Loss of the dopamine-producing neurons in the substantia nigra causes the nerve cells in the striatum to fire out of control, resulting in an inability to control movements in a normal manner. Studies have demonstrated that the brain loses approximately 80% of the dopamine-producing cells in the substantia nigra before the cardinal features of Parkinson disease manifest. The cause of this cell death or impairment is not known, but significant findings by research scientists continue to yield important new clues.

One theory about the cause of Parkinson disease is that free radicals – unstable and potentially damaging molecules generated by normal chemical reactions in the body – may contribute to nerve cell death, thereby leading to Parkinson disease. Free radicals are unstable because they lack one electron; in an attempt to replace this missing electron, free radicals react with neighboring molecules (especially metals such as iron) in a process called oxidation. Oxidation is thought to cause damage to tissues, including neurons. Normally, free radical damage is kept under control by antioxidants, chemicals that protect cells from this damage.

Some scientists have suggested that Parkinson disease may occur when either an external or an internal toxin selectively destroys dopaminergic neurons. An environmental risk factor such as exposure to pesticides or a toxin in the food supply is an example of the kind of the external trigger that could hypothetically cause Parkinson disease. This hypothesis is based on the fact that there are a number of toxins, such as the chemical MPTP and some drugs, known to induce parkinsonian symptoms in humans. So far, however, no research has provided conclusive proof that a toxin is the cause of the disease.

Another relatively new theory explores the role of genetic factors in the development of Parkinson disease. Fifteen to twenty percent of people with Parkinson disease have a close relative who has experienced parkinsonian symptoms such as tremor. After studies in animals showed that MPTP interfered with the function of mitochondria within nerve cells, investigators became interested in the possibility that impairment in mitochondrial DNA could be the cause of Parkinson disease. Mitochondria are found in all animal cells; they convert the energy in food into fuel for the cells.

Yet another theory proposes that Parkinson disease occurs when, for unknown reasons, the normal age-related wearing away of dopamine-producing neurons accelerates in certain individuals. This concept is supported by the knowledge that loss of antioxidative protective mechanism is associated with both Parkinson disease and increasing age.

Many researchers believe that a combination of these four mechanisms – oxidative stress, environmental toxins, genetic predisposition, and accelerated aging – may ultimately be shown to cause the disease.

Recently diagnosed patients sometimes wonder whether the onset of Parkinson symptoms could be linked to some traumatic event…an accident, surgery, or extreme emotional distress. There is no evidence to support that concern. A significant trauma might trigger symptoms earlier than they would spontaneously occur, but this should not be confused with actual causation.