RESUMEN
OBJECTIVES: Studies suggest that impairments in some of the same domains of cognition occur in different neuropsychiatric conditions, including those known to share genetic liability. Yet, direct, multi-disorder cognitive comparisons are limited, and it remains unclear whether overlapping deficits are due to comorbidity. We aimed to extend the literature by examining cognition across different neuropsychiatric conditions and addressing comorbidity. METHODS: Subjects were 486 youth consecutively referred for neuropsychiatric evaluation and enrolled in the Longitudinal Study of Genetic Influences on Cognition. First, we assessed general ability, reaction time variability (RTV), and aspects of executive functions (EFs) in youth with non-comorbid forms of attention-deficit/hyperactivity disorder (ADHD), mood disorders and autism spectrum disorder (ASD), as well as in youth with psychosis. Second, we determined the impact of comorbid ADHD on cognition in youth with ASD and mood disorders. RESULTS: For EFs (working memory, inhibition, and shifting/ flexibility), we observed weaknesses in all diagnostic groups when participants' own ability was the referent. Decrements were subtle in relation to published normative data. For RTV, weaknesses emerged in youth with ADHD and mood disorders, but trend-level results could not rule out decrements in other conditions. Comorbidity with ADHD did not impact the pattern of weaknesses for youth with ASD or mood disorders but increased the magnitude of the decrement in those with mood disorders. CONCLUSIONS: Youth with ADHD, mood disorders, ASD, and psychosis show EF weaknesses that are not due to comorbidity. Whether such cognitive difficulties reflect genetic liability shared among these conditions requires further study. (JINS, 2018, 24, 91-103).
Asunto(s)
Trastorno por Déficit de Atención con Hiperactividad/fisiopatología , Trastorno del Espectro Autista/fisiopatología , Disfunción Cognitiva/fisiopatología , Función Ejecutiva/fisiología , Inteligencia/fisiología , Trastornos del Humor/fisiopatología , Trastornos Psicóticos/fisiopatología , Tiempo de Reacción/fisiología , Adolescente , Adulto , Trastorno por Déficit de Atención con Hiperactividad/epidemiología , Trastorno del Espectro Autista/epidemiología , Niño , Disfunción Cognitiva/epidemiología , Comorbilidad , Femenino , Humanos , Estudios Longitudinales , Masculino , Trastornos del Humor/epidemiología , Trastornos Psicóticos/epidemiología , Adulto JovenRESUMEN
BACKGROUND: Evidence that different neuropsychiatric conditions share genetic liability has increased interest in phenotypes with 'cross-disorder' relevance, as they may contribute to revised models of psychopathology. Cognition is a promising construct for study; yet, evidence that the same cognitive functions are impaired across different forms of psychopathology comes primarily from separate studies of individual categorical diagnoses versus controls. Given growing support for dimensional models that cut across traditional diagnostic boundaries, we aimed to determine, within a single cohort, whether performance on measures of executive functions (EFs) predicted dimensions of different psychopathological conditions known to share genetic liability. METHODS: Data are from 393 participants, ages 8-17, consecutively enrolled in the Longitudinal Study of Genetic Influences on Cognition (LOGIC). This project is conducting deep phenotyping and genomic analyses in youth referred for neuropsychiatric evaluation. Using structural equation modeling, we examined whether EFs predicted variation in core dimensions of the autism spectrum disorder, bipolar illness, and schizophrenia (including social responsiveness, mania/emotion regulation, and positive symptoms of psychosis, respectively). RESULTS: We modeled three cognitive factors (working memory, shifting, and executive processing speed) that loaded on a second-order EF factor. The EF factor predicted variation in our three target traits, but not in a negative control (somatization). Moreover, this EF factor was primarily associated with the overlapping (rather than unique) variance across the three outcome measures, suggesting that it related to a general increase in psychopathology symptoms across those dimensions. CONCLUSIONS: Findings extend support for the relevance of cognition to neuropsychiatric conditions that share underlying genetic risk. They suggest that higher-order cognition, including EFs, relates to the dimensional spectrum of each of these disorders and not just the clinical diagnoses. Moreover, results have implications for bottom-up models linking genes, cognition, and a general psychopathology liability.
Asunto(s)
Trastorno del Espectro Autista/fisiopatología , Trastorno Bipolar/fisiopatología , Función Ejecutiva/fisiología , Esquizofrenia/fisiopatología , Adolescente , Trastorno del Espectro Autista/clasificación , Trastorno Bipolar/clasificación , Niño , Femenino , Humanos , Estudios Longitudinales , Masculino , Esquizofrenia/clasificaciónRESUMEN
In two experiments, participants studied two types of word lists. Direct lists were taken from the Deese-Roediger-McDermott (DRM) paradigm (e.g., water, bridge, run) and contained words directly related to a nonpresented critical item (CI; e.g., river, Roediger & McDermott, 1995). Mediated lists (e.g., faucet, London, jog) contained words related to the CI through a nonpresented mediator. After each study list, participants completed either a recall test, a recall test with a warning about the CI, arithmetic problems, or a recognition test, or they guessed the CI. On a final recognition test, both warning and guessing decreased direct false recognition but increased mediated false recognition, an ironic effect of guessing. An initial recognition test also increased final mediated false recognition. We argue that warning and guessing tasks strengthened associative pathways to the CI, increased the accessibility of associated mediators, and increased monitoring for the CI at test. Increased monitoring was able to reduce CIs from direct, but not mediated, lists.