Grant: Master's Award: Canada Graduate Scholarships

Freezing of gait (FOG) is arguably the most debilitating symptom experienced by patients with Parkinson's disease (PD). It is often described by patients as a sensation in which they feel that their feet are “glued to the floor”, despite the intention to walk. This diminishes the patient's quality of life, and leads to an increased number falls, which increases the burden to the healthcare system. Moreover, advanced FOG often does not respond well to the common treatments used for PD (1), thus demanding more effective treatment options. The mechanism underlying this phenomenon still remains unclear. However, a widely accepted model proposed by Lewis and Barker (2009) suggests FOG could be the result of an overload of activity in the basal ganglia, an area of the brain that is impaired in PD. This may be caused by additional demands from the cognitive (executive function), sensory (proprioception), or limbic (anxiety) system, which depletes the dopaminergic reserve and leads to FOG (2). Previous studies have demonstrated the role of each system in the occurrence of freezing (3-5), although the extent that these individually contribute to FOG is unknown. The model proposed by Lewis and Barker (2009) would suggest that independently treating the cognitive, sensory, or limbic system in isolation may lead to a reduction in freezing behaviour. Previous studies have evaluated different therapies that target each domain in PD and healthy individuals (6-8), however, research has yet to evaluate the therapeutic benefits to FOG. This investigation is highly warranted, as it may provide effective rehabilitation strategies to ameliorate FOG.