Movement Disorder Patients with Depression Have Altered Corticostriatal Alpha-Beta Power Response to Reward and Loss

Depression is a common comorbidity in movement disorders such as Parkinson's disease (PD) and essential tremor (ET). Altered reward signaling contributes to core depression symptoms such as anhedonia, but the specific neural activity patterns underlying these processes and how they manifest in comorbid movement disorders are incompletely understood. Fourteen PD and 16 ET patients (22 male, 8 female) participated while undergoing deep brain stimulation surgery. Subjects completed a working memory task and received visual feedback about response accuracy while signals were recorded from traversed structures [caudate and/or dorsolateral prefrontal cortex (DLPFC)]. Preoperative Beck Depression Inventory-II (BDI-II) scores of ≥14 indicated elevated depression symptoms. Using cluster-based permutation testing, we identified time and frequency ranges in which oscillatory power significantly differed during reward versus loss feedback. We then used two-way ANOVAs and linear mixed effects models to assess how these power changes differed based on movement disorder and depression severity. Caudate and DLPFC alpha-beta (8-30 Hz) power increased during reward feedback. In both regions, this increase was attenuated in depressed subjects (caudate difference = -0.22, 95% CI = -0.32 to -0.13; DLPFC difference = -0.10, 95% CI = -0.16 to -0.045). BDI-II score was a negative predictor of reward- and loss-related corticostriatal alpha-beta power (caudate estimate = -0.014, 95% CI = -0.020 to -0.0078; DLPFC estimate = -0.0075, 95% CI = -0.012 to -0.0029). Specific to PD, depressed patients had greater decreases in DLPFC alpha-beta power following loss feedback than nondepressed patients (difference = -0.10, 95% CI = -0.17 to -0.027). Our findings suggest that altered corticostriatal alpha-beta power may contribute to reward dysfunction in depression in patients with movement disorders.