Etiological pathways for developmental coordination disorder and attention-deficit/hyperactivity disorder: shared or discrete?

Attention-deficit/hyperactivity disorder (ADHD) and developmental coordination disorder (DCD) are two of the most common developmental disorders of childhood. Furthermore, children with a diagnosis of one developmental disorder are highly likely to be diagnosed with at least one other developmental disorder [1,2]. However, there are gaps in our understanding of the underlying mechanisms of these disorders and why they so frequently co-occur.

The rate of co-occurrence of DCD and ADHD has been found to be close to 50% [3]. Gillberg has published widely on deficits in attention, motor control and perception [4]. Piek and colleagues found an association between fine motor ability, in particular, and inattentive symptomatology in ADHD [5]. Fliers and colleagues proposed that ADHD with motor deficits might be a subtype of ADHD [6].

It is not surprising that a number of studies support a shared etiology for ADHD and DCD. Kaplan and colleagues argued that there is an association between developmental disorders and atypical brain development, which they proposed as the reason why they so commonly co-occur [7]. Fliers and colleagues argued a shared etiology for ADHD with co-occurring motor problems, which they attributed to genetic and/or shared environment effects [6].

The Diagnostic and Statistical Manual of Mental Disorders – Fourth Edition Text Revision (DSM-IV-TR) [8] and the International Statistical Classification of Diseases and Health-Related Problems Tenth Revision, Second Edition (ICD-10) [9] classify psychopathology on the basis of phenomenology, rather than etiology [10]. DSM-IV-TR and ICD-10 have similar classification categories for ADHD and hyperkinetic disorder, respectively. For a diagnosis of ADHD, inattention and/or hyperactivity must be more frequently displayed and be more severe than is typical for the person’s developmental stage, and symptoms must be present before the age of 7 years; there must be impairment in two or more settings, and clinically significant impairment must be present in at least one of the following – academic, occupational or social functioning. DSM-IV-TR has separate diagnostic criteria for symptoms of inattention and hyperactivity/impulsivity, with ADHD diagnosable as three subtypes: inattentive, hyperactive/impulsive and combined. It specifies that, in ADHD, symptomotology involving movement is limited to increased motor activity, and notes that children with ADHD may knock things over or fall because of their impulsivity and distractibility, rather than due to motor impairment. However, Pitcher and colleagues provided evidence to suggest that motor deficits in ADHD were a result of poor motor ability [11].

Developmental coordination disorder and specific developmental disorder of motor function are also described in DSM-IV-TR and ICD-10, respectively. DCD is defined as having motor coordination significantly lower than expected for the child’s age and intellect, which interferes significantly with activities of daily living. Both classification systems state that the movement disorder must not be due to a medical condition, such as cerebral palsy.

Attention-deficit/hyperactivity disorder and DCD have some factors in common:

• • Both disorders have similar prevalence rates. ADHD is generally thought to affect some 3–10% of school age children [12], although some estimate the prevalence rate to be as low as 1% [13]. DCD affects approximately 6% of children aged 5–11 years [8]. In their study of monozygotic (MZ) twins, discordant and concordant for ADHD and DCD, Pearsall-Jones and colleagues found similar prevalence rates of approximately 6% for both disorders [14];

• • Males are more vulnerable to both ADHD and DCD. Developmental disorders have been found to be more common in males than females [15]. ADHD has been widely reported to affect more males than females [14,16], with estimates in clinical samples varying from 2:1 to 9:1 [8]. Rhee and colleagues concluded that males were more likely to be affected by ADHD than females, as males have a lower genetic threshold for the required liability to express ADHD [16]. Some studies have shown similar numbers of females and males with DCD [14,17–19], although others have reported a higher male incidence [20–22]. Research has indicated that the male developing brain is more vulnerable than the female brain to certain types of brain injury, such as hypoxia [23], which has been associated with DCD [14,18]. This vulnerability has been related to distinct male and female chromosome complements [23];

• • Some children are said to ‘outgrow’ both disorders. The term ‘developmental’ implies that problems start early in life and interfere with ‘normal’ development [24]. The hallmark of a developmental disorder is deviation and/or delay from normal development, and each developmental disorder is characterized by a specific pattern of developmental delay [25]. Investigating the long-term prognosis of ADHD, Mannuzza and colleagues found that approximately two-thirds to three-quarters of their study participants experienced problematic symptoms of ADHD into early and middle adolescence, indicating that some children appear to ‘outgrow’ ADHD [26]. Some ‘clumsy’ children – especially those with fewer deficits – appear to ‘grow out of it’ [27]; however, it could be questioned whether this is DCD, or rather a developmental delay [28];

• • Both ADHD and DCD have been associated with other disorders. ADHD and DCD have been linked with mood disorders, such as depression, and children with comorbid ADHD and DCD are at a particular risk for depression [29]. However, Piek and Dyck found that DCD, but not ADHD, was associated with poor visuomotor processing [2].

Levy and colleagues concluded that ADHD is one of the most heritable disorders of childhood [30]. In their study of MZ twins, discordant and concordant for ADHD, Lehn and colleagues noted that with an estimated 60% heritability, environmental factors contributed 40% [31]. They found that low birth weight and delayed motor development were markers for ADHD in infancy. In their study of MZ twins discordant for ADHD, Shaw and colleagues found that in children with ADHD the developmental trajectory of cortical maturation was typical, but reached its peak thickness at a later age than was the case in normally developing children [32]. This was particularly evident in prefrontal regions of the brain, which are important in the control of attention and motor planning. ADHD children who had the DRD4 seven-repeat allele, which is frequently associated with ADHD, had a thinner cortex during childhood in brain regions that are important for attentional control, but to a great extent this resolved during adolescence [33]. This suggests that genes play an important role in brain development in children with developmental ADHD – and possibly explains why some children ‘outgrow’ ADHD. However, environmental factors, such as brain damage caused by intrauterine infection, forceps delivery, hypoxia or anoxia during pregnancy or at birth, often go unrecognized [34,35], and have been linked to secondary ADHD. van ‘t Ent and colleagues in their study of MZ twins, concordant and discordant for ADHD, concluded that MRI findings indicated a genetic etiology of ADHD in concordant high-risk sets, whereas an environmental etiology was implicated in ADHD twins in discordant sets [36]. This suggests that there might be more than one causal pathway to ADHD symptomotology.

There is conflicting evidence for etiology in DCD. Using structural equation modeling, Martin and colleagues found a strong shared additive genetic component for subtypes of DCD and ADHD [37]. On the other hand, DCD has been linked to damage to the developing or immature brain, and it has been proposed that DCD and cerebral palsy may fall on a continuum of motor disorder [14,18,28,38,39], rather than being discrete categories as defined by current classification systems. Jongmans and colleagues examined the relationship between the duration of ‘flares’ (echodensities in the periventricular white matter) in preterm infants and motor competence at 6 years of age [40]. They found that the longer the duration of the flares, the greater the decrease in motor performance, and that premature infants with extensive perceptual-motor difficulties were more likely to have shorter gestational ages and to have shown a brain lesion soon after birth [41]. An association has been found between DCD, perinatal oxygen perfusion problems, low birth weight and gestational ages of less than 37 weeks [14,18,28].

While ADHD and DCD appear to be developmental disorders that overlap in some children, they seem to have somewhat different developmental pathways, and it is likely that multiple causal pathways define both disorders. This could result from different but overlapping genetic and/or environmental influences, differentially affecting susceptibilities of neural pathways in the womb. For instance, Volpe pointed out the highly complex development of the neurological system during prenatal development [42]. Timing of exposure to infections and anoxia is important, and may have long-term cumulative effects, for example, increased sensitization to hypoxia at birth and in later life [43].

The causal pathways of developmental disorders are a combination of genetic, epigenetic and environmental factors that evolve over time. Although subtypes of co-occurring movement and attention disorders may have a shared etiology, in other instances we would argue different etiological pathways for DCD and ADHD. This has important implications for clinical practice, classification systems, such as DSM and ICD, research and policy development, and warrants further exploration of the nature of movement deficits associated with ADHD, and the nature of attention deficits associated with DCD.

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.