Abstract
BackgroundApart from a progressive decline of motor functions, Parkinson’s disease (PD) is also characterized by non-motor symptoms, including disturbed processing of emotions. This study aims at assessing emotional processing and its neurobiological correlates in PD with the focus on how medicated Parkinson patients may achieve normal emotional responsiveness despite basal ganglia dysfunction.MethodsNineteen medicated patients with mild to moderate PD (without dementia or depression) and 19 matched healthy controls passively viewed positive, negative, and neutral pictures in an event-related blood oxygen level-dependent functional magnetic resonance imaging study (BOLD-fMRI). Individual subjective ratings of valence and arousal levels for these pictures were obtained right after the scanning.ResultsParkinson patients showed similar valence and arousal ratings as controls, denoting intact emotional processing at the behavioral level. Yet, Parkinson patients showed decreased bilateral putaminal activation and increased activation in the right dorsomedial prefrontal cortex (PFC), compared to controls, both most pronounced for highly arousing emotional stimuli.ConclusionsOur findings revealed for the first time a possible compensatory neural mechanism in Parkinson patients during emotional processing. The increased medial PFC activity may have modulated emotional responsiveness in patients via top-down cognitive control, therewith restoring emotional processing at the behavioral level, despite striatal dysfunction. These results may impact upon current treatment strategies of affective disorders in PD as patients may benefit from this intact or even compensatory influence of prefrontal areas when therapeutic strategies are applied that rely on cognitive control to modulate disturbed processing of emotions.
Highlights
In addition to the characteristic motor symptoms such as tremor, hypokinesia, rigidity, and postural instability, patients suffering from Parkinson’s disease (PD) frequently encounter psychiatric syndromes, such as affective disorders, cognitive deterioration, sleep disturbances, and hallucinations [1]
Parkinson patients showed decreased bilateral putaminal activation and increased activation in the right dorsomedial prefrontal cortex (PFC), compared to controls, both most pronounced for highly arousing emotional stimuli
Our findings revealed for the first time a possible compensatory neural mechanism in Parkinson patients during emotional processing
Summary
In addition to the characteristic motor symptoms such as tremor, hypokinesia, rigidity, and postural instability, patients suffering from Parkinson’s disease (PD) frequently encounter psychiatric syndromes, such as affective disorders, cognitive deterioration, sleep disturbances, and hallucinations [1]. The majority of studies report an intact ability at the behavioral level of PD patients to explicitly recognize and categorize emotions, but an impaired ability to generate autonomic emotional responses [7,8,9,10,11,12,13,14]. Frontal-subcortical limbic regions including the amygdala, the orbitofrontal cortex (OFC), the ventral anterior cingulate cortex (ACC), the ventral striatum, and the ventrolateral prefrontal cortex (PFC) have been described to be affected in PD. Most of these structures are part of the “emotional circuitry” and depend largely upon dopaminergic projections. Apart from a progressive decline of motor functions, Parkinson’s disease (PD) is characterized by non-motor symptoms, including disturbed processing of emotions. This study aims at assessing emotional processing and its neurobiological correlates in PD with the focus on how medicated Parkinson patients may achieve normal emotional responsiveness despite basal ganglia dysfunction
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