Facial emotion recognition in Parkinson's disease: A review and new hypotheses

Abstract

Parkinson's disease is a neurodegenerative disorder classically characterized by motor symptoms. Among them, hypomimia affects facial expressiveness and social communication and has a highly negative impact on patients' and relatives' quality of life. Patients also frequently experience nonmotor symptoms, including emotional-processing impairments, leading to difficulty in recognizing emotions from faces. Aside from its theoretical importance, understanding the disruption of facial emotion recognition in PD is crucial for improving quality of life for both patients and caregivers, as this impairment is associated with heightened interpersonal difficulties. However, studies assessing abilities in recognizing facial emotions in PD still report contradictory outcomes. The origins of this inconsistency are unclear, and several questions (regarding the role of dopamine replacement therapy or the possible consequences of hypomimia) remain unanswered. We therefore undertook a fresh review of relevant articles focusing on facial emotion recognition in PD to deepen current understanding of this nonmotor feature, exploring multiple significant potential confounding factors, both clinical and methodological, and discussing probable pathophysiological mechanisms. This led us to examine recent proposals about the role of basal ganglia-based circuits in emotion and to consider the involvement of facial mimicry in this deficit from the perspective of embodied simulation theory. We believe our findings will inform clinical practice and increase fundamental knowledge, particularly in relation to potential embodied emotion impairment in PD. © 2018 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Keywords: Parkinson's disease; basal ganglia; dopamine; embodied simulation; facial emotion recognition.

Figure 1

Facial emotion recognition in Parkinson's disease: review and discussion. (1) level of impairment, (2) emotions‐specificity, (3–4) methodology, (5‐6) underlying pathophysiological mechanisms with (5) recent considerations about basal ganglia‐based circuits in emotions, (7) new hypothesis related to hypomimia, (8–11) potential clinical confounding factors.