Motor Control Abnormalities in Parkinson's Disease

Abstract

The primary manifestations of Parkinson's disease are abnormalities of movement, including movement slowness, difficulties with gait and balance, and tremor. We know a considerable amount about the abnormalities of neuronal and muscle activity that correlate with these symptoms. Motor symptoms can also be described in terms of motor control, a level of description that explains how movement variables, such as a limb's position and speed, are controlled and coordinated. Understanding motor symptoms as motor control abnormalities means to identify how the disease disrupts normal control processes. In the case of Parkinson's disease, movement slowness, for example, would be explained by a disruption of the control processes that determine normal movement speed. Two long-term benefits of understanding the motor control basis of motor symptoms include the future design of neural prostheses to replace the function of damaged basal ganglia circuits, and the rational design of rehabilitation strategies. This type of understanding, however, remains limited, partly because of limitations in our knowledge of normal motor control. In this article, we review the concept of motor control and describe a few motor symptoms that illustrate the challenges in understanding such symptoms as motor control abnormalities.T he effects of Parkinson's disease (PD) can be described at different levels. Within the brain, the major pathological change is progressive degeneration of neurons in the pars compacta of the substantia nigra, one of the nuclei that constitute the basal ganglia (BG). These neurons normally transmit dopamine to another BG nucleus, the striatum, but their degeneration leads to dysfunction of these neuronal circuits that include the BG and motor cortical areas. At the level of an individual's behavior, these changes result in movement abnormalities, which are the major manifestations of the disease. These difficulties, in turn, cause major disruptions that range from an individual's quality of life to society-wide economics. Our goal in this article is to describe motor symptoms of PD at the level of motor control. We briefly review what is meant by "motor control" and describe the process of understanding a symptom as a motor control abnormality. We then focus on selected symptoms that, among the many and varied motor symptoms of PD, have been most studied from a motor control perspective.

Focal Muscle Vibration Improves Gait in Parkinson's Disease: A Pilot Randomized, Controlled Trial

“…Early movement studies have shown that motor performance worsens in PD, particularly when patients perform simultaneous and sequential movements. In addition, patients with PD have impaired motor execution that, compared to healthy subjects, worsen dramatically when no external sensory cues are provided . Overall these findings may suggest the hypothesis of impaired sensorimotor integration as a pathophysiological mechanism contributing to motor symptoms in PD .…”

Electrifying the motor engram: effects of tDCS on motor learning and control

“…As described in the previous section, tDCS facilitates learning in these artificial tasks. However, motor performance can also be affected by aging (Leversen et al, 2012), brain lesion (Coderre et al, 2010; Tyryshkin et al, 2014) or brain disease (Mazzoni et al, 2012) and produces a decrease in motor performance. The potential of tDCS to restore motor performance in these more natural contexts has been investigated in the recent years.…”

Selenium reduces bradykinesia and DNA damage in a rat model of Parkinson's disease

“…According to one study [3], the most common signs of PD are akinesia (delayed movement initiation; paucity of movements), bradykinesia (movement slowness), hypokinesia (reduced movement amplitude), postural instability, rigidity, stooped posture, and tremor at rest. The main cause of the disease is the degeneration of dopaminergic neurons in the substantia nigra pars compacta [4], and DNA damage and oxidative stress may be involved in the pathophysiology of this neuronal degeneration [5][6][7].…”