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ADHD in children and youth: Part 3—Assessment and treatment with comorbid ASD, ID, or prematurity

Posted: Oct 24, 2018 | Reaffirmed: Jan 11, 2024

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Principal author(s)

Brenda Clark, Stacey A. Bélanger; Canadian Paediatric Society, Mental Health and Developmental Disabilities Committee

Paediatr Child Health 2018, 23(7):485–490.


Attention-deficit hyperactivity disorder (ADHD) is a chronic neurodevelopmental disorder. Three position statements have been developed by the Canadian Paediatric Society, following systematic literature reviews. Statement objectives are to:

1) Summarize the current clinical evidence regarding ADHD,

2) Establish a standard for ADHD care, and

3) Assist Canadian clinicians in making well-informed, evidence-based decisions to enhance care of children and youth with this condition.

Specific topics reviewed in Part 3, which focuses on associated autism spectrum disorder, intellectual disability, and prematurity, include the challenges of diagnostic assessment, common presentations, the role of genetics, and treatment, including the benefits of physical activity. Recommendations are based on current guidelines, evidence from the literature, and expert consensus.

Keywords: Autism; ADHD; Intellectual disability; Prematurity

GUIDE FOR CLINICIANS: Non-pharmacological interventions

Neurodevelopmental deficits associated with autism spectrum disorder (ASD), intellectual disability (ID), or premature birth mimic and overlap with ADHD symptoms that affect learning, behaviour, and daily functioning. However, ADHD symptoms may also overshadow or mask symptoms of all three conditions, leading to delayed diagnosis. Expertise in evaluating ASD, ID, and the sequelae of prematurity as well as associated comorbidities, and a multidisciplinary approach that includes environmental, behavioural, and learning interventions, are required for patients with these conditions. This position statement highlights symptom presentation and trajectories of impairment in these three distinct yet convergent conditions, to enhance understanding and help guide treatment planning. The roles of genetics and therapies (both pharmacological and nonpharmacological) are examined.


Unlike the DSM-IV-TR, the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5), refers to ASD and ADHD (now ASD+ADHD) not as mutually exclusive diagnoses but as conditions that may, and often do, coexist in the same individual [1]. ASD treatment centres on social communication and interaction skill deficits, repetitive and stereotyped behaviour, and restricted interests as core features [1]. However, more recent and increasing evidence of comorbidity with childhood-onset neurodevelopmental disorders like ADHD, with specific impacts on function and prognosis for children and youth with ASD, has broadened scope of treatment [2][4]. Comorbidity between ASD+ADHD is high. More than 50% of individuals with ASD meet criteria for ADHD, and up to 50% of children with ADHD have ASD traits [3][7].

Clinical presentation

Although ADHD+ASD each have distinct core symptoms, children with ASD can present with inattention, impulsivity, and hyperactivity, while children with ADHD often show ASD-like social deficits [4][6]. Both conditions have early onset, present more commonly in males, and have high heritability and comorbidity with other psychiatric, developmental, and neurological disorders [4][7][8]. It is common for young children with ASD+ADHD to receive their ADHD diagnosis first. In these children, there is a higher probability for a significant delay (3 years on average) in the diagnosis of ASD, compared to individuals diagnosed with ASD+ADHD concurrently or with ASD alone [9].

Children with ASD+ADHD present with more impairment in cognitive functioning, more severe behaviour problems and greater psychopathology than individuals with either disorder alone [4][8][12]. Impairments include more severe and pronounced autistic symptoms, greater difficulties with social and communication skills, self-care, adaptive and executive functioning skills, as well as problematic internalizing behaviours (such as anxiety and depression). Maladaptive disruptive behaviours (e.g., tantrums, aggression, emotional dysregulation) and stereotypic or repetitive behaviours are more common in children with ASD+ADHD [4][8][12]. Comorbid psychiatric disorders (e.g., schizophrenia, bipolar, depression, anxiety, disruptive behaviours, and sleep and tic disorders) are also more prevalent. ASD+ADHD is associated with significant learning difficulties and specific language impairment, especially in children and youth with higher functioning ASD [2][4][8][12].


ASD+ADHD share genetic factors [8][9]. Rare copy number variants (<1% population frequency), chromosomal deletions and duplications with a greater effect size are common in children with ADHD and show significant overlap with genetic abnormalities found in ASD and ID [8][12][14]. Genetic syndromes with clinical features of ASD+ADHD include fragile X syndrome, tuberous sclerosis, 22q11 deletion, and Williams syndrome [8][12][14].

Loci underlying ASD+ADHD have been identified on chromosomes 12, 16, and 18 [11][13]. Sixteen single-nucleotide polymorphisms associated with ASD have been identified from ADHD studies, while 25 single-nucleotide polymorphisms appear to be related to ADHD based on ASD studies [13]. These studies further suggest shared heritability of ASD+ADHD [8][13][14]. Research into the role of genetics in ASD is evolving rapidly, with genetic associations and causes being frequently reported. Remaining up-to-date with the literature in this area is important for treatment planning.


When medication is indicated, recent guidelines and meta-analyses concur that psychostimulants should be considered as the first-line treatment for children diagnosed with ASD+ADHD [15][16]. ADHD should be treated in individuals with ASD using the same treatment algorithm as for ADHD alone. However, children and youth with ASD+ADHD are more likely to be nonresponders and to have side effects [15][19].

Irritability with emotional outbursts is the most common adverse effect of stimulants in children with ASD+ADHD [16][19]. Increased stereotypic behaviours, agitation, dysphoria, and psychotic symptoms have also been reported [16][19]. Limited studies have suggested that atomoxetine treatment improves ADHD symptoms in individuals with ASD+ADHD. However, the length of time required for full medication response is longer than for stimulants [20].

A significant reduction of ADHD symptoms was observed in children with ASD+ADHD who were treated with guanfacine and guanfacine extended-release [21][22]. Antipsychotic medications are not indicated for treatment of core symptoms of ADHD [16]. Although stimulant medications are used most often to treat children with ASD+ADHD [22], combined pharmacology in cases complicated by comorbidities is also common, with adjunctive use of an antidepressant, antipsychotics or a mood stabilizer [22]. Because these children tend to be complex, regular multidisciplinary assessment is often needed to guide behavioural and learning goals.

Physical activity is known to alleviate ADHD symptoms [23] and improve social skills in children and youth with ASD [24], and should be integrated into daily routines. While evidence supports a broad range of behavioural interventions for children diagnosed with either ASD or ADHD, few studies to date have demonstrated efficacy for the nonpharmacological or behavioural management of individuals with ASD+ADHD [22]. Children with ASD benefit from early intense behavioural interventions, but ADHD symptoms must not be overlooked. Before initiating pharmacological management, standard evidence-based interventions for ADHD should be implemented, including behavioural parent and teacher training, with a strong school-based component, including individualized education plans (IEPs) and academic supports [8][16]. Referral to a tertiary level care centre is often required to access clinicians with expertise in a broad range of developmental and mental health disorders.


The diagnosis of intellectual disability (ID), also to be known as intellectual developmental disorder in the WHO’s most current International Classification of Diseases (ICD-11), was also revised in the DSM-5 to replace the DSM-IV diagnosis of mental retardation. ID is a chronic condition diagnosed in 2% to 3% of children >5 years of age that often co-occurs with—and affects prognosis for—other neurodevelopmental and mental health disorders. ID is characterized by developmental deficits in cognitive function (i.e., reasoning, problem-solving, planning, abstract thinking, judgment, academic learning, and learning from experience) or in adaptive functioning, such that individuals may be unable to meet developmental and sociocultural standards for personal independence and social responsibility [1]. In ID, intelligence quotient (IQ) scores are ≥2 standard deviations below the population mean [1]. Based on DSM-5 criteria, adaptive function rather than an IQ score is used to define the level of severity (mild, moderate, severe, profound ID), because support requirements depend largely on the level of adaptive function [1].

ADHD is the most common neurodevelopmental disorder comorbid with ID. Prevalence rates are three to four times higher in children or youth with ID than in the general population [25]. However, diagnosing ADHD in individuals with ID is particularly difficult because lower intellectual functioning can affect attention and behaviour [26], leading to diagnostic ‘overshadowing’ [27]. ADHD-like symptoms may also mask (or reveal) a coexisting organic or psychiatric illness [28].

Symptoms of inattention, hyperactivity and impulsivity may be present when academic requirements exceed a child’s intellectual level. In such cases, symptoms typically abate in nonacademic settings. As per the DSM-5, a diagnosis of ADHD in ID can only be made when the core symptoms of ADHD are excessive for developmental age and occur in two or more settings. No standardized behaviour questionnaires exist at the present time to measure ADHD symptoms in special populations. Although psychological tests cannot be used to diagnose ADHD, intelligence screening for children or youth with ADHD symptoms who are also experiencing significant difficulties with key academic skills (reading, spelling, math) is justified to rule out ID as a contributing factor [29]. Furthermore, a multidisciplinary approach and specific expertise in assessing behaviour disorders in children and youth with ID are required to fully determine whether inattention, hyperactivity, and impulsivity are due to comorbid ADHD rather than to ID alone [28].

Clinical presentation

Research on comorbid ID+ADHD is still sparse, but some features are clear: core symptoms of ADHD tend to be more severe [29] and less likely to remit with age [30] in individuals with comorbid ID. Moreover, higher rates of agitation, aggressive and self-injurious behaviours [31], autistic traits or stereotypic behaviours (e.g., rocking) and conduct problems [32] are common. Adaptive functioning, especially in areas of daily living and social communication, is generally impaired in children or youth with comorbid ID+ADHD [33].


At least 50% of ID cases are associated with chromosomal (e.g., fragile X, Klinefelter or Turner syndrome), metabolic (e.g., aminoacidemias, phenylketonuria, galactosemia) or neurological conditions (e.g., neurofibromatosis, tuberous sclerosis, myotonic dystrophy) [34][36]. Rare copy number variants found in children with ADHD have also been associated with ID (see the Genetics section under ASD/ADHD, above). Clinicians need to investigate patients with ID+ADHD in accordance with the companion statement published in this issue.


Optimizing environmental and academic interventions, such that a child’s or youth’s cognitive and emotional needs are addressed concurrently, is an important aspect of treatment. Coordinated therapies help to lower the medication dose required and minimize risk for adverse effects. Evidence for the beneficial effects of physical exercise in individuals with ADHD [23] suggests that exercise programs should be encouraged for children and youth with ID+ADHD.

The clinical effectiveness of short-acting methylphenidate for managing ADHD symptoms in children with comorbid ID+ADHD has been studied in randomized controlled trials [37]. A response rate to methylphenidate of 45% to 66% for the combined condition significantly exceeds that of placebo, but is below the response rate for ADHD alone [29]. An IQ above 50 predicts a better response to stimulants [29][38], while very low (severe, profound) IQ levels predict poorer response [29][39]. Moreover, children with ID+ADHD who receive short-acting methylphenidate are at higher risk for such side effects as tics and social withdrawal [40].

Recent Canadian guidelines recommend that when medication is needed to manage ADHD symptoms in children or youth with ID, psychostimulants should be used first [41]. When response to psychostimulants combined with psychotherapy is suboptimal, the use of nonstimulants is recommended. For functionally disabling behaviours not responsive to behavioural interventions and/or to stimulants and nonstimulants, neuroleptics (e.g., Risperidone) may be used, with extreme caution due to their significant burden of side effects [41]. Close monitoring for adverse metabolic and neurological events, as outlined in the Canadian Alliance for Monitoring Effectiveness and Safety of Antipsychotics (CAMESA) guidelines, is mandatory [42]. Data is sparse for the use of nonstimulants and long-acting psychostimulants in children and youth with ID+ADHD. The need for more evidence to support prescribing and monitoring of drugs in this population remains profound [43].


Since the 1990s, advances in neonatal intensive care have increased survival rates for preterm births significantly [44]. Research studies and follow-up programs now define very low birth weight and extremely low birth (ELBW) weight as <1,500 g and <1,000 g, respectively. ‘Very preterm’ (VPT) and ‘extremely preterm’ (EPT) refer to infants born before 30 weeks and 26 weeks gestation, respectively [45]. Premature infants are surviving with lower rates of disability, including cerebral palsy, severe visual or hearing impairments, and severe cognitive impairment defined by developmental quotient or IQ [45][46].

However, while major disability rates have decreased, the occurrence of sequelae associated with low birth weight and prematurity, such as milder cognitive impairment and associated neurodevelopmental and mental health difficulties during childhood, is increasing [45][47][49]. Almost 50% of children born EPT or ELBW have developmental disorders [44][45][47]. Cognitive impairment, inattention, hyperactivity, internalizing behaviour disorders, and social interaction difficulties persist well beyond the preschool period, affecting educational achievement in later childhood [44][46][49].

In a cohort of ELBW children who were followed to 6 years plus 4 months of age, an increased prevalence of disability was noted by school age, compared with same-aged peers [46]. Cognitive impairment was the most common disability (IQ 1–2 SD below the mean identified in 25% of children and IQ >2 SD below mean in 21%). The frequency of cognitive impairment rose to 41% when ELBW children were compared with contemporary classmates.

One study followed 219 ELBW children until they reached 8 years of age. The authors identified significantly more chronic conditions than in normal birth weight (NBW) controls, along with increasing need for supports and services beyond routine requirements [44].

There is also an association between gestational age (GA) or birth weight and cognitive scores by school age [45]. As GA increases >26 weeks, impairments decrease almost linearly until 32 weeks GA. Even past this point, and correcting for prematurity, the mean remains 5 SD lower than for NBW peers [44][46]. Although most school-related learning difficulties, supportive services, IEPs, and special education placements are determined by lower cognitive scores, more recent research has highlighted attentional or behavioural concerns and their impact on learning [44][49].

Behaviour outcomes in premature infants

Children born VPT or with ELBW experience significantly more neurodevelopmental difficulties and a wider range of behavioural problems at school age than NBW children [50][52].

Common difficult-to-manage behaviours relate to symptoms associated with ADHD: inattention, internalizing disorders (anxiety, depression, withdrawal, somatic complaints), and social difficulties [47][50][52]. This cluster of difficulties is collectively referred to as the ‘preterm behavioural phenotype’ [48][51][52]. Disruptive behaviour disorders, such as oppositional defiant disorder, conduct disorder, and hyperactive/impulsive presentation in ADHD, are seen less frequently [48][52].

In a 2001/2003 birth cohort of ELBW and EPT children assessed at kindergarten, approximately twice as many met criteria for ADHD combined presentation compared with NBW controls, but nearly five times as many met criteria for ADHD inattentive presentation [53].

At 8 years of age, ELBW children showed significantly more behavioural problems than NBW children, with higher rates of ADHD and anxiety disorder [47]. Almost twice as many had ADHD inattentive presentation compared with NBW controls [47]. At 14 years of age [52], the same cohort showed significantly higher rates of subnormal IQ (14% <70) and need for IEPs (45%). Previously reported symptoms of ADHD inattentive presentation, anxiety and social problems persisted through school age. These symptoms were not accompanied by comorbid oppositional defiant disorder, conduct disorder or disruptive behaviours characteristic of ADHD [47][52]. This finding is supported by other studies [51][56], which showed that EPT children are more likely to have a psychiatric disorder at 11 years compared with NBW controls [50].

A Swedish national cohort study of more than a million children followed and treated for ADHD from age 6 to 19 years [57] showed a stepwise increase in odds ratios for ADHD medication with increasing prematurity at birth, compared with term infants. This effect was not explained by genetic, perinatal or socioeconomic status, although the last factor modified risk for ADHD in moderately preterm births [57].

This research has been supported by another study [58], which compared cohorts of later preterm (34 to 37 weeks GA) and term (37 to 42 weeks GA) children. They found no statistically significant difference in the cumulative incidence of ADHD between groups, which suggests that late preterm and term infants have similar rates of ADHD.

Most provinces and territories in Canada have follow-up programs to monitor developmental outcomes in this population, for at least 2 years postbirth and sometimes longer. However, only a few jurisdictions continue surveillance to school age, when symptoms are most likely to affect function. Monitoring development and behaviour in children born prematurely, identifying concerns early, and ensuring timely interventions, supports and services can improve outcomes significantly. As yet, there is no specific literature on treating ADHD symptoms in ELBW/EPT children or those born prematurely. When medications are needed, the same protocols are followed as for children born at term, but special consideration must be given to the screening, monitoring and treatment of internalizing behaviour disorders.


  • Children and youth with ASD, ID, and born prematurely are at increased risk for ADHD and experience greater impairment due to symptoms. Clinicians must be aware of high comorbidity and assess for ADHD symptoms in children and youth with these conditions. Follow-up programs should monitor developmental, cognitive, and emotional outcomes at least until school entry and, preferably, until children are integrated and adapting well to their school environment and their academic performance is stable.
  • The diagnostic evaluation of ADHD in children and youth with concurrent neurodevelopmental conditions requires a multidisciplinary approach and an expert assessment of associated behaviour disorders.
  • When medication is indicated for treating ADHD symptoms in individuals with ASD and ID, psychostimulants should be used first and as part of a comprehensive treatment program.
  • There is a positive role for regular physical activity in mitigating ADHD symptoms, and every effort should be made to promote these activities and integrate them into daily routines.
  • Side effects of ADHD medication are more common in children and youth with ASD and ID.
  • Further research is needed to develop an evidence base for using behaviour modification, long-acting psychostimulants, and nonstimulants to treat children and youth with ASD, ID or those born premature.


This position statement has been reviewed by the Adolescent Health, Community Paediatrics and Fetus and Newborn Committees of the Canadian Paediatric Society. It was also reviewed by representatives of the Canadian Academy of Child and Adolescent Psychiatry (CACAP).


Members: Debbi Andrews MD (Chair), Susan Bobbitt MD, Alice Charach MD, Brenda Clark MD (past member), Mark E Feldman MD (past Board Representative), Johanne Harvey MD (former Board Representative), Benjamin Klein MD, Oliva Ortiz-Alvarez MD, Sam Wong MD (Board Representative)

Liaisons: Sophia Hrycko MD, Canadian Academy of Child and Adolescent Psychiatry; Angie Ip MD, CPS Developmental Paediatrics Section; Aven Poynter MD, CPS Mental Health Section

Principal authors: Brenda Clark MD, Stacey A. Bélanger MD, PhD


  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th edn. Arlington, VA: American Psychiatric Association, 2013.
  2. Mannion A, Leader G. Attention-deficit/hyperactivity disorder (AD/HD) in autism spectrum disorder. Res Autism Spectr Dis 2014;8(4):432–9.
  3. Matson JL, Rieske RD, Williams LW. The relationship between autism spectrum disorders and attention-deficit/hyperactivity disorder: An overview. Res Dev Disabil 2013;34(9):2475–84.
  4. Matson JL, Cervantes PE. Commonly studied comorbid psychopathologies among persons with autism spectrum disorder. Res Dev Disabil 2014;35(5):952–62.
  5. Pinto R, Rijsdijk F, Ronald A, Asherson P, Kuntsi J. The genetic overlap of attention-deficit/hyperactivity disorder and autistic-like traits: An investigation of individual symptom scales and cognitive markers. J Abnorm Child Psychol 2016;44(2):335–45.
  6. Kotte A, Joshi G, Fried R, et al. Autistic traits in children with and without ADHD. Pediatrics 2013;132(3):e612–22.
  7. Martin J, Cooper M, Hamshere ML, et al. Biological overlap of attention-deficit/hyperactivity disorder and autism spectrum disorder: Evidence from copy number variants. J Am Acad Child Adolesc Psychiatry 2014;53(7):761–70.e26.
  8. Antshel KM, Zhang-James Y, Wagner KE, Ledesma A, Faraone SV. An update on the comorbidity of ADHD and ASD: A focus on clinical management. Expert Rev Neurother 2016;16(3):279–93.
  9. Miodovnik A, Harstad E, Sideridis G, Huntington N. Timing of the diagnosis of attention-deficit/hyperactivity disorder and autism spectrum disorder. Pediatrics 2015;136(4):e830–7.
  10. Rao PA, Landa RJ. Association between severity of behavioral phenotype and comorbid attention deficit hyperactivity disorder symptoms in children with autism spectrum disorders. Autism 2014;18(3):272–80.
  11. Chen MH, Wei HT, Chen LC, et al. Autism spectrum disorder, attention deficit hyperactivity disorder, and psychiatric comorbidities: A nationwide study. Res Autism Spectr Dis 2015;10:1–6.
  12. Nijmeijer JS, Hoekstra PJ, Minderaa RB, et al. PDD symptoms in ADHD, an independent familial trait? J Abnorm Child Psychol 2009;37(3):443–53.
  13. Rommelse NN, Franke B, Geurts HM, Hartman CA, Buitelaar JK. Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder. Eur Child Adolesc Psychiatry 2010;19(3):281–95.
  14. Williams NM, Zaharieva I, Martin A, et al. Rare chromosomal deletions and duplications in attention-deficit hyperactivity disorder: A genome-wide analysis. Lancet 2010;376(9750):1401–8.
  15. Mahajan R, Bernal MP, Panzer R, et al.; Autism Speaks Autism Treatment Network Psychopharmacology Committee. Clinical practice pathways for evaluation and medication choice for attention-deficit/hyperactivity disorder symptoms in autism spectrum disorders. Pediatrics 2012;130(Suppl 2):S125–38.
  16. Subcommittee on Attention-Deficit/Hyperactivity Disorder, Steering Committee on Quality Improvement and Management; Wolraich M, et al. ADHD: Clinical practice guideline for the diagnosis, evaluation, and treatment of attention-deficit/hyperactivity disorder in children and adolescents. Pediatrics 2011;128(5):1007–22.
  17. Greenhill LL, Swanson JM, Vitiello B, et al. Impairment and deportment responses to different methylphenidate doses in children with ADHD: The MTA titration trial. J Am Acad Child Adolesc Psychiatry 2001;40(2):180–7.
  18. Reichow B, Volkmar FR, Bloch MH. Systematic review and meta-analysis of pharmacological treatment of the symptoms of attention-deficit/hyperactivity disorder in children with pervasive developmental disorders. J Autism Dev Disord 2013;43(10):2435–41.
  19. Pearson DA, Santos CW, Aman MG, et al. Effects of extended release methylphenidate treatment on ratings of attention-deficit/hyperactivity disorder (ADHD) and associated behavior in children with autism spectrum disorders and ADHD symptoms. J Child Adolesc Psychopharmacol 2013;23(5):337–51.
  20. Harfterkamp M, Buitelaar JK, Minderaa RB, van de Loo-Neus G, van der Gaag RJ, Hoekstra PJ. Long-term treatment with atomoxetine for attention-deficit/hyperactivity disorder symptoms in children and adolescents with autism spectrum disorder: An open-label extension study. J Child Adolesc Psychopharmacol 2013;23(3):194–9.
  21. Scahill L, McCracken JT, King BH, et al.; Research Units on Pediatric Psychopharmacology Autism Network. Extended-release guanfacine for hyperactivity in children with autism spectrum disorder. Am J Psychiatry 2015;172(12):1197–206.
  22. Politte LC, Henry CA, McDougle CJ. Psychopharmacological interventions in autism spectrum disorder. Harv Rev Psychiatry 2014;22(2):76–92.
  23. Den Heijer AE, Groen Y, Tucha L, et al. Sweat it out? The effects of physical exercise on cognition and behavior in children and adults with ADHD: A systematic literature review. J Neural Transm (Vienna) 2017;124(Suppl 1):S3–26.
  24. Sowa M, Meulenbroek K. Effects of physical exercise on autism spectrum disorder: A meta-analysis. Research in ASD 2012; 6(1):46–57.
  25. Neece CL, Baker BL, Crnic K, Blacher J. Examining the validity of ADHD as a diagnosis for adolescents with intellectual disabilities: Clinical presentation. J Abnorm Child Psychol 2013;41(4):597–612.
  26. Antshel KM, Phillips MH, Gordon M, Barkley R, Faraone SV. Is ADHD a valid disorder in children with intellectual delays? Clin Psychol Rev 2006;26(5):555–72.
  27. Reiss S, Szyszko J. Diagnostic overshadowing and professional experience with mentally retarded persons. Am J Ment Defic 1983;87(4):396–402.
  28. Ageranioti-Belanger S, Brunet S, D’Anjou G, Tellier G, Boivin J, Gauthier M. Behaviour disorders in children with an intellectual disability. Paediatr Child Health 2012;17(2):84–8.
  29. Barkley RA, ed. Attention-Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment, 4th edn. New York, NY:Guilford Press, 2015.
  30. Xenitidis K, Paliokosta E, Rose E, Maltezos S, Bramham J. ADHD symptom presentation and trajectory in adults with borderline and mild intellectual disability. J Intellect Disabil Res 2010;54(7):668–77.
  31. Cooper SA, Smiley E, Jackson A, et al. Adults with intellectual disabilities: Prevalence, incidence and remission of aggressive behaviour and related factors. J Intellect Disabil Res 2009;53(3):217–32.
  32. Ahuja A, Martin J, Langley K, Thapar A. Intellectual disability in children with attention deficit hyperactivity disorder. J Pediatr 2013;163(3):890–5.e1.
  33. Stein MA, Szumowski E, Blondis TA, Roizen NJ. Adaptive skills dysfunction in ADD and ADHD children. J Child Psychol Psychiatry 1995;36(4):663–70.
  34. Moeschler JB, Shevell M; American Academy of Pediatrics Committee on Genetics. Clinical genetic evaluation of the child with mental retardation or developmental delays. Pediatrics 2006;117(6):2304–16.
  35. Kaufman L, Ayub M, Vincent JB. The genetic basis of non-syndromic intellectual disability: A review. J Neurodev Disord 2010;2(4):182–209.
  36. Shashi V, McConkie-Rosell A, Rosell B, et al. The utility of the traditional medical genetics diagnostic evaluation in the context of next-generation sequencing for undiagnosed genetic disorders. Genet Med 2014;16(2):176–82.
  37. Handen BL, Gilchrist R. Practitioner review: Psychopharmacology in children and adolescents with mental retardation. J Child Psychol Psychiatry 2006;47(9):871–82.
  38. Aman MG, Kern RA, McGhee DE, Arnold LE. Fenfluramine and methylphenidate in children with mental retardation and ADHD: Clinical and side effects. J Am Acad Child Adolesc Psychiatry 1993;32(4):851–9.
  39. Aman MG, Buican B, Arnold LE. Methylphenidate treatment in children with borderline IQ and mental retardation: Analysis of three aggregated studies. J Child Adolesc Psychopharmacol 2003;13(1):29–40.
  40. Handen BL, Feldman H, Gosling A, Breaux AM, McAuliffe S. Adverse side effects of methylphenidate among mentally retarded children with ADHD. J Am Acad Child Adolesc Psychiatry 1991;30(2):241–5.
  41. Gorman DA, Gardner DM, Murphy AL, et al. Canadian guidelines on pharmacotherapy for disruptive and aggressive behaviour in children and adolescents with attention-deficit hyperactivity disorder, oppositional defiant disorder, or conduct disorder. Can J Psychiatry 2015;60(2):62–76.
  42. Pringsheim T, Panagiotopoulos C, Davidson J, Ho J; Canadian Alliance for Monitoring Effectiveness and Safety of Antipsychotics in Children (CAMESA) guideline group. Evidence-based recommendations for monitoring safety of second-generation antipsychotics in children and youth. Paediatr Child Health 2011;16(9):581–9.
  43. Ji NY, Findling RL. Pharmacotherapy for mental health problems in people with intellectual disability. Curr Opin Psychiatry 2016;29(2):103–25.
  44. Hack M, Taylor HG, Drotar D, et al. Chronic conditions, functional limitations, and special health care needs of school-aged children born with extremely low-birthweight in the 1990s. JAMA 2005;294(3):318–25.
  45. Marlow N. Neurocognitive outcome after very preterm birth. ArchDis Child Fetal Neonatal Ed 2004;89:F224–8.
  46. Marlow N, Wolke D, Bracewell MA, Samara M; EPICure Study Group. Neurologic and developmental disability at six years of age after extremely preterm birth. N Engl J Med 2005;352(1):9–19.
  47. Hack M, Taylor HG, Schluchter M, Andreias L, Drotar D, Klein N. Behavioral outcomes of extremely low birth weight children at age 8 years. J Dev Behav Pediatr 2009;30(2):122–30.
  48. Moore T, Hennessy EM, Myles J, et al. Neurological and developmental outcome in extremely preterm children born in England in 1995 and 2006: The EPICure studies. BMJ 2012;345:e7961:1–13.
  49. Johnson S. Cognitive and behavioural outcomes following very preterm birth. Semin Fetal Neonatal Med 2007;12(5):363–73.
  50. Johnson S, Marlow N. Growing up after extremely preterm birth: Lifespan mental health outcomes. Semin Fetal Neonatal Med 2014;19(2):97–104.
  51. Johnson S, Hollis C, Kochhar P, Hennessy E, Wolke D, Marlow N. Psychiatric disorders in extremely preterm children: Longitudinal finding at age 11 years in the EPICure study. J Am Acad Child Adolesc Psychiatry 2010;49(5):453–63.e1.
  52. Taylor HG, Margevicius S, Schluchter M, Andreias L, Hack M. Persisting behavior problems in extremely low birth weight adolescents. J Dev Behav Pediatr 2015;36(3):178–87.
  53. Scott MN, Taylor HG, Fristad MA, et al. Behavior disorders in extremely preterm/extremely low birth weight children in kindergarten. J Dev Behav Pediatr 2012;33(3):202–13.
  54. Burnett AC, Anderson PJ, Cheong J, Doyle LW, Davey CG, Wood SJ. Prevalence of psychiatric diagnoses in preterm and full-term children, adolescents and young adults: A meta-analysis. Psychol Med 2011;41(12):2463–74.
  55. Johnson S, Marlow N. Preterm birth and childhood psychiatric disorders. Pediatr Res 2011;69(5 Pt 2):11R–8R.
  56. Johnson S, Wolke D. Behavioural outcomes and psychopathology during adolescence. Early Hum Dev 2013;89(4):199–207.
  57. Lindstrom K, Lindblad F, Hjern A. Preterm birth and attention-deficit/hyperactivity disorder in schoolchildren. Pediatrics 2011;127(5):858–65.
  58. Harris MN, Voigt RG, Barbaresi WJ, et al. ADHD and learning disabilities in former late preterm infants: A population-based birth cohort. Pediatrics 2013;132(3):e630–6.

Disclaimer: The recommendations in this position statement do not indicate an exclusive course of treatment or procedure to be followed. Variations, taking into account individual circumstances, may be appropriate. Internet addresses are current at time of publication.

Last updated: May 31, 2024