Cognitive impairment among children at-risk for schizophrenia

Toward earlier identification and preventative intervention in schizophrenia: evidence from the London Child Health and Development Study

“…physical punishment [35], negative life events, and daily hassles [34]) that are more prevalent and elicit greater distress in at-risk children than typically developing children. Whilst we have found no evidence as yet that these stressful experiences elicit HPA axis abnormalities in ASz and FHx children [35,43], developmental changes may render the HPA axis more susceptible to environmental stressors. Thus, many of the components within the sociodevelopmental-cognitive model of schizophrenia [79] that are hypothesised to contribute to the development of schizophrenia are detectable in at-risk children, but further work is required to integrate these findings for testing.…”

“…For example, ASz children were characterised by increased amplitude of the MMN potential [55], and relative increases in grey and white matter in the temporal lobes [52]; it is possible that these patterns may reverse as the brain undergoes maturation in adolescence. Our investigations revealed no evidence of anticipated abnormalities such as elevated diurnal cortisol [43] or pituitary volume enlargement [35] among either ASz or FHx children, implying that HPA axis hyperactivity may emerge more proximally to illness onset. Having identified potential premorbid markers of illness (albeit these must be shown to be robust with replication in other samples), an important next step will be to determine whether these markers vary with symptom fluctuation and are responsive to intervention.…”

“…In initial cross-sectional analyses conducted in ASz and TD groups only, we observed impairments in general intelligence, verbal memory, working memory, and executive function among ASz children aged 9-12 years [39] which were less pervasive and smaller in magnitude than those characterising adults with schizophrenia [40], but similar to those observed among CHR individuals [41,42]. In subsequent analyses performed on a larger, partially overlapping sample, ASz children performed at a level intermediate to FHx children with high familial loading (C1 first-degree or C2 seconddegree relatives) and FHx children with low familial loading (one affected second-degree relative only) across a range of neurocognitive subtests [43]. Preliminary analysis of longitudinal data collected across three biennial assessments spanning 9-16 years indicates different patterns of [44], with relatively more subtle differences apparent between the high risk groups (as has been indicated also in meta-analysis of older samples of CHR youth relative to youth with family history [45]).…”

“…Nonetheless, among both FHx and ASz children, abnormal cortisol levels (i.e. higher diurnal cortisol levels and greater blunting of the CAR) were associated with poorer memory and executive function, possibly reflecting underlying dysfunction in the brain regions which mediate both HPA axis function and these cognitive functions [43]. Neither ASz nor FHx children were characterised by pituitary volume enlargements [35], which contrasts with those identified among individuals with firstepisode psychosis [66][67][68][69] and in some (but not all) studies of older individuals at-risk for psychosis [69,70].…”

Hot and cold executive functions in youth with psychotic symptoms

“…Therefore, we expect that impairments in hot executive functions will be more closely related to the propensity to experience psychotic symptoms. Previous studies in youth with psychotic symptoms have identified cognitive impairment in cold executive functions, including processing speed and working memory (Cullen et al 2010;Blanchard et al 2010, Kelleher et al 2012aDickson et al 2014). The relationship between hot executive functions and the propensity for psychotic symptoms has not yet been explored.…”