درمان شناختی رفتاری برای اضطراب دوران کودکی و استفاده از مواد مخدر در پیگیری 7.4 ساله : ارزیابی مجدد کنترل پیش بینی شناخته شده
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|34848||2011||7 صفحه PDF||سفارش دهید||5281 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Anxiety Disorders, Volume 25, Issue 5, June 2011, Pages 690–696
A previous report suggested that successful cognitive behavioral therapy (CBT) for child anxiety reduced substance use problems at 7.4-year follow-up, but that report did not include predictors of: (a) substance use disorder (SUD; e.g., attention deficit-hyperactivity disorder symptoms, negative life events, family substance abuse, additional treatment), or (b) treatment outcome (e.g., severity of internalizing pathology, age). Analyses incorporating these factors tested previously reported findings in 72 participants (ages 15–22 at follow-up; 84% of the 7.4-year follow-up sample), using parent and youth diagnostic interviews and report measures. The majority of previously reported associations between less successful treatment and later substance use problems remained significant after controlling for known predictors of SUD and treatment outcome. Our findings bolster previous conclusions that effective CBT for child anxiety may have ameliorative effects on the target disorder and later substance use problems.
Childhood anxiety disorders are associated with strained peer and interpersonal relationships, academic difficulties, and reduced psychological wellbeing (Costello et al., 2004 and Verduin and Kendall, 2008). They are common, affecting approximately 18% of children (Kessler, Chiu, Demler, & Walters, 2005) and unlikely to remit without treatment (Pine, Cohen, Gurley, Brooks, & Ma, 1998). Rather, the detriments of child anxiety are both immediate and prolonged. In addition to disrupting early functioning, childhood anxiety is a significant risk factor for later negative sequelae, such as substance use disorders (SUDs; Kaplow et al., 2001 and Pine et al., 1998). Research suggests that childhood anxiety disorders typically precede the onset of SUDs (Merikangas et al., 1998), a primacy that is compelling given the high lifetime co-occurrence of these disorders (35–45%; Kessler et al., 1996) and the deleterious outcomes associated with SUDs (Toumbourou et al., 2007). Cognitive behavioral therapy (CBT) for anxiety in youth is an efficacious treatment (Silverman, Pina, & Viswesvaran, 2008) with enduring effects (Glantz et al., 2009, Kendall and Kessler, 2002 and Kessler et al., 2007). A previous randomized clinical trial (RCT) of CBT for child anxiety reported that treatment responders (i.e., those whose anxiety diagnoses were either (a) no longer present or (b) no longer the principal diagnosis following treatment) had reduced substance use and fewer associated problems compared to treatment non-responders at 7.4-year follow-up (Kendall, Flannery-Schroeder, Safford, & Webb, 2004). Compared to responders, non-responders drank more days per month, were more likely to have unwanted social, physical/psychological consequences from drug use, gave up more activities due to drug use, used larger amounts of drugs, and made more unsuccessful attempts to control their use. Substance dependence is often viewed as chronic, requiring long-term treatment (McLellan, Lewis, O’Brien, & Kleber, 2000). Thus, the claim that CBT for child anxiety may mitigate later substance use, which may in turn lower the risk of SUDs, requires re-examination. The findings of Kendall et al. (2004) did not take into account important predictors of SUDs, such as inattention and impulsivity–hyperactivity, perceived negative life events, and family history of substance abuse. Research supports externalizing behavior and a family history of substance abuse as risk factors for later substance problems (Kendler et al., 1997 and Reinherz et al., 2000). Attention deficit hyperactivity disorder (ADHD) often predates adolescent substance use (Wilens, Biederman, Mick, Faraone, & Spencer, 1997). Likewise, increased negative life events have predicted SUDs even when controlling for other critical contributing factors such as genetic vulnerability (Connor et al., 2009 and Wills et al., 1992). Given these associations, it is unclear if the increased substance use of non-responders versus responders reported previously (Kendall et al., 2004) is attributable to their poor CBT treatment outcomes or to these other SUD risk factors. Approximately 30–45% of children treated with CBT continue to meet diagnostic criteria for an anxiety disorder following treatment (Cartwright-Hatton, Roberts, Chitsabesan, Fothergill, & Harrington, 2004). Older child age and greater internalizing pathology, but not diagnostic comorbidity, have been associated with poorer treatment outcomes (Crawford and Manassis, 2001, Rapee, 2003 and Southam-Gerow et al., 2001). Given that internalizing symptoms are also related to increased SUD risk (King, Iacono, & McGue, 2004), it seems plausible that the association between poor treatment response and later substance misuse may be a spurious association resulting from the association of internalizing symptoms with both these outcomes. Similarly, child age might account for both a child's treatment response and later substance use given that older youth are speculated to have a more chronic or developmentally “non-normative” anxiety (Southam-Gerow et al., 2001) that might also increase their risk for SUDs. The present study tested whether previously reported associations between differential CBT outcomes and substance use at 7.4-year follow-up would hold after (a) controlling for predictors of SUDs (i.e., ADHD symptoms, negative life events, family substance abuse history), and (b) controlling for predictors of CBT outcome (internalizing pathology, older age). The receipt of additional treatment between the post and 7.4-year follow-up assessment was also included as a novel control variable. Additional treatment may reflect the child's exposure to factors related to increased SUD risk, such as life stressors or emerging child or family psychopathology, or serve as a protective factor against such risk. We hypothesized that previously reported findings would be strengthened by the inclusion of these control variables.