Hypokinesia and Movement Challenges in Parkinson's Disease

Parkinson’s disease (PD) is a chronic, progressive neurodegenerative disease characterized by hypokinesia and motor dysfunction. The cardinal symptoms of PD are bradykinesia, rigidity, postural instability, and tremor. Associated deficits such as worsening handwriting (micrographia), shuffling gait, speech disturbance, dysphagia, and finger incoordination also occur frequently. In general, the combination of asymmetric presentation of symptoms and clinical improvement with levodopa treatment distinguishes PD from other movement disorders. PD is caused by dysfunctions in the basal ganglia. The basal ganglia consist of several important nuclei in the subcortical part of the brain and play a major role in initiation and control of normal voluntary movement. They do not regulate strength nor do they communicate with the spinal cord or peripheral limbs directly. They receive their primary input from the cerebral cortex and send the majority of their output, via the thalamus, back to the cortex. Neuronal loss in the substantia nigra, leading to a decrease in the level of dopamine in the striatum, is the pathophysiologic hallmark of PD. The loss of dopamine produces an imbalance of activities in the striatum and causes an increase in inhibitory signals to the thalamus. Because the thalamus is responsible for the activation of the cortical areas involved in generation of movements, the final outcome of dopamine deficiency is poverty or slowness of movements. Bradykinesia or slowness of movement can be observed in the loss of a patient’s automatic movements, such as decreased arm-swing while walking, eye-blinking, facial expression, or swallowing of saliva. Patients also complain of difficulty getting up from a chair, turning over in bed, or putting on a jacket or sweater. They feel restrained in their movements and every action becomes more effortful. There is hesitation in initiating voluntary movement, sluggishness during