Ordinarily we are in control of the initiation and perpetuation of movement; such movement is said to be volitional. However, there are disease states in which involuntary movements occur; these are referred to in aggregate as movement disorders. The best-known of these is Parkinson’s disease.
Volitional movement requires overcoming reflexes that maintain postural set. In primary Parkinson’s disease, there is a deterioration of the neurocircuitry smoothly integrating the reflexes that maintain posture with those of volitional movement. In particular, Parkinson’s disease occurs when there is drop-out of dopamine neurons collected in an anatomical structure of the brain called a nucleus. Due to its black appearance in the brain, this nucleus is called the substantial nigra. It is part of a circuit, the basal ganglia, that primarily controls the reflexes of postural set.
Parkinson's disease is readily apparent. Signs and symptoms include a tremor at rest, as opposed to an intention tremor. This means that when the hands of the Parkinson’s patient are not occupied with volitional movement (that is, at rest), a characteristic tremor is present involving the thumb and first finger. It appears as if the person is rolling a pill there, hence the name pill-rolling tremor. There is also rigidity of the limbs manifest by a ratcheting resistance to passive movement. This is why it is often called cog-wheeling. There is also a loss of spontaneous movements in general, including the face, causing the classic mask fasces. The voice and writing of the Parkinson’s patient start out strong but readily fatigue; the voice soon becomes a whisper, and the writing terminates in a tiny script called micrographia. Even reflexes responsible for handling oral secretions are impaired, leading to drooling.
Over time, the patient with Parkinson’s disease becomes stooped and the limbs flexed. Ambulation is impaired as well; some patients, when they start walking, involuntarily walk faster and faster and are unable to stop, called festination. They often run into walls or otherwise injure themselves. As the disease progresses, patients find themselves experiencing periods of immobility alternating with periods of mobility, the classic “off-on” phenomenon. In addition to moderating motor movements, the basal ganglia also play a role in mood and cognition; the deterioration of this system eventuates in depression and dementia, respectively.
Treatment for Parkinson’s involves attempts to restore dopamine functioning in the remaining dopamine-bearing neurons in the basal ganglia. Surgery is sometimes necessary. Ablating (destroying) a specific nucleus in the thalamus of the brain can mitigate tremor; often all motoric manifestations of the disease respond to Deep Brain Stimulation (DBS), in which an electrical pulse is delivered to regions of the brain affected by the disease. Finally, there are cases where the Parkinson’s disease signs and symptoms are due to the side effects of medication. Such features are said to be Parkinsonoid, and respond to careful management of the medications used to treat the primary condition.