ABSTRACT
Introduction
ADHD causes significant distress and functional impairment in multiple domains of daily life. Therefore, diagnosis and treatment are important to improve the quality of life of people. The pharmacotherapy for ADHD is well established but needs systematic evaluation in Intellectual Disability (ID) populations.
Areas covered
This paper reviews the ADHD pharmacological treatment in people with ID using the PRISMA guidance for scoping reviews to help identify the nature and strength of evidence.
Expert opinion
In the last 20 years, seven randomized controlled trials have evaluated pharmacotherapies for ADHD in people with ID; five looking at methylphenidate. Generally, studies were underpowered; all but two had less than 25 participants. Of the two larger trials one was single blinded and therefore open to bias. Only two used a parallel-group method, the remainder were mostly short crossover trials; not ideal when measuring behavioral and psychological parameters which are long standing. The remaining evidence is made up of observational studies. Methylphenidate and atomoxetine, particularly at higher doses, have shown clear benefits in people with ID. Most people with ID tolerated ADHD medications well. Benefits were seen in behavioral and/or cognitive domains. The evidence base is limited, though promising, for dexamfetamine, clonidine, and guanfacine.
Article highlights
The available evidence supports the use of methylphenidate and atomoxetine for ADHD management in people with intellectual disability.
There is evidence to support the use of higher doses of methylphenidate to treat ADHD in people with intellectual disability.
There is some evidence for dexamfetamine, clonidine, and guanfacine.
There is evidence suggesting that people with intellectual disability may respond differently to ADHD medications compared to the general population.
Further research evaluating the evidence for first- and second-line ADHD medications in people with intellectual disability is warranted.
Declaration of interest
R Shankar has received institutional and research support and personal fees from LivaNova, UCB Pharma, Eisai, Veriton Pharma, Bial, and Desitin. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.