Orthostatic hypotension, non-dipping and striatal dopamine in Parkinson disease.

Orthostatic hypotension and non-dipping are relatively common autonomic dysfunctions in patients with Parkinson disease (PD). These abnormalities have been thought to occur independently of striatal dopaminergic depletion; however, only little preliminary information is available. In this study, we investigated the association of neurocirculatory changes with striatal dopamine transporter status in 69 patients with early PD. Seventeen patients had orthostatic hypotension and 55 patients were non-dippers. A comparison between cases with and without orthostatic hypotension was insignificant for striatal dopamine transporter uptake. These insignificances continued in a comparison of dippers and non-dippers. These results suggest that sympathetic noradrenergic dysfunctions in PD are independent of striatal dopamine transporter depletion.

Combined use of ¹²³I-metaiodobenzylguanidine (MIBG) scintigraphy and dopamine transporter (DAT) positron emission tomography (PET) predicts prognosis in drug-induced Parkinsonism (DIP): a 2-year follow-up study.

DIP is a heterogeneous clinical syndrome; some patients develop persistent and worsening of parkinsonian symptoms after discontinuation of the offending drug, or Parkinson's disease (PD) reappears later after a full remission from DIP. However, it is difficult to predict the prognosis in patients with DIP. Herein, we evaluated whether the combined use of (18)F-N-(3-fluoropropyl)-2 beta-carbon ethoxy-3beta-(4-iodophenyl) nortropane (FP-CIT) PET and cardiac MIBG scintigraphy can be used to help distinguish the prognosis in patients with DIP. Among 20 patients enrolled, 16 showed normal DAT uptake and normal myocardial sympathetic innervation. After withdrawal of the suspected drugs, the patients experienced a clinical remission of parkinsonian motor symptoms within 3 months and did not experience any new movement symptoms after at least 2 years of follow-up. Two patients with a moderate decrease in DAT uptake and impaired sympathetic denervation showed worsening of motor manifestations 3 months after discontinuation of the drugs. Another two patients with normal DAT uptake and decreased MIBG uptake, presented full remission of motor symptoms within 2 months after discontinuation of the drugs. However, these two patients eventually developed parkinsonism within 2 years of the follow-up period. The follow-up scans revealed severe decreased DAT uptake in the putamen and similar ranges of cardiac sympathetic denervation. The results suggest that the combined use of these techniques can predict the prognosis of DIP and suggest a proper therapeutic plan for DIP.