شناسایی حالات صورت در افراد مبتلا به بیماری پارکینسون که با دارو و غیر دارو درمان می شوند

Recognition of facial expressions of emotion was investigated in people with medicated and unmedicated Parkinson’s disease (PD) and matched controls (unmedicated PD, n=16; medicated PD, n=20; controls, n=40). Participants in the medicated group showed some visual impairment (impaired contrast sensitivity) and performed less well on perception of unfamiliar face identity, but did not show significant deficits in the perception of sex, gaze direction, or familiar identity from the face. For both Parkinson’s disease groups, there was evidence of impaired recognition of facial expressions in comparison to controls. These deficits were more consistently noted in the unmedicated group, who were also found to perform worse than the medicated group at recognising disgust from prototypical facial expressions, and at recognising anger and disgust in computer-manipulated images. Although both Parkinson’s disease groups showed impairments of facial expression recognition, the consistently worse recognition of disgust in the unmedicated group is consistent with the hypothesis from previous studies that brain regions modulated by dopaminergic neurons are involved in the recognition of disgust.

Neuropsychological studies have shown deficits affecting the recognition of specific emotions. People with lesions involving the amygdala show differentially severely impaired recognition of facial expressions of fear [2], [3], [9] and [10]. Investigation of one of these cases also revealed impaired recognition of fear (and anger) to auditory stimuli [37] and Sprengelmeyer et al. [42] reported deficits in recognition of facially, vocally and gesturally displayed fear in a further patient with bilateral gliosis of the amygdala. These neuropsychological results are paralleled by demonstrations of activation of the human amygdala in response to facial and vocal expressions of fear in functional imaging studies of normal subjects [8], [26], [32] and [33]. In contrast, people with symptomatic Huntington’s disease [40] and [43] and pre-symptomatic Huntington’s disease gene carriers [17] are particularly poor at recognising facial expressions of disgust. The findings from Huntington’s disease point to the possibility that fronto-striatal regions and especially the basal ganglia (widely considered to form the core site of pathology in Huntington’s disease) are implicated in recognition of disgust. This hypothesis is supported by findings of impaired recognition of disgust in people with Gilles de la Tourette’s syndrome with co-present obsessive–compulsive behaviours and for people with obsessive–compulsive disorder [41], since neurophysiological and neuropsychological studies of these disorders also highlight fronto-striatal abnormalities [25] and [34]. Supporting evidence that the basal ganglia are involved in recognition of facial expressions of disgust comes from two functional imaging (fMRI) studies in which activation of the putamen in response to faces depicting disgust has been reported [33] and [39]. Because of this evidence that the basal ganglia are involved in recognition of facial expressions of disgust, we investigated recognition of facial expressions by people with Parkinson’s disease (PD). The pathology in Parkinson’s disease especially affects the dopaminergic system, allowing us to study the possible contribution of this neurotransmitter system to processes of facial expression recognition in general and to the recognition of disgust, in particular. To provide evidence concerning the involvement in face related information processing of brain regions modulated by dopaminergic neurons, we looked in detail at face perception and recognition of emotions in people with Parkinson’s disease who were and were not receiving dopamine replacement therapy using an extensive battery of tasks to explore the perception of age, gender, unfamiliar face identity, gaze direction and recognition of emotional expression from the face. We were able to compare the performance of people with medicated and unmedicated Parkinson’s disease to that of neurologically normal controls, and to compare the performance of medicated and unmedicated Parkinson’s disease groups to each other. The latter comparison is of particular interest to identifying the potential contributions of the dopaminergic system.