Our previous work revealed substantial heterogeneity in the cognitive profile of bipolar disorder (BD) due to the presence of three underlying cognitive subgroups characterized as: globally impaired, selectively impaired, or cognitively intact. In an effort to determine whether these subgroups are differentially related to genetic risk for the illness, we investigated whether cognitive deficits were more pronounced in unaffected siblings (UAS) of BD probands within identified clusters.

Cluster analysis was used to identify cognitive clusters in BD (N = 60). UAS (N = 49) were classified into groups according to their proband sibling's cluster assignment; comparisons were made across all clusters and healthy controls (HCs; N = 71).

Three cognitive clusters in BD emerged: a globally impaired (36.7%), a selectively impaired (30%), and a cognitively intact cluster (33.3%). UAS showed a qualitatively similar pattern to their BD siblings; UAS of the globally impaired BD cluster showed verbal memory and general cognitive impairments relative to HCs. In contrast, UAS of the other two clusters did not differ from HCs.

This study corroborates findings from prior work regarding the presence of cognitive heterogeneity in BD. UAS of subjects in the globally impaired BD cluster presented with a qualitatively similar cognitive profile to their siblings and performed worse than all other BD clusters and UAS groups. This suggests that inherited risk factors may be contributing to cognitive deficits more notably in one subgroup of patients with BD, pointing toward differential causes of cognitive deficits in discrete subgroups of patients with the disorder.

Executive functions have been proposed as endophenotypes for attention deficit hyperactivity disorder (ADHD); however, data regarding visual memory are lacking. We therefore assessed visual memory in adolescents with ADHD and their unaffected siblings compared with controls.

The participants included 279 adolescents with ADHD, 108 unaffected siblings, and 173 unaffected school controls. They were assessed by using the visual memory tasks of the Cambridge Neuropsychological Test Automated Battery (CANTAB): Delayed Matching to Sample (DMS), Spatial Recognition Memory (SRM), Paired Associates Learning (PAL), and Pattern Recognition Memory (PRM).

Compared with the controls, probands with ADHD had a significantly lower number of correct responses, a higher probability of an error following a correct response and following an error response in the DMS, and a lower percentage of correct responses in the SRM. Their unaffected siblings occupied an intermediate position between ADHD probands and controls in the probability of an error following a correct response and following an error response in the DMS, and in the percentage of correct responses in the SRM. In general, lower IQ and current use of and duration of treatment with methylphenidate were associated with more severe visual memory deficits.

The present results suggest that ADHD is associated with poorer visual memory function. Visual memory assessed by the DMS and SRM tasks in the CANTAB may be a useful endophenotype for ADHD.