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Psychotic Disorders - Science topic

Psychotic Disorders are disorders in which there is a loss of ego boundaries or a gross impairment in reality testing with delusions or prominent hallucinations. (From DSM-IV, 1994)
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By Trialogue, I mean Trialogue events like the Psychosis Seminar or the Borderline Trialogue in the field of social psychiatry.
How would you theoretically underpin the Trialogue? Which theories would you use?
And specifically, from the perspective of Clinical Social Work: with which theories would you connect the Trialogue?
Thanks a lot!
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The Trialogue approach in social psychiatry can be theoretically underpinned by various theories that emphasize community engagement, empowerment, and collaborative learning. Social constructionism, participatory action research, and recovery-oriented models are relevant frameworks.
In Clinical Social Work, connect the Trialogue to ecological systems theory, emphasizing the interplay between individuals, communities, and institutions. Incorporate strengths-based perspectives and person-in-environment theories to enhance understanding and intervention.
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The psychosis (break from reality) known as schizophrenia involves symptoms such as paranoia, trouble thinking logically, socially unusual behaviour, and suicidal thoughts. The “hollow mask illusion” is a common visual misconception that causes most healthy people to view the concave side of a mask as though its features were convex or sticking out in their direction. This illusion occurs because we fill in the hollows with our expectations, accumulated over a lifetime of observing and committing to memory convex faces. Curiously, people with schizophrenia see the hollow mask as just a hollow mask and have an increased ability to see hidden patterns in reality (“The Faulty Weathermen of the Mind” – Nautilus magazine, Issue 52, Page 59 – reporting the neuroscience of Paul Fletcher and Christoph Teufel.)
Many researchers believe that psychosis actually exists as a continuum, that the general population exhibits varying levels of susceptibility to it, and that these manifest in ways that do not greatly disturb the healthy person’s functioning. While full-blown psychosis or schizophrenia is obviously incompatible with a breakthrough like physically uniting everything in both space and time, a trace of it – a tiny, unrecognizable hint of its symptoms – may be vital to intuiting how unification works ie what was previously referred to as “increased ability to see hidden patterns in reality”. The hormonal and biochemical changes in the brain which accompany this barest trace of the condition conceivably result in insights into the nature and connectedness of space-time.
While this speck of psychosis would possess the great benefit of allowing discernment of the so-called “secrets of the universe” and “the mind of God”, it’d also produce problems like intermittent delusions of persecution and awkward – even totally unacceptable – social interactions. Perhaps the most well-known example in science of unacceptable interactions is Isaac Newton’s hostility towards, and clashes with, other academics. I wouldn’t be surprised if he often regretted his own hostility. Despite the tendency to be harsh and inhuman, my World Book encyclopedia says he had a sensitive nature which, besides aiding his scientific pursuits, manifested as great generosity to his nephews and nieces.
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Mental health issues definitely mirror human societies Rodney Bartlett The unifying aspect are chronified moods, which lead to certain mental pathologies and reflect human suffering in respective societies. The universal aspect may be that these societal moods are non-simultaneous, in terms of social stages of human development and medical psychology.
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Hello everyone,
I am planning to design a model that can predict individuals with high or low psychosis-proneness by looking at the brain connectivity measures in 114 regions, age, gender, IQ, SES, polygenic risk score for psychosis (PRS), and environmental risk score for psychosis (ERS). In this way, I am planning to investigate the brain regions that serve to distinguish high and low psychosis-proneness by using machine learning. However, my sample includes healthy twin and sibling data; hence, my data is not independent. I could group the sample into high and low psychosis-proneness based on weighted positive symptom severity.
Therefore, I would like to ask whether there are any codes or approaches that you can share with me.
My data looks like the image I shared (I did not add the PRS since I do not have the information yet).
Thank you for your help!
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Hello everyone!
It is not an answer to my question above. However, I found a beneficial pdf from an NCFR Workshop by Xiaoran Sun. When I looked for the answer to my question, I thought it would be helpful to understand the machine learning algorithm with family data.
Best!
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As often in medicine animals are ( SADLY) used in experiments .A new study of mice shows there are important links between human and mouse minds in how they function -- and malfunction. Researchers at Washington University School of Medicine in St. Louis devised a rigorous approach to study how hallucinations are produced in the brain, providing a promising entry point to the development of much-needed new therapies for schizophrenia.
The study that was published in the journal Science, lays out a way to probe the biological roots of a defining symptom of psychosis: hallucinations. The researchers trained people and mice to complete a computer-based task that induced them to hear imaginary sounds. By analyzing performance of the task, the researchers were able to objectively measure hallucination-like events in people and mice.
This approach allowed them to study the neural circuits underlying hallucinations, potentially fully opening up the study of mental illness to the kind of scientific studies that have been fruitful for diseases of other parts of the body. My concern is that despite the positives and even if there are similarities, can a study like this be of great value when it comes to humans who has a fundamentally different cognitive ability and brain structure? I agree that we can see tendencies and the study gives an insight, however can this ever fully be transferred to humans? also see other risks as well as grave ethical concerns that applies with all experiments on animals. What are your thoughts?
Best wishes
Henrik
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The comparative study of living organisms is standard laboratory practice, e.g. the knowledge transfer of animal experiments to humans. Concerning psychiatry, this may be the human medicine par excellence, and I personally (and methodically) doubt that, in this case, the results of veterinary medicine can be applied to humans successfully.
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There are many reports of psychosis in patients who have symptomatic COVID-19 disease. Usually there is no past psychiatric history and onset of psychosis seems sudden within first few weeks. How long should the antipsychotic used if initiated in first place?
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The psychoses that appear due to Covid-19 - which are not "Dementias" - are fortunately rare and of the "toxic" type (Psychosis of toxic and / or infectious etiology) and, therefore, their treatment is the same as in the rest: Combat and eradicate the somatic cause that originated them and, if necessary, the use of neuroleptics, controlling the possible extrapyramidal effects, and "ad hoc" psychotherapy.
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High expressed emotions is a major determinant of psychiatry disorder prognosis. Especially when it comes to schizophrenia. Research suggests that being in a developing country has better prognosis in psychosis. Partly due to low levels of EE. Is it still a truth ? Do we have enough evidence to prove this fact ?
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Thanks Sarah for your beautiful answer
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Although the relationship between alexithymia and primary psychotic disorders (e.g. schizophrenia) has been studiedad, I have had difficulties in finding any research on alexithymia in patients with schizophrenia that also have any substance use disorder. Someone knows any publications on this issue?
Thank you,
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I sincerely request all the experts working on schizophrenia to provide their valuable explanations/views on the above topic.
My concern is that PCP, MK-801, and ketamine are anesthetics, these drugs induced unconsciousness (sleep) whereas schizophrenia patients are hyperactive and do not sleep properly.
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Dr. Khan, there is such a thing as dose dependence. The above drugs are aenesthetics at substantially higher doses than they are as dissociative hallucinogens. In any case, the NMDA model of schizophrenia is still a better one than that of amphetamine 'psychosis', which does not resemble schizophrenia at all. I anticipate there may be others who comment that the depressant effects of the above drugs resemble the negative or catatonic symptoms of schizophrenia, but that is too hand-wavy and speculative for me.
The fact is that you are right to be concerned! The idea that drugs (with a variety of systemic effects on multiple receptor systems) can be a good model for a complex brain disorder should be approached with much skepticism.
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Melancholic depression is a form of depression that should be considered separately from other forms of depression. I'm interested in why this is the case? How are the mechanisms different from other forms of depression? In addition, considering the severity of the symptoms (e.g. psychomotor, psychosis (in some cases), poor concentration, slowed speech, lack of concentration) is it worth increasing physical activity levels or altering diet? Anyone performed research in this area?
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You might want to refine your question by looking at how treatments differ for male versus female clientele. Causes for dysthymia in males tend to come from struggles with identity and gender role and as such should be treated with those factors in mind. Physical activity is often effective; particularly when combined with other males suffering from similar disorders.
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Basically I`ve done a review of the literature on disengagement from Early Intervention Psychosis services using systematic methods. There was heterogeneity across the studies, no RCTs and I`ve used `vote counting` to make sense of the results
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According to Cochrane's handbook, there are two main concerns about using vote counting to make sense of results: by considering each study on its own you are not allocating different weight to them, and too much emphasis is given to significant/not-significant, without considering range of effects (e.g., CI) (https://handbook-5-1.cochrane.org/chapter_9/9_4_11_use_of_vote_counting_for_meta_analysis.htm)
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GABA- ergic interneurons are responsible for sinchronization of different neural networks ( provide balance in excitation and inhibition) in brain cortex. If there is a disruption of this balance, via excitotoxic degeneration in interneurons, are positive symptoms in schizophrenia a result of released improper activity of neural networks ? Vulnerability for excitotoxicity depends on our congenital conditions ( gene polymorphisms, enzyme conditions, et c.), maybe so, vulnerable people, prone to interneuron disturbance during first episode lose this balance and exhibit psychosis, which leads to connectopathy and brain degeneration?
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Requested 👌
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Thank you / Theresa
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It's good question Theresa.
Adding AP is safe. Sometimes I do that.
But decision is taken on the basis of complete diagnosis, I.e. if (1) It's Bipolar disorder with mood congruent or mood incongruent psychosis, then AP along with mood stabilisers is opted. If (2) it's OCD or OC Spectrum disorder with psychosis , then along with SSRI mild AP or low dose AAP is ok, if (3) it's Dysthymia with m c or m in c psychosis then add on AP will always help, if (4) it's Post parturial depression then AP addition need to be judiciously executed, if (5) it's overwhelming psychotic episode or aggressive behaviour or abnormal behavior, or with history of recurring such episodes in past then AP is a inevitable, if (6) it's with history of benzo. abuse or h o subs. abuse then also AP would be selected with priority along with Anti depressants, mood stabilizer, benzodiazepines, etc.
Other than plain pharmacotherapy, in all such patients Psychotherapy , may be integrated or solution focused or client oriented or DBT or CBT or simple psychoeducation in highly psychotic patients, or family therapy's psychoeducation session, etc takes or should take 1st seat in order of measures of intervention.
Psychotherapeutic intervention cannot be avoided.
😊
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Infectictous, metabolic, endokrinological, toxic, drug abuse, ect.
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Neuropathy is equivalent to computer CPU hardware malfunction, psychosis is equivalent to software malfunction. In my opinion, people's mental and psychological activities are a set of programs, which are similar to computer programs. Psychosis is a disorder of procedure. Enclosed are my papers on this subject
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As aripiprazole, brexpiprazole, and cariprazine are partial-dopamine agonists with potent binding affinities to the D2 receptor, do they prevent augmentation effects (or worsen psychosis) when two or more antipsychotics are combined?
Certainly, there is data suggesting worsening psychosis when aripiprazole has been added to other agents (Takeuchi and Remington, Psychopharmacology 2013). Additionally, the idea of competitive inhibition is supported by the reversal of hyperprolactinemia when aripiprazole is added to another antipsychotic.
I can find no data of this phenomenon occurring yet with brexpiprazole or cariprazine.
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Drugs work best when they are new. Hence the adage, "Be quick to use this new medication before it stops working!"
Problems of low efficacy and adverse effects take time to emerge.
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But, would not be better in the case of psychosis to talk about increased dopamine release instead of increased dopamine synthesis capacity, if we do not know directly, whether the hyperdopaminergic striatal state is caused by increased dopamine synthesis or only by increased dopamine release or even disruption of termination of synaptic dopamine action (https://www.ncbi.nlm.nih.gov/pubmed/?term=Putative+presynaptic+dopamine+dysregulation+in+schizophrenia+is+supported+by+molecular+evidence+from+post-mortem+human+midbrain)?
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@Michal Patarak. Indeed, to my knowledge every theory about psychosis is somewhat related to dopamine. And, I would suggest to the SEEK system. The antipsychotic action of clozapine, then would seem at the moment unexplained.
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I am currently looking into developing a tool which can be used clinically with young people 14yrs-25yrs who may present with both suspected ASD and psychotic symptomology. Before i begin i though it could be helpfuul to see what is already available.
Any information or pointers would be most helpful.
Thank you in advance
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Hi Lorraine, we wrote a paper on this topic in people with intellectual disability which might be useful? Here is the link, I'd be happy to share the paper:
Best wishes, Verity
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It is my understanding that from a Kraeplinian perspective, and as outlined in the DSM-V and ICD-10, cognitive dysfunction is one of the fundamental diagnostic criteria for schizophrenia, schizoaffective, and affective psychosis.
I have recently been reviewing literature regarding attempts to outline dimensional or spectral criteria for schizophrenia and other psychotic disorders. What I have taken to be the majority consensus is that it may be reasonable to postulate a schizophrenia spectrum disorder which incorporates schizophrenia, schizoaffective disorder, and affective psychosis. This view seems to generally include the caveat that it would not be reasonable to go further and propose a psychotic spectrum disorder since this would lead to the inclusion of etiologically distinct disorders such as psychosis NOS, psychosis in dementia, and drug induced psychosis.
I was curious if it would be plausible to conceptualize schizophrenia as a comorbid condition, which one could describe as “persistent psychosis with cognitive impairment” (PPCI), rather than its own entity which is distinct from other psychotic disorders. This conceptualization would permit for a possible shared etiology underlying psychotic disorders (i.e. the “psychotic core”) by placing schizophrenia along the broader psychotic axiom. To avoid overinclusion, one could assess the phenomenological characteristics of psychotic experiences associated with other disorders to differentiate symptoms which result from a “psychotic core” from psychotomimetic symptoms that are secondary to another disorder and have a separate etiology. For example, if the presence of psychosis in dementia does in fact have its own unique neurological mechanism (as compared to say schizophrenia), it would make sense to assume that it also possesses unique phenomenological qualities that could be differentiated.
This small distinction would have significant clinical implications. Since it has been shown that cognitive impairment is the most significant determinant of poor prognostic outcome in schizophrenia, conceptualizing this as a separate symptom would merit a dual approach to therapeutic intervention in which the positive and cognitive symptoms should be addressed differentially. This could be accomplished by combining therapeutic approaches, given the existence of interventions which are specific to targeting either positive symptoms or cognitive impairment. I would imagine this would also have implications for how samples are defined (i.e. construct validity) in research methodology.
If anyone reading this can understand my train of logic and would be able to provide some insight or relevant literature, it would be greatly appreciated.
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The question if psychoses are a continuum or they are not is very old and intriguing. The problem of your proposal, it s that the schizophrenia is not just persistent but sometime remittent-intermittent and the cognitive impairment in my view is not so typical and omogenous. It seems more an impairment of the personality with different aspects, sometime frankly demential, sometime a subtle shrinking of social abilities.
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Hello,
I have a question about treatment protocols and standardization of services in mental health care in the US. I am aware of numerous treatment guidelines and recommendations that have been published, for example by SAMHSA, WHO, NICE, etc. However, it would seem that theses materials function more or less as suggestions rather than as actual standard procedures.
What I would like to locate is data on the services provided in either the treatment of chronic schizophrenia or in the case of first episode psychosis. Specifically, I would like to find information on the treatment plans which are actually constructed and used in routine clinical practice. My suspicion is that there is a significant gap between the quality of services actually provided and those which have been recommended.
This question stems from a perceived overreliance on psychiatric drugs in treating psychotic disorders as well as from the recognition that there seems to be a persistent lag between psychopathology research and clinical practice. This can be seen in our current models of mental illness which is still heavily rooted in the biomedical model dating back to its initial rise to power in the 1950's. And while clinical practice still holds these views as the dominant model in the field, a recent push back against medicalization has gained popularity amongst researchers, and with it, a renewed interest in psychosocial models of treatment.
This leads me to another question about treatment standards for psychotic disorders. If you consider the poor prognosis despite available medication and the generally pessimistic attitudes toward the effectiveness of psychotherapy for psychosis, one would imagine that the development of innovative psychosocial therapies would be of great service to the unmet needs of this population. Accordingly, the literature would suggest that there has indeed been growing interest in this endeavor, and a number of therapies designed specifically for psychosis have been gaining attention. Of these approaches, a few notable examples include Metacognitive Training, ACT for psychosis, AVATAR therapy, Voice Dialogue Therapy, and IMR, among others.
So the question remains, why does it seem that CBTp is still the only intervention regularly employed in mental health care services? (I would also be interested to know how the rates of providing CBTp compare to the use of psychiatric drugs proportionally) Where is it that these alternative therapies are actually being made available to patients, and if they are not, by what process and on what timeline will they become available?
Any input on these matters would be appreciated. I would be particularly interested in locating actual statistical data on these practices. These seem to be important questions to consider, especially if my suspicions are true. From my perspective, the bias resulting from the overemphasis of a biomedical model in conjunction with a lack of enforcement of standardized protocols leads to an environment which carries significant risk of resorting to ineffective, poor quality services.
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I follow the question
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Benign hallucinations are usually non-threatening hallucinations in patients with Parkinson´s disease associated psychosis, in which the patient has a well-preserved sensorium and is aware of the hallucinations.
Minor hallucinations are: 1. a sense of presence hallucinations, which are characterized as a vivid feeling that somebody or an animal is closely present when in reality it is not. 2. Passage hallucinations are described as a person or a animal quickly passing in the peripheral visual field.
These terms are more used by neurologists as by psychiatrists.
Do you use them?
Do you also use them outside the context of Parkinson's disease?
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In Germany, neurologists have to spend one year of their specialty training in psychiatry. Besides specialty issues, questions of national or regional traditions in terminology may also arise.
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DSM-5 (2013) defines anhedonia in schizophrenia spectrum and other psychotic disorders as "the decreased ability to experience pleasure from positive stimuli or a degradation in the recollection of pleasure previously experienced."
If so, and if there is anhedonia in relation to the presence (consummatory anhedonia), and in relation to the future (anticipatory anhedonia), is there any anhedonia in relation to the individual's past? And how we can name it?
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i wish I could answer your question directly but I am not sure if there is such a phenomenon "anhedonia inn relation to the past". This resource might prove helpful in your pursuit here is the link and I attached the document. https://www.frontiersin.org/books/Reward_Processing_in_Motivational_and_Affective_Disorders/1023
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Caffeine is an antagonist of A2A adenosine receptors that are coupled to D2 receptors in striatally located heteromers. Antagonism on A2A has a similar effect as D2 agonism, so the dopaminergic effect (and also a psychostimulating one) of caffeine is mediated precisely by this mechanism. But is caffeine itself strong enough to cause psychosis?
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Thank you! It is really a very interesting and complex topic.
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From the Beatles to Bob Marley, David Hockney to Duke Ellington, artists and musicians alike have long credited cannabis with enhancing creativity. In psychiatry however, cannabis is known to be associated with an increased incidence of psychosis and schizophrenia. Does cannabis enhance creativity? And is this related to the drug’s ability to induce psychosis? Is there any research that provides empirical evidence that cannabis increases creativity that you would suggest? Are psychotic symptoms and creative outbursts mutually exclusive? Any papers/articles/meta-analyses on the topic would be highly appreciated!
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Yes. It enhances creativity, but reduces productivity.
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I am seeking databases that includes variables for women that have been diagnosed with postpartum psychosis or postpartum bipolar disorder or major depressive mood disorder with psychotic features in the first year postpartum.
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Thank you so much....
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There is some research indicating possible mitochondrial dysfunction in Psychosis.  Currently a client with psychosis has been given melatonin  for sleep in combination with therapies done by myself - Cognitive restructuring, talking to voices and cognitive therapy. This was after ALL normal (medical and psychotherapeutic) treatments had been applied for a 2 year period with little success before I received the client. The only two differences in treatment was talking to voices and melatonin prescribed by the doctor. Naturally this is not enough to propose that melatonin may have an impact, however there was a distinct improvement in cognitive processing abilities. Has anyone done any trials or research on the use of melatonin. Studies suggest that melatonin may or may not partially or fully repair mitochondria, whilst no research has been found on the possible utilisation of Gh.
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Some research from my area of interest (gynecologic psychosomatics): Anderson G. The role of melatonin in post-partum psychosis and depression associated with bipolar disorder. J Perinat Med. 2010 Nov;38(6):585-7. doi: 10.1515/JPM.2010.085 and from the area of general psychiatry: van Beveren NJ, Schwarz E, Noll R, Guest PC, Meijer C, de Haan L, Bahn S. Evidence for disturbed insulin and growth hormone signaling as potential risk factors in the development of schizophrenia. Transl Psychiatry. 2014 Aug
26;4:e430. doi: 10.1038/tp.2014.52. FULL TEXT)
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My program is experiencing an influx of re-referrals. Our assessments are showing that their cognitive levels have dropped to levels seen prior to beginning the first round of treatment. Has anyone else experienced this? 
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Is this not to be expected.
Was there any ongoing reeinforcement? .Did you examine the factors which have have changed since the first treatment? There are many possible inhibitors and promoters of effectiveness such as self-confidence.. And what of outside circumstances (like coping with institutionalization or physical disablement) drastically changing?  How long did you expect CR to be effective? Did you consider it permanent?
Did you read the following?:
Clark, D. A. 2013. Cognitive Restructuring. The Wiley Handbook of Cognitive Behavioral Therapy. Part One:2:1–22.
Beck's cognitive therapy (CT) has made a substantial contribution to current evidence-based cognitive behavioral therapy (CBT) for a variety of psychiatric disorders, most notably depression, anxiety, personality disorders, and, more recently, psychosis. A. T. Beck's (1987, 1996) cognitive model postulates that biased self-relevant thoughts, evaluations, and beliefs are key contributors to the development and persistence of psychopathological states. The biased thoughts and appraisals that characterize psychopathology are derived from maladaptive mental representations of reality stored in memory structures called schemas. Schematic content or beliefs organize and guide the selection, encoding, and retrieval of information. Given their central role as progenitors of a biased and maladaptive information processing apparatus, the cognitive model considers schematic change essential for significant and enduring symptom reduction (A. T. Beck, Rush, Shaw, & Emery, 1979; D. A. Clark, Beck, & Alford, 1999).
The term cognitive restructuring has been used to describe the schematic change mechanism articulated in CT. It refers to a structured, collaborative therapeutic approach in which distressed individuals are taught how to identify, evaluate, and modify the faulty thoughts, evaluations, and beliefs that are considered responsible for their psychological disturbance (Burns & Beck, 1978; Dobson & Dozois, 2010; Hollon & Dimidjian, 2009). In their first seminal treatment manual, Beck and associates emphasized thought self-monitoring, reality testing, external reattribution, evidence gathering, examining consequences, cost/benefit analysis, generating alternatives, and behavioral assignments as key interventions for inducing cognitive change (A. T. Beck et al., 1979). However, A. T. Beck did not refer to this suite of interventions as cognitive restructuring until the publication of his second treatment manual for anxiety disorders (A. T. Beck & Emery, 1985). Since then, various descriptions of CT have referred to the cognitive interventions utilized to achieve schematic change as cognitive restructuring (e.g., D. A. Clark & Beck, 2010; Dobson & Dobson, 2009).
In this chapter, cognitive restructuring (CR) is defined as structured, goal-directed, and collaborative intervention strategies that focus on the exploration, evaluation, and substitution of the maladaptive thoughts, appraisals, and beliefs that maintain psychological disturbance. Within this definition both cognitive and experiential or behavioral interventions are considered CR as long as the intention is cognitive or schematic change. The remainder of the chapter provides an in-depth examination of CR. I begin with a conceptual analysis of schemas and the three key components of CR. This is followed by a review of empirical research that has attempted to isolate the specific therapeutic efficacy of CR. The chapter concludes with a discussion of critical research issues pertinent to CR.
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The Nature of Cognitive Restructuring
Defining Schematic Change
Since CR is defined in terms of schematic change, a conceptualization of CR is rooted in the definition of schemas. In A. T. Beck's cognitive model schemas are meaning-making constructions of the cognitive organization that have content, structure, and function (A. T. Beck, 1964). They embody top-down processing in which schema-driven processes select, organize, and prioritize human cognition. In essence schemas have an executive function, directing information-processing resources so that schema-congruent information has priority over schema-incongruent information. In depression, for example, negative self-referent schemas of loss, failure, rejection, and hopelessness predominate. As a result the cognitive apparatus of the person with clinical depression is oriented toward processing schema-congruent negative self-referent information.
A key goal of CR, then, is to reverse this maladaptive schema-congruent processing bias by questioning the automatic acceptance of negative schema-congruent information and encouraging assimilation of more adaptive schema-incongruent data. Traditionally, a change in belief ratings is considered a measure of the client's shift from maladaptive schematic processing to more normal, adaptive schema activation (A. T. Beck et al., 1979). Thus a depressed client, in the course of therapy, demonstrates a reversal in depressotypic schema-congruent processing bias when he or she professes diminished belief in the view “I am a complete loser who will never amount to anything,” and greater belief in the idea “I have had some failures in my life but also many successes; this means I can learn from my failures and forge a brighter future for myself.” However, it is not clear how well this indicator of change applies to CR more generally. Belief ratings may be a less sensitive indicator of cognitive change for some disorders, such as anxiety, and reversal of the dominance of maladaptive schema-congruent processing is far from a monotonic, linear decline in absolute influence, as any practitioner can attest. Rather, clients often exhibit a more fluctuating pattern of shifting schematic processing that is influenced by circumstances and even mood state, with symptom improvement associated with an eventual dominance of adaptive schematic processing over the maladaptive disorder-related schemas. It must also be recognized that long-term dominance of maladaptive schema-congruent processing in distressed individuals poses special challenges for CR because these beliefs will always seem more intuitive and inherently plausible to the individual. The more entrenched the maladaptive schematic organization, the less responsive they are to initial CR efforts.
As well as executive function, schemas also have structural characteristics. A. T. Beck (1967) noted that maladaptive schemas are inflexible, closed, impermeable, and relatively concrete systems. Most often they are rooted in negative, or even adverse, early childhood experiences and are subsequently reinforced and strengthened by congruent life events in adolescence and adulthood. For example, the person with an obsessive-compulsive personality disorder will have experiences that appear to confirm his or her belief that “It is critical that I pay close attention to detail in all that I do in order to avoid making mistakes.” With repeated activation and reconfirmation, the maladaptive schemas attain a higher degree of interrelatedness so they gain greater capability of dominating the information processing system (Segal, 1988). Various studies have investigated schematic structure in depression. Using a grid task to assess schematic structure, Dozois and Dobson (2001) found that a clinically depressed group had more interconnectedness for negative self-referent adjectives and less interconnectedness for positive adjectives than nonpsychiatric controls, although the anxious and depressed groups differed primarily in their organization of positive, rather than negative, schemas. In a later study, Dozois (2007) found that clinically depressed individuals may exhibit more interrelatedness of negative interpersonal but not achievement schemas that endures even with remission of the depressive state.
The very structure of psychopathological schemas and their inherent prepotent nature makes schematic change especially difficult to achieve. In the course of conducting CR, most clients will have great difficulty recognizing schema-incongruent information, questioning their intuitively based maladaptive schemas, and accepting more adaptive beliefs. For the individual with health anxiety, the automatic maladaptive interpretation “What if the red spot on my arm is cancerous?” will feel more intuitively plausible because of underlying rigid, highly interrelated, and generalized dysfunctional schemas about death, disease, and vulnerability. Cognitive therapists using CR, then, must build into their intervention plan recognition of the relative impermeability of psychopathological schemas.
It is schematic content that is the primary focus of CR. The content or propositional elements of maladaptive schemas consist of negative idiosyncratic generalized attitudes, beliefs, and assumptions about the self, personal world, future, achievement, and interpersonal relations (Dozois & Beck, 2008; Ingram & Kendall, 1986). A. T. Beck (1976, 1987) proposed that different psychopathological conditions, as well as normal emotion states, are characterized by their own unique belief content. Known as the content-specificity hypothesis (D. A. Clark et al., 1999), the cognitive model proposes that depression is characterized by themes of loss and deprivation, anxiety by threat and vulnerability, each of the personality disorders by disorder-specific content, and psychosis by misinterpretation of subjective experience. This disorder-specific schematic content will be easily accessed by a wide range of triggering cues and readily available to guide information processing. Thus, the goal of CR is to modify schematic organization or interconnectedness, reduce the accessibility or activation threshold of maladaptive schematic content, and strengthen access to competing, more adaptive beliefs and assumptions.
In sum, the schematic change achieved by CR involves two fundamental processes. After identifying the key disorder-relevant schemas, the cognitive behavioral therapist utilizes a series of cognitive interventions to reduce the activation threshold, accessibility, and availability of the maladaptive schemas. Over time and with repeated effortful evaluation, the processing priority and interconnectedness of the maladaptive schemas are weakened and schema-congruent processing becomes less automatic. Second, CR also involves the process of learning to substitute more normal, adaptive schemas about the self, world, and future. Lowering the activation threshold and strengthening the accessibility and acceptance of competing adaptive schemas that counter disorder-related beliefs are critical objectives of CR. In the end, CR seeks to elevate normal adaptive schematic processing through evidence-based thinking so it comes to predominate the information processing system. It is through this process that CR achieves enduring symptomatic change and remission of the psychopathological state.
Key Components of Cognitive Restructuring
In order to achieve schematic change, an effective CR program has three critical components. Each of these components is necessary for the success of CR. If any component is missing, the intervention would not constitute CR but some other form of intervention. Each component may consist of various intervention strategies, but together collaborative empiricism, verbal intervention, and empirical hypothesis-testing constitute the therapeutic process involved in CR. The following provides an explanation and illustration of these three central elements of CR.
Collaborative empiricism
A. T. Beck and colleagues (A. T. Beck et al., 1979; A. T. Beck & Emery, 1985) introduced the term “collaborative empiricism” to describe the therapeutic relationship adopted in CR. The concept has been refined and elaborated by subsequent clinical researchers and is now considered a critical element in the effectiveness of CT or CBT (J. S. Beck, 2011; Kuyken, Padesky, & Dudley, 2009; Tee & Kazantzis, 2011). In essence, collaborative empiricism involves the client and therapist sharing their respective expertise in order to describe, explain, and help resolve the client's problems. In recognizing their respective contributions to the therapeutic enterprise, the therapist as an expert in the human change process, and the client as having the lived experience of the problem, work together on formulating treatment goals, setting the session agenda, and negotiating homework assignments. Therapist and client share equal responsibility for the direction of therapy, in which the therapist frequently seeks feedback and ensures understanding from the client.
A strong therapeutic alliance and client engagement in the therapy process is a necessary but not sufficient feature of effective CR. To achieve a collaborative atmosphere, the therapist (a) educates the client on the CT model to establish an agreed rationale for achieving change, (b) involves the client in identifying and prioritizing treatment goals, (c) collaborates on setting the session agenda, (d) asks questions and requests client feedback throughout the session, and (e) negotiates homework assignments. This strong emphasis on mutual responsibility and joint involvement in the therapeutic process ensures that CR does not become dictatorial, with the therapist imposing ideas and direction on the client. An authoritarian, overly didactic, and uncompromising therapist style will quickly undermine the effectiveness of CR.
Empiricism is another central feature of the therapeutic process in CR. The therapist encourages the client to take an investigative, questioning approach to long-held beliefs and attitudes. Throughout treatment, an emphasis is placed on observation, experiential evaluation, and learning (Kuyken et al., 2009). The therapist uses Socratic questioning of the client's past personal experiences to evaluate the validity of maladaptive beliefs and to introduce the possibility of a more adaptive alternative perspective. In addition, experientially based exercises are formulated that can empirically verify the veracity of the alternative belief and challenge the validity of maladaptive schemas. The cognitive therapist frequently encourages the client to “test this with your experience,” or “collect some evidence and see what can be learned.” Throughout each session the therapist places a strong emphasis on empiricism to achieve schematic change. Tee and Kazantzis (2011) argue that effective collaborative empiricism will encourage clients more readily to attribute behavioral change to their own efforts rather than external forces or the skills of the therapist. This self-determined attribution should result in better and more persistent treatment outcomes.
The importance of collaborative empiricism is especially acute when a therapeutic impasse arises. This can often happen in the treatment of the anxiety disorders, for example. Most clients seeking CBT for anxiety desire immediate relief from their heightened subjective anxiety. For them the goal of treatment is quite clear; the elimination of anxious feelings. However, CBT for anxiety involves exposure to anxious situations, intentional elevation of subjective anxiety, and a greater acceptance or tolerance of anxiety. In this case the client's and therapist's treatment objectives may collide. A strong emphasis on collaborative empiricism will be critical for overcoming these differences by helping the client identify and evaluate schemas that might threaten the effectiveness of CR (D. A. Clark, in press).
Verbal interventions
Over the years cognitive behavioral researchers and practitioners have proposed a number of verbal intervention strategies that can be used by therapists directly to modify maladaptive schematic content. These strategies, which in many respects are the essence of CR, are summarized in Table 1.
Table 1. Verbal Intervention Strategies Employed in Cognitive Restructuring
Intervention strategy
Description
1. Evidence gathering Obtaining schema-congruent and -incongruent evidence from the client's past and current experience that enables a more balanced evaluation of schematic content.
2. Consequential analysis Examining the immediate and long-term costs and benefits of continued acceptance of the maladaptive belief.
3. Cognitive bias identification Training clients in greater awareness of the cognitive biases that operate when processing schema-relevant information (e.g., dichotomous thinking, catastrophizing, mind reading, magnification/minimization, etc.).
4. Generate alternative Formulating a more adaptive conceptualization of the self or some aspect of personal experience that more accurately represents external contingencies and that enhances the client's functional adaptation.
5. Normalization Reconceptualizing unwanted thoughts, feelings, and behavior as deviations of normal human experience in order to encourage greater acceptance and confidence in dealing with schema-related subjective experience.
6. Decatastrophizing Developing a hypothetical account of a worst-case scenario, evaluating its realistic and probable effects on quality of life, and formulating a coping plan to deal with the catastrophe.
7. Problem solving Specifying a real-life problem, delineating the pros and cons of various responses to the problem, selecting a course of action, and evaluating the outcome.
8. Imaginal exposure Guiding the client in repeatedly and systematically generating a schema-related unwanted intrusive thought, image, or emotion in order to enhance client self-efficacy in dealing with unacceptable emotions.
9. Distancing Teaching clients to take a “third party” or observer stance to their unwanted thoughts and emotions; to react to their subjective experience as if it belonged to another person.
10. Reframing or perspective taking Focusing on current experience as a moment in time and situating it within a longer lifespan time frame or the totality of one's life experience.
11. Reattribution Identifying the external or situational causes of the client's difficulties in order to address exaggerated internal attributions and self-blame.
12. Positivity reorientation Refocusing the client on positive, adaptive personal coping experiences that provide schema-incongruent information.
The first four strategies are the most common verbal interventions used in CR, first introduced by A. T. Beck et al. (1979; A. T. Beck & Emery, 1985) in the original CT treatment manuals and then later refined and elaborated by other cognitive therapists (e.g., J. S. Beck, 2011; D. A. Clark & Beck, 2010, 2012; Dobson & Dobson, 2009; Greenberger & Padesky, 1995; Wells, 1997; Wright & McCray, 2012). Evidence gathering, cost/benefit analysis, identifying cognitive errors, and generating alternative explanations are such an integral part of CR that implementing these verbal interventions is what most therapists think of as cognitive restructuring. They are robust and versatile interventions that can be used in most clinical disorders. Since these strategies are well described in the sources cited, I will confine my comments to a few general observations.
In order to utilize any of these verbal interventions, clients must be willing to engage in an evaluative process. That is, they must be willing at least to consider the possibility that their maladaptive schematic thinking might be inaccurate, counterproductive, and unrealistic. Of course, clients will be considerably invested in retaining their schematic view of themselves and current circumstances, but there has to be a willingness at least to consider alternative perspectives. Clients who insist that their maladaptive beliefs are immutable facts will not be amenable to CR. Second, the therapist always begins by inviting clients simply to examine and evaluate their thoughts and beliefs in the light of empirical evidence, that is, their own personal experience. The therapist refrains from cajoling, debating, or trying to convince the client of a more adaptive alternative belief instead of clinging to the maladaptive schematic perspective. Rather, clients are encouraged to generate an alternative view that provides the best fit with “objective” external experience and would be associated with an improvement in their emotional functioning. Third, effective CR will ensure an equal emphasis on questioning the veracity of the maladaptive beliefs and evaluating the relevance of a more adaptive alternative viewpoint. The objective of CR is to raise doubts in the client's mind about long-held maladaptive beliefs (e.g., “People will notice I'm anxious and think there is something wrong with me”) and to consider the accuracy and utility of an alternative perspective (e.g., “People might notice I'm a little anxious but consider it unimportant”).
The remaining verbal interventions in Table 1 are more specific to particular clinical disorders or client situations. Normalization, for example, is used frequently in CR for anxiety in which clients are taught to view their distress as an extreme variant of normal emotion rather than as a distinct and disconnected experience. A client with health anxiety, for example, could be asked to describe other nonhealth situations in which he or she felt anxious and yet coped with the emotion very well (e.g., a job interview). The client could then be encouraged to think of his or her high anxiety associated with an unexpected physical pain in the same way that he or she thought of heightened anxiety during the job interview. In other words, the health anxiety experience is normalized rather than being considered a unique human experience.
Likewise, distancing encourages the client to consider his or her thoughts and beliefs from the perspective of another person, a third-party observer, such as a friend or work colleague. The therapist can ask the client to talk about his or her thoughts “as if they were the product of someone else's mind.” For example, a cognitive therapist might say to a client, “Imagine for a moment that your conviction, ‘I'll be alone and miserable the rest of my life’, is a belief expressed by a close friend. What would you think about her perspective on life? What would you say to her as an alternative way to view being single?” The goal of distancing is to teach the client to take a more external, observer orientation to disturbing thoughts and beliefs.
Reframing or perspective taking encourages clients to consider their emotional experience as a single moment in time and to view their current emotional state from a longer time perspective. This not only helps clients to “live in the moment” rather than the past or future, as emphasized in mindfulness cognitive therapy, but to view the present as one moment in a longer lifespan continuum. For example, a client with panic disorder who becomes completely immersed in his or her heightened anxiety while in a supermarket is encouraged to view this experience as one instance of hundreds of experiences that comprise a typical week. A person with social phobia is asked to consider his or her current speech anxiety and fear of negative evaluation in terms of the long-term consequences of this single anxious event, say, 10 years later.
Reattribution is an important verbal intervention for clients with excessive self-blame and guilt, or what Abramson, Metalsky, and Alloy (1989) call hopelessness depression. These individuals exhibit a negative inferential style in which they tend to make global, stable, and negative self-referent attributions for the cause of distressing life events. Findings from the Cognitive Vulnerability to Depression (CVD) Project indicate that a negative inferential style and endorsement of dysfunctional beliefs confers vulnerability to depression onset (Alloy, Abramson, Safford, & Gibb, 2006). Given its prominence as a cognitive vulnerability factor, it is important that the cognitive therapist helps clients become aware of their biased inferential style and teaches them how to shift their focus onto external circumstances that may have contributed to the negative life experience. A responsibility pie chart can be used to teach the client how to distribute responsibility for a bad outcome among several causes rather than narrowly attributing all blame to the self (see Greenberger & Padesky, 1995). Reattribution is an important verbal intervention in CT for depression and was first described by A. T. Beck et al. (1979) in the depression treatment manual.
The final verbal strategy listed in Table 1 is positivity reorientation. This is a term that refers to teaching clients more deeply to encode positive, adaptive experiences and information that indicates the client is able to cope with strong unwanted feelings. In most cases more positive, schema-incongruent information is not well processed and so an important goal of CR is to teach clients intentionally and effortfully to select, encode, and retrieve positive experiences. This therapeutic work is critical for reversing the heightened sense of personal vulnerability and helplessness that is commonly seen in the emotional disorders. A person with generalized anxiety disorder (GAD), for example, would be taught to process past experiences when his or her worries did not come true or when he or she successfully coped with a negative experience. The later sessions in any trial of CBT should shift from a focus on refuting maladaptive schemas to the processing of a positive orientation to self, world, and future. This will strengthen the resourcefulness of clients and prepare them for treatment termination.
Empirical hypothesis-testing
CT has always taken a strong behavioral view from its very inception and so empirical hypothesis-testing is a critical component of CR. A. T. Beck et al. (1979) described the use of activity scheduling, mastery and pleasure techniques, grade task assignment, behavioral rehearsal, assertiveness training, and role playing in CT for depression. The use of these therapeutic strategies has been well explained in the original treatment manual and numerous subsequent descriptions of CT (e.g., J. S. Beck, 2011; Dobson & Dobson, 2009; Fennell, Bennett-Levy, & Westbrook, 2004; Leahy, 2010; Wright & McCray, 2012). For the anxiety disorders, behavioral experiments mainly take the form of systematic, graded exposure to fear triggers along with prevention of escape, avoidance and safety, or compulsive responses (A. T. Beck & Emery, 1985; D. A. Clark & Beck, 2010). Behavioral interventions in CR for personality disorders often involve observations about the real-life effects of long-held and exaggerated beliefs about the self or others, which may be supplemented with experiential techniques such as reliving childhood events and imagery (A. T. Beck, Freeman, Davis, & Associates, 2004). CR for psychosis again involves setting up behavioral experiments that test the accuracy of clients' erroneous interpretations of reality and help them adopt more effective coping responses to hallucinations, delusions, and thought disorder (A. T. Beck, Rector, Stolar, & Grant, 2009; Kingdon & Turkington, 2005).
Empirical hypothesis-testing can be defined as “planned experiential activities, based on experimentation or observation, which are undertaken by patients in or between cognitive therapy sessions” (Bennett-Levy et al., 2004, p. 8). The authors note that behavioral experiments are derived from the cognitive case formulation and are designed to test the validity of disorder-related schematic beliefs and contribute to the construction of more adaptive schemas. The critical difference between traditional behavior therapy and CT lies in the purpose of the behavioral intervention. In standard behavior therapy the focus remains on behavior change, whereas CT utilizes behavioral experiences as a means to achieve schematic restructuring. For this reason, behavioral experimentation or empirical hypothesis-testing is a key element of CR.
When using behavioral experimentation in CR, there are seven steps that the therapist follows in order to achieve schematic change (D. A. Clark & Beck, 2010; Rouf, Fennell, Westbrook, Cooper, & Bennett-Levy, 2004). First, a rationale or purpose of the behavioral experiment must be discussed with the client. The experiment will be derived from the case formulation and is introduced as a way of testing a maladaptive belief that contributes to the persistence of the disorder. For example, a student with pathological worry may believe that worry about “failing an exam” is helpful because it strengthens her motivation for studying. A behavioral experiment would be introduced as a means of testing out the positive and negative consequences of exam worry. The second step involves a clear statement of the maladaptive belief and its alternative. In our case example, the therapist would record the maladaptive belief as “worrying about my exams is actually helpful because I'll study more” and an alternative belief as “worrying about my exams is more detrimental than good because it distracts me from studying.”
In the third step the therapist and client collaborate in designing the experiment. It is important that clients feel invested in devising the experiment. Noncompliance is likely higher when clients do not understand the rationale for the experiment or do not feel responsible for its design and implementation. In the current experiment, the client and therapist decided that the best way to test out the utility of the “exam worry belief” was to pick two midterm exam courses. For one she would purposefully worry about her performance for at least one hour per day, and for the other course she let her worries come and go with the intention that less time would be spent worrying. Specific details about the time, place, and responses associated with the exercise were elaborated and recorded for the client's benefit.
The fourth step involves a clear statement of the experimental hypothesis. In the present example the client was to record study hours associated with both courses and to rate her level of motivation to study. If worry facilitated study behavior, the client would record more study time for the “worry course,” whereas if worry interfered with study, the client would record more study time for the “nonworry course.”
In the fifth step, the client conducts the experiment, usually as a between-session homework assignment, and records the outcome. It is important that the therapist write out details of where, when, and how to carry out the experiment so there is no misunderstanding on what outcome constitutes evidence for or against the maladaptive belief. It is often helpful to have clients predict beforehand the outcome they expect from the behavioral activity. In addition, it is important that a written record of the outcome is made so the therapist is able to review the outcome at the next therapy session.
The sixth step involves consolidation of the results of the empirical hypothesis-testing experiment at the subsequent session. The therapist explores with clients their thoughts and feelings while conducting the experiment, and whether their experience confirms the maladaptive belief or its alternative. In the present example the client discovered that the more she worried about her course the less time she spent studying that evening. On the other hand, letting go of her worries resulted in less worry time and, surprisingly, more time spent studying the course material. The therapist was able to use this experience to challenge the client's belief that “worry motivates me to study more.”
The final phase is to summarize the findings from the experiment and to draw out the broader implications. It is important to emphasize how a maladaptive schema can be modified in light of the findings from the behavioral experiment and how schematic change will lead to treatment goals and ultimately symptom reduction. As well, the outcome of a behavioral experiment should lead to further planning for the next empirical hypothesis-testing experiment (Rouf et al., 2004). In this way each behavioral experiment plays an important role in moving the client toward schematic change and achieving significant symptom improvement.
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Empirical Evidence for Cognitive Restructuring
Over the years there has been considerable interest in empirically testing the effectiveness of CR in achieving symptom improvement. Many of these studies have attempted to contrast “purely” behavioral interventions with “purely” cognitive interventions. Unfortunately such comparisons are misleading because it can be difficult to ensure external validity of the treatment conditions (Rodebaugh, Holaway, & Heimberg, 2004) and, as previously discussed, behavioral experiments are a key component of CR. Stripping CR of its behavioral elements would be tantamount to testing the effectiveness of fear hierarchies with some proxy to actual hierarchy exposure in real life. Nevertheless, it is reasonable to ask whether an intervention that emphasizes schematic change (i.e., CR) is more or less effective than an intervention that omits reference to schemas (i.e., behavioral activation or exposure alone).
There are two types of psychotherapy process studies that bear on the effectiveness of CR. The first is component analysis in which CR is compared with a non-CR intervention. This design represented some of the earliest dismantling studies that examined the incremental contribution of CR to symptom reduction. The second is mediation analysis which examines whether cognitive or schema change precedes symptom reduction. If CR is an effective intervention, one would expect that schematic change should be a key mechanism in symptom improvement. Most studies on cognitive mediation have examined changes across baseline, posttreatment, and follow-up intervals, although a few studies have conducted a more refined analysis of session-by-session changes in cognitions and symptoms. Another question addressed by mediation research is whether cognitive change is specific to cognitive interventions such as CR, or whether it is also evident in noncognitive treatments such as exposure alone or pharmacotherapy.
Component Analysis
One of the earliest component studies compared behavioral activation (BA), automatic thought modification (AT), and full CT in 152 individuals with major depression randomly assigned to 12–20 sessions of treatment (Jacobson, Dobson, Truax, Addis, & Koerner, 1996). CT was the only condition to focus specifically on identification and modification of core beliefs, whereas BA primarily focused on behavioral change. Analysis of outcome measures at posttreatment and 6-month follow-up revealed no significant differences between treatment conditions. Moreover, none of the treatments had a significant differential effect on specific cognitive or behavioral change variables. That is, CT did not produce significantly more change in depressogenic schemas nor did BA result in a significantly greater increase in mastery or pleasure activities. The authors concluded that BA alone was equally effective to the full CT treatment protocol. Given equivalence across treatment conditions, Jacobson and colleagues questioned whether verbal interventions (i.e., CR) were necessary in the treatment of depression and whether schematic change was as critical to depressive symptom remission as proposed by Beck's model.
A subsequent 2-year follow-up revealed that all three treatment conditions were equally effective in preventing depressive relapse (Gortner, Gollan, Dobson, & Jacobson, 1998). Again the authors concluded that their findings raised questions about the validity of the cognitive model and more specifically the clinical utility of verbal interventions such as CR. In other words, it would appear that schematic change is not necessary for long-term depressive symptom remission and prevention of relapse. However, a significant limitation is the one-sided evaluation of the additive effects of CR without also testing the additive effects of BA. In other words, the finding indicated that CR may not add significantly beyond the therapeutic benefits of BA, but we do not know whether BA would have incremental benefits beyond a “purely” cognitive intervention. It is possible that the treatments are equally efficacious and their combination confers no added benefit. Nevertheless, the results do suggest that one therapy (i.e., BA) is just as effective as another therapy (i.e., CT), and the findings call into question the necessity of CR in the treatment of depression.
A more recent randomized controlled trial (RCT) based on the Jacobson studies compared an expanded version of BA to standard CT, paroxetine alone, and an 8-week pill placebo condition in 241 adults with major depression (Dimidjian et al., 2006). Cognitive interventions were excluded from the BA condition but the CT condition presented the full range of CT interventions including CR and behavioral activity scheduling. At posttreatment all three active treatments were equally effective for depression in the mild to moderate range of severity, but BA and medication were both significantly more effective in treating those with severe major depression than was CT. However, a 2-year follow-up revealed that CT may have a more enduring effect than BA, and both treatments were at least as efficacious over the long term as maintaining individuals on antidepressant medication (Dobson et al., 2008).
What then can be concluded about the role of CR in the treatment of depression? The dismantling studies have shown that CR is effective in the treatment of depression but it is clearly not necessary for achieving immediate symptom improvement. However, there is more recent evidence that CR might contribute to improved endurance of depressive remission. Thus in terms of depression, CR is effective but not superior to other “noncognitive” interventions, and it appears not to be a necessary treatment component for effective psychotherapy of the acute phase of major depression.
Several studies have compared the effectiveness of cognitive interventions and exposure in the treatment of anxiety disorders. In studies of panic disorder, CR alone can lead to a significant reduction in panic symptoms (Bouchard et al., 1996; Margraf & Schneider, 1991; see Gould, Otto, & Pollack, 1995), although exposure alone appears to be as effective as exposure plus CR (Bouchard et al., 1996; Öst, Thulin, & Ramnerö, 2004; van den Hout, Arntz, & Hoekstra, 1994). However for social anxiety, CR may play a more critical therapeutic role. In their RCT for social anxiety, D. M. Clark et al. (2006) found that CT was more effective than exposure plus applied relaxation at posttreatment and 3-month and 6-month follow-up. In an earlier study, Mattick and Peters (1988) found that therapist-assisted exposure plus CR was more effective than therapist-assisted exposure alone, although this finding was not replicated in a later study (Feske & Chambless, 1995). Hofmann (2004) randomly assigned 90 individuals with social anxiety to group CBT, exposure without cognitive restructuring, or a wait list control. Although both active treatments produced similar symptom improvement at posttreatment, only the CBT group exhibited continued symptom improvement after treatment termination. Thus CR, with its focus on the identification and modification of maladaptive beliefs, may be a key treatment ingredient for social anxiety disorder.
Numerous studies have compared exposure and response prevention (ERP) with a combination of ERP and CR in the treatment of obsessive-compulsive disorder (OCD). Like other anxiety disorders, a CBT approach to treatment of obsessions and compulsions that includes a strong CR component does lead to significant immediate and long-term symptom reduction (e.g., Freeston et al., 1997; McLean et al., 2001; van Oppen et al., 1995; Whittal, Robichaud, Thordarson, & McLean, 2008; Whittal, Thordarson, & McLean, 2005). Furthermore, it is apparent that CR alone can have a significant treatment effect even in the absence of systematic, intensive ERP (Cottraux et al., 2001; Whittal et al., 2005; Wilson & Chambless, 2005). Although some studies have found CBT equivalent to ERP (Cottraux et al., 2001; Whittal et al., 2005), others reported that intensive ERP alone is more effective than CBT (McLean et al., 2001) or that adding CR to ERP did not significantly improve treatment outcome (O'Connor et al., 2005). Moreover, Whittal, Woody, McLean, Rachman, and Robichaud (2010) found that CBT and stress management were equally effective in treating individuals who experienced obsessions without overt compulsions. This finding has led to the conclusion that cognitive strategies alone are less effective than ERP alone and that adding CR to ERP does not boost the effectiveness of treatment for OCD (Abramowitz, Taylor, & McKay, 2005).
Component analysis of CR, per se, has not been conducted with GAD. However, outcome studies comparing CBT with applied relaxation or pharmacotherapy alone have concluded that CBT has equivalent or superior treatment effectiveness (see Fisher, 2006; Mitte, 2005). In posttraumatic stress disorder (PTSD) there has been considerable research on whether CR adds any treatment effectiveness beyond prolonged trauma exposure. Several meta-analyses have concluded that individual trauma-focused CBT that includes exposure to an individual's memory of the trauma and its personal meaning is an effective treatment for PTSD (e.g., Bisson & Andrew, 2009; Seidler & Wagner, 2006; see also discussion by Ehlers et al., 2010). However, there is considerable controversy over whether CR of trauma-related thoughts and beliefs adds any therapeutic effectiveness over prolonged imaginal exposure to the trauma memory. In their systematic review, Ponniah and Hollon (2009) concluded that trauma-focused CBT that included exposure and/or CR was an efficacious treatment for PTSD. However, other researchers have concluded that cognitive interventions may be unnecessary in the treatment of anxiety disorders including PTSD (Longmore & Worrell, 2007).
Recently, Hassija and Gray (2010) conducted a thorough review of component studies comparing CR and prolonged exposure in PTSD. These researchers found sufficient evidence that CR is an effective intervention for PTSD and that the effects are generally comparable to prolonged exposure. Moreover, CR may produce more enduring effects than does imaginal exposure alone (Tarrier & Sommerfield, 2004) and may differentially affect associated features of PTSD such as detachment, catastrophic cognitions, and guilt (Hassija & Gray, 2010). Outcome and dismantling studies of cognitive processing therapy (CPT), which involves intense CR of beliefs and negative cognitions, indicate that the therapy is as effective as prolonged exposure in the immediate and longer term (Resick, Nishith, Weaver, Astin, & Feuer, 2002; Resick, Williams, Suvak, Monson, & Gradus, 2012). In addition, CPT may have some superiority over trauma-focused exposure alone in treatment of chronic PTSD in military samples (Alvarez et al., 2011). Recent CPT dismantling studies indicate that CR may be the more potent component of the treatment package (Resick et al., 2008; Stein, Dickstein, Schuster, Litz, & Resick, 2012). At this point the most parsimonious conclusion is that the CR component of CPT and prolonged exposure produce similar changes in PTSD so that the average person with PTSD can benefit from either treatment (Stein et al., 2012).
Before concluding this review of component studies, it is worth considering the most recent meta-analysis on the efficacy of exposure and CT in treatment of anxiety disorders. Ougrin (2011) identified 20 RCTs that directly compared CT and exposure alone. Studies of CT versus CT plus exposure, or the reverse, were excluded. Analysis revealed equivalent short- and long-term effect sizes for PTSD, OCD, and panic disorder. However, there was a statistically significant difference in effect size favoring CT for immediate and long-term outcomes for social anxiety disorder.
In summary, the component studies clearly indicate that CR is an effective treatment intervention for anxiety and depression, and in some cases may convey a distinct therapeutic advantage. This is very different from the conclusion reached by Longmore and Worrell (2007) in their review of CBT component analysis studies for anxiety and depression, in which they stated that “for a range of clinical problems, specifically cognitive interventions do not produce superior outcomes to the behavioral components of CBT” (p. 180). The failure of cognitive interventions to add significant therapeutic value beyond exposure or behavioral activation alone was a significant factor in leading the authors to question whether challenging negative thoughts was necessary in CBT. The present review considers this a misguided conclusion, although it is true that the general finding of equivalence of cognitive and behavioral interventions provides little practical guidance for the clinician who must decide how much emphasis should be placed on CR when treating an individual client with anxiety or depression.
Mediation Analysis
Cognitive mediation is a fundamental hallmark of CT and CBT (D. A. Clark et al., 1999; Garratt, Ingram, Rand, & Sawalani, 2007; Maxwell & Tappolet, 2012). It is the assertion that symptom improvement and recovery from a disorder is the result of change in underlying maladaptive thoughts and beliefs, and biased information processing. It is change in the functioning of the cognitive apparatus that mediates symptom amelioration. Although CT acknowledges that modification in physical processes, emotions, behavior, and experiences can result in cognitive change, it is assumed that CR provides a more direct means to modify the faulty information processing apparatus. Thus, there are two fundamental questions in cognitive mediation. Is schematic change a significant causal mechanism of symptom improvement, and is CR unique in its ability to produce change in schematic content (Garrett et al., 2007; Hofmann, 2008)? I turn now to the initial question of mechanisms of therapeutic change.
Longmore and Worrell (2007) reviewed a select number of early CBT treatment process studies and concluded that there is limited evidence that cognitive variables mediate therapeutic change in CBT. Hofmann (2008), however, was critical of the Longmore and Worrell (2007) discussion of cognitive mediation, noting that several recent CBT process studies that employed more rigorous data analytic procedures in support of cognitive mediation were missing from their review. Interestingly Garrett et al. (2007) arrived at a different conclusion in their review of cognitive mediation in treatment of depression. They stated that in CT, change in cognition does predict changes in depressive symptoms, although it appears that studies are divided on whether cognitive change is specific to CT or also evident in other psychosocial treatments or even pharmacotherapy.
There have been several rigorous tests of cognitive mediation in CBT for the anxiety disorders. Hofmann (2004) found that group CBT, and exposure alone, produced equivalent improvements in social anxiety disorder at posttreatment, but at 6-month follow-up only CBT was associated with continued symptom reduction. Using linear regression analyses, he demonstrated that change in the estimated social cost associated with 20 hypothetical negative social events predicted pre-post difference scores in self-reported social anxiety symptoms, especially for the CBT group at 6-month follow-up. Smits, Rosenfield, Telch, and McDonald (2006) found evidence of cognitive mediation for exposure-based treatment of social anxiety using growth modeling analysis and a cross-lagged panel design. Change in probability judgmental bias predicted later self-rated fear during exposure, although the reverse relationship was also found and judgments of cost bias did not predict fear.
Based on an RCT comparing CBT and pharmacotherapy for panic disorder, Hofmann et al. (2007) used multilevel modeling to show that change in catastrophic cognitions was a significant mediator of change in panic symptoms for those receiving CBT but not for participants in the imipramine alone condition. A recent study of one session exposure versus CBT-based exposure for spider phobia revealed that change in maladaptive cognitions mediated posttreatment and follow-up reductions in self-report phobic symptoms (Raes, Koster, Loeys, & De Raedt, 2011). Finally, a systematic review of CBT studies of anxiety disorders concluded that change in threat reappraisal has a causal effect on reduction in anxious symptoms, although it was not possible to support the stronger position that threat reappraisal is responsible for the efficacy of CBT (Smits, Julian, Rosenfield, & Powers, ).
Several studies have examined session-by-session change in cognitions and symptoms in order to investigate temporal precedence. Tang and DeRubeis (1999) found that CT sessions involving sudden gains (i.e., large depressive symptom reduction during a single between-session interval) were associated with cognitive changes in the previous session. A subsequent reanalysis of the Jacobson et al. (1996) data set again confirmed that significantly more cognitive change occurred in the pregain than control sessions (Tang, DeRubeis, Beberman, & Pham, 2005). However, another study using multivariate hierarchical linear modeling of session-by-session changes in Beck Depression Inventory symptoms found similar trajectories of change for cognitive and vegetative symptoms for depressed outpatients randomly assigned to CT or pharmacotherapy (Bhar et al., 2008).
In a stringent test of cognitive mediation in CBT for obsessions, Woody, Whittal, and McLean (2011) found that maladaptive appraisals of the primary obsession significantly accounted for improvement in obsessive symptoms. Although this finding supported the cognitive mediation hypothesis, a session-by-session analysis using latent change modeling revealed that prior obsession severity led to subsequent change in appraisals for both CBT and stress management treatment conditions. In this study, then, symptom change had temporal precedence over cognitive change. However, a multivariate time series analysis of session-by-session data for CR versus exposure treatment for panic disorder indicated that changes in dysfunctional beliefs and self-efficacy preceded change in panic apprehension (Bouchard et al., 2007). Overall the research on temporal precedence presents a mixed picture, with some studies showing cognitive change is a cause of symptom change, others cognitive change is a consequence of symptom change, and still others a co-occurring change with bidirectional effects.
Before concluding this review on cognitive mediation, it is worth considering several lines of research that demonstrated that a specific focus on cognitive change does have an impact on symptom remission. For example, Segal and colleagues found that depressed participants treated with CT were less cognitively reactive during sad mood induction at posttreatment than those treated with medication alone, and this in turn predicted probability of relapse (Segal, Gemar, & Williams, 1999; Segal et al., 2006). Furthermore, a study of CT plus medication versus medication alone for major depression found that both treatments produced a significant reduction in depressive symptoms and negative cognitions, but only the CT plus medication group evidenced increased organization of positive schema content and reduced interconnectedness for negative schema content (Dozois et al., 2009). The specific type of automatic thought targeted during group CBT for social anxiety also appears to influence treatment outcome (Hope, Burns, Hayes, Herbert, & Warner, 2010). Finally, patients' competence in acquiring CR skills in CT predicted lower 1-year relapse in one study (Strunk, DeRubeis, Chiu, & Alvarez, 2007), although the evidence is mixed on whether therapist adherence to or competence in the CT protocol is significantly related to outcome (Strunk, Brotman, DeRubeis, & Hollon, 2010; Webb, DeRubeis, & Barber, 2010). Overall, then, considerable progress has been made in understanding the mechanisms of change in CBT. It is clear that the quality of the cognitive intervention, its focus, and the degree of subsequent cognitive change does have a significant impact on treatment outcome.
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Concluding Remarks
CR is a multifaceted therapeutic intervention that seeks symptom reduction by modifying the maladaptive schematic content considered crucial in the etiology and maintenance of psychological disorders. Since its first conceptualization by A. T. Beck and colleagues in the 1970s (A. T. Beck et al., 1979), considerable progress has been made in elaborating, refining, and applying CR to a variety of psychiatric disorders. Psychotherapy process research has indicated that CR is an effective intervention for anxiety and depression, and that CR's most significant contribution might be in conferring more enduring treatment effects or mediating change in specific disorder symptoms. However, it is also clear that CR is at best equivalent to, and at worst less effective than, “noncognitive” interventions such as exposure or behavioral activation, at least in terms of short-term symptom reduction. Although there is substantial evidence in support of cognitive mediation in symptom improvement, the direction of causality is still a matter of debate and it is evident that cognitive change is not specific to CR.
There are several issues that remain unresolved about the effectiveness and mechanism of change in CR. At the schematic level, the effects of CR remain relatively unknown. Does CR alter existing maladaptive schema content or does it introduce more adaptive schemas that compete with or inhibit activation of disorder-related schemas? There have been no dismantling studies of CR itself to indicate the relative importance of collaborative empiricism, verbal interventions, and empirical hypothesis-testing to determine the effectiveness of the intervention. Most of the component and mediation research has relied on symptom measures taken at limited time intervals throughout treatment (i.e., baseline, posttreatment, follow-up). What is needed are more session-by-session studies that use specific cognitive and symptom measures employing multilevel modeling techniques to chart the trajectories of cognitive and symptom change. It is also unclear which clinical, client, and therapist variables might moderate the effectiveness of CR, and we are only just beginning to learn the role that therapist competence and client acquisition of CT skills might play in the effectiveness of CR. Unfortunately the treatment process research has not yet matured to the point where it can provide guidelines to clinicians on when to use CR, when to combine it with other interventions, or when to refrain from its use. Until then, clinicians can consider CR an effective intervention that should hold a prominent place in their treatment armamentarium.
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1. What is it include in schizophrenia spectrum? are those the same with psychotic disorder?
2.Is it ok if I  say that schizoaffective is part of schizophrenia spectrum? or schizoaffective is part of psychothic disorder?
3. In DSM V, why schizotypal personality disorder include in schizophrenia spectrum and other psychotic disorder?
4. Schizotypal personality disorder is categorized as personality disorder or schizophrenia spectrum disorder?
Thank you 
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Thank you for the explanation :D
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For example, using the Aberrant Salience Inventory (ASI)? 
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Cognitive Remediation Therapy appears to be a much recommended approach although aberrant salience is only infrequently measured. ( See previous response by B M Evalds-Kvist). Are you seeking to relate the rate of learning to the level of aberrant salience, evaluate the efficacy of therapy in another study...?
Also see:
Gould RA, Mueser KT, Bolton E, Mays V, Goff D:
Cognitive therapy for psychosis in schizophrenia
Schizophr Res 2001; 48: 335-342
Kurtz MM, Moberg PJ, Gur RC, Gur RE
Approaches to cognitive remediation of neuropsychobiological deficits in schizophrenia
Neuropsychol Rev. 2001;11 (4): 197-210
Cognitive Rehabilitation for Schizophrenia and the Putative Role of Motivation and Expectancies
Dawn I. Velligan1,2,
Robert S. Kern3 and
James M. Gold4
1To whom correspondence should be addressed; e-mail: velligand@uthscsa.edu
 
Abstract
Cognitive rehabilitation (CR) approaches seek to enhance cognitive processes or to circumvent cognitive impairments in schizophrenia in an effort to improve functional outcome. In this review we examine the research findings on the 8 evidence-based approaches to cognitive remediation listed in the 2005 Training Grid Outlining Best Practices for Recovery and Improved Outcomes for People With Serious Mental Illness, developed by the American Psychological Association Committee for the Advancement of Professional Practice. Though the approaches vary widely in theoretical orientation and methods of intervention, the results are, for the most part, encouraging. Improvements in attention, memory, and executive functioning have been reported. However, many persons with schizophrenia are more impaired in real-world functioning than one would expect given the magnitude of their cognitive deficits. We may need to look beyond cognition to other targets such as motivation to identify the reasons that many persons with schizophrenia demonstrate such marked levels of disability. Although a number of current CR approaches address motivation to varying degrees, treating motivation as a primary target may be needed to maximize CR outcomes.
Introduction
Cognitive impairment is a core feature of schizophrenia.1 Deficits in cognitive functioning, including those in psychomotor speed, attention, memory, and executive functions, are thought to underlie the severe functional disability associated with this illness.2–11 This relationship between cognitive deficits and poor functional outcome has prompted the development of cognitive rehabilitation (CR) approaches focused specifically on treating the cognitive deficits of schizophrenia.12--The field continues to struggle to reach agreement in terminology to describe existing CR approaches. The restorative versus compensatory distinction has been popularized in the traumatic brain-injured but not the schizophrenia literature. As not all programs of cognitive rehabilitation aim to “restore” the individual to his or her premorbid state or “restore” the function of neurons and neural circuits, it may be more accurate to describe such programs as “cognition enhancing” efforts, in that they all seek to improve cognitive functioning through a set of specified training interventions. In contrast, compensatory approaches aim to bypass or “compensate” for cognitive deficits to promote skill acquisition or functional outcome.--In the schizophrenia literature there are several independent and competing CR approaches being developed concurrently. These approaches vary in their theoretical underpinnings, methodologies, and targets of outcome. An appreciation of the different theoretical approaches and methods of intervention, and their corresponding strengths and weaknesses, may inform future efforts.--Previous Reviews
The CR literature in schizophrenia has been, and continues to be, a difficult literature from which to draw firm conclusions. Studies vary considerably in teaching methods, patient samples and sample sizes, outcome measures, intervention dose (amount of training), inclusion of control or comparison groups, blinded procedures, level of professional education and experience of trainers, and reliance on theoretical models. Even the reviews of this literature vary considerably.13–20 They differ according to criteria for study inclusion, conceptual organization of studies, and interpretation of findings. These range from highly conservative reviews such as provided by Pilling et al.,14 which examined 5 randomized controlled trials in schizophrenia, to more liberal efforts such as those by Kurtz et al.,13 which encompassed the extant literature at the time. Overall, the reviews have been mostly positive, with the exceptions of the Pilling et al. review,14 which was decidedly negative, and Suslow, Schonauer, and Arolt's review20 of attention studies. We focused our review on 8 evidence-based approaches of CR. The selection was based on their inclusion in the 2005 Training Grid Outlining Best Practices for Recovery and Improved Outcomes for People With Serious Mental Illness, developed by the American Psychological Association Committee for the Advancement of Professional Practice.21 These approaches have been used in clinical trials of schizophrenia and best illustrate the differing emphases in this continually developing area of rehabilitation. To our knowledge, this is the first review article to include a presentation of all 8 approaches. The second aim of this review is to stimulate a discussion on the role of motivation in CR. A section at the end of the article deals specifically with this issue. When appropriate, motivation issues are discussed within the context of the CR approaches presented in this review.--Integrated Psychological Therapy (IPT22) was one of the first clinically based CR programs that was specifically designed for persons with schizophrenia. IPT is based on a building-block model that assumes that elementary, basic neurocognitive functions are necessary prerequisites for higher-order complex social functions. Training is conducted in small groups of 5–7 patients in 30–60 minute sessions 3 times per week and proceeds through 5 subprograms arranged in a hierarchical order according to complexity of function. The first 3 subprograms represent the cognitive training component and include training of abstraction, conceptual organization, and basic perception and communication skills. These are named Cognitive Differentiation, Social Perception, and Verbal Communication. These abilities are believed to be prerequisite skills, essential for carrying out effective social interactions. The fourth and fifth components represent the behavioral level of social interaction and are similar to skills training approaches used elsewhere.23 These are named Social Skills and Interpersonal Problem Solving. Training is highly structured and manual-driven. Completion of the subprograms is accomplished in about a 6-month period though successful completion of a series of graduated activities.--IPT appears to convey benefits compared with less extensive psychosocial treatments on social functioning. However, the beneficial effects of IPT on neurocognition are more equivocal. Further, it is not clear from the studies of IPT whether changes in neurocognition are necessary to produce changes in social functioning.--In one of the more methodologically rigorous studies of IPT, Spaulding et al.24 tested the effects of the cognitive component of IPT on social problem-solving ability in a sample of schizophrenia inpatients. Participants were randomized to 2 groups: a group that received the first 3 subprograms of IPT plus skills training versus a group that received supportive therapy plus skills training. Hence, the primary difference between groups was the IPT cognitive training component. The results from the study showed a differential treatment effect favoring the IPT plus skills training group on the primary outcome measure of interpersonal problem-solving (AIPSS). Interestingly, the study produced relatively few differential treatment effects on cognition. Only 2 out of 13 neurocognitive variables (Span/Continuous Performance Test [CPT] and Wisconsin Card Sorting Test [WCST] random errors) showed a differential treatment effect. However, the IPT plus skills training group did show significant pre-post gains on 7 of the 13 measures compared with 4 out of 13 in the control group. Somewhat paradoxically, the results suggested that participation in the neurocognitive component was necessary to enhance gains in social problem-solving ability, yet there was little evidence of a differential treatment effect on neurocognition. A failure to find support for the “building block” model of IPT has been found in other studies as well.25--Cognitive Enhancement Therapy
Cognitive Enhancement Therapy (CET) is based on a neurodevelopmental model of schizophrenia that proposes that disturbances in neurodevelopment result in delays in social cognition. Social cognitive milestones such as perspective taking are the focus of treatment. According to the model, the brain's neuroplasticity reserve can be enriched through cognitive experiences provided through training. The conceptualization of training within CET was influenced by Ben-Yishay and colleagues'26 work with traumatic brain-injured patients, Brenner's IPT,22 and contemporary theories of human cognitive development. The emphasis in training is to shift from concrete cognitive processing of information to “gistful” spontaneous abstraction of social themes. There are 2 main components to training: (1) computer-based cognitive exercises that focus on attention, memory, and problem-solving abilities and (2) small group training of social cognition. CET involves social interaction at every stage. The computer sessions are conducted in pairs of patients with the therapist providing oversight. Patients take turns using the computer software programs and assist each other by providing strategies and offering encouragement. The curriculum for the social cognition groups consists of categorization exercises, formation of gistful, condensed messages, solving real-life social dilemmas, abstraction of themes from newspaper articles (eg, USA Today), appraisal of affect and social contexts, initiating and maintaining conversations, playwriting, and center stage exercises (eg, introducing oneself or a friend). The groups involve structured but unrehearsed in vivo social interactions. Sessions include a homework review, a psychoeducation topic, an exercise by a patient or pair, feedback from other patients and coaches, and a new homework assignment based on the education topic. Training is individualized to the cognitive-processing style deficit of the participant.
CET is one of the more time and resource demanding of the CR programs in schizophrenia. In a 2-year randomized trial of CET,27 participants in the CET group received 75 hours of computerized training on attention, memory, and problem-solving exercises combined with 56 sessions (1.5 hours per week) of training on social cognition exercises. Participants were selected based on meeting criteria for cognitive disability, which consisted of impairments, functional disabilities, and social handicaps associated with 1 of 3 dysfunctional cognitive styles, and the criteria for social cognitive disability. At the 12-month follow-up assessment, differential treatment effects of CET compared with enriched supportive therapy (EST) were found for composite indices of neurocognition and processing speed, and marginal differences were found for the behavioral composites of cognitive style, social cognition, and social adjustment. At the 24-month assessment, differential effects were found on all composite indices. The control group was not matched to the experimental group for amount of training exposure, which makes it difficult to interpret the contribution of participation in a structured rehabilitation activity. Also, the neurocognitive battery used to assess outcome shared similar methods with the computerized training tasks. Hence, the study's findings could be due to shared method variance and not the training per se. Still, the reports from this group over the years have been highly encouraging. The conceptual model underlying CET is well developed, and the approach targets a deficit highly relevant to the overall well-being of persons with schizophrenia.--Neurocognitive Enhancement Therapy
The Neurocognitive Enhancement Therapy (NET) program of Bell and colleagues28 is similar to CET, except that the focus is on work rehabilitation. Like CET, NET includes computer-based cognitive training. NET uses software programs developed specifically for this group by Odie Bracy, which are similar to that used by Hogarty and colleagues27 and were specifically designed for use in the treatment of persons with compromised brain function. They have been widely used in the rehabilitation of persons with traumatic brain injury, and in more recent years they have been used with persons with schizophrenia. The software programs include a number of specific training exercises that differ by cognitive target and difficulty level. Training begins with relatively simple exercises and proceeds to more complex ones. During training, participants work at their own pace and move from one training exercise to another. Once a participant attains 90% accuracy at a given difficulty level, the parameters of the task are changed to make the task more challenging and enhance the motivation to perform optimally. Training focuses on attention, memory, and executive functions. The other components of NET include biweekly feedback based on results from an on-the-job assessment, using the Cognitive Functional Assessment scale, and participation in a weekly social processing group. The Cognitive Functional Assessment scale is a measure of cognitive function that consists of ratings of attention, memory, and executive functioning while the participant is performing his or her job. Feedback is provided to participants during their weekly work therapy support group.--In a study of 65 schizophrenia or schizoaffective disorder patients, participants were administered a baseline cognitive assessment and then stratified by level of cognitive impairment and randomly assigned to NET plus work therapy versus work therapy alone.28 Participants received up to 5 hours of computerized cognitive training each week over the 26-week protocol. At the end of training, the NET plus work therapy group showed significantly greater gains than the work therapy alone group on measures of executive functioning, working memory, and affect recognition. Approximately 60% of participants in the NET plus work therapy group showed improvement in neurocognitive performance and were 4 to 5 times more likely than participants in the comparison group to show improvements in neurocognitive function of a large effect size (Cohen's d > .80). Improvements in working memory were, perhaps, most impressive. The percentage of patients showing working memory performance within the normal range changed from 45% to 77% in the NET plus work therapy group, compared with a decrease from 56% to 45% in the work therapy alone group. Moreover, Bell et al.28 found that patients participating in NET plus supported employment had better vocational outcomes than those in supported employment alone.
This group has conducted 2 long-term studies to evaluate the effects of adding NET to vocational programs. The first study, described above, was conducted in a VA setting with participants placed at jobs within the VA.28 A second study,29 which is ongoing, used a community-based supported employment program. Training in the second study was twice as long (12 months). Preliminary data on 54 participants who completed training revealed the NET plus supported employment group to show significantly greater improvement on executive functioning and trends in the expected direction on the other cognitive factors (working memory, thought disorder, and visual and verbal recall). Employment data attained from these 2 studies showed that participants assigned to NET either maintained or increased the number of hours they worked during the follow-up period. Participants receiving only work therapy or supported employment showed a decrease in hours worked. Results were similar when considering the percentage of participants employed. The group differences were more modest in the VA-conducted study perhaps because of the high rates of employment with veterans placed in noncompetitive jobs. In the supported employment study with preliminary data on 43 participants who completed the 12-month follow-up period, the differences were more marked. Twelve months after training, 57.5% of participants in the NET plus supported employment group were still employed compared with only 21.0% of participants in the supported employment alone group. The results from the latter study provide preliminary evidence that the beneficial cognitive and vocational effects of NET can be extended to competitive jobs in community settings.
Individual Executive Functioning Training/Cognitive Remediation Therapy
Another approach to cognitive rehabilitation in schizophrenia is based on an understanding of the cognitive processing deficits common to persons with schizophrenia and how these are linked to deficits in complex behavior such as social functioning. An example of a formal clinical program using this approach was developed in Australia by Ann Delahunty and Rod Morice (1993)30 and has been adopted for use in the United Kingdom by Til Wykes and colleagues, and it is now referred to as Cognitive Remediation Therapy (CRT).6,31,32 The training program targets deficits in executive processes and consists of 3 modules: cognitive flexibility, working memory, and planning. This program places a strong emphasis on teaching methods and uses procedural learning, principles of errorless learning, and other evidenced-based methods. In contrast to CET and NET, this program uses paper-and-pencil exercises for training instead of computerized tasks, and there is greater emphasis placed on the trainers' role in working with patients during the cognitive exercises. Similar to CET and NET, training proceeds through a series of exercises, graduated in level of difficulty, beginning with simpler exercises and progressing to more complex ones. Training is individualized and proceeds at each subject's own pace. The exercises share conceptual features with neurocognitive tests, but they are methodologically different to reduce shared method variance between training exercises and outcome measures. For example, during training for cognitive flexibility, participants are asked to cross out all even numbers, then odd numbers. This requires maintenance and then shifting of cognitive set, similar to that required on the WCST but distinctly different from training to the test.--Results of this approach have been mostly positive. In a study using only the cognitive flexibility module, Delahunty et al.30 found improvements in WCST performance immediately after training, and the gains were maintained at a 6-month follow-up assessment. In a separate study using all 3 training modules, Wykes et al.33 found evidence for a differential treatment effect favoring the cognitive training group over a control group that received intensive occupational therapy. Training was conducted 1 hour per day, 3 to 5 days per week, over 40 sessions. A differential training effect was found on measures from the WCST and a planning test (modified 6 elements). An interesting secondary analysis of the data showed that participants who met a certain threshold for improvement on cognitive flexibility showed improvements in social functioning within the 3-month duration of the trial. In a 6-month follow-up study of 33 outpatients to address the durability of CRT effects, Wykes et al.32 examined stability of gains on 3 primary cognitive outcome measures (WCST, Digit Span, and Tower of London) and a number of secondary cognitive outcome measures. Of the primary outcome measures, only Digit Span performance showed durable gains with CRT over the 6-month follow-up. For the secondary outcome measures, there was a differential treatment effect favoring the CRT group on measures within the memory domain, but not the cognitive flexibility or planning domains. The results suggest good durability for improvements in memory but not for the other 2 targeted domains.
Neuropsychological Educational Approach to Rehabilitation
The manualized Neuropsychological Educational Approach to Rehabilitation (NEAR) program developed by Medalia34 is founded on teaching techniques developed within educational psychology that are designed to promote intrinsic motivation and task engagement. The NEAR conceptual model favors a top-down approach that emphasizes higher-order, strategy-based methods of learning over drill-and-practice exercises that focus on learning of elementary cognitive skills (bottom-up approach). Training involves participation in computer-based cognitive exercises that are designed to be engaging, enjoyable, and intrinsically motivating and that require the recruitment of several cognitive skills within a contextualized format.--Medalia et al.35 investigated a component of the NEAR program in a sample of 54 inpatients with schizophrenia. Participants were randomly assigned to problem-solving remediation, memory remediation, or a control group. CR participants worked with either problem-solving or memory-enhancing computer games in 2 weekly 25-minute sessions for 5 weeks. The group assigned to problem-solving training worked with the “Where in the USA is Carmen Sandiego?” software program. This program is colorful, cognitively challenging, and provides strategy-oriented feedback. Memory training involved a less engaging computer-based program (Memory Package software) that emphasized verbal and visual memory. Participants in the problem-solving group improved to a greater extent in problem solving than those in the memory or control groups. However, participants in the memory training group did not show any differential training effect on memory. The effects of remediation on problem solving persisted 4 weeks after training.36--In an earlier study Medalia et al.37 examined the effects of individual computer-based training of attention using a software program developed out of Ben-Yishay's lab.26 The study included 54 inpatients with schizophrenia who were randomly assigned to computer-based cognitive training using the Orientation Remedial Module or a control condition that involved the viewing of video documentaries. Training within each module followed a test-train-test sequence and lasted approximately 20 minutes. The tests administered at the beginning and end of each session measured visual reaction time. In between, participants worked on 1 of 5 training modules. Progression through 1 module was believed to build skills necessary for successful mastery of later ones. After 18 sessions the results showed significantly greater improvement in the cognitive training group compared with the control group on the primary outcome measure, a computerized continuous performance test. Results of the studies conducted by Medalia et al. suggest that intrinsic motivation may be an important consideration for promoting rehabilitation success.--In an interesting extension of their work, Medalia and Richardson38 reported on moderating variables of rehabilitation outcome. Data were collected from 3 of their studies (total N = 117) that used NEAR or elements of it. Three broad categories were examined: patient characteristics, illness characteristics, and treatment characteristics. Patients were dichotomized as “improvers” or “non-improvers” according to whether they showed reliable improvement in at least 1 cognitive domain. The change index was calculated by dividing change scores on each dependent measure by its standard error of measurement. The results showed that illness factors were least related to training outcome. However, patient and treatment factors differentiated improvers from non-improvers. Specifically, treatment intensity, type of cognitive remediation program, therapist qualifications, patient's motivation for treatment, and baseline work habits differentiated improvers from non-improvers. These findings suggest that a host of variables, including motivation and dosing, may be important considerations in formulating CR training.--Attention Process Training
Attention Process Training (APT) was developed by Sohlberg and Mateer39 as an approach to CR for persons with traumatic brain injury. Four areas of attention are targeted for training: sustained, selective, dividing, and alternating attention. Four different types of material (auditory and visual cancellation tasks, mental control tasks, and daily life tasks) are used. The training exercises are arranged in hierarchical difficulty; participants progress through training exercises after establishing mastery at each stage. Like CET and NET, APT follows a building block approach. Skills acquired in earlier stages are viewed as prerequisite for skill development in later training stages.--Though APT has been used successfully in studies of brain-injured patients, there is little data on its efficacy with schizophrenia patients. Lopez-Luengo and Vazquez40 examined the efficacy of APT in a sample of 24 schizophrenia patients. Participants were randomly assigned to APT or treatment as usual. Participants in the APT group received training twice per week; however, the number of weeks of training varied considerably across patients (range = 8 to 76). Training sessions were on the average less than 1 hour. A large number of attention measures were included in the battery. These were specifically designed to capture the 4 areas of attention that were targets of training in APT. Measures of memory and executive functioning were also included. Despite the number of measures, the study yielded only 1 significant finding on attention, and it was in the unexpected direction (the control group showed greater pre-post improvement than the APT group). The APT group did show a differential treatment effect on the measure of executive functioning (WCST) but not on the Spanish-translated version of the California Verbal Learning Test (CVLT) (the measure of memory). There was no statistical control for the number of comparisons in the study, so the WCST results have to be viewed somewhat cautiously. In sum, the findings are largely negative from this study.--There is a small study of APT in schizophrenia that examined APT and Prospective Memory Training (PROMT).41 Three patients were assigned to cognitive rehabilitation training using APT and PROMT; data for 3 other patients were drawn from the University of Pennsylvania Schizophrenia Center database. APT preceded PROMT training. Training was conducted 2 times per week in 1-hour sessions over a 5 to 7-month period. The 3 subjects who received training were administered an attention battery before and after training. There were no formal analyses of the data. Subjects #1 and #3 were described as showing improvement on measures of sustained attention (cancellation tasks). Subjects #1 and #2 were described as showing improvement on the measure of divided attention (auditory consonant trigrams). There were no other noteworthy observations of pre-post differences for any of the three patients on the other attention measures (Digit Span, Stroop, CPT).--Attention Shaping
Behavioral-based approaches for modifying behavior, even cognition, are not new.42,43 Shaping involves the differential reinforcement of successive approximations toward a target behavior. Behaviors that approach the desired target are reinforced; nondesired behaviors are not. Initially, training focuses on behaviors that have a high likelihood to occur within an individual's existing behavioral repertoire (eg, sitting up for 30 seconds). Once that behavior becomes established (ie, occurs regularly), the criterion for reinforcement is advanced so that the individual must perform a behavior that is closer to the end goal. The new behavior is then selectively reinforced, and these steps are repeated until the target behavioral goal is attained. Behavioral shaping procedures share methodological procedures with other training approaches such as errorless learning. One key difference is that in shaping, training is not explicitly designed to prevent mistakes or undesired behaviors from occurring, whereas in errorless learning the trainer takes active steps to prevent them.--Silverstein et al.44,45 demonstrated that a group of 6 treatment-refractory schizophrenia inpatients' attention span during participation in a skills training group could be improved by pairing primary or secondary reinforcers (such as tokens) with the desired behavioral response. A set of individualized verbal and nonverbal behaviors was targeted for training. Nonverbal behaviors included behaviors such as keeping eyes open, keeping head up, and making eye contact with the group leader. Verbal behaviors included responding within 5 seconds and making spontaneous comments. After a baseline assessment and identification of individualized attention goals, shaping procedures were initiated during the group. Two observers who were not involved in conducting the group recorded the frequency of target behaviors during 15-minute intervals. After each interval, patients who met or exceeded their target goal received a token that could later be exchanged for 25 cents. Shaping procedures initially targeted relatively simple attention goals (eg, eyes open for 30 seconds) that were easily met, and they increased in difficulty as mastery was attained over time. Results indicated that all participants in the study showed significant pre-post gains in attentive behavior. Similar positive findings are reported from earlier studies with severely impaired schizophrenia patients.42,46--Behavioral shaping is the only evidence-based cognitive rehabilitation treatment for severely impaired, treatment-refractory schizophrenia patients. One concern with behavioral shaping procedures is that training gains are lost once reinforcement is discontinued. However, there is some data to suggest that gains may be more durable in clinical settings than would be anticipated.42 The durability may be due to the fact that in treatment settings the reinforcing qualities of the originally trained-on reinforcer (a token) are transferred to other, perhaps more potent reinforcers (eg, social praise for engaging in the desired behavior, increased self-efficacy on the part of the patient). In the Silverstein et al. studies, patients may attain greater mastery and sense of success as they are able to meet behavioral goals through proscribed shaping procedures. Interestingly, though the behavioral shaping program initially begins with primary and secondary reinforcers aimed at gaining traction on the target behavior (ie, attention span), a secondary outcome of training may be improvement in self-efficacy and self-esteem. Arguably, promoting self-efficacy through training success is a goal in virtually all cognitive rehabilitation training programs.--In an interesting study with a complicated design, Silverstein et al.47 examined the efficacy of individually administered APT (described above) followed by attention shaping administered within a skills training group. Participants were schizophrenia patients randomly assigned to APT plus attention shaping versus a control condition. The 2 groups were matched for training time. For the experimental group, training included 6 weeks of APT followed by 16 sessions of skills training with attention shaping. For the control group, training included 6 weeks of group treatment followed by 16 sessions of skills training without attention shaping. The behavioral outcome measure was a summary of the daily ratings of attentiveness for each participant. Neuropsychological measures included the Digit Span Distractibility Test, Sustained Attention Test, California Verbal Learning Test, and the Micro-Module Learning Test. The study yielded rather fascinating results. The experimental group showed dramatic improvement on the behavioral observational data of attention versus the control group. After training, the experimental group showed periods of attentiveness of an average duration of approximately 19 minutes compared with approximately 2 minutes for the control group. There were no group differences on the neuropsychological measures of attention, perhaps because of the lack of sensitivity of these measures at detecting behavior change. The study design did not allow for a direct comparison of the specific contributions of APT versus attention shaping, although relatively low levels of attentiveness were observed after APT that increased substantially with attention shaping. The slope of attentional improvement during the attention shaping phase was similar to that observed in previous studies.45--These findings underscore a key conceptual dilemma in cognitive rehabilitation, namely, “What are the most appropriate CR outcome measures?” Wilson,48,49 in her work with brain-injured patients, has noted the poor relationship between cognitive impairment measured by neuropsychological tests and cognitive disability reflected in reduced ability to perform real-world tasks. Similarly, she has noted that reductions in cognitive disability occur in the absence of improvement on neuropsychological tests in patients involved in CR. These observations bring into question the selection of outcome measures used in studies of CR and warrant a reexamination of the field's goals for treatment (ie, disability reduction versus cognitive impairment reduction). Neuropsychological measures were not specifically designed to assess treatment changes in behavioral outcome. Hence, they may lack the necessary sensitivity to assess improvements in cognitive disability.
--Compensatory Approaches
Unlike the approaches reviewed above that attempt to enhance cognition, compensatory approaches place primary emphasis on bypassing cognitive impairments to improve broader aspects of function. Impairments in cognition are circumvented either by recruiting relatively intact cognitive processes or by utilizing environmental supports and adaptations to cue and sequence target behaviors. Two illustrative compensatory programs are described.--
Errorless learning is a training approach based on the theoretical belief that the commission of errors adversely affects learning in certain neurologically impaired groups. Two reports provide evidence that the commission of errors during learning is particularly problematic for persons with schizophrenia.50,51 In an errorless learning approach, the task to be trained is broken down into small component parts with the simplest tasks trained first, followed by more complex ones. During training, a wide variety of teaching methods and instructional aids are implemented to prevent errors from occurring. Each component skill is then overlearned through repetitive practice. In errorless learning 2 procedural principles are emphasized: (1) prevention of errors during learning and (2) automation of perfect task execution.--Kern et al.52 found that cognitive deficits were not related to vocational task performance in patients who were trained using errorless learning methods, but that cognitive deficits predicted performance in those trained by conventional means. This finding provides some evidence that errorless learning may in fact compensate for deficits in cognitive functioning in patients with schizophrenia. Kern et al. speculate that by utilizing this approach, the patient is not called upon to monitor mistakes and correct them. In addition, errorless learning may make use of implicit memory processes that may be relatively spared in schizophrenia patients in comparison to explicit memory processes. In a study of 65 clinically stable outpatients, Kern et al.53 found errorless learning to improve performance of entry-level job-training tasks relative to conventional training. Moreover, Kern et al.54 have extended the use of errorless learning to more complex tasks, such as social problem solving, with positive results.--
Cognitive Adaptation Training (CAT) is a compensatory approach using environmental supports and adaptations such as signs, checklists, medication containers with alarms, and the organization of belongings to prompt and sequence target behaviors such as taking medication and taking care of living quarters. Treatment strategies are based on a comprehensive assessment of cognitive functioning, behavior, and environment. CAT is based on the idea that impairments in executive functioning lead to problems in initiating and/or inhibiting appropriate behaviors. Using behavioral principles such as antecedent control, environments are set up to cue appropriate behaviors, discourage distraction, and maintain goal-directed activity. In addition, adaptations are customized for specific cognitive strengths or limitations in attention, memory, and fine motor control (eg, changing the color of signs frequently to capture attention, using Velcro instead of buttons for someone with fine motor problems). In 2 studies Velligan et al.55,56 randomized a total of 90 medicated individuals with schizophrenia to 1 of 3 treatment groups: (1) CAT, (2) a control condition involving home visits and environmental changes not related to functioning (eg, bedspreads), and (3) treatment as usual. Participants in CAT improved in severity of symptoms and level of adaptive functioning compared with the other treatments groups. Effect sizes for improvements in adaptive functioning were large (Cohen's d > 8.0).
Summary
In general, the results from the review of these cognition enhancing and compensatory approaches to CR are encouraging. Improvements in cognition have been found using different theoretical and conceptual approaches and using computer- and noncomputer-based methods. The findings are not uniformly positive, but one would not expect them to be so at this stage of CR development. Few approaches have more than 3 data-based studies supporting their efficacy in schizophrenia. With respect to broader outcomes, more data is needed, but there is evidence that participation in CR can lead to improvements in social and vocational functioning.--One issue that remains to be clarified concerns dosing—that is, how often and how long does a participant need to be involved in training to show meaningful gains. This appears particularly germane given the recent findings from Medalia's lab concerning the relationship between training intensity and training outcome. At present, there are no agreed upon guidelines for levels of intensity and duration of training.
--Looking Beyond Cognition: Motivation and Expectancies
The preceding review reflects a diverse and ever-growing movement aimed at addressing cognitive dysfunction in schizophrenia. Given the robust literature showing a relationship between neurocognition and functional outcome (see reviews2–4), most would argue that cognition is a worthwhile treatment target. However, despite its attractiveness, it is by no means obvious that the extent of disability that is prototypical of schizophrenia would be expected simply on the basis of the extent of cognitive impairment. That is, the functional disability of schizophrenia appears to be more severe than would be expected solely on the basis of general cognitive impairment on the order of 1–1.5 standard deviations below the normal mean (as revealed in the meta-analysis of Heinrichs and Zakzanis10). Clearly multiple factors contribute to this “excess” disability, including the burden of residual symptoms, the social stigma of mental illness, and illness onset disrupting the acquisition of the education, vocational skills, and normative experience needed to navigate the transition to adult independent role functioning, among others. Insofar as these “noncognitive” variables contribute to disability, it stands to reason that they will also likely limit the direct translation of gains in cognitive performance achieved through rehabilitative techniques into enhanced functional status. However, even after considering the contribution of the above social and symptomatic factors, it is our clinical view that the illness typically includes a compromise in motivation that is responsible for some of the “excess” disability and is therefore a critical treatment target.--Motivation can be defined as an internal state or condition that serves to activate or energize behavior and give it direction. Clinical observation of many patients suggests a profound lack of active, adaptive engagement with the environment. Although many patients possess certain cognitive skills and routines when assessed formally, these skills are often not brought to bear on events and challenges encountered in daily life. In essence, standard environmental cues do not appear to reliably activate the effort of patients, and many fail to adjust their performance in the face of changing contingencies. Similarly, the experience of success, and of failure, often does not lead to behavioral adaptation as one might expect in a non-ill group. Thus, the essential impairment in schizophrenia appears to be focused at the intersection of cognitive and motivational processes, where the consequences of actions serve to shape changes in behavior leading to more successful adaptation.--Recent basic neuroscience research has suggested that the dopamine system plays a critical role in precisely this type of ongoing behavioral activation and regulation.57 Two lines of research are particularly germane for the clinical phenomenology of schizophrenia and a consideration of rehabilitation. Based on a large body of animal research, Berridge and Robinson58 have argued that the dopamine system plays a critical role in the generation of reward-seeking behavior rather than of hedonic experience itself. That is, dopamine is involved in how much an animal “wants” a reward, not how much they “like” a reward, as shown in studies where the administration of dopamine-blocking drugs reduces the amount of effort/work that an animal will make to receive a reward but does not alter actual reward consumption. This conceptualization of the role of dopamine has been captured in the term “incentive salience,” suggesting that dopamine cell firing serves to increase the salience or desirability of a stimulus or action that is associated with a rewarding outcome. This notion is particularly relevant for schizophrenia, as a large body of research clearly demonstrates that patients experience surprisingly normal responses to a wide array of emotionally evocative stimuli.61–66 In essence, many patients with schizophrenia are not truly anhedonic: the observable muted emotional expressiveness and lack of goal-directed behavior cannot be attributed to an actual decrease in emotional experience or pleasure. Instead, it appears that many patients do not “want” the things that they “like.” The extent to which this is intrinsic to the illness versus an adverse outcome of treatment with dopamine-blocking drugs is a critical issue for future research.67–69 However, this basic science highlights an important clinical challenge: insofar as the “wanting” system is compromised in patients, it can be expected that positive outcomes and experiences achieved in rehabilitation settings will drive learning in a less than optimal or expected fashion. Indeed, it is possible to conceptualize the efficacy of behavioral treatment approaches through the use of the salience framework. One of the hallmarks of social learning and token economy approaches is that these interventions serve to highlight the “value” associated with various behaviors. This explicit and externally provided mapping of action outcomes may well compensate for a patient deficit in the ability to use internal representations to serve this function. The success of these approaches demonstrates that the reward system in schizophrenia is not completely shut down and unavailable; the system can be activated with vigorous external cueing.
The incentive salience line of pharmacological research is complemented by single cell recording studies of behaving nonhuman primates that have detailed the role of dopamine cell firing patterns in ongoing behavioral regulation and learning. Studies in behaving nonhuman primates have shown that phasic increases in dopamine cell firing occur when events are better than expected or predicted.57,70–72 Similarly, transient decreases in dopamine cell firing occur when events are worse than expected. These phasic increases and decreases in dopamine cell activity have been shown to correspond with those generated by temporal difference error learning algorithms widely used in the area of machine learning and computational modeling.57,73,74 In these models the error signal is used as a means of optimizing ongoing behavioral performance, and applied to behaving primates or humans, it is hypothesized that the dopamine error signal (DA) is broadcast to multiple striatal and frontal areas and serves to guide reinforcement learning and activate cognitive control. This reinforcement learning “system” is obviously relevant in the case of highly salient rewarding stimuli and experiences. However, several recent computational modeling and event-related potential studies have suggested that this same basic mechanism is involved in mediating human cognitive control, error monitoring, decision making, and managing the contents of working memory.75 McClure et al.76 have argued that the different emphases of temporal difference error models versus the salience model of Berridge and Robinson are more apparent than real and can be reconciled within a unified computational approach. In essence, this is a transactional system, where learning occurs in relationship to both external outcomes and expectancies, and which deals with extended sequences of behavior. If schizophrenia were to compromise the functioning of this system, the results would be profound (a notion addressed from a different perspective 35 years ago by Stein and Wise77). In essence, patients would have difficulty initiating behavior to pursue valued goals, leading to a failure to develop the competencies needed to achieve them. Further, they would fail to make behavioral adjustments in the face of negative outcomes.
If the functional disability of schizophrenia is caused, at least in part, by dysfunction within this cognitive/motivational system, this system may be a critical, explicit target for remediation efforts. CR interventions are often designed in an effort to attenuate the negative impact of motivational deficits on the task at hand—improving cognitive skill. For example, many approaches use high levels of positive social feedback or actual token reinforcers for on-task cognitive performance. Another design strategy includes manipulating expectancies for success. It will be important to identify which types of external manipulation of reinforcement contingencies best address the underlying systems' level of dysfunction.
One model, the NEAR program,34 has been designed with a specific focus on motivational issues, building on a large body of educational research that has emphasized the importance of intrinsic motivation. Intrinsic motivation occurs when task performance, in and of itself, is rewarding. Such tasks elicit high levels of engagement and active interest on the part of the learner. Indeed, there is a large, and somewhat controversial, literature that suggests that extrinsic rewards may actually serve to decrease intrinsic motivation, at least in specific task environments. Three aspects of the NEAR model are designed to enhance intrinsic motivation. First, the program utilizes educational software packages that are highly engaging. Thus, rather than the repetitive “drill and practice” of cognitive routines that is common to other computer software programs, the NEAR software is chosen to engage cognitive routines in a visually interesting, interactive context. Second, patients are encouraged to choose the programs and activities that are the focus of the rehabilitation sessions. Although the leader can be helpful in assisting the patient to make a selection, the patient is free to choose what he or she may like to do best, thereby increasing the role of intrinsic motivation. Further, the NEAR leader serves as more of a coach than a teacher; rather than teaching a specified curriculum, the leader provides prompts and tips that serve to help the patient get further along the path he or she has chosen. Thus, the overall clinical model is designed to enhance the motivational salience of the activities and the role of the patient as an independent agent in the rehabilitation process.
Available data to date suggest that the NEAR model does yield measurable significant cognitive benefits. These benefits are largest in the participants who were most actively engaged in the program as reviewed by Medalia and Richardson.38 Patients who completed the same number of sessions over a much longer period demonstrated much more modest cognitive benefits. Two hypotheses are suggested by these data. First, it is possible that the results simply reflect an effect of more “massed” rather than spaced practice. Alternatively, it is the activation of intrinsic motivational processes that serves to enhance the cognitive benefits of NEAR. While speculative, the latter idea can be seen as consistent with the role of dopamine in enhancing learning through the selective reinforcement of successful cognitive routines.
Other models of CR, though not designed around the issue of intrinsic motivation, address motivation in different ways. For example, in Cognitive Adaptation Training it is possible that the environmental supports that prompt and sequence appropriate behavior may bypass deficits in intrinsic motivation, as they tend to rely more on basic stimulus-response learning. All the models described herein provide a great deal of positive reinforcement for participation, including social support and praise. In addition, some offer money for time spent in remediation. The extent to which such externally mediated rewards serve to increase the level of intrinsic motivation that can persist after withdrawal of the treatment sessions is an important issue. That is, the question of interest may not be the persistence of trained cognitive/behavioral response repertoires but the likelihood that such responses are likely to be elicited on the basis of internal representations and goals. Silverstein and Wilkniss18 and Silverstein et al.78 have suggested that this process can be aided by making the goals of treatment more personal and making the process of therapy more goal-directed and understandable for the participant. Silverstein et al.78 describe a model of increasing the base rate of a desired behavior through extrinsic reinforcement, which then leads to a positive gain spiral of improved self-efficacy, intrinsic motivation to perform the behavior, and increased task engagement and performance. While evidence for simple durability of training effects is scant, the question of the persistence of motivational gains has not been investigated explicitly.
The issue of expectancies appears to be addressed to some extent by many of the models described herein. Standardized computer tasks allow for very precise alteration of the level of task difficulty based on an individual's performance. As performance improves, the difficulty of the task is increased, keeping expectations for success fairly constant and at a high level. Similarly, with errorless learning and environmental supports, the expectations for success are kept high. With errorless learning in particular, training is designed to minimize and if possible eliminate the occurrence of errors during the learning of new tasks and skills. These procedures function to bypass the need to make adaptive changes to environmental feedback (eg, developing an alternative response following a mistake). As noted above, there is reason to suspect that the usage of negative feedback may be an important area of deficit in schizophrenia linked to dysfunction of the dopamine system, where such error information is encoded as a transient cessation of dopamine cell firing. In addition, increasing patients' expectancy of success in the performance of these tasks may help motivate patients to continue task performance and develop competencies that he or she would be unable to develop in an unstructured environment with a higher probability of failure.
Though this discussion is speculative, it is clear that issues of motivation and expectancies have potentially important implications for conceptualizing the conduct and targets of CR. Targeting cognition alone may restrict the ability to see meaningful gains from rehabilitation efforts. For example, if the target of remediation is verbal memory, but a patient's functional disability is not in the capacity to remember information but in the ability to use memory in the pursuit of goals, enhancements in memory per se, while welcome, may be insufficient to produce clinically meaningful change in behavior. Second, the role of affective and motivational factors, particularly in how these intersect with cognitive processing, may need to be more deliberately addressed in CR interventions. These processes are briefly discussed in a recent review by Silverstein and Wilkniss.18 Simply providing salient stimuli (perhaps as in social, role-playing-type exercises) may be useful in the conduct of CR sessions, but it is unknown if this results in increased responsiveness to the salience of events outside of CR. We concur with the recommendation made by Barch 200579 that the field focus its energy on defining motivation and on the development and testing of assessments for use with patients with schizophrenia. Perhaps utilizing a measure of treatment engagement or working alliance would help to clarify the relationship between motivation to engage in CR and outcomes from cognitive rehabilitation. Third, if part of the essential deficit in the illness is a form of disengagement from the environment, the emphasis on a trainer-driven curriculum of exercises, as is typical of the field, is also open to question. That is, such approaches may not challenge the passivity that is characteristic of the illness, unless care is taken to engage the patient in a fully collaborative fashion. It is possible that the extent to which models are trainer-driven versus driven by the individual may be related to the variation in effect sizes between studies. Some evidence suggests that studies that adopt a more strategic approach to learning versus drill and practice seem to produce larger treatment effects.19,80 As should be clear, we are far more certain that motivational deficits are a critical part of the illness that need to be targeted by CR than we are confident that we know how to treat them at present. Current intervention approaches all acknowledge the importance of these problems in the conduct of CR. We suggest that the cognitive gains achieved through CR are likely to be consequential for functional outcome to the extent that these underlying motivational and self-regulatory mechanisms are altered in the context of CR.
Good luck.
 
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Hi all 
OPCRIT is a reliable diagnostic algorithm known to produce valid ICD-10 (and other) diagnoses of psychotic disorders, based on standardised case note review of 90 symptom items. 
Using OPCRIT to produce ICD-10 diagnoses is useful for the major psychotic disorders including schizophrenia (F20), schizoaffective disorders (F25) and bipolar disorder (F30-31) and psychotic depression (F32-33). However, substance-induced psychotic disorders are not assigned their own category under the algorithm used to produce ICD-10 diagnoses, instead being lumped with other psychotic disorders, nos (i.e. F21-29 + F1X.5, excluding F25). 
How would you go about teasing out people with a substance induced psychosis? Is this even possible? Various papers have noted this limitation, but I have not seen a workaround. Within the 90 OPCRIT items there is a section on lifetime dependence to alcohol, cannabis and other drugs (with or without affecting psychopathology), and I also have separate clinical ratings of ICD-10 diagnoses, so I could combine these with OPCRIT to code anyone who receives an OPCRIT non-affective diagnosis NOS AND a clinical diagnosis of F1X.5 to indicate a SIP. Would I be on safe ground here? 
Thanks to the community,
James
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Dear John and Andrei 
Thank you both for your responses. 
John, I agree that taking a more detail substance misuse battery, perhaps including a biological test, would be one way of getting at this problem. Unfortunately, I only have access to case notes and clinical diagnoses, and cannot return to the original participants (indeed, even if I could your idea would need to be administered prospectively). 
Andrei - I'm thinking about FEP rather than lifetime, so that makes things a bit easier. Your point about checking the agreement between clinical and research based diagnoses is an important one in this regard. 
Other views still welcomed
Thanks 
James
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In my thesis, which I am currently writing, I'm focusing on the links between (risky) sexual behaviour and Kernberg's concept of personality organization.
I have found information about sexual behaviours in patients with neurotic and borderline personality organization. However, when it comes to the psychotic personality organization I have not found any satisfactory information.
Would be grateful for any tips!
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I think there is a large qualitative/clinical literature concerning sexuality in people with psychotic disorders, mostly deriving from the psychoanalytic tradition. You'll find a good deal about "chaotic" or "poorly differentiated" sexuality, "polymorphous perversity," and so forth. As is usual with this literature, it is descriptively rich and often accurate, but contains less supporting evidence than one might wish - and of course the causal inferences are invalid.
In PsycINFO, I tried running a search with these parameters: (schizophrenia or psychotic) AND (sexual*) NOT trauma NOT abuse NOT antipsychotic
This yielded 1,769 "hits," including 1,311 journal articles. Limiting the search to English-language sources trimmed the total by about 300 more. Not all of these will be relevant to your work, I'm sure, but it's a starting place. Frankly, it's too many for me to sift through on your behalf while taking a break from my own academic duties. (And of course some of the many articles that do treat of abuse or trauma will also turn out to be relevant.) I wish I could offer an easier solution, but at least you aren't "high and dry."
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We use many agents "off label" (eg carbamazepine for bipolar) yet given history of abuse and psychotic reactions to both ketamine and phencyclidine we need to be cautious. In what situations should clinicians cross the line and administer ketamine?
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Great article thanks Devin (I cant work out how to attach articles as I just get an error message!) - I think it is fairly obviously a secondary cascade following ketamines acute effect on the nmda subset of glutamate.  I found this article discussing the meta plasticity changes particularly in the structure and function of the hippocampus to be illuminating as that would have implications on recovery from trauma ie inducing resilience (NMDA Receptors and Metaplasticity: Mechanisms and Possible Roles in Neuropsychiatric Disorders. Neurosci Biobehav Rev. 2012 March ; 36(3): 989–1000)
.  We are about to publish a case report postulating that ketmine could be an adjunct to psychological interventions to deal with depression associated with trauma.
Incidentally all this concern over psychosis being caused by Ketamine - I am concerned that people are confusing the acute dissociation effects for psychosis and they are very different - Oxford have seen zero zilch psychotic effects as have we ie none!! But dissociation certainly!!
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In psychiatry, mindfullness has been mostly used for mood and anxiety disorders. It seems that researchers and clinicians have been more reluctant to examine the effects of mindfulness in people with psychotic disorders.
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Dear Jérôme and Pier-Maria - Many thanks for your input. Much appreciated!!
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This refers to the various ways in which individuals and their families understand the "process of healing"  in the process of recovery
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the aim is to build a map of the patients about their energies. so we could understand the main differences between patients and their main similar features. it will be easy to diagnostic the patients.
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Can we devise a quasi-quantitative solution that establishes a formula to show the threshold or statistical probability for sz or sz-like disorders to manifest? The formula might look something like this: Gene A, allele a (all components weighted, perhaps a beta-weight in a regression equation) + Gene B, allele a + Gene C, allele b + Environmental factor (Env) A + Env B + Interaction of Env A & Gene A, allele a = the statistical probability that a sz-like disorder will manifest.
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Many epidemiological studies have linked diverse infections, both prenatally and in adulthood with schizophrenia http://www.ncbi.nlm.nih.gov/pubmed/?term=infection+schizophrenia. Recent data from the Danish register showed that about 45% of recently diagnosed schizophrenics had a hospital contact with some kind of infection prior to diagnosis - a large effect that did not seem to related to any specific pathogen. Nielsen et al, 2013 http://www.ncbi.nlm.nih.gov/pubmed/24379444
Many SZ genes (particularly from the MHC region in GWAS) Corvin and Morris 2014 http://www.ncbi.nlm.nih.gov/pubmed/24199664 are related to the immune system and many are also related to pathogen life cycles (toxoplasmosis/ herpes and others) http://www.ncbi.nlm.nih.gov/pubmed/23913659,23533776,18552348 suggesting a gene/environment interdependence
Infections are impossible to predict, so I doubt whether any statistical formula would be able to factor this in. Some are however preventable or treatable and perhaps the answer lies in identification and prior detection of the major culprits.
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Will the new diagnostic criteria improve differential diagnoses, and thus make treatment more effective?
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For example, the subtypes of schizophrenia (paranoid, catatonic, disorganized, undifferentiated) have been eliminated in DSM-V. These subtypes have been "eliminated due to their limited diagnostic stability, low reliability, and poor validity. These subtypes also have not been shown to exhibit distinctive patterns of treatment response or longitudinal course. Instead, a dimensional approach to rating severity for the core symptoms of schizophrenia is included in Section III to capture the important heterogeneity in symptom type and severity expressed across individuals with psychotic disorders." (Highlights of Changes from DSM-IV-TR to DSM-5, 2013, American Psychiatric Association).
Higher stability, reliability, and validity are going to be beneficial to a diagnostic system. How might this improvement in diagnostic accuracy and specificity be helpful in the treatment of psychotic disorders?