The high co‐occurrence of somatic symptom disorder (SSD) in Parkinson's disease (PD) patients suggests overlapping pathophysiology. However, little is known about the neural correlates of SSD and their possible interactions… Click to show full abstract
The high co‐occurrence of somatic symptom disorder (SSD) in Parkinson's disease (PD) patients suggests overlapping pathophysiology. However, little is known about the neural correlates of SSD and their possible interactions with PD. Existing studies have shown that SSD is associated with reduced task‐evoked activity in the medial prefrontal cortex (mPFC), a central node of the default‐mode network (DMN). SSD is also associated with abnormal γ‐aminobutyric acid (GABA) content, a marker of local inhibitory tone and regional hypoactivity, in the same area when SSD co‐occurs with PD.
               
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