral ischemia, modeled±depression, to help inform clinical trial design. We performed a systematic review and meta-analysis of data from experiments testing the efficacy of antidepressants versus no treatment to reduce infarct volume or improve neurobehavioral or neurogenesis outcomes in animal models of stroke. We used random-effects metaregression to test the impact of study quality and design characteristics and used trim and fill to assess publication bias. We identified 44 publications describing the effects of 22 antidepressant drugs. The median quality checklist score was 5 of a possible 10 (interquartile range, 4-7). Overall, antidepressants reduced infarct volume by 27.3% (95% confidence interval, 20.7%-33.8%) and improved neurobehavioral outcomes by 53.7% (46.4%-61.1%). There was little evidence for an effect of selective serotonin reuptake inhibitors on infarct volume. For neurobehavioral outcomes there was evidence of publication bias. Selective serotonin reuptake inhibitors were the most frequently studied antidepressant subtype and improved neurobehavioral outcome by 51.8% (38.6%-64.9%) and increased neurogenesis by 2.2 SD (1.3-3.0). In line with current clinical data and despite some limitations, antidepressant treatments seem to improve infarct volume and neurobehavioral outcome in animal models of ischemic stroke.

A Prospective Study on the Prevalence and Risk Factors of Poststroke Depression

Background and Purpose: Poststroke depression (PSD) is common. Early detection of depressive symptoms and identification of patients at risk for PSD are important as PSD negatively affects stroke outcome and costs of medical care. Therefore, the aim of this study was to determine incidence and risk factors for PSD at 3 months after stroke. Methods: We conducted a prospective, longitudinal epidemiological study aiming to determine incidence and risk factors for PSD at 1, 3, 6, 12 and 18 months poststroke. The present data analysis covers the convalescent phase of 3 months poststroke. Participants in this study were inpatients, admitted to a stroke unit with first or recurrent stroke. Demographic data and vascular risk factors were collected and patients were evaluated at baseline and 3 months poststroke for functional and cognitive deficits, stroke characteristics, stroke severity and stroke outcome. Signs and symptoms of depression were quantified by means of the Cornell Scale for Depression (CSD) and Montgomery and Åsberg Depression Rating Scale (MADRS). Significantly associated variables from univariate analysis were analyzed by using multiple linear and logistic regression methods. Results: Data analysis was performed in 135 patients who completed follow-up assessments at 3 months poststroke. Depression (CSD score ≥8) was diagnosed in 28.1% of the patients. Patients with PSD were significantly more dependent with regard to activities of daily living (ADL) and displayed more severe physical and cognitive impairment than patients without PSD. A higher prevalence of speech and language dysfunction and apraxia were observed in patients with PSD (36.8 and 34.3%, respectively) compared to non-depressed stroke patients (19.6 and 12.4%; p = 0.036 and p = 0.004, respectively). Applying multiple linear regressions, cognitive impairment and reduced mobility as part of the Stroke Impact Scale were independently associated with PSD, as scored using CSD and MADRS (r² = 0.269 and r² = 0.474, respectively). Conclusions: The risk of developing PSD is increased in patients with more functional and cognitive impairment, greater dependency with regard to ADL functions and with occurrence of speech and language dysfunctions and apraxia. Multiple regression models indicated that the most determining features for depression risk in the convalescent phase after stroke include reduced mobility and cognitive impairment. Further studies on risk factors for PSD are essential, given its negative impact on rehabilitation and quality of life. Identification of risk factors for PSD may allow more efficacious preventive measures and early implementation of adequate antidepressive treatment.

Prevention of Poststroke Depression: Does Prophylactic Pharmacotherapy Work?

Given the negative influence of poststroke depression (PSD) on functional recovery, cognition, social participation, quality of life, and risk for mortality, the early initiation of antidepressant therapy to prevent its development has been investigated; however, individual studies have offered conflicting evidence. The present systematic review and meta-analysis examined available evidence from published randomized controlled trials (RCTs) evaluating the effectiveness of pharmacotherapy for the prevention of PSD to provide updated pooled analyses. Literature searches of 6 databases were performed for the years 1990 to 2011. RCTs meeting study inclusion criteria were evaluated for methodologic quality. Data extracted included the antidepressant therapy used, treatment timing and duration, method(s) of assessment, and study results pertaining to the onset of PSD. Pooled analyses were conducted. Eight RCTs were identified for inclusion. Pooled analyses demonstrated reduced odds for the development of PSD associated with pharmacologic treatment (odds ratio [OR] 0.34; 95% confidence interval [CI] 0.22-0.53; P<.001), a treatment duration of 1 year (OR 0.31; 95% CI 0.18-0.56; P<.001), and the use of a selective serotonin reuptake inhibitor (OR 0.37; 95% CI 0.22-0.61; P<.001). The early initiation of antidepressant therapy, in nondepressed stroke patients, may reduce the odds for development of PSD. Optimum timing and duration for treatment and the identification of the most appropriate recipients for a program of indicated prevention require additional examination.

The symptomatology of post‐stroke depression: comparison of stroke and myocardial infarction patients

Depression is a frequent problem in stroke patients but, all too often, the problem goes unrecognized. How depression-like symptoms in post-stroke depression (PSD) should be interpreted is still subject to debate. If PSD has a distinct symptom profile of depression accompanying other chronic vascular somatic conditions then this could imply that PSD is a specific disease entity. To study whether depressed stroke patients exhibit other signs and symptoms than patients suffering from depression after myocardial infarction (MI). Depressive signs and symptoms were measured using the Hospital Anxiety and Depression Scale and the 17-item Hamilton Depression Rating Scale. The results of 190 stroke patients were compared with the results of 198 MI patients every 3 months during the first year after the event. Depressed stroke patients exhibited more loss of interest, psychomotor retardation, and gastro-intestinal complaints as compared to depressed MI patients. However, in multivariate analyses including both depressed and non-depressed stroke and MI patients, no specific symptom profile was found to differentiate between the two depressive syndromes by looking at the modifying effect of stroke vs MI on the occurrence of specific symptoms in depression. Although in their clinical presentation, depressed stroke patients exhibit a symptom profile different from depressed MI patients, this is not due to differences in the depressive syndrome in these two patient groups but it reflects differences between stroke and MI patients in general.

Success and failure of mirtazapine as alternative treatment in elderly stroke patients with sleep apnea—a preliminary open trial

More than two thirds of stroke patients suffer from sleep apnea. A recent study showed that mirtazapine reduced the respiratory disturbance index (RDI) of a stroke patient by 80%. These promising results prompted us to offer mirtazapine to non-depressed stroke patients who suffered from sleep apnea and refused treatment with a continuous positive airway pressure (CPAP) device. Polysomnography was performed between 2200 and 0600 hours. We examined ten inpatients [nine male, one female; mean age of 68.7 +/- 1.5 years +/- SE; body mass index of 26.1 +/- 1.2 kg/m(2), basal ganglia bleeding (n = 3), middle cerebral artery ischemia (n = 4), basal ganglia ischemia (n = 1), cerebellar bleeding (n = 2)] in the Neurologic Clinic's sleep laboratory. The mean duration of illness before the first polysomnography was 52.6 +/- 11.4 days. Mirtazapine effectively consolidated sleep in all patients, i.e., sleep efficiency significantly increased from 63.1 +/- 4.8% to 75.7 +/- 5.0%. A moderate increase in RDI (137.4 +/- 15.3% of baseline) occurred during initial mirtazapine administration (intake duration 15.8 +/- 5.5 days). After 51.9 +/- 8.4 days, the RDI was either reduced (51.9% in "responders" who were identified arbitrarily by a reduction in RDI >or= 25% at any time point of the investigation) or increased (154.4% in "non-responders"). Mirtazapine administration was stopped in the four patients with increased RDI. Mirtazapine may be a probably effective treatment in stroke survivors with obstructive sleep apnea who refuse nasal CPAP treatment. As it may worsen central and mixed sleep apnea, patients who receive mirtazapine to alleviate sleep apnea or to control post-stroke depression with sleep disturbances should be monitored for changes in breathing parameters during sleep.

Extended Evaluation of Serotonin Transporter Gene Functional Polymorphisms in Subjects with Post-Stroke Depression

As an extension of our previous observation, relating a serotonin transporter gene-linked promoter region (5-HTTLPR) diallelic functional polymorphism (short [S] and long [L] alleles) to the risk of post-stroke major depression (PSD), this study investigated the role of 2 other functional polymorphisms of the serotonin transporter gene (5-HTT) in the same sample of subjects with PSD. In a clinical sample of 26 patients with PSD and 25 unrelated nondepressed stroke patients of Caucasian descent, we examined the frequencies of a functional single nucleotide variant (A/G) within the promoter region (rs25531) and located in L (16-repeat) and S (14-repeat) alleles of 5-HTTLPR, and a variable number tandem repeat (VNTR) polymorphism in intron 2. There were significant intergroup differences in the allelic frequencies of 5-HTTLPR/rs25531 (SA, LA, and LG) (P < 0.05) and in the combined frequencies of lower-expressing alleles (SA and LG) and higher-expressing alleles (LA) (P < 0.025) between subjects with PSD and nondepressed stroke. However, the differences in the combined frequencies of lower-expressing (SA/SA, SA/LG, and LG/LG), intermediate-expressing (SA/LA and LA/LG), and higher-expressing (LA/LA) genotypes of 5-HTTLPR were not significant. Further, no significant intergroup differences were found in the allelic and genotypic frequencies of the intron 2 VNTR. These findings strengthen the support for an association between PSD and lower-expressing alleles of 5-HTTLPR.

Rates of Depression at 3 and 15 Months Poststroke and Their Relationship With Cognitive Decline: the Sydney Stroke Study

To investigate the frequency and correlates of depression at 3 and 15 months after stroke. A total of 164 consecutive eligible stroke patients and 100 comparison subjects received extensive medical, psychiatric, and neuropsychological assessments; a subset also received magnetic resonance imaging scans. Comprehensive assessments included ratings for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition major or minor depression at 3-6 months (index assessment) and 15 months (follow-up assessment) after stroke. The comparison subjects, who were similar in age and sex, were similarly assessed twice, 12 months apart. Major or minor depression was present in 12.0% of stroke patients at index assessment and in 20.7% at follow-up which included 18 new cases (13.4%). By follow-up, stroke patients with depression had significantly greater impairment of functional ability and global cognition than nondepressed stroke patients or comparison subjects. Depression was not associated with age, intellectual decline prior to stroke or side or severity of stroke. Patients who experienced a TIA or stroke during the follow-up, who had developed dementia by three months or who were not living with a relative or partner were more likely to be depressed at follow-up. Dementia at 3 months predicted depression, but the reverse did not hold. Depression may be less frequent after stroke than previously reported and is related to cumulative vascular brain pathology rather than side and severity of single strokes. Clinicians should strive to slow the progression of cerebrovascular disease and encourage greater social support.

Preventing Depression After Stroke

We designed this study to determine whether the daily treatment of nondepressed acute stroke patients with sertraline reduced the incidence of depression at follow-up. 111 patients with recent stroke (< 2 weeks; International Classification of Diseases, Tenth Revision criteria) were randomly assigned to treatment with placebo (N = 56) and sertraline (N = 55, 50 mg once daily) in this double-blind, placebo-controlled 24-week clinical trial. Subjects were recruited from the 2 largest teaching hospitals of Western Australia between June 2002 and June 2004. The primary endpoint of interest was development of clinically significant depressive symptoms as assessed by a Hospital Anxiety and Depression Scale-depression subscale score of 8 or above, or as diagnosed by the treating physician during 24 weeks. There was no significant difference in the incidence of depressive symptoms during 24 weeks of treatment (16.7% [8/48] sertraline vs. 21.6% [11/51] placebo, rate ratio = 0.8, 95% CI = 0.3 to 2.1, p = .590). The trial medication was discontinued by 51.8% (29/56) of patients assigned placebo and 47.3% (26/55) assigned sertraline (p = .634), most often because of perceived side effects or because the treating physician introduced an antidepressant medication. Twenty-four-week treatment with 50 mg of sertraline once daily initiated within 2 weeks of onset of acute stroke is not a significantly more effective strategy to prevent 6-month depression than usual care plus placebo among nondepressed stroke patients. New pharmacologic and nonpharmacologic strategies need to be developed to reduce the health and financial burden associated with depression after stroke.

The sensitivity of somatic symptoms in post‐stroke depression: a discriminant analytic approach

Somatic and neurocognitive symptoms of depression may overlap with the physical symptoms of stroke, and thus make the diagnosis of post-stroke depression difficult. To assess the sensitivity of individual depressive symptoms and their contribution to the diagnosis of post-stroke depression. Two hundred and six patients with first-ever stroke, participating in a longitudinal study, were administered the Structured Clinical Interview for DSM-IV and the Hamilton Depression Rating Scale (HAM-D). In a discriminant analysis the relative contribution of the individual HAM-D items to the diagnosis of major depressive disorder was evaluated. The cumulative incidence of post-stroke major depressive disorder was 32%. The discriminant model based on HAM-D item scores was highly significant (p<0.001) and classified 88.3% of patients correctly as depressed or nondepressed. As expected, 'depressed mood' discriminated best between depressed and non-depressed stroke patients. 'Reduced interests' had a relatively low sensitivity and may in part reflect 'apathy', which often is considered a separate construct. With the exception of 'suicidal thoughts', most psychological symptoms, such as 'hypochondriasis', 'lack of insight' and 'feelings of guilt', were not very sensitive. Some somatic symptoms, such as 'reduced appetite', 'psychomotor retardation', and 'fatigue' had high discriminative properties. Psychological, neurocognitive and somatic symptoms of depression differ among themselves in terms of diagnostic sensitivity, and should be considered individually. Some somatic symptoms are highly sensitive for depression and should not be neglected by following an 'exclusive' or 'attributional' approach to the diagnosis of PSD.

Depression in stroke patients 7 years following stroke.

To study the frequency of depression in stroke patients many years following stroke, most previous studies having concentrated on the first few years. Participants of a previous study of post-stroke depression (99 stroke patients and 28 control subjects) were re-examined 7 years later. Depression was diagnosed using research diagnostic criteria. The test battery comprised the Mini Mental State Examination, the Raven Matrices A+B and Word Pair Learning. Subjective experience of changes in memory, concentration, mood, irritability and fatigue during the 7-year period was also examined. Twenty per cent of the stroke patients fulfilled the criteria for major or minor depression compared with 11% of the control subjects. No differences in cognitive function were found between depressed and non-depressed stroke patients. The stroke patients reported experiencing more lability of mood and irritability during the 7-year period following stroke than the control subjects. Depressed stroke patients experienced more impairment of concentration and memory function than non-depressed stroke patients. Affective symptoms are common among stroke patients 7 years following stroke.

A neuroendocrine study of serotonin function in depressed stroke patients compared to non depressed stroke patients and healthy controls

Objectives: We employed a neuroendocrine challenge paradigm to study serotonergic abnormalities associated with poststroke depression. Method: Twelve depressed stroke patients (major depression N=5, minor depression N=7), 8 nondepressed stroke patients and 12 healthy volunteers completed a single-blind, placebo-controlled, challenge tests. Baseline cortisol (CORT) and prolactin (PRL) values, and these hormonal responses to 30 mg of oral d-FEN and placebo over a 4 hour period were measured in the three groups. Results: There were intergroup differences for baseline adjusted PRL responses (change scores from baseline) to d-FEN (group effect F=4.38, df=2,29, p=0.02) while these responses to placebo were comparable between groups (group effect F=1.82, df=2,29, p=0.18). Peak PRL responses (post d-FEN maximal PRL change from baseline scores) in depressed stroke patients were significantly greater than in nondepressed patients ( p=0.005) but comparable to healthy normals ( p=0.47). However, these responses between major and minor depression were not significant ( p=0.34). There was a trend suggesting a negative correlation between peak PRL response and severity of depression ( p=0.056). Depressed patients were younger than the controls ( p=0.054). Also, the depressed group was more functionally impaired ( p=0.04) and more likely to have right-sided lesions ( p=0.009) compared with the nondepressed group. Differences in baseline adjusted PRL changes between depressed and nondepressed groups became non significant when the influence of laterality of lesions was covaried, whereas covariation of functional scores and age did not alter the significance. CORT responses did not show intergroup differences. Limitations: The study group was small and was heterogenous in lesion characteristics, time since stroke and type of depression. A fixed-order design was used in the challenge test paradigm. Conclusions: When laterality of stroke lesion was taken into account, depressed and nondepressed stroke patients did not differ in PRL responses to d-FEN.

Incidence of post‐stroke depression during the first year in a large unselected stroke population determined using a valid standardized rating scale

This study describes the development of post-stroke depression (PSD) prospectively during the first year post-stroke in 285 unselected stroke patients. An appropriate unselected population-based control group without cerebral pathology is included for comparison. Psychiatric assessment with the Hamilton Depression Rating Scale (HDRS) was undertaken unmodified. PSD was defined as HDRS > or = 13. The one-year incidence of PSD among the 209 survivors able to communicate reliably at 1 month was 41%. Most cases develop within the first months following stroke (79%), the frequency of new cases of PSD at one year being 5%, a level comparable to that in the control group. Depressed and nondepressed stroke patients consistently scored 4 points greater on total HDRS than in the corresponding controls.

The Pharmacokinetics of Paroxetine (PAR) in Elderly Depressed and non-Depressed Stroke Patients

The Pharmacokinetics of Paroxetine (PAR) in Elderly Depressed and non-Depressed Stroke Patients