Hyposmia
Olfactory detection, identification or discrimination deficits have consistently been found in approximately 80% of patients with PD [56, 57]. Although many patients retrospectively report smell loss prior to noting the first motor problems [7, 9], to date there are only two population based studies that have investigated prospective risk for PD in relation to baseline smell function [16, 17]. In the Honolulu-Asia Aging study (HAAS), a large cohort of more than 2000 men of Japanese ancestry was prospectively followed for PD incidence with respect to baseline olfactory performance using the Brief Smell Identification Test (B-SIT) [17]. After adjustment for age and other potential confounders, the odds ratio for incident PD within four years in those with the lowest quartile of B-SIT scores at baseline was 5.2 and 3.1 in the second lowest quartile as compared with the top two quartiles. However, hyposmia was not associated with PD risk beyond four years. Intriguingly, a clinicopathologic study in a subsample from the HAAS, found an association of olfactory dysfunction with incidental Lewy bodies in the SN [25]. Likewise, the PRIPS study, a large population-based cohort study on risk factors for incident PD (see imaging biomarkers), found a relative risk ratio of 6.5 in hyposmic participants over 3 years [16]. More recently, several studies have addressed the potential of hyposmia as a risk marker for PD in subjects with increased apriori risk for PD. For example, two recent prospective cohort studies of idiopathic RBD patients found that baseline olfactory dysfunction predicted incident Lewy body disorders over 5 and more years of follow-up [14, 58].