Error data, correct trial RT data, and secondary measures were subsequently included in between-group analyses. Error analyses are reported in Table 2 and illustrated in Figure 1. As predicted, there was a significant group effect and a group–by–trial type interaction. A priori contrasts of overall AY and BX errors across groups showed the predicted differences between patients and controls (F1,81 = 14.70, P<.001) and between patients and siblings (F1,81 = 8.50, P<.01), but no overall performance difference between siblings and controls (F1,81 = 0.41, P = .52). The interaction of AY and BX trials with group was significant when comparing patients with controls (F1,81 = 10.73, P<.005) and siblings with controls (F1,81 = 9.58, P<.005), but there was no interaction of trial type and group in patients and siblings(F1,81 = .027, P = .87). These effects were due to increased BX errors in parallel for patients and siblings and increased AY errors in controls relative to siblings (Figure 1A). This predicted pattern of contrast effects provides strong interpretive leverage for describing the nature of context-processing impairments. The lack of an overall error effect between siblings and controls and the highly significant disordinal (x-shaped) interaction with trial type is suggestive of a double dissociation. In fact, controls made significantly more AY errors (t57.62 = −2.03, P<.05), while siblings made significantly more BX errors(t25.48 = 2.16, P<.05)(both 2-tailed tests for unequal variances). The difference between subjects' BX and AY errors was a useful metric that capitalized on this double dissociation, and subtracted out generalized deficits that were measured in both conditions. As expected, there were large mean differences on BX−AY between controls and both patients and siblings (effect sizes, 0.88 and 0.80, respectively), but patients were nearly equal to siblings (effect size, 0.05) (Figure 1B). The 3-way interaction in the omnibus tests was not interpretable(Table 2).