SASA: A Sensory Reactivity Measure for Severely Affected Individuals with Global Developmental Delay and/or Autism Spectrum Disorder

Background:  

There is no consensus on how to reliably measure sensory reactivity in autism spectrum disorder (ASD), despite the addition of sensory reactivity abnormalities, such as hyperreactivity, hyporeactivity and sensory seeking behaviors, as a new DSM-5 criterion. Tools to identify sensory reactivity abnormalities are especially important in severely affected individuals who cannot verbally report their sensory experiences. One of the more common single locus forms of ASD is Phelan-McDermid Syndrome (PMS), which is caused by haploinsufficiency of the SHANK3 gene and characterized by global developmental delay and severely delayed or absent speech. Children with PMS also present with significant sensory reactivity abnormalities that have not yet been thoroughly investigated. 

Objectives:  

The objectives of this study were to (1) develop an objective sensory reactivity measure and (2) test it in individuals with idiopathic ASD and in a single-locus form of ASD; PMS.

Methods:  

The Seaver Autism Sensory Assessment (SASA) is a novel assessment, which was administered by a clinician. The SASA is a standardized sensory observation and parent interview, appropriate for severely affected individuals. The SASA consists of five minutes of unstructured play followed by a standardized presentation of various sensory stimuli (e.g. flickering lights). The child’s behavioral responses such as discomfort, under responsiveness or seeking behavior are rated by a trained administer. Parents also completed the widely used Short Sensory Profile (SSP) parent report (Dunn & Westman 1997).

Results:  

All participants successfully completed the SASA observation. On the Sensory Profile children with PMS (n=5) or idiopathic ASD (n=18) both demonstrate more sensory reactivity issues compared to typically developing children (n=16) (p=.0001). Interestingly, using the SASA, children with PMS showed more hyporeactivity compared to children with idiopathic ASD and typically developing (TD) controls (p=.01). Children with idiopathic ASD did not differ from TD children on hyporeactivity or hyperreactivity. However children with idiopathic ASD had higher scores on seeking behaviors compared to children with PMS and TD children (p=.05). In contrast, children with PMS showed no difference on hyperreactivity or seeking behaviors compared to TD children. The SASA total score significantly correlated with the SSP score (r=-.65, p=.004). Data collection is ongoing to further explore the utility of SASA.

Conclusions:

The SASA, a newly developed sensory observation and parent interview, is feasible even in severely affected, minimally verbal children. The assessment allowed us to identify sensory reactivity subtypes (hyporeactivity, hyperreactivity and sensation seeking) and to differentiate between PMS and idiopathic ASD. This is the first study on sensory reactivity abnormalities in children with PMS, which could eventually support diagnosis, aid in treatment recommendations, and serve as a potential outcome measure in clinical trials. The SASA will be useful for ASD and other neurodevelopmental disorders.