Parkinson's disease

The disease once known as "shaking palsy," recognized by physicians for hundreds of years, was first described in detail by the English physician James Parkinson (1755-1824) in 1817. As a result of his work, shaking palsy graduallybecame better known as Parkinson's disease. By some estimates, more than 1.5 million Americans suffer from Parkinson's Disease, which primarily afflicts older people and usually develops slowly over a period of years causing slowness of movement (bradykinesia), gradual loss of muscular control, resting limb tremors, and gait disturbance (difficulty walking). Eventually the condition becomes so severe that the person becomes incapacitated. The cause of Parkinson's disease is usually not known; however, symptoms can appear after a stroke, encephalitis, carbon monoxide or manganese poisoning, and head injury.

James Parkinson was born in London on April 11, 1755, the son of a surgeon. He studied under the famous physician John Hunter (1728-1793) and later openeda thriving medical practice. In 1817, Parkinson completed his exhaustive study of shaking palsy, describing in detail the characteristics of the disorderand outlining the stages by which it develops. Based largely on a single post-mortem examination, he also hinted at a cause for the condition--a swellingof the medulla. This line of investigation was largely abandoned, however, for well over a century. Not until the 1970s did scientists obtain evidence for a possible cause of Parkinson's disease. Then, researchers began to receivereports of Parkinson's disease among users of certain types of illegal synthetically manufactured drugs. Eventually it became clear that Parkinson's disease results from the death of brain cells in the substantia nigra, a small area deep within the brainstem that produce the neurotransmitter, dopamine. With this knowledge, scientists began to explore methods for controlling symptoms of Parkinson's disease.

One approach is to provide patients with a drug known as L-dopa, a compound that is converted into dopamine in the brain. This therapy has been fairly successful, although it decreases in efficiency as the disease develops. In 1985, the Israeli researcher, Joussa Youdim, found that a compound called deprenyl slows the progress of Parkinson's disease; this drug has been used with considerable success on patients. However, eventually, these drugs produce dyskinesia--uncontrollable movements of the head and limbs. Thus, without drugs, the patient becomes rigid and cannot move; with them, certain movements are uncontrollable.

One promising treatment involves the grafting of brain cells to replace the dopamine-producing ones that have died. This procedure was first attempted byscientists from the United States and Sweden in the late 1970s using cells from fetal rats because the cells were still immature and capable of developinginto the type of cell needed in the brain of the patient. In recent years, the procedure has been modified by the use of human fetal tissue, tissue takenfrom another part of the patient's body, and tissue genetically engineered to produce the missing dopamine. Another promising treatment is surgery called"stereotactic pallidotomy," first introduced by Dr. Lars Leksell in 1952 andreintroduced in the 1980s by a Finnish surgeon working in Sweden, Dr. LauriLaitinen, who had worked with Leksell. In this procedure, a needle-fine probeis inserted through a tiny hole in the skull, positioned in a small area within the globus pallidus, and an electrical current is applied to destroy cells. Of 38 patients Laitinen treated in January, 1992, 80-90% had long-term relief of symptoms.

In 1997, researchers identified a gene thought to produce defective proteinswhich accumulate in the brain killing dopamine neurons and causing early-onset Parkinson's disease. Current research also shows that people who smoke mayhave only half the risk of contracting Parkinson's disease as do nonsmokers because monoamine oxidase B (MAO B), which breaks down dopamine, was found tobe 40% lower in smokers than in nonsmokers. Researchers therefore speculate they would have more available dopamine and thus be less prone to Parkinson's.Which ingredient in cigarettes lowers MAO B is not yet known.

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