Objective: To investigate amygdala subregional alterations associated with impulse control disorders (ICD) in Parkinson’s disease (PD) and to clarify the mechanistic role of the superficial amygdala in the development of ICD.

Background: Impulse control disorders are common neuropsychiatric complications of PD and are closely linked to dysregulated reward and emotional processing. The amygdala plays a central role in processing socially and emotionally salient stimuli and integrating reward-related signals with higher-order cognitive control networks.

Method: Seventy-five patients with PD, including 35 with ICDs (PD-ICD) and 40 without ICDs (PD-NICD), and 40 matched healthy controls underwent multimodal MRI during the ON-medication state. Microstructural alterations were quantified using free-water (FW) imaging and FW-corrected diffusion metrics. Seed-based functional connectivity (FC) and intrinsic neural timescale (INT) analyses were performed for amygdala subregions exhibiting significant microstructural abnormalities. Associations with ICD severity were examined using QUIP-RS scores.

Results: Compared with PD-NICD patients and healthy controls, PD-ICD showed increased FW in multiple right amygdala subregions, with the most prominent alterations observed in the right superficial amygdala. This region also demonstrated reduced corrected fractional anisotropy and increased corrected radial diffusivity, indicating compromised microstructural integrity. Functionally, PD-ICD patients exhibited increased connectivity between the right superficial amygdala and higher-order networks involved in reward and cognitive control, including the posterior cingulate cortex and middle frontal cortex, as well as enhanced coupling with visual processing regions. Furthermore, PD-ICD showed prolonged intrinsic neural timescales in the right superficial amygdala, suggesting altered temporal integration of emotionally salient information. Both FW and INT values in the superficial amygdala were positively correlated with ICD severity.

Conclusion: These findings indicate that the superficial amygdala is a key neural substrate underlying PD-ICD. Structural degeneration and altered temporal dynamics in this region may amplify the processing of reward-related and emotionally salient stimuli while disrupting regulatory interactions with frontal control networks, thereby facilitating impulsive behaviors.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/microstructural-and-functional-abnormalities-of-amygdala-subregions-in-parkinsons-disease-with-impulse-control-disorder/