In patients with newly diagnosed Parkinson disease (PD), caudate assessment of dopamine transporter availability may be helpful in identifying the risk for cognitive impairment, depression, and gait issues. This is according to a study published in the Journal of Neurology, Neurosurgery, and Psychiatry.

The Parkinson Progression Markers Initiative database was used to obtain data of patients with PD (n=397) and healthy controls (n=177). Clinical ratings and N-omega-fluoropropyl-2-beta-carbo-methoxy-3-beta-(4-[123]iodophenyl)nortropane (123I-FP-CIT) single photon emission-computed tomography data were analyzed in this cohort. Clinically significant caudate dysfunction was defined as 123I-FP-CIT binding <–2 standard deviations compared with the mean for controls. Patients were categorized into 3 groups: no reduction (n=205), unilateral reduction (n=103), and bilateral reduction (n=89).

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After 4 years, a greater proportion of patients had bilateral vs unilateral reduction (61.4% vs 22.5%, respectively). A total of 6 of 8 patients whose diagnosis changed to atypical parkinsonism had a bilaterally reduced caudate at baseline. At 4-year follow-up, patients with bilateral caudate involvement at baseline had a significantly higher frequency of cognitive impairment vs patients with normal caudate function at baseline (P <.001). Additionally, patients with baseline bilateral caudate involvement had more depression (P <.001) as well as worse ratings on cognitive (P <.001), depression (P <.05), and gait (P <.001) scales.

Limitations of the study include the relatively small sample size as well as the inclusion of only caudate and putamen dopamine transporter availability in the follow-up analysis.

The researchers concluded that these findings suggest caudate quantification of transporter availability after diagnosis of PD may play a significant role in identifying patients at risk for clinical progression. Further these data “might allow better prediction of disease course for patients with early PD and could also provide the potential to stratify cases for early targeted disease-modifying therapies.”

Reference

Pasquini J, Durcan R, Wiblin L, et al. Clinical implications of early caudate dysfunction in Parkinson’s disease [published online May 11, 2019]. J Neurol Neurosurg Psychiatry. doi:10.1136/jnnp-2018-320157