Motor Learning Deficits in Parkinson's Disease (PD) and Their Effect on Training Response in Gait and Balance: A Narrative Review
Parkinson’s disease (PD) is a neurological disorder traditionally associated with degeneration of the dopaminergic neurons within the substantia nigra, which results in bradykinesia, rigidity, tremor, and postural instability and gait disability (PIGD). The disorder has also been implicated in degradation of motor learning. While individuals with PD are able to learn, certain aspects of learning, especially automatic responses to feedback, are faulty, resulting in a reliance on feedforward systems of movement learning and control. Because of this, patients with PD may require more training to achieve and retain motor learning and may require additional sensory information or motor guidance in order to facilitate this learning. Furthermore, they may be unable to maintain these gains in environments and situations in which conscious effort is divided (such as dual-tasking). These shortcomings in motor learning could play a large part in degenerative gait and balance symptoms often seen in the disease, as patients are unable to adapt to gradual sensory and motor degradation. Research has shown that physical and exercise therapy can help patients with PD to adapt new feedforward strategies to partially counteract these symptoms. In particular, balance, treadmill, resistance, and repeated perturbation training therapies have been shown to improve motor patterns in PD. However, much research is still needed to determine which of these therapies best alleviates which symptoms of PIGD, the needed dose and intensity of these therapies, and long-term retention effects. The benefits of such technologies as augmented feedback, motorized perturbations, virtual reality, and weight-bearing assistance are also of interest. This narrative review will evaluate the effect of PD on motor learning and the effect of motor learning deficits on response to physical therapy and training programs, focusing specifically on features related to PIGD. Potential methods to strengthen therapeutic effects will be discussed.