Authors: Lucy Anne Livingston, Francesca Happé.
Publication: Neuroscience & Biobehavioral Reviews (Elsevier). Volume 80, Pages 729-742 2017 | DOI: 10.1016/j.neubiorev.2017.06.005
- • 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.
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.
Livingston, L. A., & Happé, F. (2017). Conceptualising compensation in neurodevelopmental disorders: Reflections from autism spectrum disorder. Neuroscience and biobehavioral reviews, 80, 729–742. https://doi.org/10.1016/j.neubiorev.2017.06.005
Developmental dyslexia is characterised by a specific impairment in
reading, not otherwise accounted for by intellectual or visual abilities… [A] subset of individuals, referred to as ‘compensated dyslexics’ (Lefly and Pennington, 1991), eventually establish typical reading skills by the time they enter adulthood (Callens et al.,2012; Gallagher et al., 1996).
Amongst highly ‘compensated’ dyslexics, who do not exhibit measurable spelling or reading difficulties (e.g., those in higher education), significant phonological processing deficits are revealed when tapped with sensitive enough cognitive probes, such as rapid picture naming (Gallagher et al., 1996; Ingvar et al., 2002; Parrila et al., 2007; Swanson, 2012). Further, these individuals’ reading abilities are not necessarily comparable to those of typically developing individuals under certain contexts; for example, their reading speeds are significantly slower than typically developing individuals’ when put under a time constraint (Parrila et al., 2007), or when exposed to substantial background noise (Varnet et al., 2016)
A more plausible explanation is that ‘typical’ reading ability is
achieved via one or more atypical routes that bypass phonological
processing. These alternative processes may be sufficient in certain
contexts, but ultimately, are not as fine-tuned as phonologically-based routes to reading. This is in line with empirical findings and self-reports of alternative cognitive strategies amongst dyslexics; for example, fitting the orthographic forms of unfamiliar words to familiar ones where spelling of the two is similar (Cavalli et al., 2016; Parrila et al., 2007) and relying upon visual imagery (Bacon and Handley, 2014) and the semantic context of words (Corkett and Parrila, 2008; Pugh et al., 2001). This notion of non-phonological routes to ‘typical’ reading is further corroborated by evidence at the neural level, such as findings of neural signatures that are unique to ‘compensated’ (versus ‘un-compensated’) dyslexics when performing phonological tasks (Ingvar et al., 2002; Shaywitz et al., 2003). Amongst ‘compensated’ dyslexics, neuroimaging findings generally support hypoactivation of areas implicated in phonological function, e.g., left parieto- and occito-temporal areas (Cao et al., 2008; Hoeft et al., 2007), and hyperactivation of additionally recruited areas, e.g., right inferior frontal gyrus (Hoeft et al., 2011; Shaywitz et al., 2004). Greater functional connectivity between posterior visual regions has also been reported (Koyama et al., 2013), perhaps reflecting the potential compensatory role of visual strategies (for an exhaustive review of compensatory neural pathways, see Pammer, 2014)