Abstract

The exact cause of the parkinsonism gait remains uncertain. We first focus on understanding the underlying neurological reasons for these symptoms through the examination of both static functional network connectivity (SFNC) and dynamic functional network connectivity (DFNC). We recruited 64 postural instability and gait disorder-dominated Parkinson's disease (PIGD-PD) patients, 31 non-PIGD-PD (nPIGD-PD) patients, and 54 healthy controls (HC) from Nanjing Brain Hospital. The GIFT software identified five distinct independent components: the basal ganglia (BG), cerebellum (CB), sensory networks (SMN), default mode network (DMN), and central executive network (CEN). We conducted a comparison between the SFNC and DFNC of the five networks and analyzed their correlations with postural instability and gait disorder (PIGD) symptoms. Compared with nPIGD-PD patients, the PIGD-PD patients demonstrated reduced connectivity between CEN and DMN while spending less mean dwell time (MDT) in state 4. This is characterized by strong connections. Compared with HC, PIGD-PD patients exhibited enhanced connectivity in the SFNC between CB and CEN, as well as the network between CB and DMN. Patients with PIGD-PD spent more MDT in state 1, which is characterized by few connections, and less MDT in state 4. In state 3, there was an increase in the functional connectivity between the CB and DMN in patients with PIGD-PD. The nPIGD patients showed increased SFNC connectivity between CB and DMN compared to HC. These patients spent more MDT in state 1 and less in state 4. The MDT and fractional windows of state 2 showed a positive link with PIGD scores. Patients with PIGD-PD exhibit a higher likelihood of experiencing reduced brain connectivity and impaired information processing. The enhanced connection between the cerebellum and DMN networks is considered a type of dynamic compensation.

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