INTRODUCTION The concept of comorbidity in neurodevelopmental disorders like autism is sometimes ambiguous. The co-occurrence of anxiety and autism is clinically significant, yet it is not always easy to determine whether it is a ‘real’ comorbidity, where the two comorbid conditions are phenotypically and aetiologically identical to what that anxiety would mean in persons with a neurotypical development, whether it is an anxiety that has been phenotypically modified by the pathological processes of the autism spectrum disorders, thus resulting in a specific variant of these latter, or whether we are dealing with a false comorbidity resulting from rather inaccurate differential diagnoses. DEVELOPMENT. The article puts forward two hypotheses to explain this co-occurrence, which provide each other with feedback and are little more than our reflections on the scientific evidence we have available today, but expressed aloud. The first is the ‘social error’ hypothesis, which considers that the maladjustments in the social behaviour of persons with autism (which arises from alterations affecting the processes involved in social cognition) help to aggravate anxiety in autism. The second hypothesis, referring to allostatic load, holds that anxiety is a response to chronic stress, wear or exhaustion that is produced by the hyperactivation of certain structures in the limbic system.
CONCLUSIONS The prototypical manifestations of anxiety present in the person with autism are not always related with the same biopsychosocial variables as those observed in persons without autism. Evidence points to hyper-reactive flee-or-fight responses (hypervigilance) when the person finds him or herself outside their comfort zone, and supports the hypotheses of ‘social error’ and of decompensation of the allostatic mechanism that makes it possible to cope with stress.
KeywordsAllostatic loadAnxiety disordersAutistic spectrum disordersCo-occurrenceComorbidityCategoriesNeuropediatríaNeuropsiquiatríaTécnicas exploratorias
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