Striatal dopamine loss and discriminative sensory dysfunction in Parkinson's disease

Abstract

Patients with Parkinson's disease (PD) have higher-order discriminative sensory dysfunction including prolonged somesthetic temporal discrimination threshold (sTDT). We studied the effect of striatal dopamine loss on the prolongation of sTDT and also studied the impact of prolonged sTDT values on the various parkinsonian motor deficits. In 30 patients with PD, the severity of parkinsonian motor deficits was evaluated using the Unified Parkinson's Disease Rating Scale (UPDRS) motor scores during levodopa off and on periods. The UPDRS motor subscores were calculated, representing bradykinesia, rigidity, tremor, and axial motor deficits. During levodopa off and on periods, the sTDT value of each index finger was studied. Using [(18) F]-N-3-fluoropropyl-2-beta-carboxymethoxy-3-beta-(4-iodophenyl) nortropane (FPCIT) positron emission tomography studies, caudate and putaminal dopamine transporter uptake levels were measured. Multiple regression analysis covariated with age was used for statistical analysis. During the off period, the striatal FPCIT uptake levels had an impact on the sTDT values (P<0.01). The sTDT values had an impact on the UPDRS subscores for axial motor deficits (P<0.05), but had no impact on those for bradykinesia, rigidity, and tremor. The sTDT values as well as UPDRS total motor scores and all UPDRS subscores were improved by a single oral levodopa treatment. Striatal dopamine deficiency and consequent basal ganglia dysfunction may prolong sTDT, and higher-order discriminative sensory dysfunction seems to contribute in part to the development of axial motor deficits in patients with PD.