acparian issue 2 dec 2011 the depression...the history of cognitive therapy: aaron beck acceptance...

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CONTENTS

Presidents AddressEditors ReportBoard ReportFeature ArticleResearch Article ReviewClinican Perspective

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910111112 Editorial Guidelines

AcparianA PACTHE AUSTRALIAN

CLINICAL PSYCHOLOGYASSOCIATION THE OFFICIAL NEWSLETTER OF THE AUSTRALIAN CLINICAL PSYCHOLOGY ASSOCIATION

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THE DepressionISSUE

In this issue

The History of Cognitive Therapy: Aaron Beck

Acceptance and Commitment Therapy

Interpersonal Therapy

Psychodynamic Therapy

Mindfulness

Non-psychological Treatment

Neuropsychotherapy

Assessing Bi-Polar A�ective Disorder: The practical stu� that’s not in the DSM

Workplace depression

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Editor

Assoc. Editors

Copyeditor

Design

ACPARIAN Editorial Board

Kaye Horley, PhD

Giles Burch, PhD

McLytton Clever, DPsych (Clin)

Bronwyn Williams, MPsych (Clin)

Ben Callegari, MPsych (Clin)

CONTENTSEditorial

From the President

Board Report

Feature Article: The History of Cognitive Therapy

Acceptance and Commitment Therapy for Depression

A Neurobehavioural Rationale for the use of Mindfulness

Meditation in Psychological Treatment of Emotional

Disorders

Comment: Cognitive Therapy? Is this as good as it gets?

Interpersonal Therapy for Depression

Psychodynamic Therapy for Depression

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Electroconvulsive Therapy

Neuropsychotherapy and Depression

Assessing Bipolar A�ective Disorder: the practical stu�

that’s not in the DSM

Workplace Depression

Client’s Perspective

Research Review: Exercise as a treatment for Depression

The Ethics of Suicide

Towards Compentency-Based Training in Clinical

Psychology

ACPA Mentoring Program

Editorial Guidelines

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Kaye Horley, PhDEditord

Thank you for all the very positive responses to our �rst edition of ACPARIAN. A warm welcome to our second edition, where our focus is on depression. We hope you �nd it interesting and useful.

Depression is one of the most common conditions we encounter as clinicians, and is a major contributor to morbidity and mortality in our community. The 2007 National Survey of Mental Health and Wellbeing (from 8,841 households across Australia) indicated that of the 3.2 million people who had a 12-month mental disorder, 6.2% (995,900) experienced an A�ective Disorder1. A�ective Disorders comprised Depressive Episode (Mild, Moderate or Severe (4.1%), Dysthymia (1.3%) and Bipolar Disorder (1.8%). Women experienced higher rates of A�ective Disorders (7.1% and 5.3% respectively). Women in the age group 16-24 years had nearly twice the prevalence compared with men in the same age group (8.4% and 4.3% respectively). Because of the widespread incidence of depression, research into treatment for this insidious condition is crucial.

Our contributors detail major treatments in this edition. Aaron Beck, our distinguished guest contributor and a leading pioneer in the development of cognitive behaviour therapy (CBT), gives a fascinating account of his move away from the dominant psychoanalytic interpretation of depression of the time. His emerging theory focused on negative thinking as the basis of depression, leading him towards more scienti�c measurement and treatment. He was most interested in contributing to the depression theme of our publication. During our lively correspondence he celebrated his 90th birthday!

More recently, a number of commonly called “third wave” cognitive therapies have emerged. Articles by Robert Zettle and Bruno Cayoun, leading proponents in their �eld, outline how Acceptance and Commitment Therapy (ACT) and Mindfulness-based Cognitive Therapy (MBCT) respectively di�er from conventional CBT with perceived limitations. In examining the e�ectiveness of CBT, Lucius Arco places emphasis on the use of single case research designs versus randomised controlled trials (RCTs) in attaining more e�ective individualised treatment.

Another psychological therapy with demonstrated e�cacy for depression, outlined by Paul Rushton, is Interpersonal Therapy (IPT) with emphasis upon mood and interpersonal relationships.

The latest information on electroconvulsive therapy (ECT), as an essential treatment for those who have not responded to either pharmacological treatment or psychotherapy, is explored by Coleen Loo. The potential for exercise as a treatment for depression is explored in the Research section. Knowledge of neuroscience necessarily helps us to understand and treat depression, and advances in this area are presented by Pieter Rossouw. Karen Hallam articulates the inherent di�culties in the detection of bipolar disorder and the importance of correct diagnosis. As a signi�cant part of our lifetime is spent in the work place, contributing factors and the consequences of depression in this area are reviewed by Giles Burch. As clinical psychologists it is important that we have some understanding of the experience of depression. However, unless we have experienced depression ourselves, we can never really know what it is like. Bernie’s story highlights his experience and gives us some insight in to how it has a�ected him. The risk of suicide in depressed individuals is of priority concern for those in our care and its aetiology is often imperfectly understood. The Ethics and Legal Dilemmas section raises some interesting philosophical issues in presenting arguments for and against suicide. In caring for depressed and individuals clinicians need certain competencies in risk assessment. Some of the inherent di�culties associated with both the training and assessment of competencies are explored in Student and Training Matters.

Many thanks to our guest contributors, especially Bernie. Critical comments, suggestions and contributions for our next edition are most welcome.

Reference

1 Australian Bureau of Statistics (2007). National Survey of Mental Health and Wellbeing: Summary of Results. ABS. Cat No. 4326.0. Canberra: ABS.

Editorial

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From the PresidentJudy Hyde, PhDACPA Presidentd

The last quarter has seen ACPA become more broadly known within the community and a steady rise in membership numbers. The major series of event to impact on ACPA and bring us to the notice of politicians and the media was our involvement in the Senate Inquiry into the Commonwealth Funding and Administration of Mental Health Services. The ACPA submission, developed with the membership, now stands as a platform of policy for our organisation.

The separation of the College of Clinical Psychologists’ representation from the APS at the Senate Hearing to present with ACPA was symbolic of the need for clinical psychologists to have a voice of their own, separate from other professional bodies in psychology that primarily represent those without accredited clinical quali�cations. The consistent support for clinical psychologists bypsychiatrists, both from the RANZCP and psychiatrists individually, was heartening.

One of the more disappointing results of the Inquiry was the Senate Committee’s concerns about the unprofessional behaviour of our profession as represented by those explicitly wishing to have returned to them the status they held prior to National Registration: AAPi and the APS. The APS came under particular �re, requiring three letters plus phone calls to settle their internal disputes, followed by several minutes of questioning at the Hearing. This questioning stated several times that APS’ behaviour was ‘appalling’ and that the APS Board clearly did not represent clinical psychologists. ACPA sat on the sidelines in this, its only role being to bring to the attention of the Committee concerns about the AAPi newsletter, as members quickly expressed anxieties about making submissions if they were to be publicly ‘named and shamed’ for standing up for their training.

The Senate �ndings were mixed for our speciality. Clearly, we have a long way to go in representing the expertise of clinical psychologists to politicians. The paucity of the evaluation of the Better Access program was clearly identi�ed and what became clear was our need to provide evidence for our claims of the value of our training. The ACPA Board is currently developing a strategic plan for this that incorporates the use of media, advertising, Government, various professional and non-government

organisations, and the academic arena to bring our value to the awareness of policy makers.

The other major event was the annual ACPA conference held at the University of Melbourne, titled, Building Clinical Expertise. This was well attended and very much appreciated by an audience of clinicians of varying experience. The expert clinical focus that has marked both of ACPA’s conferences was a delight. The extremely high quality of presentations and workshops were delivered by distinguished senior members of the profession who brought a great deal of knowledge, experience and expertise to us all. Of particular note was the presentation of Professor Brin Grenyer, perhaps best known as the Chair of the Psychology Board of Australia, but here sharing with us his passion for clinical psychology, his joy of research, and his reverence for the important history of our profession in his presentation, Psychotherapy works: Findings from the analysis of therapist and patient interactions inside the therapy session. It was a delight to see these qualities of our profession’s leading proponent of standards and policy take centre stage!

Looking to the future, ACPA’s leading role in the campaign for specialist title has already born fruit with this issue being clearly placed on the agenda of the Health Ministers, who are establishing guidelines for all professions to meet for the granting of this privilege. Given that Western Australia has held this status for more than 35 years and its removal represents a downgrading of the standards of the profession in that state, and that the concept of endorsement is not well understood by the public who are hindered in making informed choices about practitioners, this is a claim we must win. In the �rst half of 2012, the Psychology Board of Australia will release a consultation paper putting forward di�erent models of specialist title for the profession to consider. It will be vital for clinical psychology to gain recognition of the quality of our specialist training and expertise in mental health.

Finally, I would like to again express gratitude to the editor of the ACPARIAN, Dr Kaye Horley, and the dedicated editorial committee for an outstanding publication that showcases ACPA and strongly advances our sense of community and shared purpose.

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The AGM also saw members vote on the proposed new Constitution. I soon discovered that my knowledge of the Corporations Act and formal procedural matters was not as strong as it could be, but luckily we were not short of expertise in these matters at the meeting, and we saw plenty of goodwill in �nding the best way forward. Despite the somewhat muddled approach, we proceeded with advice from the �oor of the meeting, a vote was taken, and the resolution to accept the new constitution failed to pass. The votes were 68 for the motion, and 66 against, but we needed a 75% majority for resolutions related to a company’s constitution. We will continue to act under the current constitution, and in the meantime, ACPA’s constitution committee will work towards developing recommendations that will best meet ACPA’s needs into the future. It was clear from the various conference discussions that there is widespread support for a strong National-based organisation with a structure that will allow both the Board to govern e�ectively, and members to contribute in a signi�cant way to the aims and ongoing operations and activities of the company.

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Left to Right: Lesley Bretherton, Suzanne Midford, Caroline Hunt (Vice President), Ann Wignall, Judy Hyde (President), Absent: Marjorie Collins.



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Caroline Hunt, PhDACPA Vice President

On the 15th October ACPA held its �rst AGM, incorporating the Presidential Address and several other important items of business. The �nancial reports were accepted without any opposition, as was the election of our two new members of the Board, Lesley Bretherton and Ann Wignall. For those who don’t know Lesley or Ann well, I can assure you that they will bring a wealth of expertise, clear-headedness, and enthusiasm to the Board.

Lesley is a past member of the APS and was on the executive of the Victorian Section of the APS College of Clinical Psychologists for �ve years; representing Victoria on the National Committee of the APS Clinical College for two years. She is currently Deputy Director of Psychology and Head of Clinical Psychology at Royal Children’s Hospital, Melbourne. As Clinical Associate Professor in Psychological Sciences, University of Melbourne, she convenes the Child Psychopathology program in the Master/PhD clinical program and supervises clinical and research students from this program in the areas of language, learning and child psychopathology.

Ann is the Director of Child and Adolescent Mental Health, North Shore Ryde and Principal Psychologist for Northern Sydney Local Health District, NSW. She has worked in a range of clinical, management and policy roles in public mental health. Ann has clinical, training and research interests in the treatment of child and adolescent anxiety. She established the Child and Adolescent Anxiety Clinic at RNSH and co-authored parent and therapist books and the Cool Kids treatment program. She was also involved in the development of treatment and early intervention programs for adolescent depression.

It was with great sadness that we saw three founding Board members step down at the AGM; all will be sorely missed. Leanne Clarke, our inaugural Public O�cer, was also responsible for developing ACPA’s Medicare Taskforce, and continues to build on her work developing our Mentoring Program. Leanne’s steady and calm work certainly helped steer us solidly through the early establishment of the organisation. Alice Shires, our company secretary, brought an important perspective to the early setting up of ACPA from her previous role as the Chair of the NSW Section of the APS College of Clinical Psychologists. Her good humour and clear thinking was a tremendous asset to our work.

Last but not least, Samantha May’s exceptional organisational skills stopped us all from being lost in a mountain of forms, policies and procedures. She has also left ACPA with a well-functioning “Find A Clinical Psychologist” website, and is much appreciated for her tireless coordination of the NSW-based CPD activities, including the inaugural National Conference in 2010.

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Professor Aaron Beck is emeritus Professor of Psychiatry at the University of Pennsylvania, emeritus President at the Beck Institute for Cognitive Therapy, and Research and Honorary President of the Academy of Cognitive Therapy. His development of cognitive therapy in the 1960’s led to widespread application in the treatment of depression and other disorders. Professor Beck has multiple publications associated with his research in psychotherapy and psychopathology. He is also noted for the development of numerous psychometric scales, particularly the Beck Depression Inventory (BDI), one of the most widely used instruments for measuring depression. Professor Beck has received many awards and is considered one of the most in�uential psychotherapists of all-time. He kindly gave his permission for ACPARIAN to reproduce his 2009 Rhoads lecture1 for this edition on depression.

detecting hostility in the dreams of depressed patients. Marvin then scored these dreams blindly for the presence of hostility in dreams of both groups. To my surprise and disappointment, the depressed patients showed less hostility than the nondepressed patients. This was di�cult to reconcile with my theory. Some of my colleagues said I simply did not go deep enough. Nonetheless, I did not know how much deeper to go. However, we did notice a particular theme in the dreams of the depressed patients. Mainly, they perceived themselves in very negative ways in the dreams and were subject to negative experiences. Their own self-image was of being defective, defeated, or diseased, and bad things would happen in the action of the dreams. For example, a patient dreamed of being alone in the desert with nothing to drink. He then came upon a coke machine, put a nickel in, and all he got was �zz – no liquid and no syrup. Another patient, who was going to a formal dance, discovered that both his shoes were for the left foot. Other patients dreamed of being abandoned, rejected, or humiliated. I then hit upon the hypothesis that, perhaps, this negative image and the negative dream experiences were still a manifestation of hostility against the self – a form of masochism. Only sometime later did I arrive at a di�erent formulation. Later, we con�rmed these �ndings in a large sample of hospitalized patients.

Concurrently, of course, I was seeing patients in therapy, and I had my second surprise. A woman in therapy was regaling me with stories of various sexual escapades. At the end of the session, I asked her how she was feeling. She said she was feeling quite anxious and depressed. I then suggested to her that, undoubtedly, the anxiety was due to her unacceptable sexual ideas and experiences coming to the surface, which triggered anxiety and guilt. She responded, “Of course, you are right Doctor. I can see that.” However, I noticed that she did hesitate a bit when she said this, and I brought that to her attention. She then said, “Well, to tell you the truth, I was thinking throughout the session that I was boring you.” I was surprised that she had never mentioned this. She said, “I always think I am boring you.” More importantly, there had been a stream of self-critical thoughts. On further exploration, her big problem in life was that she felt she was unattractive and boring and self-critical. In order to impress people, she would be melodramatic. It then was obvious to me that there was

THE HISTORY OF COGNITIVE THERAPY

Professor Aaron T. Beck

Actually, I never planned to create a new system of psychopathology or psychotherapy. The theory and therapy just grew like Topsy. My research �ndings, clinical observations, theoretical ideas and therapy were so intertwined at the beginning that it is hard to disentangle them. In retrospect, however, it is possible to tease out the various strands and see where they all come together. In my next project, the study of suicide, I was able to be more systematic in my approach.

My early work contained one surprise after another. I was intrigued by the phenomenon of depression because it seemed to contradict all the accepted norms of human nature: the pleasure principle, maternal instinct, and survival instinct.

My �rst venture into the study of depression was a research project attempting to con�rm the prevailing notion of depression as due to retro�ected hostility. According to this thesis, the patient has unconscious hostility towards a loved object; this is unacceptable – in the terms of the time “ego-alien” – and thus, the hostility is repressed and turned against the self. This formulation seemed to be quite logical and it could account for various symptoms of depression. For example, the hostility against the self could be manifested by self-criticism, inability to experience pleasure, loss of interest in other people and important goals, and, ultimately, in suicide.

It seemed to me that the best way to �nd this unconscious hostility, since it was not conscious, by de�nition, would be to explore the “Royal Road to the Unconscious”, namely dreams. So, I started to collect dreams from depressed and nondepressed patients. Then, in collaboration with a psychology student, Marvin Hurvich, we prepared a manual for

Distinguished Guest



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Right: Professor Aaron T. Beck

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This thought made him feel even more sad and suicidal. He went on to say that his house was falling apart, that his marriage was dead, and that his business was deteriorating. Applying the scienti�c method, I asked, “What is the evidence regarding your deteriorating house?” He replied, “The roof is leaking and there are some termites.” He recognized that he was incredibly magnifying the extent of the problems, which were essentially solvable. In regards to his marriage being dead, his evidence was that his wife rushed o� without saying goodbye. I asked for an alternative explanation for his interpretation that the marriage was dead, he recalled that his wife had told him that she was in a great hurry because she was late and she had to run o�. His alternative explanation in regards to his business deteriorating was that his business had always been subject to the business cycle, and it was a known fact that business is slow during the o� season but picks up in the fall, and there was no reason to believe that this year was di�erent from any other year. The interesting point is that, when he was trained to generate more realistic explanations, his depressed mood and hopelessness improved, although this kind of work had to be repeated continuously since he tended to slip back – until he emerged totally from his depression.

My third major surprise arose from the fact that, as I used this more direct kind of intervention, the patients started to improve much more rapidly. Whereas previously, I could count on a patient being in treatment for at least year, and frequently much longer, the patients started to improve after 10 to 12 weeks. Consequently, they started to say such things as “Doctor, you’ve helped me a lot, but I don’t see any reason for taking up any more of your time because I am feeling much better.” As a result of this, my practice rapidly shrunk, and I was facing a serious economic crisis! Fortunately at this point, Mickey Stunkard, who was Chairman of the Department of Psychiatry, suggested that I come on full-time in the department, and, from then on, my work consisted primarily of training residents and conducting research projects.

As I started to supervise residents in this new approach, I found that their patients were starting to improve just as they had in my practice. At one point, John Rush, who was also a resident, told me “You know, Tim, this therapy really works, but if you don’t do a clinical trial, nobody is every going to believe it.” I told John that clinical trials were really back-breaking, and I could not envision myself doing one. John then volunteered that he would do all of the work involved in the trial if I would only train the residents. As it happens, again a surprise, in a randomized trial comparing cognitive therapy with imipramine over a period of 12 weeks, cognitive therapy performed signi�-cantly better and, as it turns out, did better in 6-month and one-year follow-ups.

My approach to suicide was far more systematic. In contemplating research in this area, I planned in advance to proceed to look at the following dimensions: classi�cation, assessment, prediction, and intervention. This was an ambitious project that actually continued for the next 35 years. Studies like this need to be started when one is young and is

certain material in the patient’s mind that they did not report in the free association. I found that most of these had to do with monitoring these self-critical thoughts such as “I sound stupid” or “I should try to impress him.”

I found that the patients were having a whole stream of thoughts that they were not reporting to me. I noted that the stream largely had to do with self-monitoring, self-evaluations, and self-criticism. Depressed patients, in particular, would attach negative meanings to how they perceived they were doing in therapy, and would have thoughts such as, “I sound stupid”, “I’m not getting anywhere”, “I don’t have any thoughts”, and so on.

I decided that I was missing a great deal in the free association and decided that I could get a better idea of what the patients were thinking by sitting them up. I then made my next discovery, which was that depressed patients attached negative meanings to almost any experience. However, they were frequently unaware of the negative meanings but only of the bad feelings they had. For example, they would have negative thoughts about various experiences, which took forms such as “She doesn’t like me”, “I look foolish”, “I won’t be able to do this”, “I can’t handle this” or “I’m all alone”. I then discovered that the patients seemed to interpret all experiences through a negative-colored prism – that is, they could only see the dark side of every experience and could not see anything that was positive.

At this point, I was able to put together these two strands: from the dreams and from the verbalizations. It occurred to me that what the patients were reporting in their dreams actually were a symbolic representation of their beliefs and attitudes in their waking life. Thus, the dreams of being defective or abandoned were also expressed in their statements such as “I’m stupid” and “Nobody cares about me”.

I soon discovered that a key factor in the patients’ depression was the fact that their beliefs about themselves shaped the excessive or erroneous meanings they attached to their experiences. These errors were represented in what I called a “thinking disorder”, in which they would overgeneralise, selectively extract, or greatly maximize or exaggerate problems. Driving these excessive interpretations or misinterpretations was a negative view of themselves, their future, their current experiences, and their past. It was as though they were seeing things through a dark-colored prism, blocking out the positive and seeing only the negative.

By this time, I was already enamored with the scienti�c method and started to apply the scienti�c method to what the patients were telling me. I would ask questions, such as “What is the evidence?”, “Does your interpretation necessarily follow what you observed?”, “Are there alternative explanations?”, “Do you think your basic assumption may be incorrect?” An example was a successful businessman who had become depressed and suicidal and, during one particular session, he said that he had the automatic thought, “I am a total failure.”



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“Were you sad or glad that your suicide attempt did not end in your death?” it turned out that those who were unhappy about the failure of their attempt were signi�cantly more likely to eventually commit suicide than those who were glad that the attempt had not succeeded. This �nding validated both the Hopelessness Scale and the Suicide Ideation Scale as predictors of suicide.

Finding a successful intervention was a di�erent problem. It was not until 2007 that Greg Brown and I completed a study on a short-term intervention of cognitive therapy (10 visits) of 120 patients – 60 in the experimental group and 60 in the control group – of suicide attempters. We found, at a follow-up, that twice as many patients in the control group reattempted as compared to the experimental group, so we were able to cut down the reattempt rate by 50 percent with a very short-term intervention. We presume that the longer term intervention would have produced even stronger results.

In a recent communiqué to ACPARIAN, Dr Beck made the following comments:

Cognitive therapy remains in a state of transition. More and more information is being garnered from clinical work, as well as from other branches of psychology, such as cognitive psychology and social-cognitive psychology. There also has been a great deal of work correlating various aspects of the cognitive model with neurobiological �ndings. All of this work should help to accelerate the progress of cognitive theory and cognitive therapy.

Reference

1 Source: The Eleventh Jonathan E. Rhoads Commemorative Lecture. Delivered September 15th, 2009. Sponsored by the American Philosophical Society and the University of Pennsylvania Department of Surgery. A previous version of this lecture was printed in Cognitive Therapy Today, the newsletter of the Beck Institute for Cognitive Therapy.

willing to stay with a particular subject for a professional lifetime.

In 1970, I headed up a task force on the Classi�cation of Suicidal Behaviors. At that time, there was no classi�cation of suicidal behaviors, but there was a conglomerate of con�icting and ambiguous terms, and, in many of the studies, completed suicides, suicide intent, and suicide attempts were all merged together. We came up with a classi�cation of Completed Suicides, Suicide Ideation, and Suicide Intent. Each of the categories was classi�ed by two qualitative terms, speci�cally “Degree of Intent” and “Degree of Lethality”. Lethality actually referred to the biological/medical damage or medical dangerousness of intent or actual attempt.

My next venture was to devise various instruments to measure these attributes. I, thus, prepared the Suicide Intent Scale for attempters, Suicide Ideation Scale for ideators, and then the Lethality Scale to measure the medical consequences of the suicide attempt. In short, I found that we could measure each of these variables. There was a large correlation between suicide intent, as measured by the Suicide Intent Scale for attempters, with the degree of lethality. Since I had observed that hopelessness seemed to be the most powerful generator of suicidal urges, I developed the Hopelessness Scale to measure this variable.

The validation of the Ideation Scale was �rst carried out with individuals who were hospitalized because of severe suicide intent. This was a high-risk population, and, therefore, the base rate of ultimate suicides would be high enough to make a valid prediction. We had approximately 100 patients with suicidal ideation in this group. We followed them for �ve to 10 years, and we found that the patients who scored high on our scale of suicide ideation were the most likely to commit suicide. Even more signi�cant was the fact that the patients who were high scorers on hopelessness were about 10 times more likely to commit suicide than lower scorers. This provided two valuable tools for estimating suicidal risk: the Suicide Ideation Scale and the Hopelessness Scale.

Suicidal outpatients were a di�erent story because they have a relatively low base rate for ultimate suicide. In 1989, however, we had collected enough cases of suicide ideators – over 1,000 – to conduct a validation study. Again, we found that the Suicide Intent Scale discriminated between those who ultimately committed suicide and those who did not. Also, the high scorers on the Hopelessness Scale were 10 times more likely to commit suicide than the low scorers. Thus, once again, we found that the Suicide Ideation Scale and the Hopelessness Scale were valuable instruments for predicting future suicides or for determining suicidal risk.

The study of suicide attempters, however, apparently was a di�erent story. When we studied this group, neither of our scales seemed to predict ultimate suicide. However, we later noted a signi�cant fact: namely, by asking the question,



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Third Wave Therapies

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ACCEPTANCE AND COMMITMENT THERAPY FOR DEPRESSION

Professor Robert D. Zettle

Professor Robert D. Zettle is a licensed clinical psychologist and professor of psychology at Wichita State University. He is a pioneer researcher in the development of ACT. He has conducted workshops and published several journal articles, chapters, and a 2007 book on acceptance and commitment therapy in treatment of depression. Professor Zettle also serves on the editorial boards of two psychological journals.

Acceptance and commitment therapy (ACT) is a cognitive-behavioural therapy based on a functional contextualistic account of human language and cognition known as Relational Frame Theory1. As a member of the third generation within the CBT family, ACT combines second-order change strategies, such as acceptance and mindfulness exercises, in altering how individuals relate to their own troublesome thoughts, emotions, and bodily sensations, along with e�orts to more directly activate value-directed behaviour2. ACT originally was developed as a transdiagnostic approach that has been extended to assisting those who struggle with various forms of su�ering, including depression3. ACT is recognized by the Society of Clinical Psychology within the American Psychological Association as having modest empirical support based on research showing that it compares favourably to cognitive therapy (CT) in treatment of depression4,5,6 while initiating improvement through distinct and theoretically speci�ed processes that di�er from those of CT7, 8.

Within the ACT model of human su�ering, depression is seen as a “secondary” condition that results from the inability to successfully avoid or escape from more primary a�ective states that are the inevitable consequences of being fully engaged in life - such as sorrow, guilt, and sadness - as well as the contexts that give rise to them. Loved ones die, marriages break up, and career aspirations fall short. Unfortunately, time and energy that could remain invested in valued living may instead be reallocated to support rumination and other rigid experiential avoidant strategies, resulting in disengagement from life. The primary goal of ACT is to promote psychological �exibility as the ability to make adjustments necessary to sustain value-directed behaviour. The two fundamental questions that it seeks to address in approaching this goal with each client are: (a) What do you want your life to stand for? and (b) What is standing in your way? The �rst question is about commitment to values, while the second concerns acceptance of psychological barriers to committed action.

Values within ACT are construed most simply as consequences that give meaning to life. Values encompass ongoing patterns of behaviour, such as being a loving parent, that are themselves intrinsically reinforcing and which can be realized through an in�nite number of goal-related activities, both small (e.g., telling children a bedtime story) and large (e.g., saving for their college education)9. Early on within ACT, client values are identi�ed, clari�ed, and veri�ed through a number of related means, ranging from the administration of formal questionnaires to experiential exercises, such as asking clients to imagine what they would like to have engraved on their tombstone or have friends and family members eulogize about them. Once core values are arrived at for each client, they can be used to reframe ongoing behaviour (e.g., list all of the ways the client is already acting as loving parent) as well as guide and plan further commitment to value-directed actions (i.e., what are some other things you could do to be the kind of parent you want to be to your children?).

Unwanted thoughts, feelings, memories, bodily sensations, and even the sense that certain actions would be “out of character,” are common psychological obstacles that clients encounter in moving their lives in a valued direction. At this juncture, alternative ways of responding to these barriers are introduced through a series of experiential exercises, metaphors, and practices. For example, believing a thought, such as “I can’t do this,” would not be dealt with via cognitive restructuring within ACT, but with defusion (e.g., restate the thought in an altered voice), acceptance (e.g., carry the thought written on a card), and mindfulness practices (e.g., visualize the thought being carried on a leaf �oating by on a stream). Overidenti�cation or fusion with self-referential thoughts (e.g., “I am depressed”) and related narratives or life stories (e.g., “anyone mistreated as I have been would be depressed”) that function as barriers to value-directed behaviour may be addressed indirectly through mindfulness interventions (i.e., just notice what your mind is telling you about you and your life) and more directly through experiential exercises designed to strengthen perspective taking (i.e., just notice who is noticing this).

A number of resources and materials are available to those of you who may wish to learn more about ACT for depression and possibly incorporate it into your clinical practice, including guidebooks for both therapists10 as well as clients11. A particularly rich source of both assessment and therapy materials for use in ACT as well as related research articles is available through the website of the Association for Contextual Behavioral Science (ACBS; go to www.contextualpsychology.org/). ACBS is an international organization with value-based dues (you pay what you deem your membership to be worth) and with one of its largest and vibrant a�liated chapters located in the southern hemisphere. The Australian and New Zealand Chapter of ACBS (see www.anzact.com) recently held their �fth annual conference in Brisbane in which both introductory and advanced training workshops in ACT were o�ered. The ACT community and related basic and applied research continues to grow rapidly, but has ample room remaining on the bus for additional fellow travelers who would like to join us in our exciting journey.

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References

1 Hayes, S. C., Barnes-Holmes, D., & Roche, B. (Eds.). (2001). Relational frame theory: A post Skinnerian account of language and cognition. New York: Plenum.

2 Hayes, S. C., Strosahl, K. D., & Wilson, K. G. (2003). Acceptance and commitment therapy: An experiential approach to behavior change. New York: Guilford.

3 Zettle, R. D. (2005). The evolution of a contextual approach to therapy: From comprehensive distancing to ACT. International Journal of Behavioral Consultation and Therapy, 1, 77-89.

4 Forman, E. M., Herbert, J. D., Moitra, E., Yeomans, P. D., & Geller, P. A. (2007). A randomized controlled e�ectiveness trial of acceptance and commitment therapy and cognitive therapy for anxiety and depression. Behavior Modi�cation, 31, 772-799.

5 Zettle, R. D., & Hayes, S. C. (1986). Dysfunctional control by client verbal behavior: The context of reason giving. Analysis of Verbal Behavior, 4, 30-38.

6 Zettle, R. D., & Rains, J. C. (1989). Group cognitive and contextual therapies in treatment of depression. Journal of Clinical Psychology, 45, 436-445.

7 Hayes, S. C., Luoma, J. B., Bond, F. W., Masuda, A., & Lillis, J. (2006). Acceptance and commitment therapy: Model, processes, and outcomes. Behavior Research and Therapy, 44, 1-25.

8 Zettle, R. D., Rains, J. C., & Hayes, S. C. (2011). Processes of change in acceptance and commitment therapy and cognitive therapy of depression: A mediation reanalysis of Zettle and Rains. Behavior Modi�cation, 35, 265-283.

9 Wilson, K. G. (2008). Mindfulness for two: An acceptance and commitment therapy approach to mindfulness in psychotherapy. New Harbinger: Oakland, CA.

10 Zettle, R. D. (2007). ACT for depression: A clinician’s guide to using acceptance and commitment therapy in treating depression. New Harbinger: Oakland, CA.

11 Strosahl, K. D., & Robinson, P. J. (2008). The mindfulness and acceptance workbook for depression: Using acceptance and commitment therapy to move through depression and create a life worth living. New Harbinger: Oakland, CA.

A NEUROBEHAVIOURAL RATIONALE FOR THE USE OF MINDFULNESS MEDITATION IN PSYCHOLOGICAL THERAPY OF EMOTIONAL DISORDERS

Bruno A. Cayoun, DPsych

Dr Bruno Cayoun is Director of the MiCBT Institute in Hobart, Tasmania, a registered training organisation which trains, accredits and supports MiCBT practitioners. He is a clinical psychologist in private practice and the principal developer of Mindfulness-integrated Cognitive Behaviour Therapy (MiCBT), which he has been teaching to mental health professionals internationally for the past eight years. He has undergone intensive training in mindfulness centres in France, Nepal, India, and Australia for the past 22 years. Dr Cayoun is the author of two books, including “Mindfulness-integrated CBT: Principles and Practice” (Wiley, 2011). He is also an Honorary Research Associate at the University of Tasmania where he supervises mindfulness research.

Mindfulness meditation has been taught by Buddhist monks for over 25 centuries. The consensus in both Eastern and Western literature is that mindful attention requires a deliberate and sustained focus on events experienced from moment to moment with a non-judgemental and non-reactive attitude. The main purpose of teaching mindfulness skills in the clinical context is to help clients develop a greater degree of self-awareness, self-acceptance, and greater sense of control over emotional reactivity. This short article provides a brief account of the co-emergence model of reinforcement, as a neurobehavioural rationale for the inclusion of mindfulness meditation in the psychological treatment of emotional disorders.

Essential Limitation Of Traditional CBTWhen we are upset, we tend to over-identify with the perceived problem, often misinterpreting the sensory cues and disregarding other interpretations that are just as valid, despite our ability for logical and rational thinking. More often than not, these interpretations are repeated over time and can be identi�ed as habitual patterns of thinking, or schemas, triggered by certain kinds of events. The cognitive theory of emotional disorders suggests that core beliefs learned since early childhood, and reinforced throughout life, are at the origin of this switch in cognition and its unhelpful consequences in daily life1,2. Accordingly, with conditions such as depression, cognitive-behaviour therapists do their best to help clients reappraise their deep-seated beliefs and unhelpful assumptions about life through reasoning and behavioural tasks.

People who undergo a course of traditionally delivered Cognitive Behaviour Therapy (CBT) need to rely heavily on the so-called “executive functions” to bene�t from it3. Executive functions are mostly located in various regions of the prefrontal parts of the cerebral cortex and include our ability for focused and sustained attention, goal-directed action, regulation of emotions, behavioural control, problem solving, and motivation4. There is well-established evidence that the more we are depressed or anxious, the less we can access executive functions (e.g., Siegle, Thompson, Carter, Steinhauer, & Thase, 2007), making the use of CBT di�cult and less e�ective during crisis, when we need it most5. Metaphorically speaking, the amygdala ‘hijacks’ the processing needed for rational thinking and generates an emotional experience instead. Worse, in chronic depression, the amygdala’s inhibiting e�ect on prefrontal executive functions does not even require being distressed5.

Although there is abundant evidence that CBT is a useful approach (e.g., Whit�eld & Williams, 2003), it is limited in both its scope and depth in dealing with emotions, leading numerous clinicians using CBT to be eclectic in their therapeutic approach6. Their increasing interest in learning acceptance and mindfulness approaches partly re�ects the need to �nd more e�ective or easier ways of addressing clients’ emotional reactivity.

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Figure 1. Components in the co-emergence model of reinforcement7.

The Co-Emergence Model Of ReinforcementThe co-emergence model of reinforcement7 is a model of embodied cognition8 derived from the so-called “�ve aggregates of the mind” described in the Abhidhamma, which is central to the Buddhist psychological system9,10. The model extends our understanding of learning principles through an analysis of the actual experience of reinforcement mechanisms. It is an integrated conceptualisation of how mind and matter “co-emerge” to produce an experience. The model is anchored in modern Learning Theory and the phenomenology of mindfulness meditation and principles, and its operationalisation is entrenched in a cognitive-behavioural framework. It is presented in a simple form by means of generic functional components, rather than a complex conceptual architecture, and very brie�y in this article (see Cayoun, 2011, for a comprehensive description).

Components of behaviour maintenance and changeThe non-pathological functioning of the overall information system necessary for the reinforcement of learned behaviour is presented in Figure 1. Following each component, an internally or externally-generated stimulus (Stimulus) is perceived by the senses (Sensory Perception) in the form of smell, sight, touch, taste and sound, body sensation or thought emerging from memory, and converted to a cognitive process of evaluation (Evaluation). The Evaluation component �lters perceived information according to one’s judgement, uniquely a�ected schemas, values, personality, culture, needs, autobiographic memories and other �lters, in order to make sense of the situation. Our judgement can be conscious or subconscious and learned (“automatic”).

Drawing on Teasdale and Barnard’s terminology in their Interactive Cognitive Subsystems approach11, the model suggests that our evaluation can be placed on a continuum of “implicationality”, where thoughts are increasingly “propositional” (factual) towards one end and increasingly “implicational” (personally important) towards the other end. The more implicational is a thought, the more spontaneous interoceptive changes co-emerge and are experienced consciously or subconsciously as sensations in the body (Interoception). This is because information judged as more important, such as the expectation of threats, creates deeper brain processing that sends feedback to somatosensory

pathways. This implies that the more implicational a thought is, the more intense is the co-emerging body sensation, whether pleasant or unpleasant. Cognition is thus embodied.

One of the di�erentiating factors of this model is its assertion that Reaction, the next component, is a direct response to Interoception, not to the stimulus. Accordingly, the extent to which body sensations are intense, to that extent we can predict a reaction, conscious or subconscious, expressed or unexpressed. Moreover, the extent to which sensations are pleasant, to that extent the reaction will be an attempt to increase both the duration and frequency of the sensation, and the extent to which the sensation is unpleasant, to that extent the reaction will be an attempt to decrease both the duration and frequency of the sensation. Craving behaviour is positively reinforced each time a pleasant body sensation is successfully maintained or increased. Aversive behaviour is negatively reinforced each time an unpleasant body sensation is successfully decreased, typically through avoidant behaviour.

System in disequilibrium and psychopathologyWhen we experience mental turmoil or emotional distress, a state of attentional disequilibrium between these four information-processing components takes place. Our attention is depleted from our senses (Sensory Perception and Interoception), and is reallocated to making judgement and reacting (Evaluation and Reaction). Figure 2 represents a state of disequilibrium in the attention system, pictorially highlighted by the disproportionate size of boxes representing each stage of the model.

A stress response typically results in disequilibrium. While the central nervous system is geared to handle a discrete stress response and usually recovers well from it, a disequilibrium state in the attention system can be learned and can become the most habitual state of the system, resulting in a continual cycle of negativity and emotional reactivity. We become over judgemental and over-reactive (as shown in Figure 2), facilitating the emergence and/or maintenance of psychopathology.

REACTION (OR CHOSEN RESPONSE)

SENSORY PERCEPTION EVALUATION

(FACTUAL OR IMPLICATIONAL, CONSCIOUS OR AUTOMATIC

INTEROCEPTION

(BODY SENSATIONS)

STIMULUS INTERNAL/EXTERNAL

Figure 2. The co-emergence model of reinforcement during disequilibrium in information processing.

SENSORY PERCEPTION

EVALUATION

Factual information is minimised Implicational information is

maximised

!

REACTION

STIMULUS

INTEROCEPTION



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Moreover, the co-emergence model also implies that, since early childhood, every important memory is encoded and stored with a coupled bodily experience. Hence, body sensations that co-emerge with our judgements are fundamental memory cues that help us recognise important stimuli, such as implicit memories of threats, and are essential for e�ective survival purposes. This is the fundamental principle for the perpetuation of schemas. The maintenance of schema relies on our reactivity to body sensations and can persist when the therapy approach used does not take body sensations into account.

The relevance of mindfulness meditationTraining in mindfulness meditation requires deliberate sustained attention on sensory processes with unconditional acceptance of the sensory experience. Consequently, mindful attention also requires a deliberate e�ort to prevent our usual reactions and develop greater objectivity (less implicationality), acceptance and detachment with each experience, a skill known as “equanimity”7.

When clients undergo a course of Mindfulness-integrated CBT (MiCBT)7 they �rst learn to sustain attention to their breath and learn to quickly recognise thoughts that emerge spontaneously in consciousness (metacognitive awareness), inhibit any reaction to these thoughts, and refocus attention on the breath as soon as possible. Technically, this practice requires the training of three executive functions: sustained attention to a target (breath), response inhibition to the intrusive stimulus (e.g., thoughts) and cognitive �exibility through switching attention back to the target. Rather than trying to modify the content of thoughts (as suggested by cognitive therapy), clients develop a degree of control over the process of thinking.

During MiCBT, clients are also taught to pass their attention systematically throughout (“scan”) their body and develop an increasing ability to feel body sensations consciously while purposefully inhibiting habitual judgements and learned reactions. Executive functions are now used to regulate emotions by preventing reactivity to body sensations, which are the building blocks of all emotions — indeed emotions cannot exist without body sensations.

Accordingly, the rationale for the integration of mindfulness meditation into CBT is that mindfulness practice trains the individual to reallocate attention from over-emphasised components (Evaluation and Reaction) to under-emphasised or avoided components (Sensory Perception and Interoception), thus re-establishing equilibrium in the system. According to this model, a more balanced allocation of attention across the information processing system helps regulate attention and emotion, and cannot co-exist with psychopathology. Thus, it helps prevent relapse. There is now a body of evidence that the integration of mindfulness skills with cognitive and behavioural models of therapy can generate greater therapeutic bene�ts than applying these models alone7,12,13.

ConclusionThe co-emergence model has helped clinicians understand the rationale for the use of mindfulness meditation in therapy for over ten years, as it makes two major contributions to the �elds of behavioural science and clinical psychology. The �rst is the understanding that our reactivity is uniquely triggered by body sensations and not by mere thoughts or stimuli in the environment. This alone has implications for treatment methods. The second is the understanding that using mindfulness meditation helps address the emotionality of our beliefs by re-establishing and maintaining attentional equilibrium across four broad information processing components and is therefore advantageous to therapeutic interventions for a broad range of psychopathologies.

References

1 Beck, A. T. (1976). Cognitive therapy and the emotional disorders. New York: International University Press.

2 Beck, A. T., Emery, G., & Greenberg, R. L. (1985). Anxiety disorders and phobias: A cognitive perspective. New York: Basic Books.

3 Mohlman, J., & Gorman, J. M. (2005). The role of executive functioning in CBT: a pilot study with anxious older adults. Behaviour Research and Therapy, 43, 447-465. 4 Fuster, J. M. (1989). The prefrontal cortex. New York: Raven Press.

5 Siegle, G. J., Thompson. W., Carter, C. S., Steinhauer, S. R., & Thase, M. E. (2007). Increased amygdala and decreased dorsolateral prefrontal BOLD responses in Unipolar Depression: Related and independent features. Biological Psychiatry, 61, 198-209.

6 Whit�eld, G., & Williams C. (2003). The evidence base for cognitive–behavioural therapy in depression: Delivery in busy clinical settings. Advances in Psychiatric Treatment, 9, 21-30.

7 Cayoun, B. A. (2011). Mindfulness-integrated CBT: Principles and practice. Chichester, UK: Wiley-Blackwell. 8 Isanski, B., & West, C. (2010). The body of knowledge: Understanding embodied cognition. Retrieved from http://www.psychologicalscience.org/observer/getArticle.cfm?id=2606. 9 Narada, M. (1968). A manual of Abhidhamma. Kandy, Sri Lanka: Buddhist Publication Society. 10 Nyanaponika, T. (1996). Abhidhamma studies: Researches in Buddhist psychology. Kandy, Sri Lanka: Buddhist Publication Society. 11 Teasdale, J. D., & Barnard, P. J. (1993). Interacting cognitive subsystems: A systematic approach to cognitive-a�ective interaction and change. Cognition and Emotion, 5, 1-39. 12 Baer, R. A. (2003). Mindfulness training as a clinical intervention: A conceptual and empirical review. Clinical Psychology: Science and Practice, 10, 125-143. 13 Teasdale, J. D., Segal, Z. V., Williams, J. M. G., Ridgeway, V. A., Soulsby, J. M., & Lau, M. A. (2000). Prevention of relapse/recurrence in major depression by Mindfulness-based cognitive therapy. Journal of Consulting and Clinical Psychology, 68, 615-623.



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COGNITIVE-BEHAVIOURAL THERAPIES FOR DEPRESSION: IS THIS AS GOOD AS IT GETS?

Lucius Arco PhD

Dr Lucius Arco is a self-employed specialist clinical psychologist at Praxis Research in Perth and experienced in treating a wide range of psychological problems associated with mental, neurological, and developmental disorders in adults, families and children. He has expertise in clinical behaviour analysis and single-case experimental research. Dr Arco is a former university lecturer and researcher with a Masters in (Clinical) Psychology from Flinders University and PhD from Murdoch University.

Major Depressive Disorder (MDD) in adults is a common and increasingly prevalent disorder in many communities. In many instances it can be refractory or recurrent, and thus di�cult to treat. Courses and prognoses of depression are associated with various conditions such as genetics, age and severity of onset, presence of comorbid disorders (e.g., anxiety, substance abuse), stressful life events, and poor social supports. Fortunately, many psychological treatments are available, but none seem to be as demonstrably e�ective as the cognitive-behavioural therapies. However, evaluating e�ectiveness can be contentious. More and more clinicians and researchers are voicing concerns about the established practice of evaluating e�ectiveness in terms of statistical signi�cance or e�ect size, or simply comparing treatments with no treatments or simple interventions (e.g., relaxation training, support counselling). Such comparisons report observations of reliable di�erences or magnitudes of change, but do not inform how changes are clinically signi�cant. Of course, a clinician’s primary aim is to achieve remission or recovery and not just observable responses to therapy or improved symptomatology. Remission and recovery are de�ned as periods during which clients are asymptomatic, with the latter extending over long periods, typically several months. Remission and recovery indicate more normal functioning and are usually associated with increased durability of outcomes and decreased likelihood of relapse or recurrence1. However, recent research that has reported remission or recovery from depression shows limited e�ects from cognitive-behavioural therapies, and highlights the need for more creative and incisive research.

To best illustrate the strengths and limits of cognitive-behavioural therapies and the challenges ahead, consider four exemplary studies2, 3, 4, 5 that directly compared Beck’scognitive therapy with the resurgent functional analytic therapies (also known as “third wave therapies” or behaviour analysis6), namely, behavioural activation, functional analytic psychotherapy, and acceptance and commitment therapy.

These studies are exemplary because of their comprehensive-and state-of-the-art interventions (15 to 20 sessions) delivered by competently trained and experienced therapists whose adherence to their respective treatment protocols was measured and shown to have integrity; randomised allocations of large samples of clients to various conditions; comparisons with antidepressant medications; robust measures of remission, recovery, and attrition rates; and extensive follow-up analyses up to 2 years7, 8, 9. For clients who successfully completed therapy, post-treatment results showed remission rates ranged from 61% to 36% with no di�erences between therapies and comparable to rates obtained with antidepressant medication. Post-treatment attrition rates were similar across therapies (approximately 15%), but lower than those of antidepressant medication (more than 40%). However, follow-up data showed lower rates of recovery. After a year, recovery rates were less than 50%, and after 2 years, rates decreased further, ranging from 35% to 25%. Also, results showed that clients with chronic or severe depression reported slightly higher remission or recovery rates with the functional analytic therapies, although the data are preliminary and in need of replication3, 4, 8. Such results are typical of current research outcomes.

Is this as good as the cognitive-behavioural therapies get? At best, many clients with depression should bene�t from conventional cognitive-behavioural therapies, but a large number is unlikely to recover. How can research proceed to attain higher rates? A solution may lie in reconsidering the predominant use of randomised controlled trials (RCTs). Such research designs tend to compare groups of clients in a particular therapy with other therapies or no-treatment control conditions, and typically, clients who do not attain remission or recovery are not followed-up with alternative techniques – foregoing valuable research opportunities for improving therapies.

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Conventional therapies usually consist of packages of speci�c techniques accompanied by manuals, but how these techniques should be mixed or con�gured for the individual client is largely unclear. Indeed, although many cognitive-behavioural therapies claim that techniques are individualised the published research shows little evidence of such practice. It seems that RCTs are not the most e�cient designs for identifying potent therapeutic techniques.

As mentioned earlier, depression results from various biopsychosocial conditions. For some, antidepressant medication may help, for others it won’t; improving interpersonal relations may help some, for others it won’t; enhancing spiritual behaviour or self-awareness may help some, for others it won’t. Clearly, individual analyses of clients’ complaints, symptoms, and strengths are critical for identifying likely conditions that maintain depression and for determining e�ective treatment. Individual analysis implies the use of various formats and components such as amounts or frequencies of sessions; sessions with spouses, groups, mentors, or parents; various goals for change (e.g., self-regulation, social and communicative skills, work competencies, lifestyle activities, health routines, social and interpersonal relations, work habits); various emphases on cognitive or behavioural changes (e.g., less introspection and more action), and so on.

Ultimately, undi�erentiated results between cognitive-behavioural therapies invariably leave clinicians and researchers wondering which speci�c formats and components were actually responsible for treatment e�ects, and how these a�ected individual clients. Rami�cations include many clinicians and researchers selecting therapies based on their training, knowledge of packaged therapies, experience, and preferences, rather than basing therapy on knowledge of the individual client, resulting in numerous and similarly e�cacious forms of cognitive-behavioural therapies.

An alternative approach is using more single case research designs that emphasise individual analysis. When therapeutic progress is unsatisfactory, formats and components can be readily modi�ed by experimentally introducing, adding, omitting or withdrawing speci�c formats or components, and e�ects evaluated over time10. Indeed, with severe, refractory or recurrent depression, time is essential for experimenting with additional or di�erent formats or components for attaining remission or recovery. Some recent examples of single case studies illustrate how depression was alleviated by increasing various behavioural activities or altering in-session therapeutic interactions; furthermore, the studies showed how these interventions a�ected individuals di�erently over time, thus aiding a better understanding of what clinicians should consider during therapy11, 12, 13.

This can’t be as good as it gets. Many clients with depression are not likely to recover from conventional cognitive-behavioural therapies, or from antidepressant medications for that matter. Clearly, such clients need more time, di�erent treatment formats or components, or both. The historical record shows

that from the 1950s to the 1970s, starting with the pioneering work of Joseph Wolpe (in South Africa), Charles B. Ferster (in USA), and Monte B. Shapiro (in UK), the cognitive-behavioural therapies had a major impact on clinical psychology by researching therapeutic e�ects on individual clients. Much has been learnt since then, but in the past 25 years or so much keeps being repackaged or recycled in RCT research without clear advances in outcomes. It is time to restore the “analysis of the individual” as a main research strategy for developing more potent and e�ective therapies in attaining higher remission and recovery rates from depression.

References

1 Hollon, S. D., Thase, M. E., & Markowitz, J. C. (2002). Treatment and prevention of depression. Psychological Science in the Public Interest, 3, 39-77.

2 Jacobson, N. S., Dobson, K. S., Truax, P. A., Addis, M. E., Koerner, K., Gollan, J. K., Prince, S.E. (1996). A component analysis of cognitive-behavioral treatment for depression. Journal of Consulting and Clinical Psychology, 64, 295-304.

3 Kohlenberg, R. J., Kanter, J. W., Bolling, M. Y., Parker, C. R., & Tsai, M. (2002). Enhanc-ing cognitive therapy for depression with functional analytic psychotherapy: Treatment guidelines and empirical �ndings. Cognitive and Behavioral Practice, 9, 213-229.

4 Dimidjian, S., Hollon, S. D., Dobson, K. S., Schmaling, K. B., Kohlenberg, R. J., Addis, M. E., et al. (2006). Randomized trial of behavioral activation, cognitive therapy, and antidepressant medication in the acute treatment of adults with major depression. Journal of Consulting and Clinical Psychology, 74, 658-670.

5 Forman, E. M., Herbert, J. D., Moitra, E., Yeomans, P. D., & Geller, P. A. (2007). A randomized controlled e�ectiveness trial of acceptance and commitment therapy and cognitive therapy for anxiety and depression. Behavior Modi�cation, 31, 772-799.

6 Kanter, J. W., Busch, A. M., Weeks, C. E., & Landes, S. J. (2008). The nature of clinical depression: Symptoms, syndromes, and behavior analysis. The Behavior Analyst, 31, 1-21.

7 Gortner, E. T., Gollan, J. K., Dobson, K. S., & Jacobson, N. S. (1998). Cognitive-behavioral treatment for depression: Relapse prevention. Journal of Consulting and Clinical Psychology, 66, 377-384.

8 Co�man, S., Martell, C. R., Dimidjian, S., Gallop, R., & Hollon, S. D. (2007). Extreme nonresponse in cognitive therapy: Can behavioral activation succeed where cognitive therapy fails? Journal of Consulting and Clinical Psychology, 75, 531-541.

9 Dobson, K. S., Hollon, S. D., Dimidjian, S., Schmaling, K. B., Kohlenberg, R. J., Gallop, R., et al. (2008). Randomized trial of behavioral activation, cognitive therapy, and antidepressant medication in the prevention of relapse and recurrence in major depression. Journal of Consulting and Clinical Psychology, 76, 468-477.

10 Blampied, N. M. (1999). A legacy neglected: Restating the case for single-case research in cognitive-behaviour therapy. Behaviour Change, 16, 89-104.

11 Gaynor, S. T., & Harris, A. (2008). Single-participant assessment of treatment mediators: Strategy description and examples from a behavioral activation intervention for depressed adolescents. Behavior Modi�cation, 32, 372-402.

12 Busch, A. M., Kanter, J. W., Callaghan, G. M., Baruch, D. E., Weeks, C. E., & Berlin, K. S. (2009). A micro-process analysis of functional analytic psychotherapy’s mechanism of change. Behavior Therapy, 40, 280-290.

13 Bailey, D. L., & Arco, L. (2010). E�ects of a brief behavioural activation treatment on activities of various di�culty and depression. Behaviour Change, 27, 184-197.

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INTERPERSONAL THERAPY FOR DEPRESSION

Paul RushtonBPsych(Hons)

Paul is a clinical psychologist in private practice on the Gold Coast. He has held adjunct academic appointments as Clinical Assistant Professor at Bond University, Lecturer at Gri�th University (Gold Coast Campus), and sessional Lecturer with the Medical School at the University of Queensland. He is a member of the Clinical College of the APS. Paul is considered one of the leading authorities on IPT training in the Paci�c region having conducted over seventy workshops in �ve countries.

Interpersonal Psychotherapy (IPT) is a psychological therapy that was developed in the 1970s, and rose to prominence when it compared favourably to CBT and medication in the National Institute of Mental Health (NIMH) Treatment of Depression study conducted in the mid-1980s. The e�cacy of IPT as an adjunct or alternative treatment for depression has since been con�rmed in numerous studies from adolescents to the elderly. Despite the evidence-base, and the inclusion of IPT within Medicare funded programs such as the Better Access, many practitioners within Australia have received little exposure to IPT education and training. This article outlines the targets, theories, tactics and techniques of IPT. For practitioners with specialisations in other therapies, IPT can be a useful alternative or adjunctive approach to current practice.

About IPTIPT is a time-limited, psychodynamically informed psychotherapy that facilitates change in the here and now. Assessment and intervention within IPT, therefore, focuses on the ‘interpersonal context’, which refers to interpersonal/relational factors that are involved in predisposing, precipitating and perpetuating the client’s problems or illness and also protecting the client1. Certain conditions are tailor-made for IPT intervention. For example, interpersonal factors are commonly associated with the genesis and maintenance of depression. These factors include the death of signi�cant others, relationship discord, poor social support, and con�ict with family and friends. Consequently, IPT was �rst developed for depression and research has focused on depressive presentations to a large degree. That said, there is an evidence-base for a range of conditions including bulimia and sexual dysfunction2. IPT does not o�er itself as a sole or primary treatment modality for all psychiatric presentations, especially where interpersonal factors are not directly implicated in the genesis and maintenance of the problem.

The de�ning elements of IPT are categorised into targets, theories, tactics and techniques2. Whilst elements of IPT are shared with other psychotherapies, their unique combination de�nes IPT2. The targets of IPT are symptom resolution, improved interpersonal functioning, and increased social support3. IPT is based on the premise that interpersonal distress is connected with psychological symptoms and distress. The interpersonal triad is used to explain this connection. The triad is based on an acute interpersonal stressor beginning the process. The ability of the client to manage the crisis psychologically and biologically is heavily in�uenced by the client’s biopsychosocial vulnerabilities (diatheses). These include their genetic vulnerability to illness, attachment style, and personality features, which may modulate or exacerbate the e�ect of the stressor2. Social factors such as the client’s current signi�cant relationships and social support provide the context in which the stress-diathesis interaction occurs, and further in�uence the client’s ability to cope with their distress2. Together, these elements form the interpersonal triad.

TheoriesThe primary theories underpinning IPT are attachment theory, communication theory and social theory3. Attachment theory has been a focus of literature and research for decades, and highlights the importance of internal working models for forming and maintaining relationships that are naturally implicit and highly automatised. Communication theory highlights the relationship between meta-communications and disordered interpersonal relationships3. Social theory and social psychiatry highlight the relationship between our current relationships and the genesis and course of psychological distress3. All three combined highlight the importance of relationships for healthy functioning across the lifespan. Therefore, interventions that improve current social relationships will lead to improved functioning. Furthermore, relationships are a protective factor. Conversely, disordered relationship patterns are an important risk factor and are directly implicated in conditions such as depression. Social research has highlighted that those with less secure attachment are more prone to depression. Disruption of attachment increases vulnerability to depression, and depression frequently occurs in an interpersonal context3. IPT, therefore, addresses the interpersonal context with the aim of alleviating the presenting illness or problem. Whilst symptom alleviation is a primary goal, the client should learn more e�ective ways of accessing social support, resolving interpersonal di�culties, and managing emotions courtesy of the IPT approach, thereby achieving much more than symptom relief.

TacticsThe tactics of IPT refer to the concepts applied during treatment2. A biopsychosocial assessment is a central tactic for IPT assessment, including a clinical interview and conducting an interpersonal inventory; e�ectively an audit of the client’s key current and past relationships. The aim of the inventory is to identify healthy and unhealthy patterns in forming and maintaining relationships, and responding to the changes in relationships that invariably occur. The inventory also assesses the extent of available social support.

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The biopsychosocial model is used within the assessment process to understand the interaction between interpersonal factors and the genesis and maintenance of the client’s presenting problems, as per the interpersonal triad. The focus of IPT intervention is one or more of four IPT problem areas: (1) grief which is complicated bereavement following the death of a signi�cant other; (2) role transitions, which involves di�culties arising from transitions in life such as changing jobs and relationships dissolving; (3) role disputes (often referred to as interpersonal disputes) which are overt or covert disputes with another person(s) and (4) interpersonal de�cits (sometimes referred to as ‘interpersonal sensitivity’), which is de�ned as di�culty forming and maintaining relationships resulting in loneliness and social isolation3. Decisions regarding the duration of treatment, and which problem areas are addressed and in what order, are made collaboratively with the client4.

TechniquesThe techniques of IPT refer to what the IPT therapist does or says during the treatment2. Along with common micro-counselling skills, key IPT techniques include communication analysis and role playing. These are designed to identify unhelpful methods of communicating and to develop more adaptive methods to assist the client in having their attachment needs met. IPT di�erentiates content a�ect, talking about a feeling, and process a�ect, experiencing the feeling1. The IPT therapist helps their client express, understand and manage process a�ect, through the therapeutic goals of increasing engagement in the therapeutic process, facilitating recognition and acceptance of a�ect, using a�ect to bring about change in emotion and cognition, and assisting the client to communicate their a�ect more e�ectively3. Whilst successful IPT involves mastery of these techniques by the therapist, the therapeutic alliance is considered pivotal to the process of change.

IPT was initially designed for 12-16 sessions. However, courses of IPT commonly range from 6-20 sessions with provision for maintenance treatment as necessary2. The structure of IPT is broken down into four distinct phases. In the assessment phase, the therapist determines whether or not the client is a suitable candidate for IPT, conducts a biopsychosocial assessment including an interpersonal inventory, develops an interpersonal formulation, negotiates a contract with the client and creates the IPT focus for treatment. During the intermediate sessions, the therapist and client work at resolving the relationship problems using one or more of the four IPT problem areas using the key IPT techniques. When concluding acute treatment, the therapist and client review progress in the problem areas and plan for future problems, including relapse prevention of symptoms and skills developed during IPT. If maintenance sessions are indicated, the therapist and client contract for further sessions that are usually less frequent, but maintain the interpersonal focus3.

TasksOverall, the IPT therapist has four key tasks: (1) to create a therapeutic environment in which there is a high degree of inclusion and a�liation; (2) to identify and conceptualise the client’s maladaptive communication and attachment patterns and help the client become aware of them, so they can be modi�ed; (3) to resolve the di�culty within the relevant problem area(s) using the key techniques and (4) to assist the client in building a better social support network, and to utilise the social supports that are currently available3.

ConclusionAccording to the International Society of IPT there are over 250 empirical studies supporting the e�cacy and e�ectiveness of IPT2. IPT research for depression has been conducted with clients of all ages and with di�ering presentations, including acute and chronic depression. In terms of depression speci�cally, the standard IPT format is used. Essentially the same format used for depression is used for non-depressive presentations with minor modi�cations including terminology, therapist expectation of change, age considerations, and therapeutic style.

Critics of IPT highlight the lack of focus on cognition and speci�cally cognitive change, central to the cognitive therapies. However, IPT has been compared to CBT on numerous occasions in randomised controlled trials, particularly for depression, and the results have been comparable4. These results are open to interpretation, but open up the possibility of multiple pathways to a�ect change. The apparent strengths of IPT include its applicability to a wide range of presentations either as a mono or adjunctive therapeutic approach, its emphasis on the importance of relationships and social support regardless of whether the initial presenting issue is relational or not, and provision of an evidence-based structure to address interpersonal and a�ect-related issues. The reader is directed to the International Society of IPT website and the clinician’s guide included in the reference list for further reading.

References

1 Robertson, M., Rushton, P., & Wurm, C. (2008). Interpersonal psychotherapy: An overview. Psychotherapy in Australia, 14 (3), 46-54.

2 Stuart, S., & Robertson, M. (2003). Interpersonal psychotherapy: A clinician’s guide. London: Edward Arnold (Oxford University Press).

3 International Society of IPT. http://www.interpersonalpsychotherapy.org/about-ipt.au.

4 Weissman, M.M., Markowitz, J.C., & Klerman, G.L. (2007). Clinician’s quick guide to interpersonal psychotherapy. New York: Oxford University Press.

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PSYCHODYNAMIC THERAPY FOR DEPRESSION

Professor Robert King

Professor Robert King is a clinical psychologist and Fellow of the Australian Psychological Society. He is Professor in the School of Psychology and Counselling at Queensland University of Technology where he coordinates the Clinical Psychology training program. He is Peer Review Editor for the journal Psychotherapy in Australia. In addition to his teaching and research, Professor King is active in clinical practice and also provides professional workshops and seminars in Australia, Europe and North America.

The term psychodynamic therapy refers to a range of both brief and long term therapeutic interventions. Psychodynamic therapies are widely practiced and form at least part of the therapeutic repertoire of a large number of psychologists1. The focus of this article is brief psychodynamic therapies as the evidence-base for these interventions is relatively well-established and they are more suitable for routine practice with people experiencing depression. The Treatment Improvement Protocols published by the US Substance Abuse and Mental Health Administration (SAMHSA) and Centre for Substance Abuse Treatment (CSAT) list 9 brief psychodynamic therapies, including Interpersonal Therapy (which is treated as a separate therapy in this issue).

Given the breadth of therapies designated ‘psychodynamic’ it is not easy to identify their common or de�ning characteristics. Shedler argued that psychodynamic therapies aim to achieve changes at the level of personality and functioning rather than symptom relief and that there are seven distinctive features: 1. Focus on a�ect and expression of emotion, 2. Exploration of attempts to avoid distressing thoughts and feelings, 3. Identi�cation of recurring themes and patterns, 4. Discussion of past experience (developmental focus),5. Focus on interpersonal relations,6. Focus on the therapy relationship and 7. Exploration of fantasy life2.

While some of these features are likely to be present in many therapies, psychodynamic therapies tend to be saturated by these features. Psychodynamic therapies may also be characterized by: focus on unconscious wishes, impulses or fears and by the use of the client’s experience of the therapeutic relationship (transference) for in vivo exploration of how these unconscious wishes, impulses or fears impact interpersonally.

The theoretical framework underpinning psychodynamic therapy proposes that humans have the capacity to exclude from conscious experience (repress), ideas, memories and associations that evoke painful emotions. While unconscious, these ideas, memories and associations continue to a�ect behaviour and experience and can be the cause of symptoms of anxiety, depression and some somatic complaints. Psychodynamic theory proposes that developing conscious awareness of repressed material in a safe therapeutic environment enables the person to tolerate and deal with what had previously been too painful or di�cult. Trauma, loss and intrapsychic con�ict are key concepts in psychodynamic theory.

Supportive-Expressive Therapy (SET)3,4, is a good example of a brief psychodynamic therapy. It was originally developed as a more supportive and less intensive treatment for people who were seen as lacking the emotional or �nancial resources for a full classical psychoanalysis. However, early research found that it was just as e�ective as the more intensive therapy and its e�cacy has been con�rmed in more recent well-designed trials.

In SET, the client and therapist focus on relationship episodes. These are client experiences interacting with people – especially experiences that have been emotionally challenging

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or disturbing. The aim is to identify what are known as ‘core con�ictual relationship themes’ (CCRTs) that characterise client experience 4.

Each episode is carefully analysed to identify unconscious as well as conscious elements. This analysis is guided by three questions:

1. What was the client’s wish in relation to the other person? (W or wish)

2. What was the response of the other person? (RO or response of other)

3. How did the client internalize the response of the other? (RS or response of self )

Relationship episodes may include current or recent relationships, early relationships or relationships with the therapist (transference). CCRTs are most stable and central when they are evident in each of these domains. Over the course of the therapy, the client develops an increasing awareness of aspects of CCRTs that had hitherto been unconscious and is thus able to begin to approach relationships di�erently.

The following vignette provides a clinical illustration.

Marie is struggling with clinical depression. During her session she tells her therapist that she called her sister because she was feeling lonely. The conversation started out �ne but, after she kept telling her sister how down she was feeling, her sister said something like ‘you are always so negative … you need to get a life.’ She felt angry and hopeless because it seemed her sister was not really interested in her. Later in the session she told her therapist ‘I don’t think I am getting anywhere in therapy. Maybe I should just stick with medication or try ECT like my doctor suggested’.

Marie’s therapist initially focused on helping her identify the wish that motivated her to call her sister. It was clear that she was seeking support and that she was hoping her sister would recognise that she was feeling down and provide her with comfort (W). However, her experience (RO) was that her sister pushed her away and this made her feel abandoned and worthless (RS). Later she told her therapist that she was feeling negative about the therapy. Her wish was that the therapist would make it clear that she wanted her to continue – signalling that the therapist cared about her. Initially the therapist felt disheartened in response to this communication and was inclined to agree that perhaps Marie was not bene�ting from psychotherapy. However, she held back from her initial response and instead shared with Marie her understanding that Marie was feeling as if no-one cared about her at present and was hoping that she (the therapist) really did believe in her and wanted to help her. The therapist also linked

Marie’s experience with her sister and the feelings she had conveyed about the therapy and invited her to think about how aware she was of what she was wanting in the relationship and how she was conveying her wishes.

The evidence base for the e�ectiveness of brief psychodynamic therapy for depression has been summarised in three meta-analyses. Gibbons, Crits-Christoph and Hearon concluded that the evidence available at the time of their review suggested psychodynamic therapy was e�ective for treatment of depression5. Abbas, Town and Driessen found that short term psychodynamic therapy was e�ective for treatment of depressive disorders with comorbid personality disorder and that the e�ect size was at least equivalent to that obtained by other therapies6. Driessen and colleagues found that short term psychodynamic psychotherapies were e�ective for treatment of depression7. While they were marginally less e�ective by end of treatment they were equivalent in e�ectiveness to other therapies at 3-month follow up. These meta-analyses provide a strong evidence base to support the use of psychodynamic therapy for depression. Longer term psychodynamic therapy may be indicated when depression forms part of a more complex psychological disorder8.

The main limitation of psychodynamic therapy for depression is that the typical number of sessions (16-20) is approximately twice the amount that is usually e�ective when treatment is by cognitive-behaviour therapy9 or behavioural activation and exceeds the amount of therapy funded under the Better Access (Medicare) program. This means that psychodynamic therapy would usually be provided, either in response to client preference or because a longer-term treatment was indicated given the complexity of client problems.

References

1Cook, J., Biyanova, T., Coyne, J., Schnurr, P., & Elhai, J. (2010) What do psychotherapists really do in practice? An internet study of over 2,000 practitioners. Psychotherapy: Theory, Research, Practice, Training, 47, 260 – 267.

2 Shedler, J. (2010). The e�cacy of psychodynamic psychotherapy. American Psychologist, 65, 98-109.

3 Luborsky, L. (1984). Principles of Psychoanalytic Psychotherapy: A Manual for Supportive-Expressive Treatment. NY: Basic Books.

4 Book, H. (1998). How to Practice Brief Psychodynamic Psychotherapy: The Core Con�ictual Relationship Theme Method. Washington, DC: American Psychological Association Press.

5 Gibbons, M.B., Crits-Christoph, P., & Hearon, B. (2008). The empirical status of psychodynamic therapies. Annual Review of Clinical Psychology. 4, 93-108

6 Abbass, A., Town, J., Driessen, E. (2011). The e�cacy of short-term psychodynamic psychotherapy for depressive disorders with comorbid personality disorder. Psychiatry, 74, 58-71

7 Driessen, E., Cuijpers, P., de Maat, S., Abbass, A., de Jonghe, F., & Dekker J. (2010). The e�cacy of short-term psychodynamic psychotherapy for depression: A meta-analysis. Clinical Psychology Review, 30, 25-36

8 Leichsenring, F., & Rabung, S. (2011). Long-term psychodynamic psychotherapy in complex mental disorders: Update of a meta-analysis. British Journal of Psychiatry, 199, 15-22.

9 Shapiro, D.A., Rees, A., Barkham, M., Hardy, G., Reynolds, S., Startup, M. (1995). E�ects of treatment duration and severity of depression on the maintenance of gains after cognitive-behavioral and psychodynamic-interpersonal

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ELECTROCONVULSIVE THERAPY

Associate Professor Colleen Loo

Associate Professor Colleen Loo is a psychiatrist, researcher and academic with the University of NSW, based at St George Hospital, a�liated with the Black Dog Institute (Sydney). She is the Medical Director of the ECT service at Wesley Hospital (Kogarah, Sydney). Colleen is internationally recognised for her research in Electroconvulsive Therapy and other novel forms of physical treatments: Transcranial Magnetic Stimulation and transcranial Direct Current Stimulation. She has received highly competitive research grants from the Australian National Health and Medical Research Council for her work.

Professor Loo is active in ECT practice and education, and has advised the Royal Australian and NZ College of Psychiatrists and NSW Health on ECT policy and practice. She continues to research in methods to improve ECT and conducts research trials of new brain stimulation treatments at the Black Dog Institute in Sydney.

What is ECT?Electroconvulsive therapy (ECT) is a medical treatment that involves therapeutic induction of a seizure while the patient is under general anaesthesia. It is used to treat a range of psychiatric disorders, most commonly depression. The treatment involves passing a brief, carefully calibrated electrical stimulus across the brain for several seconds, inducing a generalized seizure that typically lasts for about half a minute. When used in treatment of an acute disorder, ECT treatments are typically given 2-3 times per week, in a course of 8-12 treatments. After an acute course of ECT, other treatments are usually given to maintain improvement (medications, psychological therapy). In some patients who relapse after ECT despite other treatments, maintenance ECT can be a useful prophylactic treatment. This consists of treatments given at less frequent intervals (e.g. monthly) to prevent future relapse.

Evidence for the Use of ECT Since the �rst ECT treatment in 1937, many studies have reported on the outcomes of ECT treatment. A thorough review of this evidence was undertaken by the highly respected and conservative National Institutes of Clinical Excellence in the UK, which convened a multidisciplinary review panel for this purpose. The review concluded that ECT was clearly better than a placebo comparison and also substantially more e�ective than medications in treating depression: “In conclusion, there is a reasonable evidence base for the use of ECT: it does not rest simply on anecdote, habit, and tradition.”1 ECT is also used in the treatment of other disorders such as schizophrenia.

Review of this literature according to the stringent Cochrane evidence-based approach, also supported the use of ECT: “The evidence in this review suggests that ECT, combined with treatment with antipsychotic drugs, may be considered an option for people with schizophrenia, particularly when rapid global improvement and reduction of symptoms is desired.”2 Though most studies have been conducted in adults, published reports and clinical evidence suggests that ECT is an e�ective treatment across the age range.

ECT is appropriately used in depression and other psychiatric disorders: • As a preferred treatment option of the patient and physician, due to the higher likelihood of response and faster response time. • As an essential treatment in patients who have not improved with medication and other treatments. • As a life-saving treatment for patients who require urgent treatment due to high suicide risk or serious incapacitation (e.g. refusing food and �uids).

Formal assessments of quality of life and function before and after ECT found that 87% of patients reported improvement immediately after ECT, and 78% reported improvement 6 months later3.

Safety of ECT ECT is a safe treatment; the reported risk of death is 1: 50,000 treatments4. It can a�ect memory and cognitive function, though this impairment is mostly transient and resolves within a few weeks of completing ECT treatment. A recent systematic review and meta-analysis found that much of the cognitive impairment had improved by three days after ECT5. Occasionally, memory for past events prior to ECT can be lost. There is no evidence that ECT impairs future IQ or intelligence. It is not uncommon for patients who have improved with ECT to report that their memory and thinking have improved after ECT, as depression and psychiatric illness also impair memory and thinking. Importantly, recent research on ECT outcomes in typical clinical settings showed that while e�cacy was high and did not di�er signi�cantly between treatment centres6

cognitive side e�ects varied from minimal to severe, depending on the treatment approach used7. This has led to focussed research e�orts on treatment modi�cations that minimise cognitive side e�ects.

Treatment ApproachesSubstantial advances in ECT treatment technique have occurred in Australia over the last 20 years, based on research �ndings. These include:• Individualizing the dose of the ECT treatment for each patient and each treatment.• Monitoring brain activity/seizure quality during ECT treatment. • The option of different treatment approaches, depending on the clinical situation.

There are 2 main variations in treatment technique:

Electrode placement - treating electrodes are placed to stimulate mainly one side of the head (unilateral ECT) or both sides (bilateral ECT). Bilateral ECT is more e�ective but is also

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more likely to cause memory side e�ects – it is typically used where unilateral ECT has not worked, or where an urgent treatment response is needed.

Standard or ultrabrief pulse stimulus - ultrabrief pulse width ECT is a new approach which is emerging in clinical practice in Australia. The ECT pulse is tailored to be much closer to the natural �ring pattern of the brain’s own nerve cells, and hence seizures are induced with much lower levels of stimulation. Two of three key studies of ultrabrief pulse width ECT found high e�cacy with no memory or cognitive changes on detailed testing after a whole course of ECT treatment8,9. On some tests, cognitive function had improved relative to baseline levels. The third study10 (from Australia) reported a minimal level of cognitive impairment that was nevertheless markedly reduced compared with standard ECT. Thus, this represents a signi�cant new development in ECT treatment. However, not all patients will respond to ultrabrief pulse ECT and some may need to receive standard pulse ECT, which remains an important treatment option. Further research into improving ECT is actively occurring, including in Australia.

How Does ECT Work?Many studies have examined the neurobiological outcomes of ECT, including e�ects on neurotransmitters, hormone levels, brain metabolism and functioning. The most recent research suggests that ECT has positive neurotrophic e�ects and may reverse the hippocampal atrophy that occurs with depression11,12. It acts more strongly to promote neurogenesis than any other agent or treatment. These �ndings are consistent with the prevailing model of depression, that chronic stress leads to negative trophic e�ects on hippocampal neurons, evidenced both from histopathological �ndings and neuroimaging studies13. This body of evidence suggests that ECT acts to reverse detrimental changes in brain structure and function that occur with depression.

Novel Brain Stimulation TreatmentsA number of novel brain stimulation approaches are also being examined as treatments for depression. These are not necessarily replacements for ECT, but may be developed as other physical treatment options alongside ECT. Two promising non-convulsive treatments are repetitive Transcranial Magnetic Stimulation (rTMS) and transcranial Direct Current Stimulation (tDCS). rTMS involves the use of weak, pulsed magnetic �elds to stimulate the surface of the brain. Treatment sessions are usually conducted every weekday for several weeks and can be done on an outpatient basis.

Over 30 placebo-controlled trials have shown that rTMS has antidepressant e�cacy without any cognitive side e�ects, though it is not as e�ective as ECT14. Recent trials of tDCS suggest that it is a very promising treatment option15,16. It uses currents 1/500 the strength of ECT, which are barely percepti-ble. Unlike rTMS, there is no risk of accidental seizures and stimulation may actually enhance cognition. Trials of this treatment are ongoing at the Black Dog Institute and University of NSW in Sydney16.

ConclusionECT is a highly e�ective treatment for depression and other psychiatric disorders. Conventional forms of ECT carry a risk of cognitive side e�ects, though impairment is usually transient. Newer forms of treatment, such as ultrabrief pulse ECT, are highly e�ective but have minimal cognitive side e�ects. The practice of ECT continues to be developed and improved through ongoing research.

References

1 UK ECT Review Group. (2003). E�cacy and safety of electroconvulsive therapy in depressive disorders: A systematic review and meta-analysis. Lancet, 361, 799-808.

2 Tharyan, P., & Adams, C.E. (2005). Electroconvulsive therapy for schizophrenia. Cochrane Database of Systematic Reviews, 2, CD000076.

3 McCall, V., Prudic, J., Olfson, M., & Sackeim, H. (2006). Health-related quality of life following ECT in a large community sample. Journal of A�ective Disorders, 90(2-3), 269-274.

4 Tess, A.V., & Smetana, G.W. (2009). Medical evaluation of patients undergoing electroconvulsive therapy. New England Journal of Medicine, 360(14), 1437-44.

5 Semkovska, M., & McLoughlin, D.M. (2010). Objective cognitive performance associated with electroconvulsive therapy for depression, A systematic review and meta-analysis. Biological Psychiatry, 68(6), 568-577.

6 Prudic, J., Olfson, M., Marcus, S., Fuller, R., & Sackeim, H. (2004). E�ectiveness of electroconvulsive therapy in community settings. Biological Psychiatry, 55, 301-312.

7 Sackeim, H., Prudic, J., Devanand, D., Fuller, R., Keilp, J., Lavori , P., & Olfson, M. (2007). The cognitive e�ects of electroconvulsive therapy in community settings. Neuropsychopharmacology, 32, 244-254.

8 Sackeim, H., Prudic, J., Nobler, M.S., Fitsimons, L., Lisanby, S.H., Payne, N., Devenand, D.P. (2008). E�ects of pulsewidth and electrode placement on the e�cacy and cognitive e�ects of electroconvulsive therapy. Brain Stimulation, 1(2), 71-83.

9 Sienaert, P., VAnsteelandt, K., Demyttenaere, K., & Peuskens, J. (2009). Randomized comparison of ultra-brief bifrontal and unilateral electroconvulsive therapy for major depression: Clinical e�cacy. Journal of A�ective Disorders, 116, 106-112.

10 Loo, C.K., Sainsbyrt, K., Sheehan, P., & Lyndon, B. (2008). A comparison of RUL ultrabrief pulse (0.3 ms) ECT and standard RUL ECT. International J Neuropsychopharmacology, 11(7), 935-946.

11 Marano, C., Phatak, P., Vemulapalli, U., Sasan, A., Nalbandyan, M., Ramanujam, S., Soekadar, S., Demosthenous, M., … Regenold, W.T. (2007). Increased plasma concentration of brain-derived neurotrophic factor with electronconvulsive therapy: A pilot study in patients with major depression. Journal of Clinical Psychiatry, 68(4), 512-7.

12 Nordanskog, P., Dahlstrand, U., Larsson, M., Larsson, E.M., Knutsson, L., Johanson, A. (2010). Increase in hippocampal volume after electroconvulsive therapy. Journal of ECT, 26(1), 62-67.

13 Pittinger, C., & Duman, R.C. (2008). Stress, depression and neuroplasticity: A convergence of mechanisms. Neuropsychopharmacology, 33, 88-109.

14 Slotema, C., Blom J., Hoek H., & Sommer I. (2010). Should we expand the toolbox of psychiatric treatment methods to include repetitive transcranial magnetic stimulation (rTMS)? A meta-analysis of the e�cacy of rTMS in Psychiatric Disorders. Journal of Clinical Psychiatry, 71(7), 873-874.

15 Boggio, P.S., Rigonatti, S P., Ribeiro, R.B., Myczkowski, M. L., Nitsche, M. A., Pascual-Leone, A., & Fregni F.(2008). A randomized, double-blind clinical trial on the e�cacy of cortical direct current stimulation for the treatment of major depression. International Journal of Neuropsychopharmacology, 11(2), 249-54.

16 Loo, C., Alonzo, A., Martin, D., Mitchell, P., Galvez, V., & Sachdev, P. (2012). A three-week, randomized, sham-controlled trial of transcranial direct current stimulation in depression. British Journal of Psychiatry; 200, 1–8. doi: 10.1192/bjp.bp.111.097634.

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NEUROPSYCHOTHERAPY AND DEPRESSION

Pieter Rossow, PhD

Dr Pieter Rossouw is a member of the Australian Psychological Society and the APS College of Clinical Psychologists. Dr Rossouw was a Professor in Clinical Psychology for 11 years and lectured at Universities in Canada, Holland and South Africa. He is a member of the Global Association for Interpersonal Neurobiology Studies, the International Society for Traumatic Stress Studies, the International Association for Family Therapy and the Professional Association for Drug and Alcohol Workers. Dr Rossouw is the Director of Mediros – a company that provides training in neurobiology and neuropsychotherapy. He is also actively involved in clinical research. For further information, please contact Dr Rossouw at: Dr [email protected] or visit www.mediros.com.au

Psychotherapy is a process where a skilled clinician assesses and treats clients experiencing a wide range of psychological and behavioural challenges. Others de�ne psychotherapy as an intentional interpersonal relationship used by trained psychotherapists to aid a client in problems of living1. Neuropsychotherapy is a specialised �eld of psychotherapy. The primary focus of neuropsychotherapy is to utilise information derived from neurobiological and neuroscienti�c research in psychotherapeutic practice.

Neurobiological ResearchSince the 1950s the study of the brain became more and more the focus of research in pharmacology when scientists realised how the introduction of chemicals can alter brain functioning. Huge �nancial empires arose as result of introducing medications to address a range of mental illnesses. The golden era for psychopharmacology started in the 1980s and early 1990s. The biggest breakthrough came with the introduction to the market of Fluoxetine (Prozac) in 1986. This product, an anti-depressant or “SSRI” (selective serotonin reuptake inhibitor) discovered between 1970 and 1974, changed the world of well-being in a short space of time2. Since then a large number of SSRI’s and SNRI’s (serotonin norepinephrine reuptake inhibitor), mood stabilizers (anti psychotic medications) and benzodiazepines (sedating medications) have been introduced – all with the aim to “promote mental well being.

Since the late 1970s, the brain regained some importance in psychology in terms of assessment for certain disorders and levels of functioning, such as dementia, intellectual disabilities,

and autism. The role of the brain in treatment of mental disorders remained on the backburner. Medication became the �rst line intervention for all “signi�cant” conditions due to the focus on restoring the “chemical imbalances” in the brain3,4.

Neurobiology and the BrainIn the meantime neurobiologists made extraordinary discoveries regarding the brain.

• They discovered how different brain areas process different signals from the environment in unique ways5;

• They discovered how different neurotransmitters operate;

• They discovered how neurotransmitters work together but can also work against each other in certain conditions;

• They discovered how certain transmitters inform certain structures in the brain and eventually change the structures leading to changes in expression (behaviour);

• They discovered how the brain operates in different conditions by following the path of activity with MRI and Pet scans6;

• They discovered how external stimuli (experiences e.g. trauma) inform brain activity and brain structure and even how it changes certain structures and may cause neural atrophy in certain areas;

• They discovered how unhelpful thinking patterns can change the brain and form neural loops and changes cortical blood flow resulting in information not being processed effectively5;

• They discovered how the brain is plastic and how it can reshape itself to establish new neural pathways;

• They discovered how, by activating frontal structures in the brain (the pre-frontal cortical regions) physical distressing symptoms can change (such as headaches, stomach aches, blushing, sweating and many more) as well as emotional distressing symptoms such as anxiety or depression;

• They discovered how psychotherapy (talking) informs the brain on many levels and is more effective in changing the structure of the brain than chemical interventions7.

Neuropsychotherapy is the natural result of neurobiological research. It informs us that the brain is not �xed, but can change (neural plasticity). It informs us that the brain is not static and does not exist in isolation – it is “wired” with its environment and the brains of others, and changes its structure according to the messages that it receives from the outside as well as its internal messages to itself. (Some implications of this are that brain scans reveal how the hardware of the brain changes for the better when we are in a good frame of mind and do good things, and how the brain changes negatively when we are constantly anxious, worried or depressed all the time).

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Neuropsychotherapy is the “language” used in the interaction between the clinician and the client to guide the client in the process of restructuring the brain towards higher levels of functioning and well-being8. It uses information from neurosciences to assist clients su�ering from a wide range of biological, psychological and social challenges to apply strategies to shift cortical blood �ow away from unhelpful neural looping (being constantly worried, anxious, depressed and so on), to activate left prefrontal cortical structures (to problem-solve more e�ectively), to facilitate neural plasticity and neural growth (through cognitive and physical-behavioural activities), change neuro-chemical reactions (such as an overactive hypothalamus, pituitary or adrenal stress response), to establish new neural pathways, and deconstruct unhelpful neural patterns and structures. Many studies show neural changes in the brain years after treatment9,10.

Depression ResearchOver the past 30 years huge emphasis has been placed in research to understand the neurobiological underpinnings of depression. Currently all four major hypotheses of depressions have fundamental neurobiological components:

• The monoamine hypothesis of depression

• The genetic and environmental hypothesis of depression

• The dysfunction of the hippocampus and hypothalamus- pituitary-adrenal system theory of depression

• The neurotrophic hypothesis of depression

Limitations to the length of this paper do not allow us to elaborate on the fascinating research and even more fascinating implications for psychotherapy in the treatment of depression. These hypotheses are not mutually exclusive and demonstrate how nature and nurture are much closer linked than considered before; how genetic predispositions do not necessarily express due to changes in “nurture”; how attachment and caring change gene expression, and ultimately how neurochemicals, neural �ring and neural structure can reorganise as result of psychotherapeutic interventions5, 11 .

The Neuroscience of TherapyNeedless to say, neuropsychotherapy is an exciting science. It is encouraging to see positive changes in neural growth and neural activity in PET and fMRI scans as result of talking therapy interventions12,13,14. It is important to be aware of studies indicating that changes to neural structure are more enduring and speci�c than chemical interventions6. This does not mean that neuropsychotherapy nulli�es the use of chemical interventions. Research clearly show the role of well structured, guided therapeutic interventions as primary intervention mode in comparison to the use of chemical that cannot

discriminate between the target area and other brain areas resulting in side e�ect pro�les. Also - research shows the bene�t of talking therapies and the practical application of cognitive decisions in behaviours to facilitate new neural growth –pathways and positive changes in neural structure.

In 1998, psychiatrist and neurobiologist and winner of the Nobel Prize for medicine, Eric Kandel, wrote about the role of neurobiology in light of modern psychotherapy and indicated a “remarkable scienti�c revolution” that will forever change the practice of mental health care15. This “revolution” has indeed happened in the last decade and has come to fruition11.

The challenge for clinical psychologists is to engage in utilising these research �ndings in their clinical practice and assist their clients su�ering from the debilitating e�ects of depression to experience new neural �ring in new e�ective pathways and shift the default �ring patterns. More and more studies are conducted and published demonstrating neural changes due to talking therapies. Much more research is needed to understand the neural speci�cs of certain conditions as well as more e�ective and more targeted strategies to further improve the existing trajectory of recovery7.

References

1 “Psychotherapy”. Oxford English Dictionary. (2004). New York: Oxford University Press. 2 Wong, D., Horng. J., Bymaster, .F, Hauser, K., Molloy, B. (1974). A selec tive inhibitor of serotonin uptake: Lilly 110140, 3-(p-tri�uoromethylphenoxy)-N-methyl-3-phenylpropylamine. Life Sciences, 15(3), 471–479.

3 Linford, L., & Arden, J.B. (2009). Brain-based therapy and the ‘Pax Medica’. Psychotherapy in Australia, 15, 16-23. 4 Turner, E.H., Matthews, A.M., Linardatos, B.S., Tell, R.A., & Rosenthal, R. (2008). Selective publication of antidepressant trials and its influence on apparent e�cacy. New England Journal of Medicine, 358(3), 252-260.

5 Cozolino, L. (2010). The Neuroscience of Psychotherapy. Healing the Social Brain. New York: Norton.

6 Kumari, V. (2006). Do psychotherapies produce neurological e�ects? Acta Neuropsychiatrica, 18, 61-70.

7 Rossouw, P.J. (2011). The neurobiological underpinnings of the mental health renaissance. In The Mental Health Services (Book of Proceedings). Sydney: SOS, 184-189.

8 Walter, H., Berger, M., & Schnell, K. (2009). Neuropsychotherapy: Conceptual, empirical and neuroethical issues. European Archives of Psychiatry and Clinical Neuroscience, 259(2), 173-182.

9 Lambert, M.J., & Ogles, B. (2004). The efficacy and effectiveness of psychotherapy. In Lambert, M.J. (ed.) Bergin and Gar�eld’s Handbook of Psychotherapy and Behavior Change (5th ed., 139-193). Hoboken: Wiley.

10 Furmark, T., Tillfors, M., Marteinsdottir, I., Fischer, H., Pissiota, A., Långström, B., & Fredrikson, M. (2002). Common changes in cerebral blood �ow in patients with social phobia treated with citalopram or cognitive-behavioral therapy. Archives of General Psychiatry, 59, 425-433.

11 Kandel, E. (2006). In search of memory: The emergence of a new science of mind. New York: W.W. Norton.

12 Siegel, D. (2007). The mindful brain: Re�ection and attunement in the cultivation of well-being. New York: W.W. Norton.

13 Siegel, D. (2010a). Mindsight: The new science of personal transformation. New York: Bantam Books.

14 Siegel, D. (2010b). The mindful therapist: A clinician’s guide to mindsight and neural integration. New York: W.W. Norton.

15 Kandel, E.R. (1998). A new intellectual framework for psychiatry. American Journal of Psychiatry, 155, 457-469.

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ASSESSING BIPOLAR AFFECTIVE DISORDER: THE PRACTICAL STUFF THAT’S NOT IN THE DSM.

Dr Karen T. Hallam, PhD

Dr Karen Hallam is an academic/practitioner with twelve years experience in the �eld of mood and bipolar disorders. Dr Hallam has a research and professional interest in young adults, particularly in the context of mood (with a focus on bipolar) disorders, eating disorders and self harm behaviour. She has published over 25 peer reviewed papers in the �eld of mental health with an emphasis on the aetiology and treatment of Bipolar Disorders. Dr Hallam shares her time between teaching and supervision within the Victoria University Clinical Psychology Postgraduate Program and PhD programs, conducting research through her collaboration with The University of Melbourne and the First Episode Mania Team at ORYGEN Youth Health and running a private clinical psychology practice. She can be contacted at [email protected]

Bipolar disorder is an illness that seems to truly re�ect a need for a biopsychosocial aetiology, case formulation and treatment approach with contributions from genetic through to psychological and social factors. Around 1% of the adult Australian population meets a clinical diagnosis of bipolar disorder and up to 3% some bipolar spectrum disorder. The assessment of this chronic, chaotic and often life threatening illness is often di�cult. The goal of this article is to further elucidate the rationale and some strategies to address the why, how and when aspects of diagnosis.

Why is it so important to get the diagnosis of BPAD right anyway?Over recent years, evidence has been mounting that having bipolar episodes (depressed, manic, hypomanic or mixed) is not good for the brain. It causes a range of chemical changes including a phenomenon called oxidative stress that releases toxic free radicals that may a�ect the brain in the long term. This may lead to cognitive and memory problems, as well as what we call ‘sensitisation’, which essentially means a person needs less and less psychosocial stressors to become unwell because they become more biologically vulnerable for future episodes. Importantly, medication typically prescribed for bipolar disorder can help protect against this e�ect, particularly ‘mood stabilisers’ (e.g. lithium). These are medications which also treat the symptoms of the illness and reduce relapse risk. Mood episodes have signi�cant interpersonal, occupational and �nancial e�ects that persist long after the episode has stabilised or remitted. For many, a diagnosis and associated psycho-education about the biopsychosocial aetiology and associated distal and proximal antecedents to speci�c episodes is empowering and explanatory as the individual learns both ‘why?’ and ‘what can I do to stay well?’ Finally, it allows for the opportunity to adjust when a client is faced with reconciling and integrating illness behaviours with their core beliefs and personal constructs of identity, particularly important as onset generally occurs in adolescence and young adulthood. The earlier these biopsychosocial interventions are commenced, the better the outcome for the client in terms of mental health and overall functioning.

Why is it so hard to diagnose bipolar disorder? Bipolar disorder is a chameleon of the psychiatric world with presentations that may look similar to unipolar (major) depression, psychosis (during manic or mixed episodes) and Axis II conditions, such as borderline personality disorder, due to mood instability and potentially a chaotic lifestyle. As a consequence, there is often a signi�cant time delay in arriving at a clear diagnosis. However, research from the University of New South Wales has demonstrated a unique “bipolar signature” that may assist in diagnosis of bipolar depression. Speci�cally, they identify “psychomotor retardation; melancholic symptoms such as worthlessness, unvarying mood and marked anhedonia; atypical depressive symptoms such as hypersomnia and leaden paralysis; a past history of psychotic depression; and the absence of anxiety, initial insomnia, the tendency to blame others and tearfulness”1. In relation to the observation of psychotic features during mood episodes, some clinicians are hesitant to diagnose mania, preferring a diagnosis of schizoa�ective disorder to somehow denoting the perceived increased severity of this diagnosis and related psychotic features. In reality, some clients with bipolar disorder may show �orid psychotic symptoms with the speci�er in this case that the psychotic features are present during the mood episode (manic, depressed or mixed). Importantly, while clients with bipolar disorder may show mood congruent delusions (such as grandiosity), other types of delusions may also be experienced in this illness (e.g. persecutory delusions or delusions of reference) and are not necessarily characteristic of a schizoa�ective or other psychotic disorder unless falling outside the mood episode.

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When considering severity, I have assessed many clients displaying delusions, hallucinations, agitation, pressured speech, sleeplessness and occasional aggression with a diagnosis of bipolar disorder. Notably, with appropriate medication, acute symptoms resolved well in most cases, often better than observed in psychotic disorders.

Finally, in relation to Axis II presentations, life charting provides an opportunity to characterise the client’s illness history and observe when and under what circumstances episodes occur. Conducting such an analysis may reveal earlier episodes of depression, hypomania, mania and mixed episodes that may have been considered di�erently in isolation. The long sequential course of illness development from sub-syndromal to syndromal depression to mania or hypomania is more characteristic of a bipolar trajectory2. It is occasionally worthwhile to suspend (or defer) judgement on the Axis II diagnosis to see how the presentation appears once the bipolar disorder is managed, as symptom resolution may be one of the few ways to assess the relative contribution of Axis II traits.

What else can I do to get a better idea of this client’s episodes, and risk times using assessments?If you like something on paper (and most of us do), there are a range of assessment schedules that you may �nd e�ective in further assisting diagnosis and assessment of illness severity. The Young Mania Rating Scale3 is freely available open access on line and is one of the most commonly used measurement tools for assessing severity of mania and mixed states. It is an 11 item, clinician administered measure that provides a total score with scores over 10 often considered in the mild range. It can be easily completed after any thorough mental state exam. In relation to severity of bipolar depression, the Montgomery Asberg Rating Scale4 is widely used, and the Australian-made Bipolar Depression Rating Scale5 is also available open access from www.barwonhealth.org.au/bdrs. Finally, many clients and clinicians �nd mood charting helpful to observe patterns over days, weeks and seasonal change (risk times for relapse). Mood charts are most e�ective when done collaboratively and identify which potential triggers relate to mood variation to form both a record for future reference and a list of target areas for treatment (e.g. managing stress and sleep issues around examination times).

Bipolar disorder is a predictably unpredictable disorder, especially when untreated or undermanaged. Recent evidence indicates that accurate diagnosis and treatment is imperative to improve short, medium and long term outcomes. The impor-tance of diagnosis falls into two broad categories, getting the clinical diagnosis correct to allow commencement of treatments and assessment of mood state to maximise treatment e�cacy and the therapeutic alliance. And, most importantly, helping people stay well.

Resource Links

Young Mania Rating Scalehttp://www.outcometracker.org/library/YMRS.pdf

Bipolar Depression Rating Scalehttp://www.barwonhealth.org.au/app_cmslib/media/lib/0809/m7378_v1_bdrs%20form.pdf

References

1 Mitchell, P.B., & Mahli, G.S. (2004). Bipolar depression: Phenomonological overview and clinical characteristics. Bipolar Disorders, 6, p. 534.

2 Berk, M., Dodd, S., Callaly, P., Berk, L., Fitzgerald, P., de Castella, A.R., Filia, S., Filia, K., Tahtalian, S., Bi�n, F., Kelin, K., Smith, M., Montgomery, W., & Kulkarni, J. (2007). History of illness prior to diagnosis of bipolar disorder or schizoa�ective disorder. Journal of A�ective Disorders, 103, 181-186.

3 Young R. C., Biggs, J. T., Ziegler, V. E., Meyer, D.A. (1978). A rating scale for mania: Reliability, validity and sensitivity. British Journal of Psychiatry, 13, 429-435.

4 Montgomery, S. A. & Asberg, M. (1979) A new depression scale designed to be sensitive to change. British Journal of Psychiatry, 13, 382-389

5 Berk, M., Malhi, G.S., Cahill, C., Carman, A. C., Hadzi-Pavlovic, D., Hawkins, M. T., Tohen, M., Mitchell, P. B. (2007). The Bipolar Depression Rating Scale (BDRS): Its

development, validation and utility. Bipolar Disorders, 9(6), 571-57.

WORKPLACE DEPRESSION

Giles Burch, PhD

Dr Giles Burch, a UK-registered occupational psychologist, is a management consultant and associate senior lecturer in HRM (University of Auckland). He is also completing the Doctor of Clinical Psychology at Sydney University, where he is carrying out research into labour-management processes, mental health and work productivity.

Back in 2002, Jay Thomas and Je�rey Hite, in the Handbook of Mental Health in the Workplace, suggested that until that point there had been little need for such a handbook, and primarily put this down to two factors: (1) a lack of awareness of psychopathology within the organizational context on the behalf of managers and those involved in the design of organizations, and (2) the ease of eradicating such problems by “eliminating the a�ected employee”1.

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Over the last decade there has been some progress made on this front, more often than not in�uenced by more informed human resource policy and employment legislation. Whilst this may be driven by increased concern for the welfare of employ-ees, the more cynical may believe this to be driven by a management concern to maximize productivity or even a fear of litigation! Alongside of this, there is growing interest in workplace psychopathology in academic psychology and human resource management (HRM); however, more practical interventions need to happen if sustainable change is to occur. Given the focus of this edition of ACPARIAN, this article will concentrate on points surrounding depression in the workplace.

Given the prevalence rates for depression and given that work plays a signi�cant part in the lives of a great many people, it is not surprising to see the impact that depression can have in the workplace. For example, it has been suggested that in Australia, undiagnosed depression in the workplace can cost $4.3 billion in lost productivity, there is an organizational cost of $9,665 for every full-time employee with undiagnosed depression, there is an equivalent to six million working days lost per year due to time taken o� work by employees with depression, and more than 12 million days of reduced productivity per year are accounted for by depression, excluding absenteeism2. It has been suggested that depression is a leading cause of workplace disability3 and that dysthymia can have more signi�cant longer-term e�ects on work than an acute major depressive episode4.

So what are the signs of depression in the workplace? Alongside of the more typical clinical symptoms, depression can be identi�ed by reduced productivity (e.g., not �nishing projects), increased absenteeism and conversely, increased presenteeism (which may be the result of avoiding non-work factors or an anxiety of ‘losing’ one’s job), an increase in the number of accidents or errors made on the job, and increased inter-personal di�culties.

Next it is necessary to consider the causal factors of depression in the workplace. As we are all aware, the aetiology of depression is complex and a number of factors may come into play, including genetics and personal ‘characteristics’, in addition to environmental factors. However, when we observe depression in the workplace, it is useful to understand whether and/or how work may be implicated. When depression may be due to non-work-related factors, it is likely to impact the ability of employees to perform e�ectively at their job. Additionally, the nature of the work (and/or the working context) in itself may be a contributing or compounding factor. For example, a number of workplace stressors have been identi�ed as increasing the risk of depression, such as: shift work, reward systems, role ambiguity and con�ict, burnout, relationships at work and job insecurity5.

Going beyond this, there is growing interest within the HRM literature in the relationship between High-Performance Work Systems (HPWSs) and psychological well-being. The notion of HPWSs refers to a bundle of complementary HRM practices, and is the term often used when referring to ‘best practice’ in HRM. These systems emphasize management processes that reduce control over employees and enhance employee welfare, such as training and development, reward, team-working and involvement. Despite Neo-Fordist/Marxist claims from some industrial relations academics that HPWSs may actually intensify work and subsequently have a negative impact on worker experience and mental health, the research shows HPWSs to generally have a positive impact on employee psychological well-being, particularly those processes that emphasize employee involvement and participation. For example, Mackie, Holahan and Gottlieb found that employee-involvement management practices were negatively related to depression (mediated by ‘sense of coherence’)6.

It has been suggested elsewhere that organisations may adopt one of two di�erent labour-management strategies, one of high-involvement or one of intensi�cation, with high involvement processes having a negative relationship with stress and depression, and intensi�cation having a positive relationship7. The implications of this for management should be clear: reduce stressors in the workplace, including work intensi�cation, and implement high-involvement work processes, which will provide a more positive experience for the employee. However, the question that is typically asked is whether the investment in such processes is worth the pay-o�? Finance directors and clinicians are likely to have opposing views on this point! This aside, the important question is also raised as to whether it is realistic, or naïve, to believe that work depression can be eliminated altogether? Given the complexity of the aetiology of depression, as pointed out by Goldberg and Steury, “it may be that workplace stressors are contributors to rather than the sole cause of depression”(p. 1642)8. Thus, while (at the organizational-level) the removal of work-place stressors and changes in labour-management processes will help facilitate a more positive experience for employees, this is no panacea.

So what else can be done? Clearly there is a critical role for clinical psychologists in helping individuals manage workplace depression in identifying and targetting the implicated work-related stressors alongside of symptoms. But clinical interventions will only be e�ective at the individual-level if the individuals actually present for treatment, and as early as possible. However, the perceived and actual stigma associated with depression remains, and most certainly so in the workplace, which is recognised as a barrier to seeking help9; in particular, the concern that the identi�cation of depression will lead to negative employment/career decisions on behalf of management regarding the employee (e.g., Goldberg & Steury, 2001). Thus, preventative/protective organisational-level interventions (e.g., educating managers, resilience training) remain a useful way forward in an attempt to reduce stigma and bring about (organisational) cultural changes, which will hopefully lead to increased readiness of individuals to ‘seek help’. This is a gradual process, and we are not there yet, but in-roads are being made.

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References and Further Reading

1 Thomas, J.C., & Hite, J. (2002). Mental health in the workplace: Toward an integration organizational and clinical theory, research and practice. In J.C. Thomas & M. Hersen (Eds.), Handbook of Mental Health in the Workplace. Thousand Oaks, CA: Sage Publications.

2 BeyondBlue National Workplace Program. (2011). Retrieved from www.beyondblue.org.au/index.aspx?link_id=4.1028

3 Langlieb, A.M., & DePaulo, J.R. (2008). Etiology of depression and implications on work environment. Journal of Occupational and Environmental Medicine, 50, 391-395.

4 Kahn, J.P. (2008). Diagnosis and referral of workplace depression. Journal of Occupational and Environmental Medicine, 50, 396-400.

5 Traux, P., & McDonald, T. (2002). Depression in the workplace. In J.C. Thomas & M. Hersen (Eds.). Handbook of Mental Health in the Workplace. Thousand Oaks, CA: Sage Publications.

6 Mackie, K.S., Holahan, C.K., & Gottlieb, N.H. (2001). Employee involvement management practices, work stress, and depression in employees of a human services residential care facility. Human Relations, 54, 1065-1092.

7 Macky, K., & Boxall, P. (2008). High-involvement work processes, work intensi�cation and employee well-being: A study of New Zealander worker experiences. Asia Paci�c Journal of Human Resources, 46, 38-55.

8 Goldberg, R.J., & Steury, S. (2001). Depression in the workplace: Costs and barriers to treatment. Psychiatric Services, 52, 1639-1643.

9 Couser, G.P. (2008). Challenges and opportunities for preventing depression in the workplace: A review of the evidence supporting workplace factors and interventions. Journal of Occupational and Environmental Medicine, 50, 411-427.

INSIDE THE BRAIN OF A DEPRESSANT

Bernie is a 77 year old retired Bank Manager with a history of chronic multiple illnesses including diabetes and asthma and this year was diagnosed with Major Depressive Disor-der. BackgroundI consider that I had a rather stable upbringing. I was a rather shy boy and would consider myself to be a loner. I had very few friends, but leaving home aged sixteen years I had to become self-su�cient and joined the Bank of NSW in 1949.

I married in 1959 and it was not a happy marriage. My wife committed suicide in 1998. Her death was not traumatic for me as no love existed between us. It was not a real marriage, but she would not divorce me. I married again in 2001 and lived in England for ten years. This marriage is most successful. Whilst in England I su�ered considerable ill health and had both kidneys operated on for cancer. I have always been a pessimist, but apart from mood swings I did not have depression. We came back home in 2009 and my problems commenced. I had worked in London until I was 72 years old and I feel that leaving work contributed to my depression.

The Event October 2009Coming back home was in itself traumatic. The tenants had desecrated our place and as my wife worked full time I had to make sure that tradespeople did the right thing as my wife has very high expectations. This also resulted in �nancial worries. I found all this very stressful and I gradually sank deeper and deeper into a mental black hole. I felt that my brain was going to burst. I had suicidal thoughts and wished I was dead. I had no energy, motivation or drive and did not even wish to get out of bed of a morning. I also ate very little and my weight went from 73 kgs to 64 kgs. Finally, in February 2011, my doctor put me in hospital and I remained there for approximately one month. I was �rstly put on Lexapro, which proved unsatisfactory, and then Zoloft, which was compatible. My wife, a pharmacist, did not want me to take anti-depressants because of possible side-e�ects.

My period in hospital turned me around and I now have time and a clear mind to recall the dreadful things that I said and did during my out of body experience when very depressed. Gradually I will mend all the fences that require �xing.

The Road to RecoveryI do not consider that I am back mentally to what I was and may never be, which is sad. I still �nd life a bit surreal, especially when I �rst wake up, and don’t feel quite me, but I do not insult people and am certainly in charge of my faculties. I have little control over my legs and I go where they want to go. My doctor assures me it is just old age.

Finally I would like to thank my doctor and psychologist for their assistance in my rehabilitation.

Client ’s Perspective

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Call for contributions for

March 2012 (Vol 2, Issue 1), featuring:

EATING DISORDERSACPARIAN invites members to contact the Editor, Kaye Horley [email protected] regarding contributions for the next edition. Contributions may be from clients and from members with research, psychotherapeutic or other clinical expertise in this area. Final articles should observe the word limit detailed in the Editorial Guidelines and should be submitted by 11th February 2012.



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Research ReviewEXERCISE AS A TREATMENT FOR MAJOR DEPRESSIVE DISORDER

Kaye Horley, PhD

Depressed a�ect is one of the cardinal symptoms of major depressive disorder (MDD). Exercise, as a possible mood regula-tor for those with major depression, has been the subject of much interest in recent research. Various neurotransmitters implicated in depression have been shown to be a�ected by exercise. These include elevations of endorphins, produced by the pituitary gland and the hypothalamus, norepinephrine, serotonin, dopamine and brain-derived neurotrophic factor, with resultant feelings of well-being1. Exercise, therefore, appears to regulate all of the neurotransmitters targeted by antidepressants. Ratey posits that antidepressants appear to work from a bottom-up processing from the brainstem and through the limbic system to the pre-frontal cortex, suggesting this is why physical e�ects (increased energy) are felt before mind e�ects (decrease in sadness)1. This is in contrast to the top-down process of psychotherapy where the initial e�ect in modifying thinking stems from the prefrontal cortex. The exact mechanisms of exercise on the brain remains unclear2 as does knowledge of the pathophysiology of MDD3.

A number of large meta-analyses with both clinical and unselected samples have been conducted, with �ndings indicating a signi�cant reduction in depressive symptoms following engagement in structured exercise4, 5, 6, 7. Cox, for example, examined randomised experimental studies conducted between 2000-2006 in clinically depressed older adults5. A signi�cant pre–post e�ect indicated that the depressed adults had -0.46 of a standard deviation reduction in clinical depression from baseline compared to individuals who did not exercise. Compared to other standard treatments, exercise was as e�ective in reducing depression, with no di�erence found between aerobic, resistance or a combination treatment. However, few studies have explicitly involved individuals with MDD. In addition, methodological limitations means that results must be interpreted with caution.

Investigators have examined the e�ects of exercise upon depression in various clinical populations, particularly those with cardiovascular (CV) disease and associated depression. Poor CV recovery post-exercise appears indicative of CV problems and death. In a study by Gordon et al.8, those with MDD had slower heart rate recovery, suggestive of a slower parasympathetic exercise recovery rate. Providing a regular exercise regime that will overcome the lack of motivation in depressed individuals is an inherent di�culty in this approach. The in�uence of both negative a�ect and motivation on exercise was examined in individuals at high risk of coronary heart disease over 6 months9. In comparison to a control group

receiving standard care (SC), two life-style counselling group interventions included motivational interviewing. The life-style counselling plus group (LC+), also received a CBT negative-a�ect reduction intervention to assist recognition of negative a�ect on exercise and strategies to counter it. Both the life-style counselling groups were more motivated to exercise post-treatment than the SC group. The LC+ group had decreased levels of stress, but no decrease in depression or anxiety post-treatment. Higher levels of baseline stress and depression were associated with lower levels of exercise in all 3 groups.

Other examined conditions have included menopausal women. In a large Korean study, menopausal women who regularly exercised more than three times a week, were found to experience signi�cantly less depression and had less menopausal symptoms10.

The importance of monitoring mood before and after exercise has been stressed11, along with an understanding of the relationship between mood and motivation and the importance of the exercise environment in reducing the e�ort needed. Although �nding improvement in depressed individuals immediately post-exercise, increased negative mood 30 minutes post-exercise has been found, suggesting that exercise resulting in increased negative mood may in part explain reduced adherence in depressed individuals12. An e�ect associated with type of activity has also been found, with decreased depression scores associated with leisure-time physical activity in women, particularly high intensity activity, in comparison to occupational and household activity13.

Inadequate assessment of depressive symptomatology presents another di�culty. It has been pointed out by Mata14 that both positive (PA) and negative a�ect (NA) change associated with exercise needs to be measured, rather than, for example, a total score on the BDI-II, as well as the e�ects of frequency, intensity and duration of activity on depressive symptoms. Addressing these issues with prompted daily questioning regarding everyday physical activity and mood, Mata found that a MDD group and a control group reported higher levels of PA after physical activity, but no e�ect upon NA. Longer duration and and/or greater intensity of activity compared to short duration and/or lower intensity activity signi�cantly increased PA in the MDD group. NA was not a�ected in either group.

Despite individually-targeted treatment, remission rates of over 60% meet criteria for treatment-resistant depression15. Exercise e�ects on treatment-resistant patients with MDD were examined in a recent study16. One group received pharmacology, the second group received pharmacology and engaged in 30-45 minute walks of moderate intensity 5 days a week for 12 weeks. In comparison to the �rst group who showed no response or remission, the second group showed a 21% improvement in depression and functioning, and remission in 26%.



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In conclusion, methodological limitations lead to di�culties in interpreting studies examining the e�ects of exercise on depression. Nevertheless, there appears an increasing research base validating the importance of exercise in countering depression in MDD. The available evidence is su�cient to recommend regular moderate exercise as an adjunct with other depressive treatment3, 17 and, therefore, implicit within treatment regimes by clinical psychologists.

References1 Ratey, J.J. (2008). Spark: The revolutionary new science of exercise and the brain. London: Little, Brown and Company.

2 Krishnan V., & Nestler, E.J. (2008). The molecular neurobiology of depression. Nature 455(7215), 894–902.

3 Helmich, I., Latini, A., Sigwalt, A., Carta, M.G. Machado, S., Velasques, B., Ribeiro, P. Budde, H. (2011). Neurobiological alterations induced by exercise and their impact on depressive disorders (Erratum). Clinical Practice and Epidemiology in Mental Health, 7, ArtID 106.

4 Conn, V.S. (2010). Depressive symptom outcomes of physical activity interventions: Meta-analysis �ndings. Annals of Behavioral Medicine, 39, 128-138.

5 Cox, J. G. (2008). Is exercise an evidence-based intervention for clinical depression in older adults: A meta-analysis of randomized studies 2000-2006. Dissertation Abstracts International Section A: Humanities and Social Sciences, 69(2-A), 753.

6 Mead, G.E., Morley, W., Campbell, P., Greig, C.A., McMurdo, M., & Lawlor, D.A. (2009). Exercise for depression. Mental Health and Physical Activity, 2(2), 95-96.

7 Reed, J. & Ones, D.S. (2006). The e�ect of acute aerobic exercise on positive activated a�ect: A meta-analysis. Psychology of Sport and Exercise, 7, 477-514.

8 Gordon, J., Ditto, B., Lavoie, K.L., Pelletier, R., Campbell, T.S., Arsenault, A., & Bacon, S.L. (2011). The e�ect of major depression on postexercise cardiovascular recovery. Psychophysiology, 48(11), 1604-1609.

9 Corace, K. M. (2008). Does reducing negative a�ect facilitate readiness to exercise? A stage-based, cognitive-behavioural intervention for individuals at risk for primary and secondary Coronary Heart Disease. Dissertation Abstracts International: Section B: The Sciences and Engineering, 69(6-B), 3841.

10 Lee, Y., & Kim, H. (2008). Relationships between menopausal symptoms, depression, and exercise in middle-aged women: A cross-sectional survey. International Journal of Nursing Studies, 45(12), 1816-1822.

11 Otto, M. W., & Smits, J. A. J. (2011). Exercise for mood and anxiety: Proven strategies for overcoming depression and enhancing well-being. Oxford University Press: New York: NY.

12 Weinstein, A. A., Deuster, P. A., Francis, J. L., Beadling, C., & Kop, W. J. (2010). The role of depression in short-term mood and fatigue responses to acute exercise. International Journal of Behavioral Medicine, 7(1), 51-57.

13 Lin, L., Halgin, R. P., Well, A.D., & Ockene, I. (2008). The relationship between depression and occupational, household, and leisure-time physical activity. Journal of Clinical Sport Psychology, 2(2), 95-107.

14 Mata, J., Thompson, R.J., Jaeggi, S. M., Buschkuehl, M., Jonides, J., & Gotlib, I.H. (2011). Walk on the bright side: Physical activity and a�ect in major depressive disorder. Journal of Abnormal Psychology. Advance online publication. Doi: 10. 1037/a0023533.

15 Trivedi, H., & Daly, E.J. (2007). Measurement-based care for refractory depression: A clinical decision support model for clinical research and practice. Drug and Alcohol Dependence, 88(2), S61-S71.

16 Mota-Pereira, J., Silverio, J., Carvalho, S., Ribeiro, J.C., Fonte, D., & Ramos, J. (2011). Moderate exercise improves depression parameters in treatment-resistant patients with major depressive disorder. Journal of Psychiatric Research, 45(8), 1005-1011.

17 Daley, A. (2008). Exercise and depression: A review of reviews. Journal of Clinical Psychology in Medical Settings, 15(2), 140-147.

THE ETHICS OF SUICIDE

Giles Burch, PhD

Welcome to the second edition of this column. I hope you enjoyed our last column “Immunity of Court Experts: Safe no More?”, which I know stirred up interest amongst the readership.

Additionally, since our last column, ACPA has announced the formation of a new Ethics Committee with the appointment of Sonia Smuts and Lesley Bretherton to this Committee, whom we wish all the best in this important function. As pointed out by Caroline Hunt in her announcement of this Committee, the aim of the Committee is to promote ACPA’s objectives, as follows:

• to promote and maintain excellence in the professional practice of clinical psychology;

• to promote, encourage, and support members of the Association; and

• to promote competence and ethical practice amongst members of the Association.

Given that this edition of ACPARIAN is focusing on depression, I wanted to take the opportunity to brie�y present some views on the ethics of suicide. Aaron Beck, in his article in this edition of ACPARIAN, has already raised the issue of suicide, thus it seemed relevant to raise some of the key points in the literature regarding this complex topic. It is a vast topic, well beyond the scope of this column, but is worth us noting the philosophies regarding suicide given, as Camus stated, “there is but one truly serious philosophical problem and that is suicide. Judging whether life is or is not worth living amounts to answering the fundamental question of philosophy”1.

At its simplest level, the debate regarding the philosophy of suicide is one of an individual’s fundamental freedom of choice, or right (to die), versus the belief that suicide is wrong. Added to that is the debate of the role of mental health professionals (and wider society) in preventing suicide.

This is not a new debate, and if we go back to ancient Greek philosophy, we �nd that Plato considered suicide as wrong, except perhaps, when it is the consequence of shame, misfortune or a corrupted mind2. More recently, the likes of Thomas Szasz have adopted a more libertarian view. For example, Szasz in his book Fatal Freedom: The Ethics and Politics of Suicide wrote:

Accidental or sudden death notwithstanding, practicing death control – that is, dying voluntarily – should be a personal decision. The State and the medical profession no longer interfere with birth control. They ought to stop interfering with death control3.

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Perhaps most germane to clinical psychologists, is Szasz’s assertion that individuals should be free from “psychiatric coercion”, that is, people should be allowed to refuse medical treatment, including suicide prevention. What we have thus far considered are two polemic stances on suicide that exist in the philosophical debate. However, the debate is not that straightforward and there are other philosophical perspectives of which we should remind ourselves, usefully identi�ed by Chiles and Strosahl in their Clinical Manual for Assessment and Treatment of Suicidal Patients4:

1. Suicide is wrong.

2. Suicide is sometimes permissible (e.g., when the alternative is pain).

3. Suicide is not a moral or ethical issue.

4. Suicide is a positive response to certain conditions (e.g., when it is a rational decision).

5. Suicide has intrinsic positive value (e.g., hara-kiri).

This highlights the complexity and di�culty when considering the ethics of suicide, which can be considered to include not only direct suicidal acts, but also assisted suicide.

For clinical psychologists and other mental health professionals, our duty of care is concerned with suicide prevention, yet it still remains important for us to remember the arguments both for and against intervention, points that have been succinctly presented elsewhere by Bloch and Heyd5:

Figure 1: Arguments for suicide intervention and non-intervention (Bloch & Heyd 2009, p. 237)

In presenting some of the views on the philosophy of suicide in this column, I hope it provides us with an opportunity to re�ect on these issues; however, I will leave the �nal words with Bloch and Heyd (2009, p. 246), who conclude that “it is better to err on the side of preserving life than on the side of letting it be lost”.

References and Further Reading

1 Camus, A. (1975). The Myth of Sisyphus. Harmondsworth: Penguin. Cited in Bloch, S., & Heyd, D. (2009). Suicide. In S. Bloch & S.A. Green (Eds.), Psychiatric Ethics, 4th Ed. Oxford: Oxford University Press.

2 Cholbi, M. (2009). Suicide. The Stanford Encyclopedia of Philosophy (Fall 2009 Edition), Edward N. Zalta (ed.), Retrieved from http://plato.stanford.edu/archives/fall2009/entries/suicide/

3 Szasz, T. (1999). Fatal Freedom: The Ethics and Politics of Suicide. Westport, CT: Praeger Publishers, p. x.

4 Chiles, J.A., & Strosahl, K.D. (2005). Clinical Manual for Assessment and Treatment of Suicidal Patients. Washington, DC: American Psychiatric Association.

5 Bloch, S., & Heyd, D. (2009). Suicide. In S. Bloch & S.A. Green (Eds.), Psychiatric Ethics, 4th Ed. Oxford: Oxford University Press.

TOWARDS COMPETENCY-BASED TRAINING IN CLINICAL PSYCHOLOGY

McLytton N. Clever, DPsych(Clinical)Associate Editor

The current issue of ACPARIAN focuses on depression. Depression is one of the most prevalent mental health problems in our society with a lifetime prevalence of between 5-12% for men and 10-25% for women1. Research evidence suggests that major depressive episodes are treatable in 70-80% of patients with an integrative approach of pharmacotherapy and psychotherapeutic interventions. To be able to e�ectively treat mental health issues, psychologists, like their medical counterparts, have to be competent (i.e., have the skill set to assess, formulate, plan and treat), the skills of which are developed through training. This article presents a brief history of clinical psychology training models and the zeitgeist towards competency training.

The in�uence of the Boulder and Vail models in shaping the training of clinical psychologists cannot be underestimated. Many clinicians working in the �eld today have graduated through either of these models. The Boulder conference of 1949 for instance, endorsed a model of study for clinicians that, to this day, has dominated clinical programs at most University-based institutions: the scientist-practitioner model, designed to provide a rigorous grounding in research methods and a breadth of exposure to clinical psychology. The Boulder model emphasized the training of graduates who would work either in academic or clinical settings.

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Students and TrainingMatters

Intervention Non-intervention

Taking the patient’s decision as irrational, impulsive, distorted by mental illness.

Take the patient’s decision as authentic, deliberate, clear-headed and rational.

On the assumption that her [sic] decision is reversible, certain steps, which are also reversible, are taken to prolong her life.

On the assumption that her decision is irreversible, no steps are taken, thus irreversibly letting her commit suicide.

Paternalism: forcing the patient to act rationally as an expression of care for her real interests.

Respect for the patient’s autonomy and liberty to kill herself as to take any other decision, even if it seems irrational to us.

Care for the patient’s family, who usually ask for intervention.

Take the patient’s side rather than that of her family. Priority of her freedom over the family’s interests.

The price: forcing her to act against her will, prolongation of her mental and physical misery, serious loss of liberty.

The price: missed opportunities, the in�nite loss involved in death, possibility of the most ‘tragic mistake’.

Underlying assumption: the instinctive drive to save other people’s lives plus the professional duty and practice of doctors to do so.

Underlying assumption: ‘nothing in life is as much under the direct jurisdiction of each individual as her own person and life’ (Arthur Schopenhauer).



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The 1970s saw articulation for change in training from that espoused by the Boulder conference. Practitioners identi�ed the need for professional training (similar to medicine) with a focus on producing practitioners who were not necessarily researchers, but capable of utilizing research in their clinical practice. In 1973 the practitioner-scholar model and the associated doctor of psychology degree were formally recognized by the American Psychological Association at the Conference on Levels and Patterns of Professional Training in Psychology (also known as The Vail Conference). The new training pathway for clinical psychology was targeted at those who were particularly interested in clinical practice. Similar to scientist-practitioner training (Boulder model), practitioner-scholar (Vail model) training is characterized by core courses in both basic and applied psychology, supervision during extensive clinical experience, and using research to inform their clinical work.

For years, training in clinical psychology in Australia and overseas has been dominated by de�nitions of input – hours of classes or supervision and speci�c components2. However, in the last decade or so, there has been a signi�cant shift in thinking regarding changing clinical psychology training from input- based to competency-based training. In the US, a confer-ence was convened in 2002 to discuss the competencies model of training and subsequently the Commission on Accreditation (CoA) increased focus on competencies in the accreditation process at all levels of training3.

In section B (1) of guiding principles on accreditation, the CoA states:

Doctoral graduate and internship education and training in preparation for entry-level practice in professional psychology should be broad and professional in its orientation rather than narrow and technical. This preparation should be based on the existing and evolving body of knowledge, skills, and competencies that de�ne the declared substantive practice area(s) and should be well integrated with the broad theoretical and scienti�c foundations of the discipline and �eldof psychology in general. (p.3).

Following this call by CoA, training programs in the US have been gravitating more towards competency-based training.

In Canada, competency-based training for professional psychologists has existed for a number of years. The Canadian Psychological Association (CPA) states in its accreditation publication (available on its website4) that for practitioners to be licensed to practice, they need to demonstrate that they have acquired a number of core competencies within assessment and intervention. The CPA highlights that appropriate benchmarks have been developed for the evaluation of these particular competencies. However, Hunsley and Barker (2011) note that even though the Canadian system has well developed benchmarks in assessment of competencies in clinical training, competencies related to supervision are still lagging behind5. The authors also note that to date there is a dearth of literature on supervision competencies leaving the profession with no baseline data to compare what works and what does not.

In the United Kingdom, clinical psychology training moved toward the competency model of training in the mid-1990s. Clinical psychology training today is only o�ered at the doctoral level training, with regulation and accreditation done collaboratively between the Health Professions Council and the British Psychological Society. The UK, it seems, is currently leading the �eld in competency training for both students and supervisors and has clearly identi�ed key competencies that are assessed1.

With such clearly set guidelines for both trainees and supervisors, institutional focus has now been directed towards developing tools for assessing competencies, identi�ed as a major stumbling block for this model of training.

In contrast to comparable jurisdictions that have made considerable advances in competency-based training, Australia is still steeped in the input-based model (see Pachana, Sofrono�, Scott, & Helmes, 20116), although some universities in Australia (e.g., University of Queensland) have commenced trialing competence-based assessments of clinical psychology trainees. The current Australian training landscape is characterized by multiple pathways of training in comparison to similar jurisdictions. Training and licensing of psychologists in Australia is either through the apprenticeship model (or 4 +2 model), or the postgraduate route. One can agree with Pachana et al. (2011), highlighting the e�ects of variations in training as leading to a lack of cogent information for both clients and other healthcare professionals regarding practitioner status in Australia.

Pachana et al. went on to observe that in future practitioners may be asked to inform clients regarding their practitioner training, expertise, and other factors relating to practitioner skills. This would dispel the current confusion resulting from variations in training. The case for competency-based training is strengthening in Australia (see Australian Psychologist, Vol. 46). One of the main driving forces is the growing in�uence of managed health care (both through Medicare and health insurance companies). Through the Medicare Better Access program, for instance, there has been a need for practitioners to demonstrate higher levels of competency to enable them to claim specialist-service delivery and higher Medicare rebates. There is no doubt that the future of clinical psychology training is heading towards competency-based training. Already, practice regulations in various jurisdictions are being strengthened to protect the public and future clients. It appears that the Boulder and Vail models of training are in the throes of signi�cant revisions or change, consistent with the changing needs of society. As Kaslow and colleagues (2007) observe, competency training is the model of the future, but a key issue facing this movement is the nature of competency assessment7. Research evidence from the United States and Canada suggests that at present, even though clinical psychology training programs are required through the accreditation systems to o�er competency based training, ways to assess clinical competencies remain elusive.

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References

1 Sadock, B. J., & Sadock, V. A. (2005). Pocket Handbook of Clinical Psychiatry (4th ed.). Philadelphia: Lippincott Williams & Wilkins. 2 Kavanagh, J. D. (2011). Training clinical psychologists: The current situation and a way forward. Australian Psychologist, 46(2), 65 – 66.

3 Commission on Accreditation. (2009). Guidelines and principles for accreditation in professional psychology. Washington, DC: American Psychological Association.

4 Canadian Psychological Association. (2011). Accreditation standards and procedures for doctoral programs and internships in professional psychology (5th revision). Retrieved from http://www.cpa.ca/docs/�le/Accreditation/Accreditation_2011.pdf on 20 October 2011

5 Hunsley, J., & Barker, K. K. (2011). Training for competency in professional psychology: A Canadian perspective. Australian Psychologist, 46(2), 142-145.

6 Pachana, N., Sofrono�, K., Scott, T. & Helmes, E. (2011). Attainment of competencies in clinical psychology training: Ways forward in the Australian context. Australian Psychologist, 46(2), 67 – 76.

7 Kaslow, N. J., Rubin, N.J., Bebeau, M. J., Leigh, I. W., Lichtenberg, J, W., Nelson, P. D., Portnoy, S.M., & Smith, I. L. (2007). Guiding principles and recommendations for the assessment of competence. Professional Psychology: Research and Practice, 38(5), 441-451.

MENTORING OF NEWLY GRADUATED CLINICAL PSYCHOLOGISTS: A NEW INITIATIVE BY ACPA

Chris Basten, PhD and Leanne Clarke, MClinPsych

Clinical Psychology, as we all know, is an engaging and fascinating professional arena and also one that has its unique challenges. This is most apparent in the �rst two years after graduation - a period in which we undergo rapid growth and change and assimilate considerable knowledge and personal experiences.

ACPA will be launching a new mentoring program designed to respond to some of the unmet needs of clinical psychologists as they approach graduation and for their �rst two years post-graduation.

The ACPA Mentoring Program aims to increase a sense of collegiality within ACPA and the broader professional community, while providing critical support for new members of our profession.

How Does Mentoring Di�er From Supervision?A mentor is more likely to explore issues around career development, personal growth and choice, as well as problem-solving in the work-setting, rather than discussing clinical work on a case-by-case basis. The supervisory relationship is often characterised by a focus on skill-development and client issues. It may be conducted by a senior colleague within the place of work. The issues brought to supervision by the supervisee may be a�ected by narrowness of scope or by the dual role the supervisor may play in the management and appraisal of the developing clinical psychologist. The mentoring relationship di�ers, given that it aims to provide a vehicle for non-evaluative, independent discussions free from the potential bias of dual roles.

Topics for discussion suited to a mentoring relationship might include:

• career development, direction and job seeking

• professional identity development

• personal pathways into choosing this career

• work satisfaction

• guidance in a specific area of professional practice

• assistance in navigating professional settings, institutions,

structures and politics

• dealing with stressors or conflicts in the workplace

• self-care as a health professional

• ethical guidance

• personal issues arising in response to therapy - what it means

to become a 'therapist', as well as a psychologist.

Mentoring programs exist for other health professionals and have been trialled in the United States. We encourage people interested in this program to read more about how mentoring works. The American Psychological Association program guideline is thorough and descriptive of both the literature in the area and the possibilities of the process.

What are the Potential Bene�ts for Mentors and Mentees?Bene�ts to the mentee may include greater work-satisfaction, early management of problems, and enhanced career development. Bene�ts to mentors may include the opportunity to pass on wisdom and knowledge to early career professionals, thereby contributing to the development of the profession, as well as their own professional growth through being challenged with questions about ethics and professional development.

How Will It Work?ACPA will very soon be inviting new graduates and more experienced clinicians to register interest in the program. Mentees (those being mentored) need to be in the �nal stages of completing or have recently completed a post-graduate degree in clinical psychology. Mentors need to be ACPA members with at least �ve years clinical experience.

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Once you have registered, mentees will be matched with a mentor in their preferred geographical area and with common professional interests. ACPA has established guidelines and contracts to make the process as smooth as possible and mutually bene�cial. The mentoring relationship is designed to be professional, con�dential and time-limited (two years). Access to the program is free.

When?An open invitation to ACPA members will go out before the end of this year. In the meanwhile, feel free to contact us right now ([email protected]) to register your interest, ask for an application form, or to simply ask a question about the program.

ACPARIAN EDITORIAL GUIDELINES

ACPARIAN is the o�cial publication of the Australian Clinical Psychology Association and is published three times a year.

Editorial Board

Editor Kaye Horley, PhD

Associate Editors Giles Burch, PhDMcLytton Clever, DPsych (Clin)

Copyeditor Bronwyn Williams, MPsych (Clin)

Design Ben Callegari, MPsych (Clin)

Aim ACPARIAN provides for the dissemination of knowledge on topics of interest informative to clinical psychologists. Its focus is on the latest clinical theory and research relevant to clinical practice including assessment and intervention, training and professional issues.

ContentSubmissions to ACPARIAN may include:Letters to the EditorGeneral articles, viewpoints, opinions and commentsArticles of particular ethical and/or legal interest to the professionResearch reviewsTheoretical perspectivesTechnology updatesStudents’ news and viewpoints Book reviewsGeneral Information and announcements.

From time to time, ACPARIAN will focus upon topics or issues of interest and call for submissions accordingly.

The ACPA Editorial Board welcomes contributions and suggestions for topics from the membership.

ContributionsSubmissions should be made electronically, in a Word document, to the editor responsible for that section:

Student and Training Matters: McLytton Clever [email protected]

Ethics and Legal Matters: Giles Burch [email protected]

Perspectives, Research and Feature articles: Kaye Horley [email protected]

Please observe the following word limits: Letters to the Editor: 200 words.Perspectives, Research Articles, Student Matters and Ethics and Legal Matters: 750 to 1000 wordsFeature articles: 1000 - 1500 words.

Please ensure that submissions are made by the stated deadline. Late submissions may not be accepted.

Authors can expect the Editorial Board to review and change content for clarity and style. The Editorial Board will endeavour to make any signi�cant revisions in consultation with the author. The Editor reserves the right to include or reject written works at any point in the publication process.

The views expressed by authors in ACPARIAN do not necessarily re�ect those of the ACPA Editorial Board.

SubscriptionThree issues of ACPARIAN are produced each year in March, July and November and delivered electronically to ACPA members via the listserve.

© The Australian Clinical Psychology Association 2011

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Reproduced with the kind permission of Dan Piraro (2011): http://bizarrocomics.com/



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Here are some highlights from the 2nd Annual National Conference held at the University of Melbourne, October 15 - 16, 2011.

ACPAConference 2011

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acparian issue 2 dec 2011 the depression...the history of cognitive therapy: aaron beck acceptance...

Documents