Wednesday, May 20, 2014, 12:30 p.m.
Room 200, Graduate Student Centre (map)
Title: A Study of Neurocognition in OCD-Affected Youth, At-Risk Siblings, and Healthy Controls
Research Supervisor: Dr. Lynn D. Miller (ECPS)
Supervisory Committee: Dr. S. Evelyn Stewart (Psychiatry)
Supervisory Committee: Dr. Colleen Brenner (Psychology)
University Examiners: Dr. Laurie Ford (ECPS), Dr. Amori Mikami (Psychology)
External Examiner: Dr. Margaret Semrud-Clikeman (University of Minnesota)
ABSTRACT
OCD is a neuropsychiatric illness that often begins in childhood and has significant impact on family, academic, occupational, and social functioning. OCD has complex genetic underpinnings, with a 10-fold increased risk among siblings of OCD-affected youth. Attempts to identify OCD vulnerability contributory genes have had suboptimal results partially due to the heterogeneous nature of OCD that prevents the differentiation of external symptoms in genetically homogenous subgroups. Although genetic influences are greater in childhood-onset OCD, most studies have used adult samples. There is increasing interest in determining intermediate markers of brain dysfunction (endophenotypes) that are associated with vulnerability for OCD. Neurocognitive assessment has been considered an important measurement of cognitive markers in OCD.
This study examined neurocognition in OCD-affected youth in comparison to their siblings and healthy controls, in an effort to increase awareness about neurocognitive deficits in childhood-onset OCD and better understand the potential heritability of neuropsychological traits. Participants included OCD-identified youth (N=29), at-risk siblings (N=18), and healthy controls (N=31), who were assessed in the areas of executive function, attention, visual memory, intelligence, state anxiety, and OCD symptom severity. Analysis of covariance (ANCOVA) and mixed model ANCOVA with family membership as a random factor were used to assess group effects on the outcome variables.
Findings indicated that OCD-identified youth presented with significant deficits in planning in comparison to healthy controls. Siblings demonstrated poorer decision-making when compared to OCD and healthy control participants. OCD probands exhibited significant executive dysfunction on daily behaviour when compared to the other two groups. No significant group differences were found in other examined neurocognitive areas. Symptom severity was not associated with neurocognitive performance of OCD-affected youth, whereas high state anxiety was associated with poorer decision-making across all groups.
Impaired planning has been implicated as a potential endophenotype in OCD, and the current study’s results are comparable to those in previous adult studies. This study contributes to the limited research on neurocognitive functioning of OCD-affected youth and their siblings, increases awareness about neurocognitive deficits in OCD, and provides information for the advancement in school and clinical interventions and early identification of those at risk for developing OCD.