What is cognitive behavioural therapy and does it work?
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Biomedical subjects
Publications and source records attributed to S D Hollon.
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A scheme is proposed for determining when a psychological treatment for a specific problem or disorder may be considered to be established in efficacy or to be possibly efficacious. The importance of independent replication before a treatment is established in efficacy is emphasized, and a number of factors are elaborated that should be weighed in evaluating whether studies supporting a treatment's efficacy are sound. It is suggested that, in evaluating the benefits of a given treatment, the greatest weight should be given to efficacy trials but that these trials should be followed by research on effectiveness in clinical settings and with various populations and by cost-effectiveness research.
A recent survey by Consumer Reports (1994) found that people who received psychotherapy were generally pleased with their experience and that their satisfaction was unrelated to the type of treatment or the addition of medications. M.E.P. Seligman (1995) argued that these findings demonstrate the value of psychotherapy and suggested that such survey methodologies may be superior to randomized clinical trials in this regard because they study what occurs in actual clinical practice. Although such approaches provide important information, they are no substitute for controlled clinical trials when it comes to drawing causal inferences. However, the study does highlight the importance of defining outcome in the broadest possible fashion and of addressing the external validity of the findings obtained. Attention to such considerations has implications for the relative value of drugs and psychotherapy.
In these concluding comments to the exchange among N. S. Jacobson and S. D. Hollon (1996), D. F. Klein (1996), I. Elkin, R. D. Gibbons, M. T. Shea, and B. F. Shaw (1996), and R. J. McNally (1996) issues of continuing controversy are highlighted: the best ways to control for the allegiance effect, the complexities of assessing competence, and the role of pill placebos in comparisons between cognitive-behavior therapy (CBT) and pharmacotherapy. It is concluded that controlling for allegiance within site is the optimal strategy, that measures of competence must take context into account, and that pill placebo controls are optimal but not essential to comparisons between CBT and pharmacotherapy.
Recent reanalyses suggest that pharmacotherapy was superior to cognitive-behavior therapy in the acute treatment of more severely depressed outpatients in the National Institute of Mental Health Treatment of Depression Collaborative Research Program (TDCRP). At the same time, this finding was neither robust across sites within the TDCRP nor consistent with findings from other studies. D.F. Klein has argued that those other studies were inherently flawed because they did not include pill-placebo controls, an argument that he extended to drug-psychotherapy comparisons in the treatment of panic as well. It is agreed that the inclusion of such controls would have facilitated the interpretation of the findings, but it is not agreed that their omission rendered those studies uninterpretable. Cognitive-behavior therapy remains a viable alternative to pharmacotherapy in the treatment of depression and a particularly promising intervention in the treatment of panic disorder.
This study examined the effect of having a safe person present on artificially induced anxiety following a biological challenge among panic-disordered patients. Anxiety symptoms were induced using a 5.5% CO2-inhalation procedure. Panic patients underwent the inhalation procedure either in the presence or absence of their safe person. Nonanxious controls underwent the procedure without a safe person. Panic patients exposed to CO2 without their safe person present reported greater distress, a greater number of catastrophic cognitions, and a greater level of physiological arousal than did panic patients exposed with their safe person. The latter group did not differ from controls on most measures at postexposure. The attenuation of self-reported anxiety and catastrophic cognitions is consistent with the safety-signal theory and the cognitive model of panic, respectively. The results, however, are inconsistent with a biological model of panic.
Forty-eight unipolar depressed patients were randomly assigned to 12 weeks of treatment with either imipramine (IMI) (n = 32) or cognitive therapy (CT) (n = 16). Prior to treatment assignment, all patients were rated for severity of a variety of psychosocial stressors. The interaction effect between pretreatment stress and type of treatment, CT or IMI, on symptom improvement was evaluated. We hypothesized that patients with greater pretreatment stress would respond better to cognitive therapy. Patients treated with either CT or IMI showed equivalent reductions of depressive symptoms. There was no interaction effect between pretreatment stress and type of treatment on improvement of depressive symptoms. Based on this preliminary study it does not appear that depressed patients with higher pretreatment levels of stress respond better to cognitive therapy than they do to imipramine.
The majority of cases of clinical depression go unrecognized and untreated, despite the fact that depression is an eminently treatable disorder. The Agency for Health Care Policy and Research (AHCPR) recently published a set of clinical practice guidelines focused on depression in primary care settings. The review of the literature on which the guidelines are based is thorough and appropriate and should enhance the detection of depression and the quality of pharmacotherapy for depression. However, the guidelines encourage primary care physicians to provide pharmacotherapy to their depressed patients as the first line of treatment. The wisdom of this recommendation is questioned and revisions to the guidelines are suggested. Specifically, patients should be informed of the broad array of treatment options available and provided with a more balanced presentation of the potential benefits of psychotherapy for depression. Patients should decide which treatment alternative they wish to undergo.
Urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) levels in 53 depressed women were compared to current suicidal thoughts or activity. Comparisons were also made between MHPG and past suicide attempts, number of past attempts, and seriousness of the worst attempt. There was a weak trend for current but not past suicidality to be associated with decreased MHPG levels.
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Cognitive therapy has emerged as 1 of the most promising psychosocial interventions for the treatment of depression. It appears to be at least the equal of alternative interventions (including pharmacotherapy) with respect to acute treatment. In addition, there are indications that it may reduce risk of symptom return after treatment termination. Nonetheless, design limitations reduce the certainty with which such conclusions can be drawn. Furthermore, tests of its efficacy have largely been limited to nonbipolar outpatient (or subclinical) samples. At this time, cognitive therapy is best considered a promising, but as yet not adequately tested, intervention for the treatment of depression.
Cognitive therapy and imipramine hydrochloride tricyclic pharmacotherapy, each singly and in combination, were compared in the treatment of nonpsychotic, nonbipolar depressed outpatients. One hundred seven patients were randomly assigned to 12 weeks of active treatment; 64 patients completed the full course of treatment. Rates of attrition were high but not differential. Cognitive therapy and pharmacotherapy did not differ in terms of symptomatic response, either in the primary analyses or in secondary analyses restricted to more severely depressed outpatients. Initial severity did predict response within pharmacotherapy alone, but not within cognitive therapy. Combining cognitive therapy with pharmacotherapy did not markedly improve response over that observed for either modality alone, although such nonsignificant differences as were evident did favor the combined treatment. Two patients died as a consequence of suicide attempts, both of which involved study medication.
Patients successfully treated during a 3-month period with either imipramine hydrochloride pharmacotherapy, cognitive therapy, or combined cognitive-pharmacotherapy were monitored during a 2-year posttreatment follow-up period. Half of the patients treated with pharmacotherapy alone continued to receive study medications for the first year of the follow-up. All other patients discontinued treatment at the end of the acute treatment phase. Patients treated with cognitive therapy (either alone or in combination with medication) evidenced less than half the rate of relapse shown by patients in the medication--no continuation condition, and their rate did not differ from that of patients provided with continuation medication. It appears that providing cognitive therapy during acute treatment prevents relapse. Whether this preventive effect extends to recurrence remains to be determined.
Sixteen unipolar depressed patients were treated with cognitive therapy for 12 weeks. Pretreatment 24-hour urinary MHPG levels were unable to predict treatment response. There was a nonsignificant trend for cognitive therapy responders to show a decrease in MHPG during treatment when compared to nonresponders.
Forty-five depressed patients were treated with imipramine for 6 weeks. Seven of 7 patients (100%) who had plasma levels of imipramine plus desipramine greater than 500 ng/ml showed a 50% or greater improvement in Hamilton depression scores compared with 23 of 38 patients (60%) with plasma levels less than 500 ng/ml (p less than 0.057).
Cognitive therapy (CT) for depression has generated considerable interest in recent years. Comparisons with tricyclic pharmacotherapy in nonbipolar outpatients have suggested that (a) CT may be roughly comparable in the treatment of the acute episode: (b) combined CT-pharmacotherapy does not appear to be clearly superior to either modality (although indications of potential enhancement do exist to justify additional studies with larger samples), and (c) treatment with CT during the acute episode (either alone or with medications) may reduce the risk of subsequent relapse following termination. Nonetheless, for a variety of reasons (e.g., limitations in study design and execution, inadequate design power, and possible differential retention), these conclusions can be considered only suggestive at this time. More than a decade after the publication of the first controlled study involving CT, the approach remains a promising, but not adequately tested, alternative to pharmacotherapy in the treatment of depression.
Specificity designs in psychopathology research are used to examine whether a variable is unique to a given disorder. When nonspecificity is observed, it typically is assumed that the variable in question is not a cause of the disorder, but is instead a nonspecific consequence of general psychopathology. Such reasoning is flawed, however, because it fails to distinguish between testing a particular causal model containing the variable versus testing the causal status of the particular variable within the model. A variable may be nonspecific, but still causal, if it is one of several multiple interacting causes or if a nosological error has been made. A recognition of these complexities has implications for the nature of the psychopathology control group selected.
The ability of pretreatment 3-methoxy-4-hydroxyphenylglycol (MHPG) to predict response to various antidepressants is reviewed. MHPG appears to be a modest predictor of treatment response to imipramine but does not appear to be a reliable predictor for other antidepressants.