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Objective: Apathy occurs frequently following stroke and prior studies have demonstrated the negative effect of apathy on recovery from stroke. This study was a secondary analysis examining the efficacy of escitalopram, problem-solving therapy (PST), or placebo administered for 1 year to prevent the onset of apathy among patients with recent stroke., Methods: Patients within 3 months of an index stroke who did not meet DSM-IV diagnostic criteria for major or minor depression and who did not have a serious comorbid physical illness were enrolled. Patients were recruited from three sites: University of Iowa, University of Chicago, and Burke Rehabilitation Hospital. One hundred fifty-four patients without evidence of apathy at initial evaluation were included in the randomized controlled trial using escitalopram (10 mg patients ≤65 years; 5 mg patients >65 years) (N = 51) or placebo (N = 47) or non-blinded PST (12 total sessions) (N = 56) over 1 year. At 3, 6, 9, and 12 months, patients were assessed for diagnosis and severity of apathy using the Apathy Scale., Results: Using a Cox proportional hazards model of time to onset of apathy, participants given placebo were 3.47 times more likely to develop apathy than patients given escitalopram and 1.84 times more likely to develop apathy than patients given PST after controlling for age, sex, cognitive impairment, and diabetes mellitus status (adjusted hazard ratio: 3.47, 95% CI: 1.79-6.73 [escitalopram group]; adjusted hazard ratio: 1.84, 95% CI: 1.21-2.80 [PST group])., Conclusion: Escitalopram or PST was significantly more effective in preventing new onset of apathy following stroke compared with placebo., (Copyright © 2013. Published by Elsevier Inc.)

Objective: This prospective study examined the course of cognitive, physical, and social impairment among patients who developed apathy during the first year after stroke., Methods: Patients diagnosed with apathy (N = 23) were compared with patients who had no apathy (N = 33) at initial, 3, 6, 9, and 12 months after stroke for severity of global cognitive impairment as measured by Mini-Mental State Examination, severity of impairment in activities of daily living (ADLs) as measured by Functional Independence Measure, and severity of impairment in social functioning as measured by Social Functioning Exam., Results: A total of 41.1% of patients met diagnostic criteria for apathy during the first year after stroke. The mean time from stroke to onset of apathy was 3.8 (3.3 SD) months and the mean duration was 5.6 (2.3 SD) months. Using a linear mixed model, after controlling for age, initial severity of impairment, and major depression, patients in the apathy group had significantly less recovery in cognition (t(149) = -2.06; p = 0.0411) and ADLs (t(104) = -3.37; p = 0.0011) during the first year after stroke compared with nonapathic patients., Conclusion: Apathy is common after stroke and leads to less recovery in cognition and ADLs over the first year after stroke compared with similar nonapathic patients., (Copyright © 2013 American Association for Geriatric Psychiatry. Published by Elsevier Inc. All rights reserved.)

Background and Purpose: The purpose of this study was to compare escitalopram, problem-solving therapy, and placebo to prevent poststroke depression during 6 months after discontinuation of treatment., Methods: We examined for depression 33 patients assigned to placebo, 34 to escitalopram, and 41 to problem-solving therapy., Results: After controlling for age, gender, prior mood disorder, and severity of stroke, new-onset major depression and Hamilton Depression scores were significantly higher 6 months after escitalopram was discontinued compared with the problem-solving therapy or placebo groups., Conclusions: Discontinuation of escitalopram may increase poststroke depressive symptoms.

Executive function and denial of illness were examined among 24 patients who received double-blind antidepressant treatment following stroke. Between end-of-treatment at 3 months and follow-up at 2 years, significant correlation was found between improvement in executive function and decrease in denial of illness.

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.

Objective: To examine, in a post hoc analysis of an antidepressant treatment trial, correlates of irritability and aggression after stroke and changes in irritability scores associated with antidepressant treatment., Design: Aggressive patients (n=23) were compared with nonaggressive patients (n=69) on numerous measures of psychopathology, poststroke impairment, and neuroimaging findings., Setting: All patients were hospitalized at the time of the initial evaluation for acute stroke or for rehabilitation therapy., Participants: Ninety-two patients from the Iowa City Stroke Study were classified as aggressive or nonaggressive, based on symptoms elicited by the Present State Examination (PSE) and from family or caretaker reports., Intervention: All patients were randomized to receive nortriptyline, fluoxetine, or placebo using a double-blind methodology., Main Outcome Measure: The change in aggression score as elicited by the PSE at the beginning and the end of a 12-week treatment trial., Results: Twenty-five percent (23/92) of patients reported irritability or aggression. Irritable and aggressive patients had higher total PSE scores, Hamilton Depression Rating Scale scores, Hamilton Anxiety Rating Scale (HAMA) scores, and lower Mini-Mental State Examination scores. They also had lesions that were more proximal to the frontal pole. Stepwise regression analysis showed that HAMA scores and proximity of lesion to the frontal pole were significant independent predictors of irritability. Among irritable and aggressive patients with depression who responded to antidepressants, there was a significantly greater reduction in irritability after treatment, compared with patients whose depression did not lessen with treatment., Conclusions: Several factors, such as severity of impairment, other psychopathology, and neurobiologic factors, appear to contribute to irritable and aggressive behavior in stroke patients. If depression accompanies aggression, the results of this small study suggest that successful treatment of depression may reduce aggressive behavior.

Differences in the pattern of neuropsychological dysfunction associated with Alzheimer's disease (AD) and vascular dementia (VaD) were examined using the Dementia Rating Scale (DRS). We examined three groups of patients: (1) Patients with AD; (2) patients with single stroke (CVA); and (3) patients with multiple cerebral infarctions (MI). Comparisons of cognitive dysfunction were conducted on patients that met the DRS criteria for dementia. Dementia groups were similar in age, education, and severity of dementia. Comparisons of the AD and two VaD groups across the specific DRS-scales (Attention, Conceptualization, Construction, Initiation/Perseveration, and Memory) indicated that patients with AD were more impaired on the DRS-Memory while the patients with VaD were more impaired on the DRS-Construction. Additionally, patients with VaD related to MI scored lower on the DRS-Initiation/Perseveration as compared to patients with AD, and patients with AD scored lower on the DRS-Conceptualization as compared to patients with VaD related to CVA. These results are indicative of qualitative differences in the pattern of cognitive deficits associated with the two types of dementia.