Imagine trying to walk on a narrow path, but every few steps, your feet feel glued to the ground, making it nearly impossible to move forward. This is similar to what individuals with freezing of gait (FoG) experience in Parkinson’s disease (PD). A recent study sought to delve into the cortical mechanisms that contribute to FoG during walking tasks. By using functional near-infrared spectroscopy, the researchers measured changes in oxygenated and deoxygenated haemoglobin in different brain regions involved in movement control. They found that FoG patients exhibited less activation in the prefrontal cortex and premotor cortex compared to PD patients without FoG and healthy controls. Additionally, the FoG group showed a unique pattern of functional connectivity between these regions, suggesting impaired communication within the motor network. These findings provide insights into the potential underlying mechanisms of FoG in PD, which may help inform future interventions and treatments for this debilitating symptom.

BackgroundFreezing of gait (FoG) is a severely disabling symptom in Parkinson’s disease (PD). The cortical mechanisms underlying FoG during locomotion tasks have rarely been investigated.ObjectivesWe aimed to compare the cerebral haemodynamic response during FoG-prone locomotion tasks in patients with PD and FoG (PD-FoG), patients with PD but without FoG (PD-nFoG), and healthy controls (HCs).MethodsTwelve PD-FoG patients, 10 PD-nFoG patients, and 12 HCs were included in the study. Locomotion tasks included normal stepping, normal turning and fast turning ranked as three difficulty levels based on kinematic requirements and probability of provoking FoG. During each task, we used functional near-infrared spectroscopy to capture concentration changes of oxygenated haemoglobin (ΔHBO2) and deoxygenated haemoglobin (ΔHHB) that reflected cortical activation, and recorded task performance time. The cortical regions of interest (ROIs) were prefrontal cortex (PFC), supplementary motor area (SMA), premotor cortex (PMC), and sensorimotor cortex (SMC). Intra-cortical functional connectivity during each task was estimated based on correlation of ΔHBO2 between ROIs. Two-way multivariate ANOVA with task performance time as a covariate was conducted to investigate task and group effects on cerebral haemodynamic responses of ROIs. Z statistics of z-scored connectivity between ROIs were used to determine task and group effects on functional connectivity.ResultsPD-FoG patients spent a nearly significant longer time completing locomotion tasks than PD-nFoG patients. Compared with PD-nFoG patients, they showed weaker activation (less ΔHBO2) in the PFC and PMC. Compared with HCs, they had comparable ΔHBO2 in all ROIs but more negative ΔHHB in the SMC, whereas PD-nFoG showed SMA and PMC hyperactivity but more negative ΔHHB in the SMC. With increased task difficulty, ΔHBO2 increased in each ROI except in the PFC. Regarding functional connectivity during normal stepping, PD-FoG patients showed positive and strong PFC-PMC connectivity, in contrast to the negative PFC-PMC connectivity observed in HCs. They also had greater PFC-SMC connectivity than the other groups. However, they exhibited decreased SMA-SMC connectivity when task difficulty increased and had lower SMA-PMC connectivity than HCs during fast turning.ConclusionInsufficient compensatory cortical activation and depletion of functional connectivity during complex locomotion in PD-FoG patients could be potential mechanisms underlying FoG.Clinical trial registrationChinese clinical trial registry (URL: http://www.chictr.org.cn, registration number: ChiCTR2100042813).

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