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January 2007 | Back to Table of Contents

Clinical and Health Affairs

The Use of Cognitive-Behavioral Therapy in the University of Minnesota’s Outpatient Psychiatry Clinic

By Matt G. Kushner, Ph.D., L.P.

Abstract
Cognitive-behavioral therapy (CBT) refers to a group of therapeutic techniques that can be categorized broadly as psychoeducation, cognitive restructuring, and behavioral exposure. Unlike other psychotherapeutic approaches, CBT is derived from learning laboratory experimentation rather than conjecture and theorizing. This article provides background information concerning the origins and practice of cognitive and behavioral therapies and summarizes findings from a recently completed research project at the University of Minnesota that integrates new neuroscientific findings and CBT.


Since Sigmund Freud first introduced psychoanalysis more than a century ago, hundreds of “brands” of psychotherapy have been promulgated in books, manuals, and schools. Of these, cognitive (from the Latin verb cogit, meaning to think) and behavioral therapies are distinctive. Both behavioral therapy and, to a lesser extent, cognitive therapy trace their roots to the basic learning laboratories of researchers such as Ivan Pavlov and B.F. Skinner. This is in contrast to nearly all other traditional psychotherapeutic approaches, which were founded on the intuitions, conjectures, and clinical observations of a charismatic/genius founder such as Sigmund Freud, Carl Rogers, Henry Sullivan, or Milton Erickson.

The sine que non of both cognitive and behavioral therapies is a strong commitment to empiricism—that is, the requirement that treatment targets be quantified, intervention procedures be specific, and desired outcomes be reliably achieved. As early as 1969, Joseph Wolpe defined behavioral therapy as “the use of experimentally established principles of learning for the purpose of changing unadaptive (sic) behavior.”1 Stemming from this empirical/experimental substrate, cognitive and behavioral therapies are at the forefront of a movement in psychology and psychiatry to promote therapies that have been shown to be effective in randomized placebo-controlled clinical trials.2

Other features distinguishing cognitive and behavioral therapies include a present-time orientation versus a focus on the historical antecedents of problems, a short-term strategy (usually 10 and rarely more than 20 sessions), and a collaborative model in which goals are explicitly stated and mutually worked toward by the therapist and patient (versus a paternalistic model in which the therapist’s specific stratagems are not necessarily shared with the patient).

Although it is now common to refer to cognitive and behavioral therapies as if they were a single therapeutic approach—cognitive-behavioral therapy (CBT), cognitive and behavioral therapies each have a distinct history and have been integrated for only about the last 20 years. At this time, however, there are 3 relatively standard primary components of CBT: 1) psychoeducation, which is aimed at providing patients with accurate information concerning their disorder and the CBT approach to treatment; 2) cognitive restructuring, which is aimed at identifying and modifying habitual patterns of thinking that are understood to maintain the presenting problem; and 3) behavioral exposure, which involves confronting situations or stimuli that trigger the patient’s symptoms and/or avoidance behavior. During the last 20 years, dozens of books and manuals have described the application of CBT for a range of psychiatric problems; however, the primary applications are for depression, anxiety, and phobias.

Cognitive Restructuring
Cognitive restructuring techniques aim to manipulate thinking patterns that are understood to be either causing maladaptive functioning or otherwise inhibiting adaptive functioning. Aaron T. Beck, M.D., who is considered the father of cognitive therapy, argued that depression is characterized by an overly pessimistic belief system concerning the self, the future, and the world.3 This turns on its head the traditional notion that a depressed mood causes depressed thinking. According to Beck, people feel depressed or anxious because they hold unrealistically negative or catastrophic perceptions of their circumstances. In the case of panic attacks, for example, the cognitive model suggests that benign bodily sensations are interpreted in an alarming way (eg, feeling one’s heart race and thinking that one is having a heart attack, which provokes a strong fight or flight or panic reaction).4 Specific perceptual errors stemming from general or characteristic styles of thinking contribute to these erroneous ways of thinking (eg, the tendency to ignore positive information that contradicts negative or worst-case conclusions). Albert Ellis, Ph.D., a contemporary of Beck’s who independently contributed to the development of a branch of cognitive therapy called rational-emotive therapy, identified common “rules” people unconsciously live by that lead to unnecessary depression and anxiety (eg, thinking that one must be approved of by everyone or one is a terrible person; that if one doesn’t do perfectly well at everything, one is unlovable and a failure; and that one should constantly dwell on any possible threats to one’s well-being, even if they are unlikely).5

Once identified, erroneous thinking styles and rules are systematically recorded and challenged. With the help of a trained therapist, the patient is taught to recognize and critically question the validity of these upsetting thought patterns. This is done both by a systematic critical analysis initially led by the therapist and later by behavioral experiments that challenge erroneous thoughts by putting them to a critical test. The therapist will ask questions in an effort to put negative thinking to a reality test. These might include What is the evidence for and against this belief? What are some alternative ways of seeing this? and What are the real consequences involved? Then, the therapist will challenge erroneous thoughts directly with behavioral experiments. For example, benign bodily sensations such as rapid heart beat can precipitate panic attacks if taken as a sign of impending doom such as a heart attack. Anticipatory anxiety and avoidance can follow when the patient believes that certain situations, such as those involving physical exertion, place them in danger. Not only are patients asked to consider the evidence that they are having a heart attack when their heart beats fast, but they also are instructed to seek out and stay in situations they’d prefer to avoid (eg, crowds, exercise) to test the validity of their scary thoughts.

This approach to cognitive therapy is typically formulated for patients in an A-B-C-D-E structure. The earlier sessions focus on teaching the patient to distinguish 3 components of emotional distress:
A) The Activating Event—describing actual events that occurred (eg, My heart is beating fast);
B) Belief —describing thoughts surrounding the events that occurred (eg, I’m having a heart attack); and
C) Consequences—describing how they felt and what they did as a result of the event (eg, rushed to the ER with a sense of dread).
Once the patient is reliably able to do this, the therapist introduces the last 2 steps:
D) Dispute—asking the patient to consider alternative and benign interpretations for what’s happening in the scary situation (eg, My heart’s beating fast because I’m nervous not because I’m having a heart attack); and
E) Effect Change—asking the patient to eliminate avoidance and reassurance-seeking behavior based on the assumption that something terrible has or is about to happen (eg, avoiding being alone or in unfamiliar places). Obviously, this work assumes the patient is physically healthy.

Behavioral Exposure
Ivan Pavlov was the first to demonstrate that neutral stimuli such as a bell’s ring can elicit strong emotional responses if paired with survival-relevant stimuli (eg, food). Pavlov showed that not only can a bell trigger salivation after frequent pairings with food, but other neutral signals could also trigger fear when paired with pain or threat.

This classical conditioning model has been adapted to explain the origins of human phobias and, more importantly, their treatment. For example, early behavior therapists such as J.B. Watson, Ph.D., showed that pairing the presentation of an animal with a frightening noise could generate a fear of that animal in a child who previously had no such fear.6 Fortunately, this model also works in reverse.

Treatment in the form of repeated presentations of the phobic stimulus, such as a feared animal, without the dreaded outcome, such as a painful bite, can help the person overcome the fear. This model, called “extinction learning,” is the basis for a CBT technique referred to as “exposure therapy,” in which patients are asked to confront their fears to learn that catastrophic outcomes are unlikely to occur.

Research at the University of Minnesota
The University of Minnesota’s Outpatient Cognitive-Behavioral Therapy Clinic has been housed in the department of psychiatry since 1991. Here, we provide psychological services for a range of psychiatric disorders. Anxiety disorders including obsessive-compulsive disorder (OCD), social phobias, generalized anxiety disorder, and depression comprise the lion’s share of our patients’ problems. The typical treatment program entails 10 weekly one-hour therapy sessions. Patients may or may not be taking psychotropic medications. Recently, we added a virtual reality component to our anxiety-treatment program, which is used for patients who fear flying or public speaking. We also engage in research aimed at expanding knowledge in this field.

♦ Treating Obsessive-Compulsive Disorder
One of our most recent research projects has involved improving the efficacy of CBT treatment for OCD. Obsessive-compulsive disorder is an anxiety syndrome characterized by chronic intrusive and highly upsetting obsessive ideas and reactions such as fear of being contaminated, along with compulsive and repetitive ritualistic behaviors such as excessive hand washing and avoidance of possible contaminants.

Notably, OCD is one of the top 10 causes of disability in the United States. Obsessive-compulsive disorder affects approximately 2.5 percent of the U.S. population and is more common than schizophrenia and bipolar disorder.7,8 The social and economic costs associated with this disorder approach $10 billion a year.9

Cognitive-behavioral therapy has been identified by a consensus of experts convened by the National Institute of Mental Health as a first-line treatment for OCD. However, Foa and colleagues reviewed results from 18 controlled studies and concluded that only 51% of subjects who received CBT were either symptom-free or much improved; although many more were at least moderately improved.10 Further, Riggs and Foa reported that up to 25% of individuals with OCD, upon being made aware of the time, cost, and discomfort associated with CBT therapy, refuse this treatment.11 Notably, conventional medication treatments have efficacy rates comparable to that of CBT and do not notably improve outcomes when added to CBT.1

♦ Drug Augmentation to Enhance Response to CBT
With a grant from the Obsessive-Compulsive Foundation, we attempted to evaluate the use of D-Cycloserine, a drug used to treat tuberculosis, in accelerating response to CBT for OCD.13 D-Cycloserine, an NMDA-receptor partial agonist, has been found to accelerate the rate of extinction learning associated with conditioned fear responses in animals and humans.14,15 For example, Walker et al. showed that rats conditioned to fear a light because it was paired with a shock were able to learn the light was safe after only half the number of nonshocking light exposures when given D-Cycloserine versus vehicle (control) alone.14 This effect is attributed to the drug’s capacity to enhance learning-relevant neurochemical processes versus a direct anxiolytic effect. Animals given D-Cycloserine in the absence of exposure therapy do not show decreased fear in response to the light. Because extinction learning is understood to be a primary mechanism in the therapeutic benefit of CBT, D-Cycloserine should, theoretically, accelerate (by as much as 2-fold) the clinical response to CBT. In fact, this concept has been supported in 2 published placebo-controlled studies focused on the amelioration of pathological social anxiety and acrophobia using exposure therapy.16,17

In our study, we administered a 125 mg dose of D-Cycloserine or placebo in a double-blind fashion to individuals with OCD approximately 2 hours before each of up to 10 exposure-therapy sessions. D-Cycloserine decreased both the number of exposure sessions required to achieve clinical milestones (by about 2 sessions) and the rate of therapy dropout (7% versus more than 30%). After 4 exposure sessions, patients in the D-Cycloserine group reported significantly greater decreases in obsession-related distress compared with those in the placebo group. We concluded from this work that D-Cycloserine augmentation has the potential to increase the efficiency, palatability, and overall effectiveness of standard exposure therapy for OCD.

Conclusion
Cognitive-behavioral therapy is a broad term referring to therapeutic techniques primarily derived from laboratory research as well as a commitment to empirical quantification of presenting problems, procedures, and outcomes. An increasing number of therapists are receiving formal training in CBT as part of a larger movement in psychiatry toward empirically verified treatments. Our recent research suggests that CBT may be on the threshold of an exciting new stage in which the very brain mechanisms underlying therapeutic learning can be manipulated to provide maximum benefit from those treatments. MM

Matt Kushner is a professor and director of the Cognitive-Behavioral Therapy Clinic in the University of Minnesota’s department of psychiatry.
 
References
1. Wolpe J. The Practice of Behavior Therapy. New York: Pergamon Press; 1969.
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3. Beck AT. Cognitive Therapy and the Emotional Disorders. New York: International Universities Press; 1976.
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11. Riggs DS, Foa EB. Obsessive-compulsive disorder. In: Barlow DH, ed. Clinical Handbook of Psychological Disorders. New York: Guilford Press; 1993:189-239.
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14. Walker DL, Ressler KJ, Lu KT, Davis M. Facilitation of conditioned fear extinction by systemic administration of intra-amygdala infusions of D-cycloserine as assessed with fear-potentiated startle in rats. Neurosci. 2002;22(6):2343-51.
15. Richardson R, Ledgerwood L, Cranney J. Facilitation of fear extinction by D-Cycloserine: theoretical and clinical implications. Learn Mem. 2004;11(5): 510-6.
16. Hofmann SG, Meuret AE, Smits JA, et al. Augmentation of exposure therapy with D-Cycloserine for social anxiety disorder. Arch Gen Psychiatry. 2006;63:298-304.
17. Ressler KJ, Rothbaum BO, Tannenbaum L, et al. Cognitive enhancers as adjuncts to psychotherapy: use of D-cycloserine in phobic individuals to facilitate extinction of fear. Arch Gen Psychiatry. 2004;61(11):1136-44.
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