BACKGROUND: Multiple system atrophy (MSA) affects the preganglionic adrenergic neuron and Parkinson's disease (PD) involves the postganglionic counterpart. Widespread postganglionic denervation should result in denervation supersensitivity and a failure of the axon to release norepinephrine (NE). We examined if pharmacological dissection of the adrenergic neuron can distinguish between MSA and PD. METHOD: We measured blood pressure, heart rate, and plasma NE responses to direct (phenylephrine) and indirect (tyramine) acting adrenergic agonists in 15 patients with probable MSA, 16 patients with idiopathic PD, and 16 age- and gender-matched controls. RESULTS: Baroreflex sensitivity was impaired in MSA and intact in PD. Pressor responses to phenylephrine (direct acting) were higher in MSA (p<0.01) and PD patients (p=0.04) than in controls. Blood pressure responses to tyramine (indirect acting) were increased in MSA only (p<0.01). Tyramine increased plasma catecholamine levels in all groups with no significant differences between groups. CONCLUSION: There is denervation supersensitivity in PD patients that is, however, insufficient to shift the dose-response curve to the left. The excessive pressor responses to both tyramine and phenylephrine in MSA are due to baroreflex failure. We conclude that this diagnostic approach lacks sufficient sensitivity to differentiate PD and MSA.
BACKGROUND:Multiple system atrophy (MSA) affects the preganglionic adrenergic neuron and Parkinson's disease (PD) involves the postganglionic counterpart. Widespread postganglionic denervation should result in denervation supersensitivity and a failure of the axon to release norepinephrine (NE). We examined if pharmacological dissection of the adrenergic neuron can distinguish between MSA and PD. METHOD: We measured blood pressure, heart rate, and plasma NE responses to direct (phenylephrine) and indirect (tyramine) acting adrenergic agonists in 15 patients with probable MSA, 16 patients with idiopathic PD, and 16 age- and gender-matched controls. RESULTS: Baroreflex sensitivity was impaired in MSA and intact in PD. Pressor responses to phenylephrine (direct acting) were higher in MSA (p<0.01) and PDpatients (p=0.04) than in controls. Blood pressure responses to tyramine (indirect acting) were increased in MSA only (p<0.01). Tyramine increased plasma catecholamine levels in all groups with no significant differences between groups. CONCLUSION: There is denervation supersensitivity in PDpatients that is, however, insufficient to shift the dose-response curve to the left. The excessive pressor responses to both tyramine and phenylephrine in MSA are due to baroreflex failure. We conclude that this diagnostic approach lacks sufficient sensitivity to differentiate PD and MSA.
Authors: David S Goldstein; Courtney Holmes; Giris Jacob; Fernando Costa; Simi Vincent; David Robertson; Italo Biaggioni Journal: Circulation Date: 2004-01-27 Impact factor: 29.690
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Authors: A Druschky; M J Hilz; G Platsch; M Radespiel-Tröger; K Druschky; T Kuwert; B Neundörfer Journal: J Neurol Sci Date: 2000-04-01 Impact factor: 3.181