Turkington D, Morrison AP. Cognitive Therapy for Negative Symptoms of Schizophrenia. Arch Gen Psychiatry. 2011 Oct 3 ; Pubmed Abstract
Turkington D, Morrison AP. Cognitive Therapy for Negative Symptoms of Schizophrenia. Arch Gen Psychiatry. 2011 Oct 3 ; Pubmed Abstract
This study of a well-established, psychosocial treatment, which has been documented to be effective for depression, anxiety disorders, and positive symptoms of schizophrenia (Salkovskis, 1996; Kingdon and Turkington, 2004), presents credible evidence of efficacy for some, but not all, negative symptoms and possibly for social functioning in schizophrenia. The study has a number of strong methodological features; for example, protecting the “blind” for assessors, appropriate frequency and duration of treatment sessions necessary to achieve therapeutic outcomes in this population, controls for differences in types and doses of antipsychotic medication, a “standard treatment” comparison group which is consistent with the vast majority of community mental health, a sample that includes different racial and ethnic groups consistent with an inner-city population, and appropriate statistical analyses for measuring outcome. My comments address a number of concerns that may attenuate the clinical significance of the authors’ findings and interpretations.
Selection Criteria for Subjects
There is no indication whether the subjects had primary negative symptoms (i.e., the deficit state defined by enduring negative symptoms not related to positive symptoms including anxiety and depression, under-stimulating environments, side effects of medication (e.g., sedation, akathisia, akinesia, weight gain) or negative symptoms secondary to the above listed remediable interferences. In fact, it is likely that they had secondary negative symptoms because, as noted by the authors, the subjects showed significant reductions in positive symptoms and social anxiety, which often are associated with reductions of negative symptoms.
While the subjects were described as “low functioning” and “highly regressed,” the eligibility criteria for entry into the study did not use a well-established and psychometrically sound assessment instrument for measuring social functioning. For some inexplicable reason, the Global Assessment Scale was chosen as the measure of “social functioning,” despite the authors appropriately pointing out how the GAS confounds symptoms with functioning and has woefully inadequate anchor points for rating psychosocial adjustment and poor inter-rater reliability. The finding that, at baseline, their subjects were rated by the GAS in the mid- to high 40s suggests functioning that reflects “serious symptoms” and “serious impairment in social occupational or school functioning,” with the latter exemplified by “no friends” and “unable to keep a job.” This range in the GAS is hardly consistent with schizophrenia patients who are “repressed” and “severely socially impaired.” Individuals with schizophrenia who are low functioning would ordinarily fall into the 25-40 range on the GAS (e.g., “unable to work,” “socially isolated with little contact with other persons outside the family”). Many persons with schizophrenia who would not be considered “low functioning,” even those in remission of their positive and negative symptoms, have no friends and are unable to keep a job.
While the authors point out in their discussion that the GAS is a poor indicator of social functioning, it is not clear why they chose this instrument for their design, since it is well known that the GAS has poor inter-rater reliability, poor anchor points, and confounds symptoms with functioning (Dickerson, 1997).
The authors fail to describe specific improvements in social functioning that would convince readers that the cognitive therapy resulted in clinically significant improvements in work, school, friendships, family life, self-care skills, medication and money self-management, independent living, and other convincing examples of successes in community living.
The therapeutic methods as described by the authors clearly confound cognitive therapy procedures with those developed and validated for social skills training (Liberman et al. Social Skills Training for Psychiatric Patients, 1989; Bellack et al. Social Skills Training for Schizophrenia, 2006; Liberman. Recovery from Disability: Manual of Psychiatric Rehabilitation, 2008). For example, as described in the description of cognitive therapy, the following techniques were used that are key elements of social skills training in particular, and other evidence-based practices for the treatment of schizophrenia as well (e.g., supported employment, behavioral family therapy and its variants, assertive community treatment, cognitive adaptive therapy):
Specificity of Cognitive Therapy for Negative Symptoms
It is possible that the many elements in the experimental treatment condition that were similar to those used in social skills training, rather than the specific cognitive interventions, could have brought about the improvements reported in negative symptoms and social functioning.
Contrary to the assertion of the authors that “studies of other psychosocial, behavioral, or cognitive remediation interventions…[have failed]…to find that treatment effects generalized adequately to psychosocial functioning,” there are a number of evidence-based, psychosocial treatments that have been shown to significantly improve psychosocial functioning and negative symptoms. These include social skills training, behavioral family management, supported employment, and assertive community treatment (Bellack, 2004; Liberman et al., 1998; Glynn et al., 2002; Bellack and Mueser, 1993; Heinssen et al., 2000; Kurtz and Mueser, 2008; Kopelowicz et al., 1997; Falloon et al., 1987; Falloon et al., 1999; Drake et al., 1999; Drake et al., 1996; Stein and Test, 1980).
The authors give examples of how subjects’ symptoms interfered with social functioning, such as social anxiety and positive symptoms of schizophrenia. Since anxiety disorders are very common comorbidities in schizophrenia and have been shown to be responsive to cognitive therapy (Rector and Beck, 2001), it is possible that the cognitive therapy improved social interaction and adjustment by reducing anxiety. It is also possible, as noted by the authors, that the cognitive therapy brought about reductions in three of the four domains of negative symptoms secondarily as a function of rather marked decrease in positive symptoms. The reductions in positive symptoms were much greater than the rather small reductions in negative symptoms. This reverse direction of causality is acknowledged as a possible explanation of their results on negative symptoms by the authors in their Comment section.
One finding of the authors strongly suggests that the cognitive therapy did not produce improvements in psychosocial functioning by reducing negative symptoms. In Figure 3, it is clearly seen that the cognitive therapy had nil therapeutic impact on alogia, which is the critical negative symptom that would be expected to mediate improved social functioning. If subjects’ speech and conversational skills showed little improvement, it is questionable to attribute improvements in social interaction and relationships to the other three negative symptoms. The non-specific effects of 18 months and 50 sessions of community-based activities and homework assignments to attain incremental goals, instigated by competent, upbeat, and engaging therapists, would be expected to reduce apathy, anhedonia, and flat affect temporarily—which might rapidly erode once the spirited and therapeutically active sessions ended.
Also acknowledged by the authors in their Comment section is the possibility that improvements in three of four negative symptoms and marginal changes in social functioning (difficult to conceptualize without more behaviorally specific examples and typologies of goals attained in the arenas of social functioning) might be attributed to non-specific factors in the therapeutic relationships and instigative array of interventions used in the active therapy condition. As they point out, it may be appropriate to withhold an evidence-based attribution of the therapeutic benefits found in this study until a study is conducted with a comparison treatment equated for therapist enthusiasm, duration, time involvement, and other elements not specifically related to cognitive therapy.
Finally, one further cautionary note stems from the failure of the investigators to assess adherence to medication in the two treatment conditions. While the prescribed types and doses of medication did not differ between the conditions, it is well known that adherence to medication regimens is rather poor among persons with schizophrenia. Improved adherence to pharmacotherapy may have contributed to the superior therapeutic outcomes, given the fact that the therapists in the cognitive therapy program offered “personalized treatment” that included “laminated cards” and “colorful signs that patients posted at home to remind them of daily activities and other therapy assignments” which may have included concrete or implicit reminders to take their medication.
Salkovskis PM: Frontiers of Cognitive Therapy. New York: Guilford Press, 1996. Kingdon D and Turkington D: Cognitive Therapy of Schizophrenia. New York: Guilford Press, 2004.
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View all comments by Robert Paul LibermanComment by: Alan S Bellack
Submitted 10 November 2011
Posted 10 November 2011
Grant and colleagues are to be congratulated on their noteworthy trial. Anyone who has conducted clinical trials with seriously ill schizophrenia patients must be impressed by the ability of the research team to recruit a large cohort in an intensive treatment and keep them engaged over such a long period of time. The team also deserves credit for demonstrating that a psychosocial intervention can have a meaningful impact with this population. Added to the increasing literature on cognitive therapies with schizophrenia patients, and on recovery-based interventions, this report reinforces the argument that people with schizophrenia can and should be engaged as partners in the treatment process.
In a previous post, Bob Liberman identified a number of crucial limitations of this trial that raise questions about the findings and limit enthusiasm for the intervention. I concur with almost all of Bob's observations and analysis. The primary outcome variable (the GAS) has marked limitations and does not provide objective or detailed information about any changes in social or occupational functioning in the community. Thus, the authors' conclusion that "cognitive therapy can be successful in promoting clinically meaningful improvements in functioning" is not supported by the data. We simply do not know much about community functioning beyond what the patients report, and the reports are especially suspect given that subjects receiving the cognitive therapy attended weekly sessions with a study therapist in which a primary focus of discussions was enhancing community activities and role functioning. A related concern pertains to the course of change noted on both the GAS and SANS ratings. The graphic representation of the data indicates that most, if not all, of the change manifested across measures occurred before the first (six-month) assessment. This raises questions about the operating mechanism of the CT intervention, as well as the value of the succeeding 12 months of treatment. As stated in the article, "Early sessions focused on engaging the patient and strengthening the therapeutic relationship." This implies that any changes induced during that early period may have resulted from non-specific effects rather than any specific cognitive therapy activities. Given that (almost) no community program could afford to administer a weekly individual treatment for 18 months, it should be underscored that at best, the data do not support anything beyond six months of treatment.
Another important issue noted by Liberman was the multifaceted composition of the CT intervention. It included elements of cognitive therapy, skills training, behavior therapy, motivational enhancement, and cognitive remediation, among others. In fact, it is difficult to justify calling the intervention "cognitive therapy" when so little of it entails cognitive therapy per se. While most of the elements have face validity and independent empirical support, the resulting combination has two significant limitations. First, it is impossible to determine the active components of the treatment. Second, it would be virtually impossible to replicate or disseminate the intervention. This latter point is of particular concern, as the trial has been reported in the media (e.g., The New York Times) as demonstrating that cognitive therapy is effective for schizophrenia patients with negative symptoms. To the contrary, this trial does not demonstrate that CT is effective for reducing negative symptoms, or that CT is a cognitive therapy.
In sum, this is an important trial that should and will have an important heuristic role for the field. It is a trial that should have been done and probably could not have been done by any other research group. While acknowledging and applauding its strengths and value for the field, it is important to consider its limitations and be cautious about what conclusions can be drawn from the results.
View all comments by Alan S BellackComment by: Paul Grant
Submitted 31 January 2012
Posted 2 February 2012
We thank Professors Liberman and Bellack for their thoughtful critiques of our work and welcome the opportunity to answer their questions and concerns, and thereby clarify our study beyond the space limitations of the original paper.
Liberman and Bellack express several concerns regarding the number and types of techniques employed in therapy, as well as the length of therapy. Liberman states that our therapy is “confounded” with other treatment approaches because the intervention contains many treatment techniques (e.g., skills training, cognitive remediation, motivational enhancement) that overlap with other psychosocial treatments for schizophrenia; Bellack indicates that he does not believe our treatment should properly be called “cognitive therapy” because “so little of it entails cognitive therapy per se.” We appreciate that they have raised this issue because it affords us an opportunity to explain in greater detail why we use the term cognitive therapy and what we mean by it.
Our formulation of cognitive therapy is based on the cognitive model of schizophrenia (Beck et al., 2009) rather than specific techniques. Basically, we view the low-functioning problems in these patients as due to the interaction of neurocognitive deficits and negative attitudes about performance and social relations. Our basic research has shown both in cross-sectional (Grant and Beck, 2009; Grant and Beck, 2009) and longitudinal (Grant and Beck, 2010) studies that these low-functioning patients have very powerful negative attitudes about the possibility of achieving any goals (e.g., “there is no point in trying because I will only fail”), as well as negative attitudes about the desirability of social contact. In non-technical terms, these patients have given up and have walled themselves off from usual activities of everyday life because of their expectations that they are only going to fail if they try something. While there evidently is an upper limit on how much they can achieve due to their neurocognitive deficits, they do have considerable latent capacity that they are not utilizing. Since the negative attitudes seem to account for their loss of motivation, we use a variety of methods to ameliorate them. Since we frame the problems in cognitive terms, and our understanding of each case is based on a cognitive model, we utilize the term cognitive therapy. We would, therefore, expect that any change would be mediated by cognitive variables. To produce this change, we formulate each case in terms of the individual’s goals and identify the various obstacles to reaching these goals. We select specific techniques ranging from skills training, problem solving, explicit cognitive restructuring, etc., to overcome these obstacles. If the patient is blocked by social inhibition, we use assertiveness training; if the problem is fear of failing, we use cognitive restructuring. According to our thesis, each specific successful experience tends to undercut the negative attitudes that sap the patient’s motivation. Support for our formulation is based on an experimental study which showed that success experiences not only modify negative attitudes, but increase motivation and performance (Perivoliotis et al., 2011). Once the patients start to modify their attitudes, they become more engaged in real life and begin to take advantage of various rehabilitative services that are offered. The question of when and how to apply these strategies is described in the volume by Perivoliotis, Grant, and Beck (Perivoliotis et al., in press).
The multifaceted nature of our CT intervention prompts both Bellack and Liberman to wonder about the mechanism of change. In response to Bellack’s concern that it would be impossible to determine the “active ingredients” of the treatment, we propose that the beliefs targeted by the formulation-driven interventions are producing change. Mediation analysis (beliefs as mediators) would allow us to test this hypothesis. Liberman, in a similar vein, proposes several alternative explanations for our results: behavioral methods, social anxiety, positive symptoms, and medication adherence. He also proposes that, since we did not observe changes in alogia, we did not really affect social functioning. In regard of this last point, we think it is notable that the mean alogia ratings were in the questionable to mild range at baseline and remained in this range throughout the course of the trial. This finding suggests that if improvements were made, it is unlikely that they would be clinically meaningful due to a floor effect.
Additionally, it does not seem likely that the global improvement in the patients’ functioning was due to compliance with medication, since previous research has shown minimal impact from medication (Swartz et al., 2007). However, if medication compliance was improved, this would indicate a positive result from our multifaceted intervention. A similar argument extends to positive symptoms and social anxiety. Finally, while it is possible that behavioral methods could be the mechanisms of change in our study, it is also possible that cognitive change is produced by social skills training and cognitive remediation. We think that exploring beliefs in psychosocial treatments for schizophrenia is a rich area to pursue.
Bellack makes three final points regarding the CT treatment: he questions whether it would be possible to “replicate or disseminate the intervention”; he proposes that our data do not support providing more than six months of CT; and he suggests that “all of the changes induced during that early period may have resulted from non-specific effects rather than any specific cognitive therapy activities.” In regard to dissemination, we have already successfully trained masters-level community therapists in the manualized intervention, and have applied for funding to conduct a systematic study. As to the length of treatment, 50 sessions was the average for the entire group in the study: some participants completed therapy in fewer sessions and some required more. Thus, consistent with an individualized recovery orientation, we argue that some patients can benefit from shorter course of therapy whilst others will require more sessions. This is a matter for future study. And, in regard to non-specific factors, the best way to test this alternative hypothesis is to conduct a new study that compares CT to a supportive therapy control group.
Turning to the methods of the study, both authors are concerned about the measurement of functioning in our study. Liberman states that we did not use a well-established and psychometrically sound assessment instrument measuring social functioning for inclusion, while Bellack and Liberman both criticize our outcome measure as inadequate. We did not specifically describe social functioning as a key outcome, but rather global functioning. The Global Assessment Scale (GAS) was a conventional measure of global functioning at the time we initiated our study. Since that time, new measures have been developed, such as the Schizophrenia Objective Functioning Instrument (SOFI; Kleinman et al., 2009), and research by Phil Harvey’s group (Harvey et al., 2011; Leifker et al., 2011) has indicated that the preferred measure of functioning is the Specific Levels of Functioning scale (SLOF; Schneider and Struenging, 1983). In our next study, we plan to use the SLOF as the primary outcome measure.
Liberman proposes that our sample may not have been composed of patients with primary negative symptoms. In other words, the patients in the study had negative symptoms that were secondary to positive symptoms, with the observed improvement in negative symptoms being produced by improvement in positive symptoms. We did not formally assess primary versus secondary negative symptoms in the clinical trial. However, clinically, we observed that defeatist beliefs occurred independently of the presence of positive symptoms. And, as the beliefs were modified by the CT treatment, patients improved.
Finally, Bellack suggests our data do not support the conclusion that “cognitive therapy can be successful in promoting clinically meaningful improvements in functioning.” We disagree with his inference. We believe the intervention, by whatever name, produced successful results, as was evident in the collateral reports factored into the ratings of functioning.
The authors wish to acknowledge the contributions of Drs. Jessica Murakmi-Brundage and Yael Perry in developing this response.
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View all comments by Paul Grant