RESUMO
BACKGROUND: Parkinson's disease is characterized by dopamine-responsive symptoms as well as aggregation and accumulation of a-synuclein protofibrils. New diagnostic methods assess a-synuclein aggregation characteristics from cerebrospinal fluid and recent pathophysiologic mechanisms suggest that cerebrospinal fluid circulation disruptions may precipitate a-synuclein retention. Here, we test the hypothesis that cerebrospinal fluid motion at the level of the suprasellar cistern is reduced in Parkinson's disease relative to healthy participants and this reduction relates to choroid plexus perfusion. METHODS: Diffusion weighted imaging (spatial resolution=1.8×1.8×4 mm) magnetic resonance imaging with cycling of diffusion weightings (b-values=0, 50, 100, 200, 300, 700, and 1000 s/mm2) over the approximate kinetic range of suprasellar cistern neurofluid motion was applied at 3-Tesla in Parkinson's disease (n=27; age=66±6.7 years) and healthy (n=32; age=68±8.9 years) participants. Wilcoxon rank-sum tests were applied to test the primary hypothesis that the decay rate of cerebrospinal fluid signal as a function of b-value, which reflects increasing fluid motion, is reduced in persons with versus without Parkinson's disease and inversely relates to choroid plexus activity assessed from perfusion-weighted magnetic resonance imaging (Spearman rank-order correlation; significance-criteria: p<0.05). RESULTS: Consistent with the primary hypothesis, decay rates were higher in healthy (D=0.00328±0.00123mm2/s) relative to Parkinson's disease (D=0.00256±0.0094mm2/s) participants (p=0.016). This finding was preserved after controlling for age and sex. An inverse correlation between choroid plexus perfusion and decay rate (p=0.011) was observed in Parkinson's disease participants. CONCLUSIONS: Cerebrospinal fluid motion at the level of the suprasellar cistern is often reduced in adults with versus without Parkinson's disease and this reduction correlates on average with choroid plexus perfusion.
