Echogenicity of the Substantia Nigra

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Abstract
CURRENT treatment of Parkinson disease (PD) is basically symptomatic. So far, no neuroprotective strategy has proved to be effective in the clinical setting, although concepts and results of animal experiments have been promising.1 One important reason for the failure of neuroprotection may be the fact that nigrostriatal degeneration has advanced to a 60% to 70% reduction of neurons in the substantia nigra (SN) at the time when the first clinical symptoms of PD are noticed by the patient.2 It is possible that at this stage of the disease, drugs with a potential neuroprotective effect are no longer capable of arresting or slowing the course of degeneration. However, the speed of neurodegeneration might be reduced by the commencement of neuroprotective treatment in an earlier (preclinical) stage of PD.