Current Status of Psychopharmacological, Neuromodulation, and Oxytocin Treatments for Autism: Implications for Clinical Practice

Abstract

Objectives To provide an overview of the current literature regarding the neurobiological treatments of psychopharmacology, neuromodulation, oxytocin therapy, and psychological resilience, as treatments for autism-related difficulties, and to distil the research findings from those treatments for everyday clinical application. Methods Instead of producing another specific systematic summary of the efficacy of these treatments, this review took an overview of each field of research, identified its key research findings, and evaluated the treatment-ready status of each of them in terms of their evidence base. From this information, a set of recommendations were derived for their clinical applications, so as to inform practice in the field. Results These treatments represent relatively recent and neurobiologically based approaches to the challenges of autism, and are in the development stage. Each treatment is promising, and has some evidential basis for its success, but all need further research to establish their evidence-based validity for everyday clinical usage. Conclusions While most of these treatments can be applied with caution, clinicians should acknowledge their restrictive benefits and costs, that are described herein. Within those caveats, each of these treatments should be considered as an emerging therapy that clinicians should consider utilising in appropriate settings and with specific cases.

Peripheral oxytocin levels are linked to hypothalamic gray matter volume in autistic adults: a cross-sectional secondary data analysis

“…Presently, no approved pharmaceutical treatments exist for the core symptoms of ASD, and reported findings regarding the efficacy of OXT are inconsistent in both child and adult participants 107 . The shortcomings of clinical trials in OXT pharmacotherapy can be attributed to various factors, including a limited understanding of the biological basis of ASD, the absence of clinically meaningful markers to identify homogeneous patient subgroups, and the consequent absence of targeted therapeutic options 16 .…”