In the December 2000 issue of the Journal of Abnormal Child Psychology, we published a set of papers presenting secondary analyses of the Multimodal Treatment Study of ADHD (MTA), and R. A. Barkley (2000) provided a commentary. A critique of the design of the study (MTA Cooperative Group, 1999) was presented based on a theoretical perspective of a "behavioral inhibition" deficit that has been hypothesized as the core deficit of ADHD (R. A. Barkley, 1997). The commentary questioned the design and analysis of the MTA in terms of (1) the empirical criteria for selection of components of behavioral (Beh) intervention, (2) the effectiveness of the Beh intervention, (3) the methods for analyses at the group and individual level, (4) implications of the MTA findings for clinical practice, (5) the role of genetics in response to treatment, and (6) the lack of a nontreatment control group. In this response, we relate the content of the papers to the commentary, (1) by reviewing the selection criteria for the Beh treatment, as outlined by K. C. Wells, W. E. Pelham, et al. (2000), (2) by addressing the myth that the MTA Beh treatment was ineffective (Pelham, 1999), (3) by describing the use of analyses at the level of the individual participant, as presented by J. S. March et al. (2000) and W. E. Pelham et al. (2000) as well as elsewhere by J. M. Swanson et al. (2001) and C. K. Conners et al. (2001), (4) by relating some of the suggestions from the secondary analyses about clinically relevant factors such as comorbidity (as presented by J. S. March et al., 2000) and family and parental characteristics (as presented by B. Hoza et al., 2000, S. P. Hinshaw et al., 2000, and K. C. Wells, J. N. Epstein, et al., 2000), (5) by discussing the statistical concept of heritability and the lack of a significant difference in the presence of ADHD symptoms in parents of the MTA families compared to parents in the classmate-control families (as presented by J. N. Epstein, et al., 2000), and (6) by acknowledging that an ethically necessary weakness of the MTA design is that it did not include a no-treatment control group. We discuss the use of secondary analyses to suggest how, when, and for what subgroups effectiveness of the Beh treatment may have been manifested. Finally, we invite others to use the large and rich data set that will soon be available in the public domain, to perform secondary analyses to mine the meaning of the MTA and to evaluate theories of ADHD and response to treatments.
Response to commentary on the multimodal treatment study of ADHD (MTA): mining the meaning of the MTA
VITIELLO, BENEDETTO;
2002-01-01
Abstract
In the December 2000 issue of the Journal of Abnormal Child Psychology, we published a set of papers presenting secondary analyses of the Multimodal Treatment Study of ADHD (MTA), and R. A. Barkley (2000) provided a commentary. A critique of the design of the study (MTA Cooperative Group, 1999) was presented based on a theoretical perspective of a "behavioral inhibition" deficit that has been hypothesized as the core deficit of ADHD (R. A. Barkley, 1997). The commentary questioned the design and analysis of the MTA in terms of (1) the empirical criteria for selection of components of behavioral (Beh) intervention, (2) the effectiveness of the Beh intervention, (3) the methods for analyses at the group and individual level, (4) implications of the MTA findings for clinical practice, (5) the role of genetics in response to treatment, and (6) the lack of a nontreatment control group. In this response, we relate the content of the papers to the commentary, (1) by reviewing the selection criteria for the Beh treatment, as outlined by K. C. Wells, W. E. Pelham, et al. (2000), (2) by addressing the myth that the MTA Beh treatment was ineffective (Pelham, 1999), (3) by describing the use of analyses at the level of the individual participant, as presented by J. S. March et al. (2000) and W. E. Pelham et al. (2000) as well as elsewhere by J. M. Swanson et al. (2001) and C. K. Conners et al. (2001), (4) by relating some of the suggestions from the secondary analyses about clinically relevant factors such as comorbidity (as presented by J. S. March et al., 2000) and family and parental characteristics (as presented by B. Hoza et al., 2000, S. P. Hinshaw et al., 2000, and K. C. Wells, J. N. Epstein, et al., 2000), (5) by discussing the statistical concept of heritability and the lack of a significant difference in the presence of ADHD symptoms in parents of the MTA families compared to parents in the classmate-control families (as presented by J. N. Epstein, et al., 2000), and (6) by acknowledging that an ethically necessary weakness of the MTA design is that it did not include a no-treatment control group. We discuss the use of secondary analyses to suggest how, when, and for what subgroups effectiveness of the Beh treatment may have been manifested. Finally, we invite others to use the large and rich data set that will soon be available in the public domain, to perform secondary analyses to mine the meaning of the MTA and to evaluate theories of ADHD and response to treatments.
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