The Independent Influence of Apathy and Depression on Cognitive Functioning in Parkinson's Disease
ABSTRACT The purpose of the present study was to examine the independent influence of symptoms of depression and apathy, two of the most common neuropsychiatric symptoms in Parkinson's disease (PD), on executive functioning and memory in PD patients using measures designed to discriminate between these symptoms.
Participants included 68 nondemented, idiopathic PD patients, ages 56-82 years. The Apathy Evaluation Scale-Self-Rating and select items of the Beck Depression Inventory II were used to assess symptoms of apathy and depression, respectively. Cognitive function was assessed using the Wisconsin Card Sorting Test and Hopkins Verbal Learning Test-Revised. Correlations and hierarchical regressions were conducted to investigate the relationships between apathy, depression, and cognitive function. Hierarchical regression analyses were conducted to evaluate the degree of influence of depression and apathy on cognitive function.
Results revealed that symptoms of apathy, but not depression, were significantly and negatively associated with executive functioning. Immediate memory was significantly and negatively associated with both apathy and depression. However, apathy accounted for additional variance in memory performance after controlling for depression at a level approaching significance.
Apathy is not only associated with cognitive impairment, but also with impaired daily functioning, caregiver burden and distress, medication noncompliance, and increased mortality. Differentiating apathy and depression, understanding their unique effects, and appropriately identifying apathy symptoms in patients have robust implications for the development of neuropsychological models of these effects in PD as well as practical implications in guiding improvements to patient care and enhancing quality of life in patients and caregivers.
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- "Concerning other possible cognitive or perceptual troubles not related to Parkinson's disease, we made every effort to minimize the biases that might impair EFE processing. None of the patients suffered either from depression, or any significant dysexecutive syndrome , conditions that are also associated with an impaired EFE recognition   . The absence of most of the cognitive impairments was ensured by exclusion criteria. "
ABSTRACT: Background: Deep brain stimulation of the subthalamic nuclei (STN-DBS) is an effective treatment for the most severe forms of Parkinson's disease (PD) and is intended to suppress these patients' motor symptoms. However, be it in association with Dopamine Replacement Therapy (DRT) or not, STN-DBS may in some cases induce addictive or emotional disorders. Objective: In the current study, we suggest that PD patients suffer from emotional deficits that have not been revealed in previous studies because in those experiments the stimuli were displayed for a time long enough to allow patients to have recourse to perceptual strategies in order to recognize the emotional facial expressions (EFE). Methods: The aim of the current article is to demonstrate the existence of emotional disorders in PD by using a rapid presentation of the visual stimuli (200-ms display time) which curtails their perceptual analysis, and to determine whether STN-DBS, either associated or not associated with DRT, has an impact on the recognition of emotions. Results: The results show that EFE recognition performance depends on both STN-DBS ('on' vs. 'off') and medication ('on' vs. 'off'), but also that these variables have an interactive influence on EFE recognition performance. Moreover, we also reveal how these EFE impairments depend on different spatial frequencies perceptual channels (related to different cortical vs. subcortical neural structures). Conclusions: The effect of PD without therapy seems to be particularly acute for LSF emotional faces, possibly due to a subcortical dysfunction. However, our results indicate that the joint action of STN-DBS and DRT could also disrupt recognition of emotional expressions at the level of occipito-temporal cortical areas (processing HSF visual information) inducing broad global impairment of EFE at the level of HSF visual channels.02/2014; 4(1). DOI:10.3233/JPD-130256
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- "e prevalence of apathy in a CVD population has not been empirically examined. Based on the above �ndings, it is likely that apathy frequently occurs in persons with CVD and is associated with cognitive function  . e current study examined the prevalence of apathy among a sample of older adults with CVD undergoing cardiac testing and examined the association between apathy and neuropsychological test performance. "
ABSTRACT: Background. Psychiatric comorbidity is common in patients with cardiovascular disease, with the literature indicating that this population may be at risk for apathy. The current study examined the prevalence of apathy in patients with cardiovascular disease and its relation to aspects of cognitive function. Methods. 123 participants from an outpatient cardiology clinic completed a brief neuropsychological battery, a cardiac stress test, and demographic information, medical history, and depression symptomatology self-report measures. Participants also completed the Apathy Evaluation Scale to quantify apathy. Results. These subjects reported limited levels of apathy and depression. Increased depressive symptomatology, history of heart attack, and metabolic equivalents were significantly correlated with apathy (P < 0.05). Partial correlations adjusting for these factors revealed significant correlations between behavioral apathy and a measure of executive function and the other apathy subscale with a measure of attention. Conclusion. Findings revealed that apathy was not prevalent in this sample though associated with medical variables. Apathy was largely unrelated to cognitive function. This pattern may be a result of the mild levels of cardiovascular disease and cognitive dysfunction in the current sample. Future studies in samples with severe cardiovascular disease or neuropsychological impairment may provide insight into these associations.Cardiovascular Psychiatry and Neurology 01/2013; 2013:659589. DOI:10.1155/2013/659589
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ABSTRACT: The relationship between apathy, depression and cognitive impairment in Parkinson's disease (PD) is still controversial. The objective of this study is to investigate whether apathy and depression are associated with inefficient cognitive strategies in PD. In this prospective clinical cohort study conducted in a university-based clinical and research movement disorders center we studied 48 PD patients. Based on clinical evaluation, they were classified in two groups: PD with apathy (PD-A group, n = 23) and PD without apathy (PD-NA group, n = 25). Patients received clinical and neuropsychological evaluations. The clinical evaluation included: Apathy Evaluation Scale-patient version, Hamilton Depression Rating Scale-17 items, the Unified Parkinson's Disease Rating Scale and the Hoehn and Yahr staging system; the neuropsychological evaluation explored speed information processing, attention, working memory, executive function, learning abilities and memory, which included several measures of recall (immediate free, short delay free, long delay free and cued, and total recall). PD-A and PD-NA groups did not differ in age, disease duration, treatment, and motor condition, but differed in recall (p<0.001) and executive tasks (p<0.001). Immediate free recall had the highest predictive value for apathy (F = 10.94; p = 0.002). Depression and apathy had a weak correlation (Pearson index= 0.3; p<0.07), with three items of the depression scale correlating with apathy (Pearson index between .3 and.4; p<0.04). The depressed and non-depressed PD patients within the non-apathetic group did not differ. Apathy, but not depression, is associated with deficit in implementing efficient cognitive strategies. As the implementation of efficient strategies relies on the fronto-striatal circuit, we conclude that apathy, unlike depression, is an early expression of executive impairment in PD.PLoS ONE 03/2011; 6(3):e17846. DOI:10.1371/journal.pone.0017846 · 3.53 Impact Factor