[Author Affiliation]Michael G. Aman. The Nisonger Center UCEDD, Ohio State University, Columbus, Ohio.L. Eugene Arnold. The Nisonger Center UCEDD, Ohio State University, Columbus, Ohio.Jill A. Hollway. The Nisonger Center UCEDD, Ohio State University, Columbus, Ohio.Address correspondence to: Michael G. Aman, PhD, Professor Emeritus of Psychology, The Nisonger Center (OCEDD) Ohio State University, 1581 Dodd Drive, Columbus, Ohio 43210, E-mail: Michael.Aman@osumc.eduThese days, there is considerable interest in attempts to treat certain developmental disabilities pharmacologically. In this discussion, we periodically step outside the fields of psychopharmacology or autism to see what lessons can be learned for the study of core autism features. If we explore Clinicaltrials.gov, we see approximately 20 studies underway or recently completed among patients with autism spectrum disorder (ASD), Down syndrome, or Fragile X syndrome.Recently, we completed a small trial of mecamylamine in children with autism and pervasive developmental disorder not otherwise specified (Arnold et al., 2012). This trial was the occasion for reflections on the issue of how to measure change in the core symptoms of autism in the context of pharmacological intervention. The purpose of this editorial is to make some observations, pose questions, and offer some suggestions regarding the measurement of ASD core symptoms. We also comment on the clinical and research context in which such investigations must take place.Autism Spectrum Disorder as a Developmental Disability: Implications for PharmacotherapyASD is a neurodevelopmental disorder--i.e., it becomes evident in the course of development, usually within the first three years of life. As a developmental disability, we see three areas of profound social impairment involving failure to develop normally. First, there are profound deficits in social-emotional reciprocity (APA, 2013). The Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5), gives the following examples of deficits in social and emotional reciprocity: Poor social approach, failure to engage in reciprocal conversations, reduced sharing of thoughts, experiences, and emotions. Second, there are deficits in nonverbal communication, including the ability to integrate gesture, eye contact, facial expressions, and body language when communicating with others. Third, there are deficits in the development and understanding of relationships, which may include a lack of interest in others and lack of joint interactive imaginative play (APA, 2013). Also included in the diagnostic criteria are behavioral excesses encompassing restricted, repetitive, or narrow patterns of behaviors and interests, including repetitive physical movements or speech, insistence on sameness or routines, narrow or fixated interests, and odd reactions (often increased or muted) to sensory aspects of the environment.The key issue here is that these developmental deficits suggest months and (usually) years of failure to develop and progress at normal rates. When practiced in the general population, the field of psychopharmacology tends to focus on recovery to the premorbid status (i.e., on reversible symptoms, such as major depression or significant anxiety disorder). In the case of ASD, there is usually no premorbid period in which patients had essentially normal behavior or development, unless we count the first months of life before the problems are noted. The study participants have not stored up the relevant developmental information to be released later with the onset of successful pharmacotherapy. Hence, true therapeutic success for individuals with ASD is likely to require months or even years to reach the patient's new adaptive level. This has obvious implications for pharmacological trials, including matters related to duration of the trial, ideal age of the participants (younger children may be more plastic than older adults), and therapeutic medium in which participants are embedded (e. …
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