Presynaptic inhibition (PSI) at the spinal cord level is crucial for coordinating postural preparation with step initiation. People with freezing of gait and Parkinson’s disease (PD+FOG) show loss of PSI of the soleus muscle during step initiation that is associated with abnormal anticipatory postural adjustments (APA). Here, we hypothesize that increasing PSI of the soleus muscle during step initiation via wrist vibration in PD+FOG would decrease abnormally large APA. Fifteen PD+FOG performed self-initiated steps on a force platform without electrical stimulation and with test or conditioned Hoffman reflexes (H-reflex) to measure PSI of the soleus muscle under three conditions: OFF medication, OFF medication with vibration, and ON medication without vibration. Soleus H-reflexes were recorded during quiet stance (a control task) and when the amplitude of the APA under the same leg exceeded 10–20% of the mean baseline mediolateral displacement. Vibration consisted of 200-300 Hz applied to the wrist when the ipsilateral step initiation foot was on the ground. PD+FOG showed loss of PSI during APA in OFF and ON medication, but PSI was increased during vibration (P<0.05). Increased PSI was associated with smaller APA during vibration (P<0.05). Smaller APA were associated with lower subjective freezing of gait severity (P<0.05). Wrist vibration, but not levodopa, decreases abnormal APA during step initiation by increasing PSI levels of the soleus muscle. Since PSI is modulated by cortical and brainstem areas related to FOG and APA, proprioceptive drive during vibration may reorganize these brain circuits.

Freezing of gait (FOG) is a disabling feature of Parkinson’s Disease (PD) that results in a loss of automatic gait. Neuroimaging studies suggest that increased cortical involvement in gait is closely linked to a loss of automaticity. While non-invasive neuromodulation techniques, such as transcranial magnetic stimulation (TMS), show promise in targeting cortical control mechanisms involved in FOG, their effectiveness is limited by an incomplete understanding of the underlying interactions between cortical control of gait and FOG. Recent studies have brought into question whether increased cortical control of gait in people with FOG is adaptive or maladaptive. Here, we present evidence and literature supporting these two opposing frameworks. One perspective suggests increased cortical involvement serves a compensatory, adaptive role, helping to overcome the loss of automatic gait and mitigate FOG episodes. In contrast, the alternative view suggests that increased cortical control is maladaptive, resulting from a disruption of automatic motor processes that may exacerbate gait impairments. To review these conceptual models, we examine neuroimaging, non-invasive brain stimulation studies, pharmacological modulation, and physical therapy interventions in people with PD and FOG. We conclude that while the vast majority of studies have performed neuromodulation under the conceptual framework that increased cortical control is adaptive, there is limited evidence that this approach is in fact superior to the alternative framework. We encourage future studies to develop a causal, mechanistic understanding of how cortical control of gait impacts freezing behavior to advance the development of effective brain-based treatment strategies.