The Neural Basis of Postural Instability Gait Disorder Subtype of Parkinson's Disease: A PET and fMRI Study

Summary Aims The aim of this study is to further uncover the neural basis of postural instability gait disorder ( PIGD ) subtype of Parkinson's disease. Methods With F‐18 fluorodeoxyglucose PET ( FDG ‐ PET ), brain glucose metabolism of patients with PIGD (n = 15) was compared with healthy controls (n = 17) and tremor‐dominant ( TD ) patients (n = 15), and the correlation between metabolism and PIGD symptoms was also assessed. Within PIGD symptom‐correlated hypometabolic areas, the relationship of functional connectivity ( FC ) with motor and cognitive symptoms was examined by using functional MRI . Results Compared with controls, patients with PIGD displayed a distributed pattern of brain hypometabolism including striatal, frontal, and parietal areas. Relative to the pattern of TD patients, the pattern of patients with PIGD had additional metabolic decreases in caudate and inferior parietal lobule ( IPL , Brodmann area [ BA ] 40). In PIGD group, the metabolic reductions in IPL ( BA 40), middle frontal gyrus ( MFG , BA 9) and fusiform gyrus ( FG , BA 20) were associated with severe PIGD symptoms. Regions showing such correlation were chosen for further seed‐based FC analysis. Decreased FC within the prefrontal–parietal network (between the MFG and IPL ) was associated with severe PIGD symptoms. Conclusion The involvement of the caudate, FG , and prefrontal–parietal network may be associated with the prominent gait impairments of PIGD subtype. Our findings expand the pathophysiological knowledge of PIGD subtype and provide valuable information for potential neuromodulation therapies alleviating gait disorders.