Commentary on: “Motor Switching and Motor Adaptation Deficits Contribute to Freezing of Gait in Parkinson’s Disease”

More than 50% of Parkinson’s disease (PD) patients exhibit freezing of gait (FoG) characterized by a sudden and transient inability to initiate or continue walking (1). The pathophysiology of FoG is still unknown, particularly due to the difficulty in reproducing this symptom spontaneously in the laboratory, either in humans or in animal models (2, 3). A current hypothesis proposes that FoG could be caused by an asymmetry and impaired left-right coordination of the locomotor pattern (4). In a recent article published in Neurorehabilitation and Neural Repair, Mohammadi and colleagues used a split-belt treadmill that can independently control the speed of the left and right sides to evaluate gait symmetry and adaptation in healthy subjects (n= 12), non-freezer (n= 12), and freezer (n= 10) PDpatients (5). Subjects were evaluated in six conditions without interruption (each lasting 2min): (1) slow tied-belt condition (3 km/h), (2) split-belt walking following an increase in speed of one side in a random manner to 4 km/h, (3) a return to slow tied-belt condition, (4) same split-belt condition for the other leg, (5) another return to slow tied-belt, and (6) finally, a fast tied-belt condition (4 km/h). The results show that during the first tied-belt condition, freezer patients already exhibited more asymmetrical gait than non-freezer patients and healthy subjects. In addition, the changes of asymmetry during both switching to split-belt and returning to tied-belt were significantly larger in freezers compared to non-freezers and control subjects. Moreover, the adaptation of gait asymmetry during split-belt and the re-adaptation during return to tied-belt were slower in freezers. However, the most interesting result of this study is probably the fact that immediately after switching to splitbelt with the most affected leg on the faster belt, one patient experienced a FoG episode and another one exhibited a festination episode. As a result, Mohammadi et al. (5) proposed that switching to an asymmetrical walking could be a primary deficit in freezers. As stated in the introduction, it is difficult to evaluate FoG in laboratories, either in humans or in animal models (2, 3). Indeed, in a research environment, even patients with clear FoG fail to express this phenomenon during experimental testing (3). To better understand the pathophysiology of this symptom, some methods have been proposed to elicit FoG during standardized conditions. Snijders et al. (3) evaluated the effect of obstacle avoidance during treadmill walking on FoG. Of 13 PD patients, 8 exhibited FoG episodes during treadmill walking with obstacle avoidance. However, FoG episodes elicited by obstacle avoidance were brief and it was proposed that obstacle could act as a cue to rapidly help abort the episode. More recently, the same group investigated the percentage of