Revisiting the latent structure of ADHD: is there a ‘g’ factor?

Attention-deficit/hyperactivity disorder (ADHD), as defined by the DSM-IV-TR (American Psychiatric Association, 2000), is characterized by two behavioral symptom domains: inattention and hyperactivity-impulsivity. This syndrome captures a heterogeneous group of youngsters (Nigg, Willcutt, Doyle, & Sonuga-Barke, 2005) and may reflect heterogeneous inputs to the symptom domains (Sonuga-Barke, 2002). Inattention and hyperactivity convey somewhat distinct long-term risks (Fischer, Barkley, Smallish, & Fletcher, 2007; Massetti et al., 2008; Sonuga-Barke, Auerbach, Campbell, Daley, & Thompson, 2005), even though they are substantially correlated and often co-occur. Yet conceptual models of ADHD structure do not accommodate this information. For example, the subtyping scheme in the DSM-IV is likely insufficient to capture the etiological or phenotypic structure of ADHD due, in part, to the fact that small variations in symptoms levels lead to large changes in subtype classification (Lahey, Pelham, Loney, Lee, & Willcutt, 2005). There is better support for the two-dimensional model (inattention and hyperactivity-impulsivity), but that model is quite vulnerable to developmental changes in ADHD symptoms (Hart, Lahey, Loeber, Applegate, & Frick, 1995; Lahey et al., 2005). This raises a key conceptual question that is testable by statistical methods: does a multiple-component model of ADHD, specifying distinct influence on ADHD symptom domains, more accurately characterize the disorder compared to a single-component model, specifying uniform influence on the disorder? The answer to this question of phenotypic symptom structure has clear ramifications for how the disorder is conceptualized (e.g., in the DSM manuals) and for theories of etiological structure, as well as for clinical practice, assessment, and future epidemio-logical studies. Despite the fact that ADHD symptoms can wax and wane (Lahey et al., 2005) and some children do recover (Faraone, Biederman, & Mick, 2006), ADHD is generally conceptualized by clinicians and researchers as a relatively stable condition across development. That is, it is typically assumed that a latent general or ‘g’ ADHD construct holds across situations and time, with or without specific or ‘s’ factorial components that may change over time (i.e., the child ‘has ADHD’ even though the symptom display may vary with context). However, factorial support for this idea has been lacking, leaving a gap between clinical understanding and statistical models of ADHD. The factorial literature on ADHD structure does not presume a ‘g’ factor for ADHD; it assumes a one-, two-, or three-factor structure, or occasionally a second-order factor structure. Confirmatory factor analyses have tended to support a two-factor structure in clinical and population samples (Amador-Campos, Forns-Santacana, Martorell-Balanzo, Guardia-Olmos, & Pero-Cebollero, 2005, 2006; Bauermeister et al., 1992, 1995; Burns, Walsh, Owen, & Snell, 1997a; Burns et al., 1997b; Burns, Boe, Walsh, Sommers-Flanagan, & Teegarden, 2001; DuPaul et al., 1997; Gomez, Burns, Walsh, & Hafetz, 2005; Lahey et al., 1988; Pillow, Pelham, Hoza, Molina, & Stultz, 1998; Wolraich et al., 2003). Two-factor models are generally better supported than one-factor (unidimensional) or three-factor (separating impulsivity from hyperactivity) models (Burns et al., 2001). Yet none of these models are consistent with the way ADHD is thought of by clinicians or portrayed in the DSM-IV, nor do they account simultaneously for the overlap and stability, as well as distinctiveness and change, of ADHD symptom domains. A second-order factor model or a bifactor model1 would provide meaningful alternatives to these simple factor models by enabling simultaneous estimation of general and specific factors. However, second-order and bifactor models still suggest quite different assumptions about underlying structure, support different etiological assumptions, and have different clinical implications (see Table 1). A second-order factor model allows inattentive and hyperactive-impulsive symptom domains to be modeled separately with both symptom domains being entirely encompassed by a higher-order ADHD factor, as shown in Figure 1. This idea is most in line with the DSM-IV model of a single ADHD diagnostic category, perhaps with subtypes, and with a single final pathway to this disorder, influenced by overlapping etiological inputs. In addition, support for a second-order factor model suggests that clinical intervention would be similarly effective for all children with ADHD, regardless of symptom profile, and that variation of symptom profile would not be especially important for assessing long-term risk of poor outcomes or for investigating etiology. Figure 1 ADHD second-order factor model Table 1 Real-world implications of ADHD structural models A bifactor model of ADHD, with a ‘g’ factor and two (or three) specific factors of inattention and hyperactivity-impulsivity, is conceptually distinct (see Table 1). It allows for individual ADHD symptoms to simultaneously load onto an overall, or ‘general’ (‘g’), ADHD factor along with completely or partially distinct (‘specific’ (‘s’)) inattention and hyperactive-impulsive latent components, as shown in Figure 2. Support for this model might explain contradictory findings of general and specific influences on ADHD symptom domains. It would further suggest that children with ADHD are characterized by substantial interindividual heterogeneity, with some children exhibiting high inattentive and hyperactive-impulsive symptoms and other children exhibiting a different kind of symptom profile with high symptoms in only one of the two symptom domains. Thus, this model is more compatible than any other model with the current subtype structure in DSM-IV, although not identical since general and specific risk are not necessarily part of the same diagnostic category (ADHD) in this model (i.e., general ADHD might be one diagnostic category with specific inattention being a different disorder and specific hyperactivity-impulsivity being a developmentally specific manifestation of general ADHD). A bifactor model suggests that there are distinct (rather than heavily overlapping) etiological influences that converge on the same syndrome (Chen, West, & Sousa, 2006; Krueger, Markon, Patrick, Benning, & Kramer, 2007). This model would be in line with multiple-pathway, or multiple component process, conceptions of the disorder (Nigg, Goldsmith, & Sachek, 2004; Sonuga-Barke, 2005). For clinicians, this would suggest that assessment of general risk for ADHD, specific risk for inattention, and specific risk for hyperactivity-impulsivity would provide valuable information about an individual child's profile and risk over time. In addition, it suggests that treatment for ADHD might benefit from being tailored to the symptom profile of the particular child (e.g., psychopharmacology for high inattentive symptoms, behavioral treatment for high hyperactive-impulsive symptoms, and combined treatment for children with high symptoms in both domains). Figure 2 ADHD bifactor model The bifactor model approach has recently been used to describe externalizing behaviors in adults (Krueger et al., 2007). However, it has essentially not been tested for childhood ADHD, with two important exceptions. Toplak et al. (2009) fit a bifactor model of ADHD in a sample of clinic-referred adolescents. The bifactor model showed superior fit to simple factor models, although a second-order factor model was not examined. There has also been some empirical support for a bifactor model of inattention, hyperactivity, and impulsivity using the Achenbach (1991) Child Behavior Checklist (CBCL) item pool (somewhat different than the DSM-IV item pool; Achenbach, Bernstein, & Dumenci, 2005; Dumenci, McConaughy, & Achenbach, 2004). This paper attempts a comprehensive evaluation and comparison of alternative models (including single-order factor, second-order factor, and bifactor models) using DSM-IV items in a community-recruited sample of cases and controls with a wide age range. Study hypotheses were that there would be support for both a general ADHD factor and orthogonal specific factors of inattention and hyperactivity-impulsivity, consistent with DSM-IV and multiple-component conceptualization of ADHD etiology.