Our model also explains how STN-DBS may act on the pathology of FOG. Previous reports focused more on the direct improvement on motor function, suggesting that STN-DBS may exert its effect on freezing through improving overall gait speed, stride length, trunk flexion or anticipatory postural adjustments.43–46 Our model integrates motor improvement into a larger explanatory framework. Loss of dopamine can lead to changes in local and distant neural population activity.47,48 DBS can disrupt abnormal information flow in basal ganglia circuits, potentially by dissociating input and output signals of the STN.49,50 This may result in the restoration of a normalized cortical activity pattern. Besides, the antidromic activation of the cortico-STN fibres through DBS may desynchronize cortical neurons51,52 and increase their ability to transfer information individually, leading to higher information-coding capacity.53,54 These effects, presented as the improved motor function and the lower cortical PAC (analogues to lower baseline occupation), contribute to enlarged disposable computational capacity (analogues to higher available bandwidth) that can be used to deal with dynamic cognitive burdens and therefore reduces freezing probability. Notably, since the STN is also actively
