Recent years have witnessed a renewed interest in the surgical treatment of some of the symptoms of Parkinson's disease,1 and, as in most developing fields of therapeutic endeavor, there are still many unanswered questions. A more accurate conception of the surgical target, a greater precision of method, and, above all, a further understanding of the physiological mechanism of tremor and rigidity are all required.
In the production of tissue necrosis we have used two agents, alcohol and the betaemitting isotopes. It has been demonstrated in animals that a 20 mc. source of palladium-109 (Pd109) will produce in brain an area of complete necrosis 5-6 mm. in maximum diameter.2 This necrosis is first visible after 45 minutes' irradiation and reaches its maximum size after 90 minutes. Transition between necrosis and normal tissue is abrupt, and there is no evidence of neurological damage outside this area either immediately
MULLAN S. Observations on Deep Cerebral "Localization" of the Tremor of Parkinson's Disease. AMA Arch Neurol. 1960;2(3):274–280. doi:10.1001/archneur.1960.03840090038005
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