The ascertainment/enrollment strategy could also have contributed to the high degree of inter-rater reliability. By prioritizing families where OD was highly prevalent and increasing the number of OD cases in our inter-rater subsample, we may have inadvertently selected more severe (and perhaps less ambiguously affected) cases. The effectiveness of our approach, which was designed to maximize the yield of the genetic linkage study and balance the composition of the inter-rater subsample, is evident in the considerably higher rates of OD in those initially studied (i.e., approximately 42% of 123) as compared to the total sample (i.e., approximately 16% of 578). That being said, we did not find evidence of significant differences in severity (as assessed by DSM-IV symptom count) between those OD subjects enrolled initially (N=52 of 123, 5.7±1.4) as compared to subsequently (N=38 of 455, 5.8±1.4; t(88)=0.11, p=0.91). Neither can we exclude the possibility that characteristics of OD in the specific population we studied contributed to a more homogeneous phenotypic presentation. Importantly, the high (but not extreme) rates of OD in our inter-rater reliability sample would not have contributed
