History

Tremor was mentioned in the writings of Hippocrates, Celsus, and Galen, but the real history of Parkinson's disease does not start until 1817, the year Parkinson's essay on the shaking palsy was published - when he was 62 years old. Parkinson called the disease the "shaking palsy," but he also provided a Latin term: paralysis agitans. He reported on six patients. The first was personally observed, two others were noticed casually in the street; case 4 had an abscess on the chest wall but was lost to follow-up; case 5 was evidently seen at a distance, and there are no details of that patient

OA neuron available; and case 6 was a 72-year-old man who was visually inspected but evidently not examined.

In other words, by modern standards Parkinson's great essay on Parkinson's disease would not have passed muster. It is clear that the information he conveys in his essay is basically from visual inspection: He did not examine the patients personally. Despite that his paper was well received by the medical community, and subsequently, clinicians added to his description.

Armand Trousseau, in 1859, included a lecture in clinical medicine on parkinsonism and discussed the rigidity and the bradykinesia. The great French neurologist Jean Martin Charcot considered Parkinson's disease a neurosis because there was no proper central nervous system lesion to explain it, and the condition was characteristically worsened by stress or emotion. Charcot frequently commented that everything possible had been used to treat parkinsonism but with very little effect. He recommended belladonna alkaloids, especially hyoscyamine, an etropine isomer, now known to us as scopolamine. According to our modern biochemical understanding of parkinsonism, this agent should have a partial effect in improving the signs and symptoms of Parkinson's disease. In an interesting paper in 1893, Paul Oscar Blocq reported the case of a patient with hemiparkin-sonism, who at autopsy was found to have a lesion in the inferior peduncle with complete destruction of the substantia nigra. This, of course, suggested that the neuroanatomic substrate of Parkinson's disease was the substantia nigra and probably is the first description in the medical literature of a lesion that produces parkinsonism. Many other descriptions were made by William R. Gowers and other famous physicians, but these merely added to the fundamental and original observations of Parkinson.

The road to effective therapy was paved in the 1960s by A. Carlsson, who showed in animals that reserpine produces a bradykinesia that could be reversed by the administration of l-dopa, a dopamine precursor. Because it was known that reserpine administration to humans produces a condition that resembles parkinsonism, l-dopa was administered to reserpinized humans to ameliorate the signs and symptoms of the reserpine-induced parkinsonism. O. Hornykiewicz and colleagues then studied the concentration of dopamine in patients dying of parkinsonism, comparing the results to those in normal controls, and reported that there was a marked decrease in dopamine in the caudate nucleus. In 1962 André Barbeau tried the oral administration of l-dopa (100 to 200 mg), and in 1961 W. Birkmayer and

Hornykiewicz experimented with intravenous levo-dopa (50 to 150 mg), both reporting temporary benefits in parkinsonism. Others, however, were unable to confirm any major effect until George C. Cotzias and colleagues initiated the modern era of therapy in parkinsonism by showing that much larger oral doses of the l-dopa, 1.6 to 12.6 grams per day, resulted in dramatic improvement in many patients. The improvements were so dramatic that the efficacy of levodopa treatment was established beyond any doubt, and a new era in the management of Parkinson's disease began.

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