People with Parkinson's disease exhibit debilitating gait impairments, including gait slowness, increased step variability, and poor postural control. A widespread supraspinal locomotor network including the cortex, cerebellum, basal ganglia, and brain stem contributes to the control of human locomotion, and altered activity of these structures underlies gait dysfunction due to Parkinson's disease.

People with Parkinson disease (PD) who show freezing of gait also have dysfunction in cognitive domains that interact with mobility. Specifically, freezing of gait is associated with executive dysfunction involving response inhibition, divided attention or switching attention, and visuospatial function. The neural control impairments leading to freezing of gait have recently been attributed to higher-level, executive and attentional cortical processes involved in coordinating posture and gait rather than to lower-level, sensorimotor impairments. To date, rehabilitation for freezing of gait primarily has focused on compensatory mobility training to overcome freezing events, such as sensory cueing and voluntary step planning. Recently, a few interventions have focused on restitutive, rather than compensatory, therapy. Given the documented impairments in executive function specific to patients with PD who freeze and increasing evidence of overlap between cognitive and motor function, incorporating cognitive challenges with mobility training may have important benefits for patients with freezing of gait. Thus, a novel theoretical framework is proposed for exercise interventions that jointly address both the specific cognitive and mobility challenges of people with PD who freeze.

Approximately 50% of people with Parkinson disease experience freezing of gait, described as a transient inability to produce effective stepping. Complex gait tasks such as turning typically elicit freezing more commonly than simple gait tasks, such as forward walking. Despite the frequency of this debilitating and dangerous symptom, the brain mechanisms underlying freezing remain unclear. Gait imagery during functional magnetic resonance imaging permits investigation of brain activity associated with locomotion. We used this approach to better understand neural function during gait-like tasks in people with Parkinson disease who experience freezing- “FoG+” and people who do not experience freezing- ”FoG−“. Nine FoG+ and nine FoG− imagined complex gait tasks (turning, backward walking), simple gait tasks (forward walking), and quiet standing during measurements of blood oxygen level dependent (BOLD) signal. Changes in BOLD signal (i.e. beta weights) during imagined walking and imagined standing were analyzed across FoG+ and FoG− groups in locomotor brain regions including supplementary motor area, globus pallidus, putamen, mesencephalic locomotor region, and cerebellar locomotor region. Beta weights in locomotor regions did not differ for complex tasks compared to simple tasks in either group. Across imagined gait tasks, FoG+ demonstrated significantly lower beta weights in the right globus pallidus with respect to FoG−. FoG+ also showed trends toward lower beta weights in other right-hemisphere locomotor regions (supplementary motor area, mesencephalic locomotor region). Finally, during imagined stand, FoG+ exhibited lower beta weights in the cerebellar locomotor region with respect to FoG−. These data support previous results suggesting FoG+ exhibit dysfunction in a number of cortical and subcortical regions, possibly with asymmetric dysfunction towards the right hemisphere.