ABSTRACT
Introduction
Mood symptoms are common features of Parkinson’s disease (PD) and essential tremor (ET) and have been linked to worse cognition. The goals of the present study were to compare the severity of anxiety, apathy, and depressive symptoms in PD, ET, and healthy controls (HC) and to examine differential relationships between mood and cognition.
Method
Older adults with idiopathic PD (N = 448), ET (N = 128), or HC (N = 136) completed a multi-domain neuropsychological assessment consisting of memory, executive function, and attention/working memory domains. Participants also completed self-reported mood measures. Between-group differences in mood and cognition were assessed, and hierarchical regression models were conducted to examine relationships between mood and cognition in each group.
Results
Relative to the HC group, the PD and ET groups reported more mood symptoms and scored lower across all cognitive measures. There were no differences between the two movement disorder groups. Mood variables explained 3.9–13.7% of the total variance in cognitive domains, varying by disease group. For PD, apathy was the only unique predictor of executive function (β = −.114, p = .05), and trait anxiety was the only unique predictor of attention/working memory (β = −.188, p < .05). For ET, there were no unique predictors, though the overall models significantly predicted performance in the executive function and attention/working memory domains.
Conclusions
In a large cohort of ET and PD, we observed that the two groups had similar self-reported mood symptoms. Mood symptoms were differentially associated with cognition in PD versus ET. In PD, increased apathy was associated with worse executive function and higher trait anxiety predicted worse attention/working memory. For ET, there were no unique predictors, though the overall mood symptom severity was related to cognition. Our study highlights the importance of considering the relationship between mood and neuropsychological performance in individuals with movement disorders.
Disclosure statement
Dr. Okun reported grants from the National Institutes of Health (grants R01NR014852, R01NS096008, UH3NS119844, U01NS119562, and R25NS108939) outside the submitted work; received royalties for publications with Demos, Manson, Amazon, Smashwords, Books4Patients, Perseus, Robert Rose, Oxford, and Cambridge (movement disorders books); is an associate editor for NEJM Journal Watch Neurology; and had participated in continuing medical education and educational activities (past 12-24 months) on movement disorders sponsored by WebMD/Medscape, RMEI Medical Education, American Academy of Neurology, Movement Disorders Society, and Vanderbilt University. Dr. Foote reported grants from the National Institutes of Health during the conduct of the study; nonfinancial support from Medtronic (donation of closed-loop DBS devices) outside the submitted work; and grants from Medtronic, Boston Scientific, and Functional Neuromodulation outside the submitted work. No other disclosures were reported.
Supplementary material
Supplemental data for this article can be accessed online at https://doi.org/10.1080/13803395.2022.2157796