Peripheral catecholamine output in Parkinson's disease: effects of drug treatment

Recent reports have indicated depressed levels of catecholamines in the adrenal medulla of advanced Parkinson's Disease (PD) patients undergoing autologous transplant and at autopsy. Such an adrenal defect might have compromised the efficacy of autologous transplants in PD patients. The question arose whether these findings were the result of a generalized defect in catecholamine metabolism in both central and peripheral nervous systems or simply due to drug treatment with levodopa and carbidopa (L/C), the latter being an inhibitor of peripheral catecholamine synthesis. If indeed there are defects in adrenal catecholamine output in PD it might be possible to screen candidates for autologous adrenal medullary transplants. We investigated these issues by measuring 24-h urinary epinephrine (EPI), norepinephrine (NE), metanephrines (METS), and vanilmandelic acid (VMA) levels in three groups of patients: PD patients on standard treatment with L/C, PD patients not on L/C drug treatment, and control non-PD patients. There were no significant differences in 24-h urinary catecholamines, METS, or VMA among the three groups. However, trends in the present results together with previously published data suggest that parkinsonian drug treatment may lower urinary EPI excretion and increase NE excretion. The former may be related to the depressed adrenal medullary tissue levels of EPI, while the latter may reflect conversion of levodopa and incomplete suppression of sympathetic catecholamine synthesis. If there are depressed levels of tissue catecholamines in the sympathoadrenal system in untreated PD patients this is not reflected in a significantly decreased catecholamine output in 24-h urine samples.