This review proposes that implicit learning processes are the cognitive substrate of social intuition. This hypothesis is supported by (a) the conceptual correspondence between implicit learning and social intuition (nonverbal communication) and (b) a review of relevant neuropsychological (Huntington's and Parkinson's disease), neuroimaging, neurophysiological, and neuroanatomical data. It is concluded that the caudate and putamen, in the basal ganglia, are central components of both intuition and implicit learning, supporting the proposed relationship. Parallel, but distinct, processes of judgment and action are demonstrated at each of the social, cognitive, and neural levels of analysis. Additionally, explicit attempts to learn a sequence can interfere with implicit learning. The possible relevance of the computations of the basal ganglia to emotional appraisal, automatic evaluation, script processing, and decision making are discussed.

/pdf/intuition-a-social-cognitive-neuroscience-approach-41dbhtx32b.pdf

Intuition: a social cognitive neuroscience approach.

Background Parkinson's disease is a neurodegenerative hypokinetic movement disorder presenting with subcortical pathology and characterized by motor deficits. However, as is frequently reported in the literature, patients with Parkinson's disease can also exhibit cognitive and behavioral impairments. These impairments may be attributed to dysfunction of multiple systems associated with the disease process in Parkinson's disease that are not necessarily related to motor symptoms. In recent years, considerable attention has addressed the circuits connecting the frontal cortical regions and the basal ganglia (i.e., frontostriatal circuits) and how they mediate cognition and behavior in humans. It has been suggested that these same circuits are disrupted in Parkinson's disease and may be responsible for the frontal/executive deficits predominantly reported in this patient population. Objective The current survey of the literature provides a critique and analysis of the neuropsychological profile of Parkinson's disease, including cognitive impairments, behavioral alterations, and emotional processing deficits. A special feature of this paper is to ascertain how frontostriatal circuitry might provide the substrate for the neuropsychological impairments exhibited in Parkinson's disease. In so doing, studies involving nonhuman subjects, neurologically healthy adults, brain-lesioned individuals, and patients with Parkinson's disease are reviewed to provide a novel perspective in conceptualizing and categorizing the cognitive and behavioral sequelae concomitant to specific frontostriatal circuit dysfunction in Parkinson's disease. Conclusions The current review suggests that the neuropsychological profile of Parkinson's disease, which predominantly reflects frontal/executive dysfunction, may be attributed to disruption of the frontostriatal circuitry. The information generated from this review can serve as a guide in the assessment of frontal/executive dysfunction in Parkinson's disease with suggestions for a clinical neuropsychological test battery.

A review of the cognitive and behavioral sequelae of Parkinson's disease: relationship to frontostriatal circuitry.

Individuals with Parkinson's disease (PD) have shown deficits in the ability to recognize emotion. However, these results have been inconsistent. In addition, questions remain about whether any deficit in PD is secondary to depression and broader cognitive impairments, and the effects of stimulus modality, task type, and specific emotion remain unclear. A meta-analysis of 34 comparisons, using data from 1,295 individual participants, was conducted to (a) provide a reliable estimate of the magnitude of the purported deficit in emotion recognition and (b) examine the influence of several potential moderators of emotion recognition abilities in PD. Results show a robust link between PD and specific deficits in recognizing emotion, from both the face and the voice (overall effect size g = 0.52). The deficit extends across stimulus modalities and task types and is particularly acute with respect to negative emotions. Although this deficit does not appear to be secondary to comorbid depression or visuospatial impairments, the potential role of working memory constraints warrants further investigation. We highlight the potential implications of these findings for communication abilities in PD.

/pdf/a-meta-analysis-of-performance-on-emotion-recognition-tasks-hyatph96g7.pdf

A meta-analysis of performance on emotion recognition tasks in Parkinson's disease.

Deficits in decoding emotional facial expressions in Parkinson's disease.

In this study, individuals with Parkinson's disease were tested as a model for basal ganglia dysfunction to infer how these structures contribute to the processing of emotional speech tone (emotional prosody). Nondemented individuals with and without Parkinson's disease (n = 21/group) completed neuropsychological tests and tasks that required them to process the meaning of emotional prosody in various ways (discrimination, identification, emotional feature rating). Individuals with basal ganglia disease exhibited abnormally reduced sensitivity to the emotional significance of prosody in a range of contexts, a deficit that could not be attributed to changes in mood, emotional-symbolic processing, or estimated frontal lobe cognitive resource limitations in most conditions. On the basis of these and broader findings in the literature, it is argued that the basal ganglia provide a critical mechanism for reinforcing the behavioral significance of prosodic patterns and other temporal representations derived from cue sequences (Lieberman, 2000), facilitating cortical elaboration of these events.

/pdf/processing-emotional-tone-from-speech-in-parkinson-s-disease-44gj6adpjx.pdf

Processing emotional tone from speech in Parkinson’s disease: A role for the basal ganglia

Prosodic features in the speech production of 21 patients with idiopathic Parkinson's disease were tested. The appreciation of vocal and facial expression was also examined in the same patients. Significant intergroup differences were found in the prosody production tasks but, in contrast to previous results, not in the receptive tasks on the recognition and appreciation of prosody and of facial expression. The discrepancy between the production and recognition of prosodic features does not support the suggestion that dysprosody in Parkinson's disease is necessarily a disorder of processing emotional information that could be misinterpreted as a dysarthria.

https://jnnp.bmj.com/content/jnnp/54/2/145.full.pdf

O. J. S. Buruma

Papers

The interpretation of dysprosody in patients with Parkinson's disease.