Behavioural differences between EEG-defined subgroups of children with Attention-Deficit/Hyperactivity Disorder
Introduction
Attention-Deficit/Hyperactivity Disorder (AD/HD) is one of the most common psychiatric disorders treated by child and adolescent psychiatrists in the US. (Cantwell, 1996), with studies estimating the prevalence rate in children at between 3% and 6% (Lindgrean et al., 1990, Pelham et al., 1992). AD/HD is characterized by varying levels of hyperactivity, impulsivity and inattention, which may change with development from preschool through adulthood (APA, 1994). The disorder interferes with many areas of normal development and functioning in a child’s life, and predisposes a child to greater risk of social and psychiatric problems as an adult.
EEG studies of children and adolescents with AD/HD typically report increased theta activity, which is often maximal in the frontal regions (Satterfield et al., 1972, Janzen et al., 1995, Chabot and Serfontein, 1996, Lazzaro et al., 1998, Clarke et al., 1998, Clarke et al., 2001b, Clarke et al., 2001d, Clarke et al., 2002a, Clarke et al., 2002b, Clarke et al., 2002d, Clarke et al., 2003a, Clarke et al., 2003b, Clarke et al., 2006, Clarke et al., 2007, Clarke et al., 2008, Hobbs et al., 2007), increased posterior delta (Matousek et al., 1984, Clarke et al., 1998, Clarke et al., 2001b, Clarke et al., 2001d), and decreased alpha and beta activity (Dykman et al., 1982, Callaway et al., 1983, Barry et al., 2003, Clarke et al., 2006, Clarke et al., 2007, Clarke et al., 2008), also most apparent in the posterior regions (Clarke et al., 1998, Clarke et al., 2001b, Clarke et al., 2001d, Lazzaro et al., 1998, Barry et al., 2003). However, a number of studies have found several distinct EEG profiles within this disorder. Clarke et al., 1998, Clarke et al., 2001d found that between 15% and 20% of children with a diagnosis of AD/HD combined type had significantly elevated levels of beta activity in their EEG. AD/HD children with excess beta activity were further investigated by Clarke et al. (2001e), who found that this pattern was more common in patients with the combined type of AD/HD, and more common in boys than girls. As part of that study, a review of the clinical notes was also conducted, which indicated that children with excess beta activity were more prone to moodiness and temper tantrums compared to AD/HD children with the typical EEG profile of excess theta activity. That study was limited in that only clinical notes were available to evaluate behavioural differences within the different EEG-defined groups. However, the results indicated that further behavioural assessments were warranted.
Following from these initial studies that identified the presence of excess beta activity in some children with AD/HD, Clarke et al. (2001c) investigated the existence of other groups of children with distinct EEG profiles, using cluster analysis of the EEG in boys with the combined type of AD/HD. In a comparison of the total AD/HD sample with the control group, the EEG power and topography of the AD/HD group were typical of results from other studies. However, cluster analysis identified three distinct EEG-defined groups within the sample. The first cluster had greater total power, relative theta and theta/beta ratio, as well as less relative delta and beta across all regions. This profile was interpreted as indicating cortical hypoarousal. The second cluster was characterised by elevated slow wave and deficiencies of fast wave activity, which suggested the presence of a maturational lag in central nervous system (CNS) development. The third cluster had excess beta activity, and was tentatively labelled as an over-aroused group. In a follow-up study (Clarke et al., 2002c), a replication of our first cluster study was conducted in boys with the inattentive type of AD/HD. In that study, two clusters were identified, with one having a profile indicative of cortical hypoarousal, and the second suggesting a maturational lag in CNS development. The lack of an excess-beta group was compatible with our previous reports of the occurrence of that group largely within the combined type (Clarke et al., 2001d, Clarke et al., 2001e).
In a further study, Clarke et al. (2003b) investigated whether distinct EEG clusters could be found in a sample of girls with the disorder. Results indicated the presence of two clusters in girls with AD/HD. There was a large subgroup characterised by greater total power, more relative theta, and less relative delta and beta than control subjects, and a small subgroup with a substantially-greater amount of high amplitude theta activity, with deficiencies in all other bands. These results indicate that girls with AD/HD exhibit abnormalities in their EEGs, but with far less variance in their EEG profiles than boys with the disorder. Chabot and Serfontein (1996) and Chabot et al. (1999) also reported the existence of distinct EEG-defined subtypes of children with AD/HD, characterised by excess beta activity, as well as children with excess alpha and theta as the dominant abnormality.
One possible limitation of the above Clarke et al. studies was that subjects with a second comorbid condition were excluded. This was done in an attempt to ascertain the major EEG abnormalities that are specific to AD/HD. However, AD/HD is a highly comorbid disorder that is commonly found with conduct and oppositional defiant disorder, learning disabilities, and anxiety and depression (Offord et al., 1987, Offord et al., 1989, Cohen et al., 1993). Many of these disorders also have been reported to be associated with EEG abnormalities, so it is not known how robust the reported AD/HD EEG cluster profiles are in the presence of other comorbid conditions. The first aim of this study was to determine the reliability of the above EEG-defined subtypes of AD/HD in a group of children who have not been screened for other comorbid psychiatric conditions. Following from the study by Clarke et al. (2001e), the second aim was to explore whether behavioural differences exist between the EEG-defined subgroups of children with AD/HD.
Section snippets
Participants
Participants in this study were 155 boys with a diagnosis of AD/HD combined type, and 109 age-matched male controls. All children were between the ages of 7 and 13 years, and had a full-scale WISC-III IQ score of 80 or higher (range 81–136). The children with AD/HD were drawn from new patients presenting at a paediatric practice for an assessment for AD/HD. The clinical subjects had not been diagnosed as having AD/HD previously, had no history of medication use for the disorder, and were tested
Results
Cluster 1 (t(1143) = −2.826, p < .01) and Cluster 3 (t(1145) = −2.787, p < .01) had a significantly lower mean IQ than the control group. Cluster 2 (t(1122) = −3.979, p < .001), Cluster 3 (t(1143) = −2.814, p < .01) and Cluster 4 (t(1143) = −5.261, p < .001) had lower mean ages, and Cluster 5 (t(1131) = 6.985, p < .001) had a higher mean age than the control group (see Table 1).
Discussion
In our past research we found a number of different EEG profiles that suggested the presence of three different groupings of CNS abnormalities in children with AD/HD (Clarke et al., 1998, Clarke et al., 2001c, Clarke et al., 2001d, Clarke et al., 2001e, Clarke et al., 2002c, Clarke et al., 2003b). These consisted of a group with elevated slow wave activity and deficiencies of fast wave, which was labelled as maturationally-lagged, a group with elevated high amplitude theta with deficiencies of
Acknowledgement
This research was supported under the Australian Research Council’s Discovery funding scheme (project number DP0558989).
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