A.A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development, as characterized by (1) and/or (2)
1.Inattention: Six (or more) of the following symptoms have persisted for at least 6 months to a degree that is inconsistent with developmental level and that negatively impacts directly on social and academic/occupational activities. (For older adolescents/adults [age 17 and older], at least five symptom are required.)
(a)Often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or during other activities (e.g. overlooks or misses details, work is inaccurate).
(b)Often has difficulty sustaining attention in tasks or play activities (e.g. has difficulty remaining focused during lectures, conversations, or lengthy reading).
(c)Often does not seem to listen when spoken to directly (e.g. mind seems elsewhere, even in the absence of any obvious distraction).
(d)Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (e.g. starts tasks but quickly loses focus and is easily sidetracked).
(e)Often has difficulty organizing tasks and activities (e.g. difficulty managing sequential tasks; difficulty keeping materials and belongings in order; messy, disorganized, work; has poor time management; fails to meet deadlines).
(f)Often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort (e.g. schoolwork or homework; for older adolescents and adults, preparing reports, completing forms, reviewing lengthy papers).
(g)Often loses things necessary for tasks or activities (e.g. school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones).
(h)Is often easily distracted by extraneous stimuli (for older adolescents and adults, may include unrelated thoughts).
(i)Is often forgetful in daily activities (e.g. doing chores, running errands; for older adolescents and adults, returning calls, paying bills, keeping appointments).
2.Hyperactivity and Impulsivity: Six (or more) of the following symptoms have persisted for at least 6 months to a degree that is inconsistent with developmental level and that negatively impacts directly on social and academic/occupational activities. (For older adolescents/adults [age 17 and older], at least five symptom are required.)
(a)Often fidgets with or taps hands or feet or squirms in seat.
(b)Often leaves seat in situations when remaining seated is expected (e.g. leaves his or her place in the classroom, office or other workplace, or in other situations that require remaining in place).
(c)Often runs about or climbs in situations where it is inappropriate. (In adolescents or adults, may be limited to feeling restless.)
(d)Often unable to play or engage in leisure activities quietly.
(e)Is often ‘on the go’, acting as if ‘driven by a motor’ (e.g. is unable to be or uncomfortable being still for extended time, as in restaurants, meetings; may be experienced by others as being restless and difficult to keep up with).
(f)Often talks excessively.
(g)Often blurts out an answer before a question has been completed (e.g. completes people’s sentences; cannot wait for turn in conversation).
(h)Often has difficulty waiting his or her turn (e.g. while waiting in line).
(i)Often interrupts or intrudes on others (e.g. butts into conversations, games, or activities; may start using other people’s things without asking or receiving permission, adolescents or adults may intrude into or take over what others are doing).
B.Several inattentive or hyperactive-impulsive symptoms were present prior to age 12 years.
C.Several inattentive or hyperactive-impulsive symptoms are present in two or more settings (e.g. at home, school or work; with friends or relatives; in other activities).
D.There must be clear evidence that the symptoms interfere with or reduce the quality of social, academic, or occupational functioning.
E.The symptoms do not occur exclusively during the course of schizophrenia or another psychotic disorder and are not better explained by another mental disorder (e.g. mood disorder, anxiety disorder, dissociative disorder, personality disorder, substance intoxication, or withdrawal).
Specify whether:
Combined Presentation: If both Criterion A1 (Inattention) and Criterion A2 (Hyperactivity-Impulsivity) are met for the past 6 months.
Predominantly Inattentive Presentation: If Criterion A1 (Inattention) is met but Criterion A2 (Hyperactivity-Impulsivity) is not met for the past 6 months.
Predominantly Hyperactive/Impulsive Presentation: If Criterion A2 (Hyperactivity-Impulsivity) is met and Criterion A1 (Inattention) is not met for the past 6 months.
Specify current severity:
Mild, Moderate, or Severe.
ADHD can be summarized according to three subtypes or presentations: (1) ADHD combined type (ADHD-C): at least six inattention and six hyperactivity-impulsive symptoms; (2) ADHD predominantly inattentive type (ADHD-I): at least six inattention symptoms but fewer than six hyperactive-impulsive symptoms; or (3) ADHD predominantly hyperactive type (ADHD-H): at least six hyperactive-impulsive symptoms and less than six inattentive symptoms (APA, 2013). The term ‘presentation’ is used in the DSM-5, as opposed to ‘subtype’ which was used in the DSM-IV, given the fluidity of subtypes over time (Willcutt et al., 2012). ADHD-C is most commonly encountered in clinical samples, while ADHD-I is more commonly observed in community-based studies (Graetz, Sawyer, Hazell, Arney, & Baghurst, 2001).
Associated Difficulties
In addition to core symptoms of inattention, hyperactivity, and impulsivity, children with ADHD encounter significant impairments across multiple domains. They have poorer school-based functioning including academic underachievement, absenteeism, grade retention, suspensions/expulsions, and early school dropout (Barbaresi, Katusic, Colligan, Weaver, & Jacobsen, 2007a; Efron et al., 2014). Furthermore, children with ADHD have poorer social outcomes than non-ADHD peers including difficulties initiating and maintaining friendships, peer rejection and peer victimization (Harpin, Mazzone, & Raynaud, 2013; Sciberras, Ohan, & Anderson, 2012), and poorer quality of life (Danckaerts et al., 2010). ADHD also impacts negatively on families, with parents reporting higher levels of stress and mental health difficulties, less adaptive coping, higher levels of marital conflict, and lower parenting self-efficacy compared to children without ADHD (Cussen, Sciberras, Ukoumunne, & Efron, 2012; Harpin, 2005; Johnston & Mash, 2001).
The majority of children with ADHD meet diagnostic criteria for at least one comorbid psychiatric disorder including mood disorders (7–50 %), anxiety disorders (27–33 %), oppositional defiant disorder (ODD; 45–65 %), and conduct disorder (CD; 14–23 %) (Biederman et al., 1996; Busch et al., 2002; Ghanizadeh, Mohammadi, & Moini, 2008; Wilens et al., 2002). About one quarter of children with ADHD present with both internalizing and externalizing comorbidities (Abikoff, Jensen, & Arnold, 2002). Children with ADHD are also at elevated risk for learning and language disabilities (Biederman, Newcorn, & Sprich, 1991b; Pastor & Reuben, 2008; Sciberras et al., 2014), Tourette’s disorder (Biederman, Newcorn, & Sprich, 1991a), sleep problems (Sung, Hiscock, Sciberras, & Efron, 2008), poorer physical health including overweight/obesity (Nigg, 2013), and motor coordination difficulties (Cole, Mostofsky, Larson, Denckla, & Mahone, 2008).
Given the impairments experienced by children with ADHD and their increased risk for comorbidities, it is not surprising that the condition is associated with poorer long-term outcomes (Cherkasova, Sulla, Dalena, Pondé, & Hechtman, 2013; Sciberras, Roos, & Efron, 2009). Although approximately one third of individuals with ADHD will show improvements in clinical symptom severity, the impairments associated with the condition persist over time (Cherkasova et al., 2013). For example, a number of longitudinal studies have demonstrated that children with ADHD have poorer outcomes in adulthood including poorer social (e.g. relationship difficulties, divorce) and occupational functioning, as well as elevated levels of delinquency and mental health difficulties including conduct disorder, antisocial personality disorder, and substance use (Cherkasova et al., 2013; Klein et al., 2012; Sciberras et al., 2009; Silva, Colvin, Glauert, & Bower, 2014; Spencer et al., 2006). There is mixed evidence regarding whether ADHD is associated with anxiety and/or mood disorders later in life (Cherkasova et al., 2013).
Aetiology of ADHD
The precise aetiology of ADHD is unclear; however, the disorder likely arises due to a complex interplay between genetic and environmental risk and protective factors. Imaging studies have pointed to numerous functional brain abnormalities in children with ADHD, most commonly in the prefrontal cortex and striatum (fronto-striatal circuits) and the parietal cortex (Rubia, Alegria, & Brinson, 2014; Silk et al., 2005). A number of structural imaging studies have found differences between children with and without ADHD in the prefrontal cortex, cerebellum, striatum and basal ganglia, corpus callosum, and the parietal cortex (Rubia et al., 2014). On average, children with ADHD have decreased cerebral volumes and reduced cortical thickness compared to their non-ADHD counterparts (Rubia et al., 2014; Sowell et al., 2003). Brain abnormalities identified in ADHD are non-specific and overlap with those observed in children without ADHD; therefore, brain imaging techniques are not yet useful in the diagnosis of ADHD.
Family, twin, and adoption studies demonstrate that ADHD is a highly heritable disorder, accounting for approximately 80 % of cases (Faraone, Perlis, & Doyle, 2005; Thapar, Cooper, Jefferies, & Stergiakouli, 2012). No one gene conferring risk for ADHD has been identified. Candidate gene studies have implicated a number of genes within the dopamine system including the D4 receptor (seven-repeat allele), dopamine D5 receptor, and dopamine transporter gene, and the serotonin system including the serotonin transporter (5HTT) (Thapar et al., 2012). However, the amount of variance explained by these candidate genes is small. Genome-wide association studies have yet to identify any common gene variants associated with ADHD, suggesting that multiple common variants may be implicated, each exerting a small effect (Neale et al., 2010; Thapar et al., 2012). Williams and colleagues (2010) found that rare chromosomal deletions and duplications (copy number variants) were elevated in ADHD cases, yet these were common to numerous developmental disorders including intellectual disability and ASD.
A number of environmental factors have also been associated with ADHD including exposure to maternal smoking and alcohol use during pregnancy, maternal stress and/or anxiety during pregnancy, post-natal depression, low birth weight or prematurity, lead exposure, and psychosocial adversity including low parent education and poverty (Sauver et al., 2004; Sciberras, Ukoumunne, & Efron, 2011; Thapar et al., 2012; Williams et al., 2010). There are no randomized control trials which implicate nutritional deficiencies and artificial colourings in the aetiology of ADHD (Thapar et al., 2012). Like most mental health conditions, it is suspected that multiple genetic and environmental factors interact to produce risk for ADHD.
Treatment of ADHD
Treatment guidelines emphasize that the management of ADHD should be multi-modal including both pharmacological and non-pharmacological interventions (American Academy of Child and Adolescent Psychiatry, 2007; National Health and Medical Research Council, 2012; NICE clinical guideline 72, 2008; Taylor et al., 2004). ADHD is commonly managed using psychostimulant medication including short and long acting preparations of methylphenidate and amphetamine based stimulants (Feldman & Reiff, 2014). Non-stimulants such as atomoxetine and norepinephrine reuptake inhibitor are also used to treat ADHD, although less commonly and with weaker effects than stimulant medications (Wolraich et al., 2011). Most children with ADHD (~80 %) taking stimulant medication will have short-term clinically significant reductions in hyperactivity and/or inattention without adverse side effects (Biderman et al., 2003; Faraone et al., 2002; Goldman, Genel, Bezman, & Slanetz, 1998). Common short-term side effects include reduced appetite and initial insomnia (Feldman & Reiff, 2014).
The largest study investigating the efficacy of both medication and behavioural interventions for children with ADHD aged 7.0–9.9 years is the Multimodal Treatment of ADHD Study (MTA; N = 579) (The MTA Cooperative Group, 1999). This study found that stimulant medication was superior to behavioural therapy in reducing the core symptoms of ADHD in the short to medium term (i.e. 14 months later), and helped children function more effectively in the classroom and in the playground (The MTA Cooperative Group, 1999). Behavioural treatment added benefit to medication in improving broader functional outcomes (e.g. teacher-rated social skills, academic skills, parent-child relationships) and was just as effective at reducing inattention, hyperactive/impulsive, internalizing symptoms, overall impairment, social skills, and academic achievement as medication for those children with comorbid ADHD and anxiety (Jensen et al., 2007). The best overall outcomes were for children who received both medication and psychosocial (behavioural and educational) interventions and this was especially so for children with ADHD-I (Pfiffner et al., 2007; The MTA Cooperative Group, 1999). There is some preliminary evidence that medication use may be associated with improved educational functioning and reduced risk for substance abuse although further research is needed (Barbaresi, Katusic, Colligan, Weaver, & Jacobsen, 2007b; Groenman et al., 2013; Langberg & Becker, 2012).
Behavioural therapies are an essential component of ADHD management (Pelham & Fabiano, 2008). A recent meta-analysis found that there were small improvements in ADHD symptoms for non-pharmacological interventions including parent and teacher training, cognitive training, and dietary modifications including supplementation with essential fatty acids (Sonuga-Barke et al., 2013). However, when studies were restricted to those using blinded ratings of ADHD symptoms, no treatment effect was observed. Yet there is evidence that psychological therapies have more benefit in improving functional outcomes for children with ADHD. In a recent meta-analysis, Daley and colleagues (2014) found that behav ioural interventions had benefits in promoting positive parenting and reducing child conduct problems assessed using blinded outcome measures. Effectively managing sleep problems in children with ADHD is another promising non-pharmacological intervention, with a recent large-scale randomized controlled trial reporting that a two session treatment program addressing behavioural sleep problems in children with ADHD improved not only sleep but also child ADHD symptom severity, quality of life, and broader daily functioning (Hiscock et al., 2015).
Overlap and Distinctions Between ADHD and ASD
There is a growing body of research examining the overlap and distinction between ASD, ADHD, and comorbid ASD + ADHD across biological, neuropsychological, and behavioural domains. The few studies which have directly examined ASD, ADHD, and ASD + ADHD will be the focus of this section, rather than providing a comprehensive review of each domain.
Biological Findings
There is strong evidence of overlap between ADHD and ASD in regard to genes, brain function, and structure. Both ASD and ADHD are highly heritable conditions , with around 70–80 % of the phenotypic variance for each disorder explained by genetic factors (Faraone, Perlis, Doyle, Smoller, et al., 2005; Lichtenstein, Carlström, Råstam, Gillberg, & Anckarsäter, 2010). Studies suggest that around 50–70 % of the covariance of ASD and ADHD may be explained by common genetic influences (Mulligan et al., 2009; Reiersen, Constantino, Grimmer, Martin, & Todd, 2008; Rommelse, Franke, Geurts, Hartman, & Buitelaar, 2010; Ronald, Simonoff, Kuntsi, Asherson, & Plomin, 2008). This indicates that the two disorders may potentially be alternate manifestations of the same underlying risk factors. There are a number of recent comprehensive reviews of this area (Rommelse et al., 2010; Taurines et al., 2012).
Until recently individuals with ASD and ADHD had not been directly compared in brain imaging studies, with ADHD symptoms in ASD typically not controlled for and vice versa. In individuals with ADHD, structural studies show reduced volume and cortical thickness in the frontal, cingulate, and parietal regions of the brain (Bush, 2011; Durston, van Belle, & de Zeeuw, 2011) with abnormalities in the frontostriatal and fronto-cerebellar circuits (Durston et al., 2011). Together, studies suggest dysfunction in fronto-striato-cerebellar and frontoparietal networks in ADHD (Taurines et al., 2012). There have been inconsistent findings in individuals with ASD; however brain connectivity is atypical in ASD (Anagnostou & Taylor, 2011). Early brain overgrowth has consistently been found in at least a subset of individuals with ASD (Anagnostou & Taylor, 2011; Stanfield et al., 2008). This involves both increased volume of grey and white matter particularly in cerebral, cerebellar, and limbic structures and is followed by arrested or abnormally slow growth over time (Courchesne, 2004; Stanfield et al., 2008). In addition, there is reduced volume of the corpus callosum (Stanfield et al., 2008). Increased head circumference is a feature of a subset of those with ASD, but notably is also present to some degree in individuals with ADHD, but may be less stable over development (Gillberg & De Souza, 2002).
Studies directly comparing the two conditions are limited. One study of structural MRI compared ASD and ADHD but did not control for comorbidity with both the ASD and ADHD groups having similar levels of ADHD symptoms (Brieber et al., 2007). Structural abnormalities found in both ASD and ADHD groups compared to controls were grey matter reductions in the left medial temporal lobe and higher grey matter volumes in the left inferior parietal cortex. ASD-specific brain abnormalities consisted of increased grey matter volume in the right supramarginal gyrus (Brieber et al., 2007). Another recent study excluded participants with comorbidity but did not examine the comorbid presentation (Lim et al., 2015). Using structural MRI they found reduced grey matter in the cerebellar in ADHD relative to controls and ASD, and enlargement in the middle/superior temporal gyrus in ASD relative to ADHD (Lim et al., 2015). A recent study of fMRI in children with ASD, ADHD, and ASD + ADHD found both unique and overlapping brain regions (Di Martino et al., 2013). Children with ASD + ADHD shared ADHD-specific basal ganglia connectivity abnormalities, whereas connectivity in temporolimbic areas was atypical in ASD with or without ADHD comorbidity. These findings suggest there is an additive effect of having both conditions with brain connectivity abnormalities from both conditions implicated in the comorbid phenotype. Further work directly comparing the two disorders and their comorbid form is needed in this domain to better understand the neurobiological phenotypes.
Neuropsychological Findings
Attention/Executive Functioning
Executive function is an umbrella term for a range of attention components including the ability to switch attention between stimuli, sustain attention on the task at hand, and inhibit responses (Pennington & Ozonoff, 1996). Individuals with ASD are primarily thought to show difficulties related to perseveration impacting the ability to switch attention. In ADHD inhibition and atypical reward processing are primary areas of executive dysfunction.
When the two disorders are directly compared, there are equivocal findings. For response inhibition, some studies find children with ADHD show more inhibitory deficits than those with ASD, with comorbid ASD + ADHD falling in between the two groups but not significantly different to either (Bühler, Bachmann, Goyert, Heinzel-Gutenbrunner, & Kamp-Becker, 2011). In contrast, other studies indicate that children with ASD have similar or even greater inhibition deficits than those with ADHD (Corbett, Constantine, Hendren, Rocke, & Ozonoff, 2009). Sinzig, Morsch, Bruning, Schmidt, and Lehmkuhl (2008) found impairment in inhibition and working memory in ADHD but not ASD, with impairment in planning in ASD but no group differences in flexibility. Those with comorbid ASD + ADHD also showed more impairment in inhibition, but not working memory, compared to the ASD alone group. The authors concluded that the executive functioning profiles may not be useful in the differential diagnosis of ASD and ADHD. Notably, although these studies fail to consistently differentiate ASD and ADHD, they provide evidence for additive effects of having ASD + ADHD (Gargaro et al., 2014; Taurines et al., 2012).
In regard to sustained attention, there are similarly inconsistent findings. In a study which did not exclude comorbid ADHD symptoms in ASD, individuals with ADHD performed more poorly than ASD with the ASD group performing similarly to controls (Johnson et al., 2007). However, other studies have found children with ASD and ADHD (without excluding ADHD in ASD) were similarly impaired in regard to sustained attention (Corbett et al., 2009). Studies comparing ASD, ADHD, and ASD + ADHD are needed to further clarify whether sustained attention deficits are associated specifically with the presence of ADHD symptoms in ASD.
Intra-individual response variability is considered a measure of lapses of attention and therefore may be characteristic of ADHD. Again, there are mixed findings in this area. One study which did not exclude comorbid symptoms found only individuals with ADHD showed higher levels of response variability compared to ASD and typically developing children (Johnson et al., 2007). Another study which carefully differentiated ASD, ADHD, and ASD + ADHD found individuals with ASD or comorbid ASD + ADHD had more intra-individual variability on EF tasks than did individuals with ADHD (Geurts et al., 2008). This finding was taken to indicate that elevated response variability in ADHD was associated with comorbid ASD. In contrast, a more recent study found that ADHD whether comorbid with ASD or alone showed elevated response variability relative to ASD alone (Adamo et al., 2014).
Neuromotor Profile
There is an emerging literature showing that motor profiles may be a distinguishing characteristic of children with ASD versus children with ADHD. For example, using measures of gait and movement proficiency, Rinehart et al. (2006) and Papadopoulos, Rinehart, Bradshaw, and McGinley (2013) reported unique motor deficits for each disorder, and noted that children with ADHD who are carefully screened for ASD do not have motor problems. This contrasts with previous research showing that up to 50 % of children with ADHD (where the ASD status is unknown) experience motor problems (Buderath et al., 2009; Pan, Tsai, & Chu, 2009).
Social Processing
Emotion recognition and social processing deficits have been extensively studied in ASD. There have been some equivocal findings, with some studies indicating intact emotion and facial recognition performance (Bar-Haim, Shulman, Lamy, & Reuveni, 2006) and others showing deficits (Baron-Cohen, Wheelwright, & Jolliffe, 1997; Dalton et al., 2005). These task performance differences may relate to compensatory mechanisms in individuals with ASD given underlying atypical processing found via brain imaging, electrophysiological, and eye gaze studies (Harms, Martin, & Wallace, 2010). Facial emotion recognition ability has been found to be similarly impaired in individuals with ASD, ADHD, and ASD + ADHD (Bühler et al., 2011; Sinzig, Morsch, & Lehmkuhl, 2008) and not associated with autistic or ADHD symptoms but may instead relate to executive functioning deficits (Sinzig, Morsch, & Lehmkuhl, 2008). Similarly, individuals with ASD have been found to show similar Theory of Mind deficits to those with ADHD and ASD + ADHD (Bühler et al., 2011). However, ASD symptoms but not ADHD symptoms have been correlated with Theory of Mind deficits (Ames & White, 2011; Geurts, Broeders, & Nieuwland, 2010). Hence, social processing deficits appear in both children with ASD and ADHD, thus not representing a useful point of difference between the two conditions.
Reward Processing
Individuals with ADHD show delay aversion, tending to prefer smaller immediate rewards compared to larger delayed rewards (Castellanos, Sonuga-Barke, Milham, & Tannock, 2006; Marco et al., 2009). When ASD and ADHD have been compared in this area, there have been inconsistent findings. In one study individuals with ADHD but not ASD showed delay aversion (Antrop et al., 2006). In contrast, another study showed both conditions have atypical reward processing (Demurie, Roeyers, Baeyens, & Sonuga-Barke, 2011).
Overall, there are inconsistent findings regarding the executive functioning profile of ASD and ADHD, and what is unique or shared between the two disorders. Currently, executive functioning profiles are not able to reliably differentiate the two conditions and there is much work to be done in this area.
Behavioural Findings
ADHD Symptoms in Populations with ASD
The onset of ADHD symptoms and their presentation in children with ASD + ADHD appear to be similar to that found for ADHD alone (Frazier et al., 2001; Joshi et al., 2014). The ADHD combined subtype is most prevalent in ASD clinical populations compared with the primary inattentive and hyperactive subtypes (Hofvander et al., 2009; Joshi et al., 2014).
ASD Symptoms in Populations with ADHD
Social-communicative and rigid repetitive behaviours also present similarly in children with ADHD as those with ASD (Frazier et al., 2001; Martin, Hamshere, O’Donovan, Rutter, & Thapar, 2014; Reiersen et al., 2007). A proportion of children with ADHD have difficulties in social interaction and communication, similar to that seen in ASD (Clark et al., 1999). This may include lack of empathy and difficulties with peer relationships, and in their communication including deficits in imaginative ability, nonverbal communication, and maintaining conversations (Clark et al., 1999). Additionally, there is some evidence that girls with ASD have fewer symptoms of hyperactivity-impulsivity than boys with ASD, and that the symptoms of hyperactivity remit over time in children with ASD, similar to the trajectory found in ADHD (May, Cornish, & Rinehart, 2012, 2014). These findings of typical ADHD symptom presentation in ASD and vice versa have been taken to indicate a true comorbidity between the two conditions, rather than a unique ASD + ADHD phenotype (Frazier et al., 2001).
Although the symptoms of each disorder present typically when occurring in the other condition, correlations between ASD and ADHD symptoms have been found. For example, associations between hyperactive-impulsive symptoms and rigid repetitive and stereotyped behaviours (Martin et al., 2014) and communication impairment (Sinzig, Bruning, Morsch, & Lehmkuhl, 2008) have been found, and repetitive behaviours have also been correlated with inattention (Sinzig et al., 2009). Recently, Konst and colleagues (2014) examined DSM-IV-TR and DSM-5 classifications of ASD and found ADHD inattentive and impulsive symptoms correlated with the ASD symptoms as described by both DSM-IV-TR and DSM-5. Increased severity of ASD symptoms was associated with increased inattentive/impulsive symptoms, again highlighting the additive effect of the two conditions. Although one study suggested that social-communicative impairment may better differentiate the two conditions rather than repetitive and stereotyped behaviours (Hartley & Sikora, 2009), most studies have found overlap with ADHD symptoms across both social-communicative impairment and repetitive and stereotyped behaviours.
In summary, biologically shared genetic influences are indicated between the two conditions, yet emerging imaging studies suggest that unique brain structure and connectivity patterns can differentiate the two conditions with the comorbid form having additive effects. Neuropsychological testing is not able to reliably differentially diagnose the two conditions. Together, the differentiation of ASD and ADHD across biological and neuropsychological domains can be difficult. Although the symptoms of ASD and ADHD are often correlated, they are behaviourally distinct and appear to present similarly when ASD and ADHD coexist indicating true comorbidity (Frazier et al., 2001). As the following sections outline, careful examination of the presenting behavioural symptoms is necessary to differentially and comorbidly diagnose these two conditions. The next section reviews the general assessment of ADHD, followed by points of consideration in the assessment of a child with ADHD suspected of also meeting DSM-5 ASD criteria.
General Assessment of ADHD
There is no single diagnostic test for ADHD; therefore, clinicians need to rely on their clinical judgment in applying DSM-5 criteria . The key task for clinicians is to assess for the presence, duration, and impact of inattention, hyperactivity, and impulsivity symptoms on the basis of a detailed developmental and clinical history with parents and use of multi-informant standardized behaviour rating scales. Assessing ADHD symptoms can be challenging given that all children can display some of these symptoms in the context of normal childhood development; therefore, comparing the severity of symptoms to same-aged peers is essential in diagnostic decision-making, as is determining whether the symptoms are pervasive and impairing (Biel & McGee, 2011; National Health and Medical Research Council, 2012). ADHD symptoms are especially difficult to distinguish from normal development before the age of 4 years; therefore, the disorder is more commonly identified in school-aged children (APA, 2013). In particular, inattention symptoms become more observable as academic demands increase with age (APA, 2013). Agreement between parent and teacher reports can often be low; therefore, diagnosis should not be made on the basis of parent or teacher reports in isolation.
A number of clinical practice guidelines exist around the world to guide clinicians in best practice assessment for ADHD, aiming to improve the reliability of diagnosis and standardization of clinical management (American Academy of Child and Adolescent Psychiatry, 2007; National Health and Medical Research Council, 2012; NICE clinical guideline 72, 2008; Wolraich et al., 2011). Although there are some slight variations between these guidelines, key recommendations for assessment include:
(a)
Only making the diagnosis when DSM criteria are fulfilled.
(b)
Use of standardized behaviour rating scales.
(c)
Obtaining information from multiple sources (e.g. parents and teachers).
(d)
Specific assessment for comorbid developmental, medical, and mental health conditions.
The above four points form the basis for a gold standard assessment of ADHD. A comprehensive medical, developmental, and mental health assessment should be conducted, in addition to a psychosocial assessment of the child and their family. An interview with the parent/caregiver is a crucial component of an assessment for ADHD (Biel & McGee, 2011). This interview should cover:
Reason for referral
Developmental history
Detailed history of presenting inattention, hyperactivity, and impulsivity symptoms including duration and frequency
Impact of the child’s symptoms on home and school life including relationships with peers and academic/cognitive functioning
Parent and family functioning including family history of mental health or developmental difficulties and parent-child interaction
Assessment of broader mental health functioning including the presence of broader internalizing and externalizing symptoms
Child strengths, talents, and interests
The clinical history should be supplemented by use of both broad and narrowband, multi-informant rating scales in order to assess both broader mental health functioning and specific ADHD symptoms. Best practice dictates that rating scales are completed by both parents and teachers. Multi-informant broadband rating scales such as the Achenbach Child Behavior Checklist, Behavioral Assessment System for Children (BASC) , or the Strengths and Difficulties Questionnaire (SDQ) should be used to determine the child’s overall clinical profile (see section ‘Assessment Tools’ for further details). This is particularly important to identify differential diagnoses and comorbid conditions that will lead to differential treatment planning. Broadband rating scales may under-estimate the presence of less common internalizing comorbidities such as major depression and panic disorder (Bekker, Bruck, & Sciberras, 2013); therefore, it is important to remember that these should be inquired about during the clinical interview. Multi-informant narrowband or ADHD-specific rating scales should be used to assess specifically for inattention and/or hyperactivity-impulsivity symptoms and may include the ADHD Rating Scale IV, Conners Rating Scales, Vanderbilt Rating Scales, or the Swanson, Nolan, and Pelham-IV Questionnaire-Revised (SNAP-IV-R) . Given the lack of coverage of sleep issues in these scales, specific questions about the child’s sleep patterns and behaviours (including habitual snoring and sleep apneas) should also be sought.
More detailed information from teachers can be helpful in the diagnostic process including school reports and an interview with the teacher (Biel & McGee, 2011). This information supplements standardized rating scales, by providing more qualitative descriptors of the child’s symptoms and impairments in the school setting. Direct observations of the child’s behaviour in the classroom can be incredibly helpful to supplement clinical history taking and standardized rating scales but is often not feasible for clinicians not working in educational environments. An interview with the child’s teacher could cover:
Current concerns including duration, frequency, examples of behaviour, and antecedents/consequences
Impact of symptoms on classroom functioning
The child’s education history and academic performance
Interactions with peers and teachers
Strategies that have been implemented in the classroom—what works, what doesn’t work?
No medical, psychological, or neuropsychological tests are required to make the diagnosis of ADHD given their lack of sensitivity and specificity; however, a physical examination should be undertaken to rule out potential medical causes (National Health and Medical Research Council, 2012). Standardized tests of intellectual, language, and academic abilities may be utilized in situations where there are concerns about the child’s general intellectual or language ability or to assess for a comorbid learning disability (Biel & McGee, 2011) but these tests do not have the ability to confirm or disconfirm a diagnosis of ADHD. Again, neuropsychological test may be administered to help understand the nature of the child’s deficits and inform intervention strategies, but they cannot determine whether or not a child meets criteria for ADHD (National Health and Medical Research Council, 2012).
Although it is important to assess the child’s perspective during an assessment, children with ADHD often present with a positive illusory bias (Owens, Goldfine, Evangelista, Hoza, & Kaiser, 2007), which means that they tend to over-estimate their functioning relative to parents and teachers. For adolescents though, self-reports are particularly important in assessing inattention symptoms given that parent and teachers will have difficulty observing these symptoms (Feldman & Reiff, 2014). Adolescent’s views should be specifically sought during history taking and they should also complete standardized rating scales.
Clinicians should not rely on their observations of the child’s behaviour in the one-to-one clinical environment in order to make a diagnosis, given that symptoms are more likely to be more observable in naturalistic environments such as the classroom. It is quite possible that observable symptoms may be minimal or absent if the child is (APA, 2013):
Receiving frequent positive reinforcement for appropriate behaviour
Being closely supervised or in a one-to-one environment
In a new setting or is engaged in particularly interesting activities.
Has consistent external stimulation through use of electronic screens, for example.
In summary, there is no single diagnostic test for ADHD. Key components of an assessment of ADHD include a detailed developmental and psychosocial assessment and the completion of standardized behavioural rating scales. It is absolutely essential that information is collected from multiple informants in order to ensure that symptoms occur in more than one setting. Furthermore, the diagnosis of ADHD should only be made if the child meets the full criteria for ADHD, that is, that the minimum number of symptoms are present and that there is clear evidence that inattention, hyperactivity, and impulsivity symptoms are associated with impaired functioning. Finally, an evaluation for ADHD should include an assessment for developmental and mental health comorbidities, given that these predict poorer functioning over time and need to be taken into account in treatment planning (Biel & McGee, 2011; Tarver, Daley, & Sayal, 2014; Wolraich et al., 2011).
Assessment of ADHD in Children with ASD or Suspected ASD
There are a number of existing international guidelines for the clinical assessment of ASD (American Academy of Neurology, 2000; Johnson & Myers, 2007). When considering a comorbid diagnosis of ADHD in ASD, the ADHD diagnostic guidelines as previously discussed should be applied (American Academy of Child and Adolescent Psychiatry, 2007; National Health and Medical Research Council, 2012; NICE clinical guideline 72, 2008; Wolraich et al., 2011). It has been recommended that a comprehensive ADHD assessment is only undertaken in a child with ASD, if ADHD symptoms persist following the implementation of educational, speech/language, and behavioural supports which target the core ASD symptoms and language or cognitive impairment (Mahajan et al., 2012).
Potential Challenges of ADHD Assessment in ASD
There are a number of challenges faced by clinicians when considering an ADHD diagnosis in a child with, or suspected of having, ASD. A diagnosis of ASD and/or ADHD is made on the basis of observable behaviour. There are no blood tests, no single measure, no single defining symptom, and no physical characteristics that are unique to ASD or ADHD, and so clinicians must use careful observation of behaviour to determine whether a child’s difficulties are related to ASD and/or ADHD, or are better described by another condition. Importantly, clinicians conducting the assessment must have an adequate knowledge of the diagnostic features of not only ASD but also ADHD, as well as other childhood disorders. Although an individual with ASD may have symptoms of ADHD, the ADHD symptoms must be:
1.
Clinically meaningful
2.
Producing clinically significant impairment
3.
The most likely cause of the impairment
ADHD symptoms in children with ASD must produce clinically significant impairment related to excess levels of impulsivity and hyperactivity or inattention which are beyond the impairment caused by ASD symptoms alone. This can sometimes be difficult to differentiate and may only be clear with the persistence of ADHD symptoms despite interventions targeting ASD symptoms.
Other challenges are the growing differences in the typical age of diagnosis of ASD and ADHD. The timing for when a child first undergoes an ASD assessment is slowly becoming earlier in development. The gold standard ASD measures show good reliability from 2 years of age (Lord et al., 2006) with parents noting autism-related developmental problems from around 19 months of age (De Giacomo & Fombonne, 1998). In contrast, for ADHD although caregivers typically note deviations from normality at around 3–4 years of age (Lahey et al., 2004), formal diagnosis may not occur until around 7–8 years of age, with DSM-5 allowing onset to occur up to the age of 12 years (APA, 2013). Guidelines for the assessment of ADHD recommend diagnosis only from 4 years of age given that ADHD behaviours may be difficult to differentiate from typical development prior to this (American Academy of Pediatrics, 2011). Hence, children with ASD who are diagnosed between 2 and 3 years of age may not be considered for ADHD comorbidity. Potentially, these children may not undergo another comprehensive psychological assessment during childhood resulting in their ADHD symptoms remaining undiagnosed and untreated (Joshi et al., 2014). Clinicians therefore need to be vigilant in monitoring children with ASD for ADHD symptoms throughout childhood and performing additional assessment post ASD diagnosis to examine ADHD comorbidity if indicated.
A final consideration is that of the fluidity of ADHD symptoms, particularly in children under 7 years of age (Law, Sideridis, Prock, & Sheridan, 2014). Studies show that the diagnostic stability of ADHD in children under 7 following a 2-year period is anywhere from 50 to 79 % (Law et al., 2014; Srebnicki, Kołakowski, & Wolańczyk, 2013). This again highlights the importance of ongoing review and monitoring of ADHD symptoms throughout childhood.
Assessment Considerations
The ASD assessment process will vary depending on the age of the individual and the services available in the area. Assessment will ideally involve a multidisciplinary team including a psychologist, paediatrician/psychiatrist, speech pathologist, and an occupational therapist experienced in the assessment and diagnosis of ASD. A comprehensive ASD assessment will typically include the following components:
Gathering health, developmental, behavioural, and intergenerational family history.
Physical examination including laboratory investigation to search for a known aetiology or coexisting condition.
Family system assessment including understanding the roles of significant extended family, childcare/kindergarten/school, the peer group, and the wider social and cultural context.
A developmental evaluation including formally assessing adaptive, cognitive, and speech/language functioning.
Determining the presence of DSM-5 diagnoses using standardized interviews, observations, and questionnaires, established across multi-informants, and multiple settings.
These assessment components are similar to that for ADHD, and will therefore provide information relevant to the differential and comorbid diagnoses of both conditions. Formal assessment of DSM-5 symptoms will be the key informative factor when making a differential or comorbid diagnosis of ASD/ADHD. As previously discussed, research suggests that ADHD symptoms present similarly in individuals with ASD + ADHD (Frazier et al., 2001). For a comorbid diagnosis of ASD and ADHD to be given, children must meet the full criteria for each disorder. Each disorder must uniquely contribute to clinically significant impairment in functioning to be dually diagnosed.
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