The cause of Parkinson’s disease is unknown in most cases. However, studies of the extrapyramidal brain nuclei (corpus striatum, globus pallidus, substantia nigra) have established that in this disease a dopamine deficiency prevents affected brain cells from performing their normal inhibitory function within the central nervous system.

Some cases of Parkinson’s disease are caused by exposure to toxins (such as manganese dust and carbon monoxide), which destroy cells in the substantia nigra.

Common complications associated with Parkinson’s disease include injury from falls, food aspiration because of impaired voluntary movements, urinary tract infections, and skin breakdown as the patient becomes less mobile.

The patient history notes the cardinal symptoms of Parkinson’s disease, which include muscle rigidity, akinesia, and an insidious tremor known as unilateral pill-roll tremor, which begins in the fingers. Although the patient often can’t pinpoint exactly when tremors began, he typically reports that they increase during stress or anxiety and decrease with purposeful movement and sleep. He may also report dysphagia.

The patient may complain that he becomes fatigued when he tries to perform activities of daily living and that he experiences muscle cramps of the legs, neck, and trunk. He may also mention oily skin, increased perspiration, insomnia, and mood changes. You may note dysarthria and find that the patient speaks in a high-pitched monotone.

Inspection may reveal drooling, a masklike facial expression, and difficulty walking. The patient’s gait commonly lacks normal parallel motion and may be retropulsive or propulsive. In addition, the patient may demonstrate a loss of posture control when he walks. Typically, the patient who loses posture control walks with the body bent forward. These signs result from akinesia.

You may note other results of akinesia, such as oculogyric crisis (eyes fixed upward, with involuntary tonic movements) or blepharospasm (eyelids closed). You may also discover that the patient takes a long time to initiate movement to perform a purposeful action.

In addition to gait changes, musculoskeletal and neurologic assessment may point to muscle rigidity that results in resistance to passive muscle stretching. Such rigidity may be uniform (lead-pipe rigidity) or jerky (cogwheel rigidity). The patient may also pivot with difficulty and lose his balance easily.

As you assess this patient, keep in mind that Parkinson’s disease itself doesn’t impair the intellect but that a coexisting disorder, such as arteriosclerosis, may.

Diagnosis is based primarily on history and physical examination. Diagnosis is confirmed when the patient’s symptoms decrease after anti-parkinsonism drugs are initiated. Although urinalysis may reveal decreased dopamine levels, laboratory test results usually have little value in identifying Parkinson’s disease.

Computed tomography scan or magnetic resonance imaging may be performed to rule out other disorders such as intracranial tumors. A conclusive diagnosis is possible only after ruling out other causes of tremor, such as involutional depression, cerebral arteriosclerosis and, in patients younger than age 30, intracranial tumors, Wilson’s disease, or phenothiazine or other drug toxicity.

Because no cure exists for Parkinson’s disease, treatment aims to relieve symptoms and keep the patient functional as long as possible. Treatment consists of drugs, physical therapy and, in severe disease unresponsive to drugs, stereotaxic neurosurgery.
Some experimental procedures show promise as treatments for Parkinson’s disease.