To be recognized, a sufficient amount of consensus and clinical history needs to be present, and as a newly proposed condition, PDA had not met the standard of evidence required at the time of recent revisions. However, DSM-5 also moved from sub-type classification to the use of ‘Autistic Spectrum Disorder’, which allows for the behavioural traits of different profiles to be described. In 2011, the National Institute for Health and Care Excellence commented on the fact that PDA has been proposed as part of the autism spectrum but did not include further discussion within the guideline. NICE guidance also expects an ‘ASD’ diagnosis be accompanied by a diagnostic assessment, providing a profile of key strengths and difficulties. Demand Avoidance is listed as a ‘sign or symptom of ASD’ (Appendix 3).Christopher Gillberg wrote a commentary article in 2014 that reviewed recent research and stated, “Experienced clinicians throughout child psychiatry, child neurology and paediatrics testify to its existence and the very major problems encountered when it comes to intervention and treatment.”

Proposed diagnostic criteria
As of 2014 there are no recognized diagnostic criteria.
Mutation of TCIRG1 gene may arise from deletion or gene splicing defects, leading to frame-shifts of the nucleotides of the gene.TCIRG1 mutations illustrate the heterogeneity of DSS through a case study where DSS occurred due to a frameshift mutation, in conjunction with a mutation at an intron located in the gene in one of the alleles of chromosome 11 resulting in a splice site mutation. Despite a frameshift mutation altering the C-terminal of the proton pump, due to increased remnant expression of the wild type transcript, it only resulted in intermediate autosomal recessive DSS due to the partial retainment of vacuolar proton pump function. TNFRSF11A mutation
The TNFRSF11A gene is present in chromosome locus 18q21.33, which encodes for the receptor activator of NF-κB (RANK). RANK is expressed in immature osteoclasts, which facilitates osteoclasts maturation upon binding of RANK ligand (RANKL). Binding of RANK ligand mediates the RANK/RANKL/OPG signalling pathway. The pathway mediates osteoclast differentiation and activation by promoting differentiation of precursors into multinucleated osteoclasts, and activating osteoclasts, thereby contributing to bone resorption and remodelling. Health conditions related to genetic changes in TNFRSF11A includes osteopetrosis, osteolysis, and Pagets disease of bone.Multiple reports of gene mutations exists underlining the mutation of the exons and introns leading to aberrant splicing. There are five variants to the TNFRSF11A gene which produces five unique protein iso-forms. The effects of alternative splicing on each variants are unclear. However, it is suggested that such changes lead to different expression patterns of the gene in both space and time.