Faces of emotion in Parkinsons disease: Micro-expressivity and bradykinesia during voluntary facial expressions

• Published in: Journal of the International Neuropsychological Society 2006-11, Vol.12 (6), p.765-773
• Main Authors: BOWERS, DAWN, MILLER, KIMBERLY, BOSCH, WENDELYN, GOKCAY, DIDEM, PEDRAZA, OTTO, SPRINGER, UTAKA, OKUN, MICHAEL
• Format: Article
• Language: English
• Subjects: Affect; Aged; Aged, 80 and over; Basal ganglia; Brain; Changes; Digital imaging; Digitizing; Emotions - physiology; Entropy; Face; Facial Expression; Female; Humans; Hypokinesia - physiopathology; Male; Middle Aged; Movement; Numerical Analysis, Computer-Assisted; Parkinson Disease - physiopathology; Parkinson's disease; Pattern Recognition, Visual - physiology; Photic Stimulation; Reaction Time - physiology; Research methodology; Spontaneous; Studies
• ISSN: 1355-6177; 1469-7661
• DOI: 10.1017/S135561770606111X

In humans, the neural circuitry underlying facial expressions differs, depending on whether facial expressions are spontaneously (i.e., limbic, subcortical) or voluntarily initiated (i.e., frontal cortex). Previous investigators have suggested that the “masked face” of Parkinson's disease involves spontaneous, but not intentional, facial expressions. In contrast, we hypothesized that intentional facial expressions may be slowed (bradykinetic) and involve less movement, in much the same way that other intentional movements are affected by Parkinson's disease. To test this hypothesis, we used sophisticated computer imaging techniques to quantify dynamic facial movement. Relative to controls, Parkinson patients had reduced facial movement (entropy) and were significantly slowed in reaching a peak expression (i.e., bradykinesia). These findings are consistent with the view that the basal ganglia play a role in affecting intentional facial movements. This possibly occurs because of diminished efficiency and/or activation of face representation areas in the frontal cortical regions (i.e., motor, premotor, and supplementary motor area) or because of movement-based suppression secondary to dopaminergic reduction in frontostriatal pathways. Taken together, the characterization of Parkinson's disease as a model system for the neuroanatomic dissociation between voluntary and spontaneous expressions may be unjustified. (JINS, 2006, 12, 765–773.)