Exploring the impact of adolescent cognitive inflexibility on emotional and behavioural problems experienced by autistic adults

Autistic young people experience high levels of co-occurring mental health difficulties, including anxiety, depression and behavioural difficulties, across their lifespan. Understanding the neuropsychological mechanisms which underlie these difficulties is vital in developing personalised supports and interventions. Cognitive inflexibility is one candidate mechanism which is associated with co-occurring mental health comorbidities but is also associated with other features of autism such as restricted and repetitive behaviours. This study investigates the distinct longitudinal association between cognitive inflexibility, measured using objective neuropsychological measures and emotional and behavioural problems across adolescence and early adulthood. Eighty-one autistic people from a population-based longitudinal study were assessed at 16 and 23 years on measures of emotional and behavioural problems, with cognitive inflexibility, restricted and repetitive behaviours and verbal intelligence quotient measured at 16 years. We used structural equation modelling to investigate the relationship between cognitive inflexibility and emotional and behavioural symptoms at both timepoints while accounting for the severity of restricted and repetitive behaviours and verbal intelligence quotient. Our results indicate an effect of cognitive inflexibility on increased behavioural problems at 16 years and emotional problems across timepoints, which is distinct from restricted and repetitive behaviours and verbal intelligence quotient. Exploratory mediation analyses suggest that cognitive inflexibility may be one mechanism through which emotional difficulties are maintained longitudinally. Lay abstract Autistic people experience high levels of co-occurring mental health difficulties. To develop more effective treatments, a greater understanding of the thinking processes that may lead to these difficulties is needed. Cognitive inflexibility, defined as a rigid pattern of thoughts and subsequently behaviours, is one possible thinking trait which has previously been associated with both co-occurring mental health difficulties but also other features of autism such as restricted and repetitive behaviours. Restricted and repetitive behaviours include repetitive movements, ritualistic behaviours, and/or highly focused interests. This study investigates the relationship between, cognitive inflexibility, measured using neuropsychological tasks, and emotional and behavioural problems across adolescence and early adulthood. Eighty-one autistic people who were recruited to be representative of the wider autism population were assessed at 16 and 23 years on measures of emotional and behavioural problems, with cognitive inflexibility, restricted and repetitive behaviours and verbal intelligence measured at 16 years. We used statistical modelling to investigate the relationship between cognitive inflexibility and emotional and behavioural symptoms at both timepoints while accounting for the possible relationship with restricted and repetitive behaviours and verbal intelligence quotient. Our results suggest that cognitive inflexibility may be an important factor associated with emotional difficulties across adolescence and early adulthood. This suggests that developing intervention approaches targeting cognitive inflexibility may be an important step in improving the mental health of those with autism.

Experience-dependent changes in hippocampal spatial activity and hippocampal circuit function are disrupted in a rat model of Fragile X Syndrome

Fragile X syndrome (FXS) is a common single gene cause of intellectual disability and Autism Spectrum Disorder. Cognitive inflexibility is one of the hallmarks of FXS, with affected individuals showing extreme difficulty adapting to novel or complex situations. To explore the neural correlates of this cognitive inflexibility, we used a rat model of FXS (Fmr1 KO), and recorded from the CA1 region of the hippocampus while animals habituated in a novel environment for two consecutive days. On the first day of exploration, the firing rate and spatial tuning of CA1 pyramidal neurons was similar between wild-type (WT) and Fmr1 KO rats. However, while CA1 pyramidal neurons from WT rats showed experience-dependent changes in firing and spatial tuning between the first and second day of exposure to the environment, these changes were decreased or absent in CA1 neurons of Fmr1 KO rats. These findings were consistent with increased excitability of Fmr1 KO CA1 neurons in ex-vivo hippocampal slices, which correlated with reduced synaptic inputs from the medial entorhinal cortex. Lastly, activity patterns of CA1 pyramidal neurons were discoordinated with respect to hippocampal oscillatory activity in Fmr1 KO rats. These findings suggest a network-level origin of cognitive deficits in FXS.

Discounting, Cognitive Inflexibility, and Antisocial Traits as Predictors of Adolescent Drug Involvement

Cognitive impairments, such as steep delay discounting, have been correlated with substance-related disorders. However, antisocial traits, cognitive inflexibility, and loss discounting have been barely considered despite having a high relationship with problematic consumption. This study aims to identify the predictive power of these variables in four types of drug use. Fifty-two adolescents (age range of 13 to 19 years) were assessed with a substance involvement test, four discounting tasks using $3,000, a card sorting test, and antisocial screening. Discriminant analysis with simultaneous estimation and varimax rotation was carried out. Function one included discounting of both losses, function two AT and CI, and function three probabilistic gains. The three functions explained 60.1% of the variance. The results show that preference for small and soon punishments and larger and unlikely punishments distinguished non-use and experimental use of moderate consumption and problematic consumption. High antisocial traits and low cognitive inflexibility distinguished experimental use groups of non-use. Risk-taking did not discriminate effectively between moderate consumption and problematic consumption. A replication of this study with a larger sample size is recommended to verify the results.

Distress-driven impulsivity interacts with cognitive inflexibility to determine addiction-like eating

BackgroundResearchers are only just beginning to understand the neurocognitive drivers of addiction-like eating behaviours, a highly distressing and relatively common condition. Two constructs have been consistently linked to addiction-like eating: distress-driven impulsivity and cognitive inflexibility. Despite a large body of addiction research showing that impulsivity-related traits can interact with other risk markers to result in an especially heightened risk for addictive behaviours, no study to date has examined how distress-driven impulsivity interacts with cognitive inflexibility in relation to addiction-like eating behaviours. The current study examines the interactive contribution of distress-driven impulsivity and cognitive inflexibility to addiction-like eating behaviours.MethodOne hundred and thirty-one participants [mean age 21 years (SD = 2.3), 61.8% female] completed the modified Yale Food Addiction Scale, the S-UPPS-P impulsivity scale, and a cognitive flexibility task. A bootstrap method was used to examine the associations between distress-driven impulsivity, cognitive inflexibility, and their interaction with addiction-like eating behaviours.ResultsThere was a significant interaction effect between distress-driven impulsivity and cognitive flexibility (P = 0.03). The follow-up test revealed that higher distress-driven impulsivity was associated with more addiction-like eating behaviours among participants classified as cognitively inflexible only.ConclusionThe current findings shed light on the mechanisms underlying addiction-like eating behaviours, including how traits and cognition might interact to drive them. The findings also suggest that interventions that directly address distress-driven impulsivity and cognitive inflexibility might be effective in reducing risk for addiction-like eating and related disorders.

Set-shifting-related basal ganglia deformation as a novel familial marker of obsessive–compulsive disorder

The symptoms of obsessive–compulsive disorder (OCD) are suggestive of cognitive rigidity, and previous work identified impaired flexible responding on set-shifting tasks in such patients. The basal ganglia are central to habit learning and are thought to be abnormal in OCD, contributing to inflexible, rigid habitual patterns of behaviour. Here, we demonstrate that increased cognitive inflexibility, indexed by poor performance on the set-shifting task, correlated with putamen morphology, and that patients and their asymptomatic relatives had common curvature abnormalities within this same structure. The association between the structure of the putamen and the extradimensional errors was found to be significantly familial in OCD proband–relative pairs. The data implicate changes in basal ganglia structure linked to cognitive inflexibility as a familial marker of OCD. This may reflect a predisposing heightened propensity toward habitual response patterns and deficits in goal-directed planning.