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      Conceptualising compensation in neurodevelopmental disorders: Reflections from autism spectrum disorder

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          Highlights

          • Compensation may underpin improvements in symptoms in neurodevelopmental disorders.

          • The construct of compensation is poorly understood and has no agreed definition.

          • We derive a working definition and review evidence for compensation (e.g., in ASD).

          • We propose a preliminary transdiagnostic framework of compensation.

          • We discuss potential neurocognitive mechanisms and research/clinical implications.

          Abstract

          Within research into neurodevelopmental disorders, little is known about the mechanisms underpinning changes in symptom severity across development. When the behavioural presentation of a condition improves/symptoms lessen, this may be because core underlying atypicalities in cognition/neural function have ameliorated. An alternative possibility is ‘compensation’; that the behavioural presentation appears improved, despite persisting deficits at cognitive and/or neurobiological levels. There is, however, currently no agreed technical definition of compensation or its behavioural, cognitive and neural characteristics. Furthermore, its workings in neurodevelopmental disorders have not been studied directly. Here, we review current evidence for compensation in neurodevelopmental disorders, using Autism Spectrum Disorder as an example, in order to move towards a better conceptualisation of the construct. We propose a transdiagnostic framework, where compensation represents the processes responsible for an observed mismatch between behaviour and underlying cognition in a neurodevelopmental disorder, at any point in development. Further, we explore potential cognitive and neural mechanisms driving compensation and discuss the broader relevance of the concept within research and clinical settings.

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          Most cited references88

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          The age-dependent decline of attention deficit hyperactivity disorder: a meta-analysis of follow-up studies.

          This study examined the persistence of attention deficit hyperactivity disorder (ADHD) into adulthood. We analyzed data from published follow-up studies of ADHD. To be included in the analysis, these additional studies had to meet the following criteria: the study included a control group and it was clear from the methods if the diagnosis of ADHD included subjects who did not meet full criteria but showed residual and impairing signs of the disorder. We used a meta-analysis regression model to separately assess the syndromatic and symptomatic persistence of ADHD. When we define only those meeting full criteria for ADHD as having 'persistent ADHD', the rate of persistence is low, approximately 15% at age 25 years. But when we include cases consistent with DSM-IV's definition of ADHD in partial remission, the rate of persistence is much higher, approximately 65%. Our results show that estimates of ADHD's persistence rely heavily on how one defines persistence. Yet, regardless of definition, our analyses show that evidence for ADHD lessens with age. More work is needed to determine if this reflects true remission of ADHD symptoms or is due to the developmental insensitivity of diagnostic criteria for the disorder.
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            The cognitive neuroscience of ageing.

            The availability of neuroimaging technology has spurred a marked increase in the human cognitive neuroscience literature, including the study of cognitive ageing. Although there is a growing consensus that the ageing brain retains considerable plasticity of function, currently measured primarily by means of functional MRI, it is less clear how age differences in brain activity relate to cognitive performance. The field is also hampered by the complexity of the ageing process itself and the large number of factors that are influenced by age. In this Review, current trends and unresolved issues in the cognitive neuroscience of ageing are discussed.
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              Network dysfunction after traumatic brain injury.

              Diffuse axonal injury after traumatic brain injury (TBI) produces neurological impairment by disconnecting brain networks. This structural damage can be mapped using diffusion MRI, and its functional effects can be investigated in large-scale intrinsic connectivity networks (ICNs). Here, we review evidence that TBI substantially disrupts ICN function, and that this disruption predicts cognitive impairment. We focus on two ICNs--the salience network and the default mode network. The activity of these ICNs is normally tightly coupled, which is important for attentional control. Damage to the structural connectivity of these networks produces predictable abnormalities of network function and cognitive control. For example, the brain normally shows a 'small-world architecture' that is optimized for information processing, but TBI shifts network function away from this organization. The effects of TBI on network function are likely to be complex, and we discuss how advanced approaches to modelling brain dynamics can provide insights into the network dysfunction. We highlight how structural network damage caused by axonal injury might interact with neuroinflammation and neurodegeneration in the pathogenesis of Alzheimer disease and chronic traumatic encephalopathy, which are late complications of TBI. Finally, we discuss how network-level diagnostics could inform diagnosis, prognosis and treatment development following TBI.
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                Author and article information

                Contributors
                Journal
                Neurosci Biobehav Rev
                Neurosci Biobehav Rev
                Neuroscience and Biobehavioral Reviews
                Pergamon Press
                0149-7634
                1873-7528
                1 September 2017
                September 2017
                : 80
                : 729-742
                Affiliations
                [0005]MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, De Crespigny Park, London, SE5 8AF, UK
                Author notes
                [* ]Corresponding author. lucy.livingston@ 123456kcl.ac.uk
                Article
                S0149-7634(17)30173-2
                10.1016/j.neubiorev.2017.06.005
                7374933
                28642070
                36a2ec9b-aac5-4021-bb4a-0797a81a5756
                © 2017 The Authors

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 1 March 2017
                : 25 May 2017
                : 13 June 2017
                Categories
                Article

                Neurosciences
                autism spectrum disorder,neurodevelopmental disorders,compensation,compensatory mechanisms,adaptation,camouflaging,cognitive phenotype,behavioural phenotype,remediation,theory of mind,executive function,good outcome,under-diagnosis,late diagnosis,female presentation,unaffected siblings

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