Parkinson’s disease (PD) was first described by Dr. James Parkinson in a book, “An Essay on Shaking Palsy”, in 1817. He wrote that this illness was characterized by “involuntary tremulous motion, with lessened muscular power, in parts not in action even when supported, with a propensity to bend the trunk forward and to pass from walking to running pace.” This remains the prototype, and the cause is unknown. The disease progression is slow, with disability occurring 10-20 years after the diagnosis, and no obvious cause for symptom manifestations.
Much research has been done to understand the evolution of the disease that occurs in the body once Parkinson’s disease appears. Among the many chemical substances that activate the brain, neurotransmitters are among the most crucial. One of the most important produced by the human body, deep in the basal ganglia known as substantia nigra (from Latin, meaning “black substance) is dopamine. Dopamine is responsible for regulating muscular response and overall body function. The dopamine producing cells in the substantia nigra connect with the dopamine receptors in the next part of the circuit, the corpus striatum. Another chemical neurotransmitter, acetylcholine, is also found here. In order for the striatum to function effectively, a balance between dopamine & acetylcholine is necessary. This imbalance results in the symptoms of Parkinson’s disease.
This imbalance can go on for many years because at least 60 percent of nerve cells in the substantia nigra and 80 percent of the dopamine in the striatum must be lost before it is diagnosed. It appears the brain can compensate for lesser degrees of dopamine loss, until the time that symptoms appear.
In early stages of Parkinson’s disease, diagnosis is difficult. Often symptoms “come and go” and are commonly confused with normal age-related changes. Diagnosis is based on the findings of at least two of the three primary features of the disease – tremor, rigidity and bradykinesia. The Parkinsonism triad is the tendency to stand in a acetylcholine posture; walk with short shuffling steps; and to speak softly in a rapid, monotone voice.
Tremor at rest is the characteristic feature of PD that earned it the name of “shaking palsy”. It is the earliest and most prominent symptom that causes people to seek medical attention. It initially appears unilaterally in one hand or foot and may eventually involve limbs on both sides as well as head, neck and face. These tremors occur in affected limbs at rest and disappear during movement and sleep. Many PD individuals find that purposeful activity such as lifting, carrying, or pushing causes the tremors to stop.
Muscle rigidity is often not initially noticed, but discovered by the physician. Two types of rigidity are associated with PD: lead-pipe rigidity – arm or leg moves smoothly but with stiffness or cogwheel rigidity – arm or leg “catches” along the path of bending (flexion). In addition to feeling stiffness, those with PD experience
Bradykinesia, from the Latin brady (slow) and kinesia (movement) describes the slowness of movement typically seen. Symptoms may include trouble performing fine motor tasks, difficulty doing two things at the same time or switching quickly from one activity to another. They may also have difficulty insisting new movements. A common complaint is a “sense of weakness” and an inability to perform tasks that seem to require only strength. Bradykinesia does not indicate weak muscles or lack of power. Those with PD have enough power to move but cannot move rapidly. One of the most common losses of automatic movements are eye blinking, swallowing of saliva, expressive movement of the face and hands and minor movements of postural adjustment. Bradykinesia is the most disabling symptom of PD.