Gait variability seen in Parkinson's Disorders arise due to cortical changes induced by pathophysiology of the disease process. Gait rehabilitation is focused to harness the adapted connections involved actively to control these variations during the disease progression. Gait variabilities seen are attributed to the defective inputs from the Basal Ganglia. However, there is altered activation of other cortical areas that support the deficient control to bring about a movement and maintain some functional mobility.
Transcranial direct-current stimulation is a modification of the traditionally available direct current applied with 2 saline soaked electrodes (active and reference: 5-35 cm2) with active placed at the area to be stimulated and reference electrode placed at the contralateral supraorbital region in the forehead. Focality of the current passes depends upon the position of the electrode, its dimensions and the current density. The duration of the stimulation varies from 5-20 mins with intensities of 0.5-2.0 mA. It has been successfully introduced as a promising therapeutic adjuvant in various rehabilitation procedures. It alters cortical excitability of region of interest that can be harnessed to optimized motor priming and motor learning procedures involved in gait rehabilitation Mechanisms resulting in post synaptic changes to induce long lasting plasticity is like that of LTP (long-term potentiation) and LTD (long-term Depression) depending upon polarity of the current used.
Gait variabilities in Parkinson disease and related cortical changes
Biomechanical alterations and influence of dopaminergic treatment
Biomechanical and motor control alterations of gait in Parkinson's patients are due to the hypokinesia which reduces the movement speed and size. The main biomechanical changes in seen in walking are: decreased or abnormal arm rotation, decreased trunk rotation, forward stooped posture, decreased movements at hip, knee and ankle joints invariably producing decreased ground clearance, excessive knee flexion throughout gait cycle, decreased stride and step length and decreased gait speed. They face problem in taking sharp turns due to decreased double support time that controls trunk momentum during the observed large swing phase and COM is closer to the limits of stability. There is marked dysrhythmicity seen bilaterally due to variability in stride and swing time. However, with higher walking speed the dysrhythmicity seen will be due to swing time as it is independent of the walking speed. During the ON phase of the Dopaminergic treatment there is increase in gait speed and step length. Cadence and the temporal variables remain unaffected by the Dopamine treatment. However, Dopamine replacements produce inherent variability in Sensorimotor system. As a result, medicated PD patients shows more variability in their gait characteristics than the nonmedicated patients especially in cadence, step time and double support time.
Cortical Changes
People with Parkinson's disease due not lose their inherent ability to generate normal walking patterns but they have activation problems. There is under activation of left medial frontal area, right precuneus and left cerebellar hemisphere and over activity in left temporal cortex, right insula, left cingulate cortex and cerebellar vermis. Under activation of medial frontal areas is the main mechanism related to observed gait abnormalities. Gait disturbances can also result from decreased activation of cognitive network especially in right posterior parietal cortex. There is disruption of basal ganglia-thalamocortical loop due to striatal dopamine depletion which affects the LTP-like effect in human motor cortex. There is also reduction in ipsilateral corticocortical suppression decrease in excitability intrinsic inhibitory cortex leading to selectivity of cortical discharge during movement. Dopamine alters the regional metabolism of motor cortex leading to intracortical inhibition. This results in functional reorganization of motor maps and excessive corticostriatal synchrony when movement is initiated.