Parkinson’s disease (PD) is a chronic, progressive, brain disorder resulting from degeneration of nerve cells in the substantia nigra. The damaged neurons in the substantia nigra usually display a primary diagnostic marker of PD called Lewy body.1-3 This degeneration results in decreased availability of dopamine, a chemical that is partially responsible for transmitting messages to control movement and coordination in the midbrain and emotions in the forebrain.1,3-6 Typically dopamine acts as an inhibitory neurotransmitter and acetylcholine act as an excitatory neurotransmitter.3 These two neurotransmitters complement each other in individuals without PD symptoms.
The absence of dopamine leaves the dopamine receptors in the striatum inadequately stimulated and permits acetylcholine to overpower dopamine.3 As PD progresses, the amount of dopamine produced in the brain continues to decrease and individuals lose the ability to control their body movements in an ordinary manner.1,6 It is common for individuals to experience tremors, bradykinesia, gait disturbances, muscle rigidity, and postural instability.1-6 This can ultimately result in unemployment, inability to complete activities of daily living independently-including the ability to perform oral self-care, and a decreased quality of life.7
Occasionally “Parkinsonism” (secondary parkinsonism) is mistaken for PD as many of the signs and symptoms are the same; however, the underlying pathologies are different. Parkinsonism is a clinical syndrome that can result from a variety of items such as medications, repeated head trauma, brain lesions, exposure to toxins, metabolic disorders, neurodegenerative disorders, and PD. Individuals with Parkinsonism will not respond to dopamine replacement therapy.8