Attention Deficit Hyperactivity Disorder: An Overview

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Attention Deficit Hyperactivity Disorder


An Overview



Daryl Efron1,2,3,    1Centre for Community Child Health, Murdoch Children’s Research Institute, Melbourne, VIC, Australia,    2Department of Paediatrics, University of Melbourne, Melbourne, VIC, Australia,    3General Medicine, The Royal Children’s Hospital, Melbourne, VIC, Australia


Abstract


Attention deficit hyperactivity disorder (ADHD) is the most common neurodevelopmental disorder. It is a polygenic disorder with multifactorial etiology, including genetic and environmental factors. Onset occurs in childhood, but symptoms usually persist across developmental stages into adult life, at least to some extent. A range of cognitive deficits are seen in ADHD, underpinning the substantial functional difficulties experienced by individuals with the condition. Management includes both pharmacological and nonpharmacological interventions. Comorbidities such as sleep problems are common and contribute to the impairments. These need to be identified and addressed alongside ADHD symptoms. ADHD is associated with an increased risk of negative long-term outcomes however, with support many patients thrive and have successful lives.


Keywords


Attention deficit hyperactivity disorder; comorbidities; genetics; psychostimulant medication


Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by developmentally inappropriate levels of hyperactivity, impulsivity, and/or inattention. Onset occurs in childhood, but persistence into adolescence and adult life is common. Heterogeneity in symptom profile, comorbidity mix, genetic and environmental risk factors, neurocognitive deficits, and response to treatment is a notable feature of ADHD. Furthermore, the presentation and functional difficulties associated with ADHD evolve across developmental stages as demands change (Cherkasova, Sulla, Dalena, Pondé, & Hechtman, 2013). ADHD is associated with impairments in social, academic, and family functioning and poorer outcomes in childhood (Efron, Sciberras, & Anderson, 2014), adolescence and adulthood (Shaw et al., 2012).


ADHD is classified as a Neurodevelopmental Disorder in the Diagnostic and Statistical Manual of Mental Disorders-Fifth Edition (DSM-5) (American Psychiatric Association, 2013), alongside autism spectrum disorder (ASD), intellectual disability, learning disorders, and communication disorders. This represents an important conceptual shift from the DSM-IV (1994) where it was classified as a disruptive behavior disorder and is appropriate recognition of its strong neurobiological basis.




DSM-5 Diagnostic Criteria for ADHD (American Psychiatric Association, 2013)




  1. A. A persistent pattern of inattention and/or hyperactivity–impulsivity that interferes with functioning or development, as characterized by (1) and/or (2):

    1. 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:

      1. 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).
      2. b. Often has difficulty sustaining attention in tasks or play activities (e.g., has difficulty remaining focused during lectures, conversations, or lengthy reading).
      3. c. Often does not seem to listen when spoken to directly (e.g., mind seems elsewhere, even in the absence of any obvious distraction).
      4. 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).
      5. 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).
      6. 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).
      7. g. Often loses things necessary for tasks or activities (e.g., school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones).
      8. h. Is often easily distracted by extraneous stimuli (for older adolescents and adults, may include unrelated thoughts).
      9. 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. 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:

      1. a. Often fidgets with or taps hands or feet or squirms in seat.
      2. b. Often leaves seat in situations when remaining seated is expected (e.g., leaves his or her place in the classroom, in the office or other workplace, or in other situations that require remaining in place).
      3. c. Often runs about or climbs in situations where it is inappropriate. (Note: In adolescents or adults, may be limited to feeling restless.)
      4. d. Often unable to play or engage in leisure activities quietly.
      5. 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 or difficult to keep up with).
      6. f. Often talks excessively.
      7. g. Often blurts out an answer before a question has been completed (e.g., completes people’s sentences; cannot wait for turn in conversation).
      8. h. Often has difficulty waiting his or her turn (e.g., while waiting in line).
      9. 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; for adolescents and adults, may intrude into or take over what others are doing).

  2. B. Several inattentive or hyperactive–impulsive symptoms were present prior to age 12 years.
  3. 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).
  4. D. There is clear evidence that the symptoms interfere with, or reduce the quality of, social, academic, or occupational functioning.
  5. 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:



Specify if:



*For older adolescents and adults (age 17 and older), at least five symptoms are required.


In the descriptive text, DSM-5 emphasizes the importance of gathering independent information “confirming substantial symptoms across settings” from informants “who have seen the individual in those settings,” that is, parents and teachers. DSM-5 also explicitly recognizes the fact that comorbidities are the rule rather than the exception in ADHD and need to be identified and addressed.


1.1 Historical Perspective


The disorder we currently call ADHD was first described in the medical literature over 200 years ago (Lange, Reichl, Lange, Tucha, & Tucha, 2010). In 1798, Scottish physician Sir Alexander Crighton published a work entitled “An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects” in which he described individuals with either congenital or acquired mental restlessness, who were easily distracted by extraneous stimuli and had “an incapacity of attending with a necessary degree of constancy to any one object.” In the mid-19th century, German psychiatrist and author of popular illustrated children’s books Dr Heinrich Hoffman created two characters: Fidgety Phil, who drives his parents crazy with his inability to sit still at the dinner table, and Johnny Look-in-the-Air, who watches swallows and clouds as he walks and so falls into a river. These boys would be recognizable today as having the Combined and Inattentive presentations of ADHD, respectively. At the turn of the 20th century, the father of British pediatrics Sir George Still, in his Goulstonian Lectures to the Royal College of Physicians in London, described a series of 43 teenagers with “defective moral control.” They displayed symptoms such as “passionateness” (impulsivity), and “a quite abnormal capacity for sustained attention,” core symptoms of ADHD. Some of these children also demonstrated “spitefulness,” “lawlessness,” and “wanton mischievousness,” symptoms which today would suggest diagnoses of oppositional defiant disorder (ODD) or conduct disorder, which often co-occur with ADHD. The language used by Still betrays the Victorian period’s prevailing interpretation of aberrant behavior as symptomatic of character flaws and moral weakness.


In the 1920s, following the Spanish influenza pandemic, many children presented with hyperactive, disinhibited, irritable, and impulsive behavior as a sequela of encephalitis lethargica. This widespread clinical phenomenon sparked scientific interest in the neurobiology of abnormal childhood behavior. Over subsequent decades, this symptom cluster became known as “minimal brain damage.” In 1963, The Oxford International Study Group of Child Neurology suggested that the term “minimal brain damage” should not be used as there was rarely a history of a brain injury, nor were there hard neurological signs present on examination. Instead, they advocated “minimal brain dysfunction,” intended to suggest a functional disturbance rather than brain damage, presenting as “various combinations of impairment in perception, language, memory, and control of attention, impulse or motor function” (Clements, 1966).


The first incorporation of this syndrome into official psychiatric nomenclature was in the second edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-II, 1968), where it was called hyperkinetic reaction of childhood. This term suggested a primary role for environmental factors in ADHD, in keeping with the psychodynamic view of behavior popular at the time. The “biology–environment” pendulum swung radically back the other way in 1980, when the DSM-III used the diagnostic category “Attention Deficit Disorder (with or without hyperactivity).” This key moment in the history of ADHD was due in large part to Canadian psychologist Virginia Douglas, whose work emphasized that attentional problems lay at the core of this disorder, along with deficits in impulse control (“an inability to stop, look and listen”) (Douglas, 1972). Following this, there was an explosion of research into the neuropsychological basis of ADHD symptoms, and in turn neuroimaging and genetic research has proliferated.


Subsequent iterations of the DSM have made relatively minor adjustments to terminology and diagnostic criteria. The latest edition, DSM-5 (American Psychiatric Association, 2013), explicitly recognized adult ADHD for the first time, with alternate behavioral symptoms (e.g., often loses keys or mobile phone, often has difficulty completing forms and paying bills). Other changes include an increase in the age of onset criterion from 7 to 12 years, and permission to diagnose ADHD in the presence of ASD.


The first description of the use of stimulant medications to treat behavior disorders in children was by Dr. Charles Bradley in Rhode Island in 1937 (Bradley, 1937). He used benzedrine to treat headaches caused by cerebrospinal fluid leak following pneumoencephalograms performed to exclude structural brain abnormalities in institutionalized children with behavioral problems. Bradley and teachers observed striking improvements in school performance, social interactions, and emotional responses. The dopaminergic drug methylphenidate was developed by the chemist Leandro Panizzon for Ciba Geigy, and first marketed in 1954. Panizzon named it Ritalin after his wife Rita. The prescription of stimulant medication to treat hyperactive/inattentive behavior became widespread in the United States in the 1970s, and this trend has been followed in other countries to a variable extent.


Although robust debate persists about the causes and management of ADHD, it now has a prominent position in psychological, psychiatric (child and adult), and pediatric practice in most parts of the world. In recent times, updates on ADHD appear regularly in major medical journals (Biederman & Faraone, 2005; Feldman & Reiff, 2014), signifying its mainstream place in contemporary child health.


1.2 Epidemiology


The estimated worldwide-pooled prevalence of childhood ADHD is just over 5%, and has not changed over the past three decades (Polanczyk, Willcutt, Salum, Kieling, & Rohde, 2014). There is a wide variation between countries in reported prevalence. The natural history is for a reduction in hyperactive and impulsive symptoms between childhood and adolescence (Cherkasova et al., 2013). However, persistence of impairing symptoms including mental restlessness and difficulties with sustained focus and task completion is common into adulthood, with at least partial syndromic persistence occurring in approximately two-thirds of childhood cases (Faraone, Biederman, & Mick, 2006), and approximately 2.5% of adults meeting full diagnostic criteria for ADHD (Simon, Czobor, Balint, Meszaros, & Bitter, 2009).


Many individuals with ADHD are not identified (Sawyer et al., 2004; Sayal, Ford, & Goodman, 2010). Large studies of representative samples in the United States (Froehlich et al., 2007) and Europe (Ford, Goodman, & Meltzer, 2003) have found that less than half of affected children are identified. Taylor has postulated a range of factors which may underpin underdiagnosis of ADHD, including concern about stigmatization from use of diagnostic labels, lack of teacher training in recognition of ADHD symptoms, concern that diagnosis will inevitably lead to medication treatment, and underrecognition of ADHD by health services who assess referred children (Taylor, 2017). Clinician diagnostic practice has been shown to vary, both within (Efron, Davies, & Sciberras, 2013) and between (Hodgkins, Setyawan, & Mitra, 2013) countries.


Access to services is influenced by patient-level, family-level, and health-care system-level variables. A large qualitative study in the United States found that parental perceptions of the child’s illness and help-seeking behavior for ADHD symptoms varied depending on the child’s sex and the family’s race (Bussing, Koro-Ljungberg, Gary, Mason, & Garvan, 2005). Teachers have been found to be more likely to suggest referral of boys than girls with ADHD symptoms (Sciutto, Nolfi, & Bluhm, 2004). This may partially explain the higher male:female disparity in clinical samples of children with ADHD compared to community samples. A study of children aged 5–16 years with ADHD identified in the 2004 British Child and Adolescent Mental Health Survey found that ADHD severity, the presence of comorbidities and parental burden were the main determinants of service use, and that education professionals were contacted more than health professionals (74% vs 51% in the preceding 12 months) (Sayal et al., 2010). An Australian community-based study found that 37% of children aged 6–8 years meeting diagnostic criteria for ADHD had not received any professional services in the previous 12 months (Efron, Moisuc, McKenzie, & Sciberras, 2016). The strongest predictors of service use were older child age and the degree to which the child’s behavior impacted on the family.



1.3 Cognitive Deficits


Compared to controls, children with ADHD demonstrate deficits in a range of executive functions (EFs) including visuospatial and verbal working memory, planning, vigilance, and inhibitory control (Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005). However, findings vary considerably between individuals, with some having multiple measurable EF weaknesses, while others have few or none. EF deficits have a weak relationship with functional difficulties, and insufficient sensitivity and specificity for diagnostic purposes (Faraone, Asherson, & Banaschewski, 2015).


Individuals with ADHD have been observed to have deficits in other neurocognitive functions including meta-cognitive abilities such as self-talk, deduction and prediction; temporal information processing and timing (Toplak & Tannock, 2005); processing speed; response time variability; and motor control. Effortful allocation of attention is also thought to be impaired in ADHD. A pattern of “sluggish cognitive tempo” has been described in a subset of patients with ADHD. This includes symptoms such as daydreaming, reduced alertness, and slow mental activity and working speed. Barkley has argued that this may represent a distinct disorder from inattentive-presentation ADHD, with different profiles of EF problems and comorbidities (Barkley, 2013). Reward dysregulation is another feature of ADHD. Children with ADHD have been shown to overestimate the magnitude of, and disproportionately preference, immediate over more delayed rewards, leading to poor decision-making (Faraone et al., 2015).


1.4 Emotional Dysregulation


Intense emotional reactivity (often manifesting as aggressive outbursts) is a frequent characteristic of individuals with ADHD (Shaw, Stringaris, Nigg, & Leibenluft, 2014), and some have argued that emotional dysregulation/emotional impulsivity should be considered a core diagnostic feature of ADHD. Irritability is also common in ADHD. DSM-5 includes a new diagnosis, disruptive mood dysregulation disorder (DMDD), which requires not only severe, recurrent temper outbursts that are inconsistent with developmental level and occur three or more times per week, but also that the child’s mood in between outbursts must be persistently irritable or angry most of the day, nearly every day. An Australian community-based study found that over 20% of children with ADHD met diagnostic criteria for DMDD (Mulraney, Schilpzand, & Hazell, 2016).



1.5 Neuroimaging Findings and Pathophysiology


Over the past 2–3 decades increasingly sophisticated imaging techniques have revealed abnormalities in individuals with ADHD in the size, structure, and connections between brain regions involved in key EFs such as attention, working memory, response inhibition, and motor control (see Chapter 13) (De La Fuente, Xia, Branch, & Li, 2013). Structural magnetic resonance imaging (MRI) studies have demonstrated reductions in cortical thickness, total cerebral volume, and volume of some subcortical structures in individuals with ADHD compared to controls.(Cubillo, Halari, Smith, Taylor, & Rubia, 2012; Hoogman, Bralten, & Hibar, 2017; Shaw, Eckstrand, & Sharp, 2007). Regions particularly underdeveloped include the prefrontal cortex, cingulate gyri, cerebellum, and the basal ganglia. Task-based functional MRI studies have demonstrated atypical functional activation of frontal, temporal, parietal, and cerebellar regions, as well as reduced activation in brain regions involved in timing (motor timing, perceptual timing, and temporal foresight) such as the left inferior prefrontal cortex/insula and the left inferior parietal lobe (Hart, Radua, Mataix-Cols, & Rubia, 2012).


More recently, neuroimaging studies are shedding light on the important role of white matter network pathways in ADHD. Using techniques such as diffusion tensor imaging and resting state MRI, altered interregional functional connectivity has been demonstrated (Sripada et al., 2014). Reduced homogeneity in the default mode network, and dysconnectivity between the default mode and ventral attentional networks has been identified in adults with ADHD (Uddin, Kelly, & Biswal, 2008). Dysregulated modulation of synaptic plasticity and aberrations in neural communication are thought to play a role (Penzes, Cahill, Jones, VanLeeuwen, & Woolfrey, 2011).


Disordered biochemical function in affected brain regions appears to underpin the symptoms of ADHD (Faraone et al., 2015). Evidence from animal models, pharmacology research, and genetic studies suggests that abnormalities in the dopamine and noradrenaline systems in particular are important mechanisms leading to ADHD (Genro, Kieling, Rohde, & Hutz, 2010).


1.6 Causes


The ADHD phenotype is the end result of complex causal sequence pathways involving interactions between a wide range of genetic and environmental risk and protective factors, each individually of small effect size (Thapar, Cooper, Eyre, & Langley, 2013).


1.6.1 Genetics


Family, twin, and adoption studies conducted over the past 20 years have demonstrated that ADHD is highly heritable (Faraone et al., 2005). Multiple linkage studies have identified replicated associations between ADHD and polymorphisms in genes involved in catecholamine activity, including those coding for dopamine receptors and transporters (e.g., DRD4, DRD5, DAT-1), serotonergic regulation (5HTT and HTR1B), and neurotransmitter release, as well as synaptic plasticity and axonal growth (SNAP-25) (Gizer, Ficks, & Waldman, 2009). There is some evidence that a high-activity functional variant (val–val) in the gene coding for COMT, the enzyme which breaks down dopamine, may be associated with conduct disorder symptoms in individuals with ADHD (Langley, Heron, O’Donovan, Owen, & Thapar, 2010).


A large controlled chromosomal microarray study showed that a sample with ADHD (n=410) carried a mean 2.1-fold increased burden of copy number variants (CNV) compared with matched controls (n=1156, from the 1958 British Birth Cohort) (Williams, Zaharieva, & Martin, 2010). Interestingly, the CNV loci found to be enriched in this cohort of children with ADHD had been previously identified in groups with ASD and schizophrenia. A moderate genetic relationship, identified via shared single nucleotide polymorphisms, has also been reported between ADHD and major depressive disorder (Cross-Disorder Group of the Psychiatric Genetics Consortium, 2013). This is consistent with the well-recognized clinical phenomenon whereby individuals with a similar risk burden (e.g., full biological siblings) may present with different developmental or mental health disorders such as ADHD, intellectual disability, ASD, or mood disorders, a concept in developmental psychopathology known as multifinality. A recent meta-analysis of genome-wide association studies (GWAS), including 20,183 ADHD cases and 35,191 controls, identified 16 independent loci passing the statistical threshold for GWAS (Demontis, Walters, & Martin, 2017).


These genetic differences contribute to cumulative vulnerability (traits), and some research groups are developing polygenic risk scores, incorporating both rare and common genetic variants, to estimate overall pathogenic load for ADHD (“polygenic liability threshold model”) (Martin, O’Donovan, Thapar, Langley, & Williams, 2015).



1.6.2 Environment


A broad range of environmental factors have been shown to be associated with an increased risk of ADHD, however, it is methodologically challenging to definitively demonstrate a causal link (Thapar et al., 2013). Risk factors studies include exposure to embyopathic neurotoxins (e.g., smoking, alcohol, illicit substances), marked prematurity or low birth weight (gestational age less than 32 weeks or birth weight less than 1.5 kg) (Franz, Bolat, & Bolat, 2018) maternal stress during pregnancy, postnatal environmental neurotoxins (e.g., lead, organophosphate pesticides, polychlorinated biphenyls), severe early life psychosocial deprivation, harsh and coercive parenting, nutritional deficiencies (e.g., polyunsaturated fatty acids, magnesium), dietary sensitivities (e.g., artificial food colorings and preservatives) (Froehlich, Anixt, & Loe, 2011), and electronic media exposure (Montagni, Guichard, & Kurth, 2016).


Overall, there is not yet consistent evidence that any of these environmental factors play a direct role in causing ADHD. Furthermore, these risks are not specific to ADHD, rather the exposures may contribute to the general risk of developmental pathology across clinical syndromes. However, in the majority of children diagnosed with ADHD no environmental risk factors are identified.


Gene–environment interactions are also important to consider. Relevant parenting behaviors such as smoking and parenting style are likely influenced by genetic factors (Rutter, 2005). Furthermore, these risks may be epigenetically transmitted across generations (Nigg, 2018). Cross-disciplinary research integrating genetic, neurobiological, environmental, and social data will be needed to further advance our understanding of the etiological pathways leading to ADHD (Coghill, Nigg, Rothenberger, Sonuga-Barke, & Tannock, 2005).


1.7 Comorbidities


The majority of children and adolescents with ADHD have at least one comorbid developmental or mental health disorder (Larson, Russ, Kahn, & Halfon, 2011; Spencer, Biederman, & Mick, 2007), and these are identifiable from the early years of primary school (Efron et al., 2014). Common comorbidities include ODD, conduct disorder, DMDD (Mulraney et al., 2016), anxiety disorders (Schatz & Rostain, 2006), depression (Cumyn, French, & Hechtman, 2009), language disorders (Sciberras, Mueller, & Efron, 2014), learning disabilities (Mayes, Calhoun, & Crowell, 2000), ASD (Leitner, 2014), and chronic tic disorders/Tourette syndrome (Poh, Payne, Gulenc, & Efron, 2018). Moderate or severe sleep problems are reported by 45% of parents of children with ADHD (Sung, Hiscock, Sciberras, & Efron, 2008).


Comorbidities are often associated with greatly increased functional impairment in patients with ADHD (Leitner, 2014; Mulraney et al., 2016; Poh et al., 2018; Sciberras et al., 2014). However, there is evidence that comorbidities are underidentified in clinical practice (Efron et al., 2013). Identification and treatment of comorbid disorders is fundamental to good ADHD management.


1.8 Consequences


ADHD is associated with a broad range of negative functional consequences affecting the individual, siblings, and parents with flow-on effects on classrooms, workplaces, and wider society. Individuals with ADHD are at risk of academic underachievement relative to their cognitive capacity (Ek, Westerlund, Holmberg, & Fernell, 2011), as well as peer problems (Andrade & Tannock, 2013) and emotional impairments (Wehmeier, Schacht, & Barkley, 2010). Parent report of child quality of life (QoL) is consistently lower in children with ADHD compared to peers, although self-rated QoL scores by children with ADHD are not as low (Danckaerts, Sonuga-Barke, & Banaschewski, 2010). Adults with ADHD are at risk of job dismissal and relatively low occupational status (Mannuzza, Klein, Bessler, Malloy, & LaPadula, 1993), and also poor QoL (Agarwal, Goldenberg, Perry, & IsHak, 2012). Parents of children with ADHD have increased mental health problems and disturbances in marital functioning (Harpin, 2005), and are more likely to experience poorer parent–child relationships, reduced parent efficacy, and increased levels of parenting stress than controls (Podolski & Nigg, 2001).


ADHD, both treated and untreated, is associated with greatly increased health-care costs (Birnbaum, Kessler, & Lowe, 2005; Sciberras et al., 2017). When loss of work for adults with ADHD and adult family members of individuals with ADHD is factored in, the overall excess costs are enormous—estimated at US$31 billion in the United States in 2000 (Birnbaum et al., 2005).



1.9 Early Identification and Prevention


A number of studies have examined the possibility of population screening for ADHD, or for high risk of ADHD. Primary prevention strategies to minimize the risk of developmental problems, including ADHD, include optimizing maternal physical and mental health during pregnancy, reducing antenatal exposures to alcohol, smoking, and illicit drugs, and support for mothers of young infants. There has been some interest in secondary prevention of ADHD. This involves attempting to interrupt pathways to syndromic emergence by identifying young children with risk factors (e.g., prematurity, known history of antenatal exposures) and/or symptoms (e.g., hyperactivity, developmental delay), and providing parent training, developmental supports, or specific interventions to enhance self-regulation (Plueck et al., 2015). There is some evidence that early maternal “scaffolding behavior” (e.g., general support, assisting risk-taking) protects against ADHD in children with developmental delays (Baker, Neece, Fenning, Crnic, & Blacher, 2010).


1.10 Assessment


Children with ADHD may be referred for evaluation of a range of concerns, including difficulties with learning, behavior, social function, and emotional well-being. Some have risk factors in their personal or family history, such as extreme prematurity, a trauma history, delayed language development, or a sibling or parent with ADHD. Often multiple developmental and emotional problems are identified as contributing to the child’s difficulties, and the formulation commonly includes a number of diagnoses. For example, ASD, ADHD, learning disorder, anxiety disorder.


The clinical assessment involves two main elements:




  1. 1. A detailed interview with the child’s parent(s) or carer(s), in which information is gathered about the pregnancy, perinatal period, infant temperament, early childhood development, first concerns, current concerns, family history, interventions tried to date and their effectiveness, general health, diet, and sleep health. The child is included in the consultation at a developmentally appropriate level.
  2. 2. Standardized behavior rating scales, completed by parents and teachers. A number of open-access validated instruments are available, including the Vanderbilt ADHD Diagnostic Rating Scales (www.nichq.org/childrens-health/adhd/resources/vanderbilt-assessment-scales), the Swanson, Nolan and Pelham (SNAP)-IV Rating Scale (www.caddra.ca/pdfs/caddraGuidelines2011SNAP.pdf) and the Adult ADHD Self-Report Scale (www.hcp.med.harvard.edu/ncs/asrs.php).

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Jun 13, 2021 | Posted by in PSYCHOLOGY | Comments Off on Attention Deficit Hyperactivity Disorder: An Overview

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