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Depression-Bio-Psycho-Social Management and EBT Dr Sumanta Gupta Consultant Psychiatrist Oldham Outline • • • • • • NICE guideline Antidepressant Treatments Treatment Resistant Depression CBT & MCBT IPT Evidence Base for the above treatments NICE Guideline-Principles for assessment • When assessing a person who may have depression, conduct a comprehensive assessment that does not rely simply on a symptom count. • Take into account: – the degree of functional impairment and/or disability associated with the possible depression and – the duration of the episode. Effective delivery of interventions for depression (1) • All interventions should be delivered by competent practitioners. • Psychological and psychosocial interventions should be based on the relevant treatment manual(s). • Practitioners should consider using competence frameworks. Effective delivery of interventions for depression (2) For all interventions, practitioners should: • receive regular high-quality supervision • use routine outcome measures • ensure the patient with depression is involved in reviewing treatment efficacy • engage in monitoring and evaluation of: – treatment adherence – practitioner competence. NICE-The stepped-care model Focus of the intervention STEP 4: Severe and complex1 depression; risk to life; severe selfneglect STEP 3: Persistent subthreshold depressive symptoms or mild to moderate depression with inadequate response to initial interventions; moderate and severe depression STEP 2: Persistent subthreshold depressive symptoms; mild to moderate depression STEP 1: All known and suspected presentations of depression 1,2 see slide notes Nature of the intervention Medication, high-intensity psychological interventions, electroconvulsive therapy, crisis service, combined treatments, multiprofessional and inpatient care Medication, high-intensity psychological interventions, combined treatments, collaborative care2, and referral for further assessment and interventions Low-intensity psychosocial interventions, psychological interventions, medication and referral for further assessment and interventions Assessment, support, psycho-education, active monitoring and referral for further assessment and interventions Low-intensity psychosocial interventions • For people with persistent subthreshold depressive symptoms or mild to moderate depression, consider offering one or more of the following interventions, guided by the person’s preference: – individual guided self-help based on the principles of cognitive behavioural therapy (CBT) – computerised cognitive behavioural therapy (CCBT) – a structured group physical activity programme. Drug treatment –NICE guideline • Do not use antidepressants routinely to treat persistent subthreshold depressive symptoms or mild depression because the risk–benefit ratio is poor • Consider antidepressants for people with: – a past history of moderate or severe depression or – subthreshold depressive symptoms present for a long time or – subthreshold depressive symptoms or mild depression that persist(s) after other interventions. Treatment for moderate or severe depression • For people with moderate or severe depression, provide a combination of antidepressant medication and a highintensity psychological intervention (cognitive behavioural therapy [CBT] or interpersonal therapy [IPT]). Psychological interventions for relapse prevention People with depression who are considered to be at significant risk of relapse or who have residual symptoms, should be offered one of the following psychological interventions: • individual CBT: – for people who have relapsed despite antidepressant medication – for people with a significant history of depression and residual symptoms despite treatment. • mindfulness-based cognitive therapy: – for people who are currently well but have experienced three or more previous episodes of depression. Antidepressants Few Dates 1958 1958 1982 1988 1989 1994 1994 1996 Monoamine oxidase inhibitors (MAOIs) Tricyclics (TCA’s) Trazodone (Molipaxin) Fluoxetine (Prozac) Bupropion (Zyban) Nefazodone (Serzone) Venlafaxine (Effexor) Mirtazapine (Zispin) Treatment Response Categories PREVALENCE IN RCTS STATE OBJECTIVE CRITERION CLINICAL STATUS Remission HAM-D ≤ 7 No residual psychopathology ~ 40% Response ≥ 50% decrease in HAM-D without remission Substantially improved, but with residual sxs ~ 25% Partial response 25%-50% decrease Mild-moderate in HAM-D improvement ~ 10% Nonresponse < 25% decrease in HAM-D ~ 25% No clinically meaningful response Fig. 1. Survival analysis of weeks to major depressive episode relapse (MDE): comparing patients with unipolar major depressive disorder who recovered from intake MDE with residual subsyndromal depressive symptoms vs. asymptomatic status. Wilcoxon Chi Square Test of Difference=47.96; P<0.0001. Why Is Achieving Remission Important? • Residual symptoms put patients at high risk of relapse and recurrence – Patients with residual symptoms after medication treatment are 3.5 times more likely to relapse compared to those fully recovered (Judd et al, 1998) – This risk is greater than the risk associated with having ≥ 3 prior depressive episodes – Similar finding exists after response to cognitive therapy Why a temporal delay for maximal therapeutic benefit -adrenergic receptor downregulation 5-HT2 receptor down-regulation Antidepressant medications have essentially equivalent efficacy Tricyclic Antidepressants (TCAs) Characteristic three-ring nucleus Clinical effects Normalization of mood and resolution of neurovegetative symptoms Biochemical effects Inhibit monoamine uptake at nerve terminals May potentiate action of drugs that cause neurotransmitter release Temporal delay of weeks for clinical effects, although biochemical effects are immediate Mechanism of action of TCAs “Tertiary” TCAs imipramine amitriptyline clomipramine “Secondary” TCAs desipramine nortriptyline Inhibit 5-HT uptake (weaker inhibition of NE uptake) Inhibit NE uptake (weaker inhibition of 5-HT uptake) In vivo action of TCAs If one administers a tertiary TCA If one administers a secondary TCA there is always both the tertiary and the secondary amine in the circulation there is only the secondary amine in the circulation. Neuropharmacology of TCAs Inhibit monoamine uptake (NE and 5-HT) Muscarinic cholinergic antagonism H1 histamine antagonism 1-adrenergic antagonism Tricyclics-Contraindications • QTc greater than 450 msec • Conditions worsened by muscarinic blockade (eg myasthenia gravis, BPH) • pre-existing orthostatic hypotension • Seizure disorder Side effect profile of TCAs Dry mouth Constipation Dizziness Tachycardia Urinary retention Impaired sexual funtion Orthostatic hypotension Low therapeutic index of TCAs Cardiotoxicity: resulting from combination of: Conduction defects, arrhythmias Delirium Potentiation of effects of other sedating drugs Consequences Suicide requires care in prescribing monitoring drugs that might have synergistic effects on monoamine function Monoamine Oxidase Inhibitors (MAOIs) Irreversibly inhibit monoamine oxidase enzymes Effective for major depression, panic disorder, social phobia Drug interactions and dietary restrictions limit use Biochemistry of MAO Occurs as two isoenzymes MAO-A – •Oxidizes norepinephrine, serotonin, tyramine MAO-B • selective for dopamine metabolism Dietary and Drug Interactions Increased stores of catecholamines sensitize patients to effects of sympathomimetics Accumulation of tyramine (sympathomimetic) = high risk of hypertensive reactions to dietary tyramine requires dietary restrictions Interactions with other sympathomimetic drugs Antidepressants OTC cold remedies • phenylpropanolamine Meperidine L-dopa Examples of MAOIs Irreversible, non-selective MAOIs phenelzine isocarboxazid tranylcypromine Selective MAO-B inhibitors deprenyl (selegiline) loses its specificity for MAO-B in antidepressant doses Reversible monoamine oxidase inhibitors (RIMAs) Moclobemide Appears to be relatively free of food/drug interactions Selective Serotonin Uptake Inhibitors (SSRIs) Currently marketed medications Fluoxetine (Prozac). Sertraline (Lustral). Paroxetine (Seroxat) Fluvoxamine (Luvox) Citalopram (Cipramil) Escitalopram (Cipralex) Selectively inhibit 5-HT (not NE) uptake Differ from TCAs by having little affinity for muscarinic, as well as many other neuroreceptors Selective Serotonin Reuptake Inhibitors (SSRIs) Much higher therapeutic index than TCAs or MAO-I’s Much better tolerated in early therapy Equal or almost equal in efficacy to TCAs Side effects associated with SSRIs Nausea Sexual dysfunction Delayed ejaculation/anorgasmia Anxiety Insomnia Hyponatremia Serotonin syndrome Evoked by interaction between serotonergic agents e.g., SSRIs and MAOIs Combination of increased stores plus inhibition of reuptake after release Symptoms Hyperthermia Muscle rigidity Myoclonus Rapid changes in mental status and vital signs Can be lethal Selective Norepinephrine-Serotonin Reuptake Inhibitors Venlafaxine (Effexor), Duloxetine (Cymbalta), relatively devoid of antihistaminergic, anticholinergic, and antiadrenergic properties nonselective inhibitor of both NE and 5-HT uptake. Adverse effects: GI , Sexual dysfunction, hypertension (venlafaxine), hyponatremia Other antidepressants Trazodone mixed 5-HT agonist/antagonist • 1 antagonist • H1 antagonist Nefazodone (Serzone) 5 HT2 antagonist Bupropion (Wellbutrin; Zyban) Inhibits uptake of DA and NE antismoking properties probably involves parent molecule Lacks sexual side effects Seizure risk Mirtazapine 2 antagonist 5H2 and 5HT3 antagonist Net effect selective increase in 5HT1A function H1 antagonist advantages: sedation, no adverse sexual effects Antidepressants and drug interactions Pharmacodynamic – Additive effects with alcohol and other sedating drugs – MAOI interactions Pharmakokinetic – Cytochrome P450-2D6 inhibition • Fluoxetine and paroxetine • Increased levels of TCAs, antipsychotics, warfarin – Cytochrome P450-3A4 inhibition • Nefazodone and fluvoxamine • Increased levels of terfenadine, astemizole, cisapride – can cause fatal arrhythmias Treatment Resistant Depression(TRD) • When Do You Characterize a Response As Treatment Resistant? • After a patient has been on an antidepressant at for a reasonable amount of time at an adequate dose • No commonly accepted time point – Most drug trial data comes from 8 week long studies – If no onset of response by weeks 4 or 6, there is a 73-88% chance of not having onset of response by end of 8 week trial (Nierenberg et al, 2000), so 4 weeks is a reasonable point to increase dose – An 8-12 week course is consistent with acute treatment framework and allows patients 8 weeks at a dose expected to produce response A Working Definition of Treatment Resistant Depression 6-8 weeks of at least a middle range dose without remission What Are the Clinical Features Associated With TRD(1) • Incorrect primary diagnosis – Is there a secondary cause of the depressive symptoms (e.g., substance-induced mood disorder from prescription meds or ethanol, hypothyroidism, hypercalcemia ) – Is their primary psychiatric diagnosis wrong (?bipolar, schizoaffective, cluster B personality DO)? – Is there an unrecognized depressive subtype? • Psychotic depression What Are the Clinical Features Associated With TRD (2) • Patient factors -acceptance of diagnosis -compliance • Physician factors -Underdosing -Inadequate length of treatment TRD-Strategies • Level 1 – Initial Treatment: Citalopram • Level 2 – Switch To: • bupropion • sertraline • Venlafaxine – Augment With: • bupropion • buspirone • Level 3 – Switch To: • mirtazapine or nortriptyline – Augment With: • Lithium or T3 • Level 4 – Switch To: • Tranylcypromine or mirtazapine combined with venlafaxine ECT should be considered at all stages if indicated. How Effective is an SSRI in Real World Practice? • ~1/3 met criteria for remission (HAM-D ≤ 7) • ~ 1/2 met criteria for response (≥ 50% decrease in depressive severity) (Trivedi et al, Am J Psychiatry, 2006) TREATMENT OUTCOMES L-3 Switch • Mirtazapine • Nortriptyline Remission (HAM-D) 12.3% 19.8% TREATMENT OUTCOMES L-3 Augmentation • Lithium • T3 Remission (HAM-D) 15.9% 24.7% TREATMENT OUTCOMES L-4 Switch Remission (HAM-D) • Tranylcypromine 6.9% • mirtazapine + venlafaxine 13.7% • Electroconvulsive Therapy – Response rate in patients with • inadequate medication trials: 86% • adequate trials: 50% – Probably treatment of choice for catatonic states SUMMARY of Drug treatments of Depression • Patients suffering from major depression (primarily with chronic disease and multiple recurrences) in Primary and Specialty Care settings have a 30% chance of achieving full remission with an adequate dose of Citalopram • Patients who did not remit with citalopram had a 1 in 4 chance of achieving remission by switching to bupropion, sertraline or venlafaxine and a 1 in 3 chance of responding to augmentation of the citalopram with bupropion or buspirone • There was no clear advantage in switching antidepressant class although its often the only option. SUMMARY-2 • Depressed patients who fail to respond to two antidepressant trials are have a 12-20% remission rate with another single antidepressant agent and a 16-25% remission rate with T3 or lithium augmentation • While there is indisputable evidence for real world effectiveness of available antidepressant medications, many patients do not achieve remission. • There is a pressing need to develop more effective treatments for depression and also to elucidate factors that may help us choose from our currently available treatments Cognitive Behavioural Therapy (CBT) One of the most extensively researched forms of psychotherapy with over 325 outcome studies looking at CBT effectiveness published in 2006 (Butler et al., 2006). CBT encompasses a number of therapeutic cognitive and behavioural approaches. The compelling evidence base for CBT lead to an announcement in 2007 that there would be £173 million into an Improving Access to Psychological Therapies Program (IAPT) based on the finding that CBTs were more efficient than pharmacotherapy or other interventions (Rachman & Wilson, 2008). Depression-Recap Minor depression: Rumination on negative themes: Resentful, irritable, or angry Major depression: 5 or more symptoms in the last 2 weeks (Diagnostic Criteria (DSM IV) Major Depressive Episode) Emotional changes: feelings of sadness and hopelessness. Cognitive changes: low self esteem, guilt, concentration difficulties. Behavioural and motivational difficulties: feeling slowed down, reduced interest in social activities. Bodily changes: sleep, eating, loss of energy. Chronic depression occurs in 15-39% of cases with individuals still experiencing major depression one year after symptom onset (Berti, Ceroni, et al., 1984). Early experience • e.g. rejection and criticism from parents Negative core beliefs/schemas Beck’s cognitive model - Recap. From Dozois & Beck (2008) • I am incompetent Negative life event Activation of schema Cognitive biases • Nothing ever goes right for me Negative automatic thoughts Depression Structured: • Time limited • Problem orientated Role of therapist: • As a guide • As a scientist practitioner • Socratic method CBT STRUCTURE Cognitive techniques: • Hot cognitions Recording cognitions (mood diaries) • Identifying cognitive biases Behavioural techniques: • Behavioural experiments • Experiments with therapist • Experiments alone From: Westbrook, Kennerley, & Kirk (2007) Cognitive techniques Cognition: “either a thought or a visual image that you may not be very aware of unless you focus your attention on it” (Beck et al., 1979, p. 147) The C in CBT Help clients observe and record thoughts and images that run through their minds and help them to distinguish between thoughts and feelings. For example • Identifying ‘hot cognitions’: Rapid automated decisions based on significant emotions. • Identifying: ‘cognitive biases/ thinking errors’ Extreme thinking : Dichotomous thinking or unrealistic biases. Selective attention: Overgeneralization or disqualifying the positive. Example of techniques used to help people understand the link between thoughts and emotions Daily Thought Record Date & time Situation What mood were you in? How intense was the mood? 0 10 Not at all Very Thoughts Behavioural techniques/experiments The B in CBT Planned experimental activities, performed in or between cognitive therapy sessions. (Bennett-Levy et al., 2004) Their design is derived from a cognitive formulation of the problem and their primary aims are: 1. Test validity of clients existing beliefs about themselves, others, world. 2. Construct new, more adaptive beliefs. 3. Contribute to the development of the cognitive formulation. (Bennett-Levy et al., 2004) In depression, behavioural experiments may be used to test negative automatic thoughts and to re-evaluate underlying beliefs and assumptions. Behavioural experiments One example: Emma became depressed in University and dropped out when the pressure of exams became too much. She moved back to her parents’ house and felt too depressed to contact her friends. Hypothesis testing Theory A: Client’s initial belief: ‘My friends will think I am thoughtless and selfish and won’t want to know me’ - 80% belief. Theory B: Alternative belief: ‘One or two of my friends may be missing me, a couple have tried to contact me’ – 20% belief. Prediction: My best friend won’t want to know me any more. Even if we do meet I will probably feel foolish and cry all night. Outcome: After two more sessions working on the idea that the alternative belief may be true, Emma picked up the phone and rang her friend. Her friend was pleased to hear from her, they arranged to go out and Emma was surprised to find that she had fun and did not cry. Emma’s belief that her friend’s wouldn’t want to know her dropped to 10%. Common CBT goals 1.The client needs to counteract negative cognitive biases and develop a more balanced view of him/herself, the world, and the future. 2. Restore activity levels, especially of activities that bring a sense of pleasure and achievement. 3. Increase active engagement with problem solving. Efficacy of CBT for depression • Based on clinical trials evidence – NICE recommends CBT for depression http://www.nice.org.uk/cg90 • Important questions to consider when thinking about efficacy: 1. What is CBT compared to? Drug treatments, other therapeutic approaches, nothing? 2. Long term outcomes: Are treatment gains maintained over time? • CBT is more effective than no intervention – Based on meta-analysis of 97 studies, d = 0.67, Cuijpers et al., 2011 • Is equally effective as other types of psychological therapy – Based on meta-analysis of 56 studies, d = 0.03, Cuijpers et al., 2011 • CBT is equally effective to antidepressant medication, and may be more effective at preventing relapse (De Rubeis et al., 2005) Efficacy of CBT for depression De Rubeis et al (2005) Study comparing cognitive therapy with antidepressant medication in adults No difference in outcomes at 16 weeks Cognitive Therapy was associated with lower rates of relapse Mindfulness Based Cognitive Therapy (MBCT) MBCT aims to prevent depressive relapse by developing awareness of and changing the relationship with unwanted negative thoughts, feelings and bodily sensations. In this way previously depressed individuals respond to negative thoughts not in an automatic way, but in a skilful intentional way. Ma & Teasdale (2004) Mindfulness “Paying attention in a particular way: on purpose, in the present moment , and nonjudgmentally ” Kabat-Zinn (1990) Core assumptions of MBCT MBCT assumes that once in a mode of recovery from depression, previously depressed individuals will still be vulnerable to experiencing low mood and patterns of negative thinking. Reactivation of depression related thoughts, feelings, and physical sensations is often automatic – and can trigger relapse. Model underlying development of MBCT for depressive relapse Negative thinking: Depressive episode Nonnegative thinking: Remission Potential RELAPSE Negative thinking patterns “nipped in the bud ” Negative thinking patterns re-established. From: Segal, Williams, & Teasdale (2002), p. 37 LOW MOOD Reactivation of negative thinking How does it work? “The aim of the program is freedom, not happiness” (Segal, Williams, & Teasdale, 2002, p.91) 8 week manualised course : Mindfulness practices and traditional cognitive therapy techniques AIM: To prevent re-establishment of patterns of negative thinking Core themes • Recognition of patterns of negative thinking e.g. ‘automatic pilot’ & ‘attachment to achieving happiness’. • How to step out of old cognitive routines e.g. ‘decentring & ‘mindful awareness’. • Experiential learning e.g. engaging in ‘being’ not ‘doing’ mode (in class and through homework. • Empowerment and acceptance/kindly awareness. Comparing MBCT and CBT Practical differences: MBCT delivered in a group format whereas CBT is often 1:1 MBCT is based on an 8 week program Theoretical differences: CBT encourages individuals to identify and change maladaptive thoughts by challenging the accuracy of their beliefs. MBCT teaches individuals to recognise the occurrence of depressive thoughts without emotionally responding to them. (Manicavasgar, Parker, & Perich, 2011) MBCT includes techniques and exercises from cognitive behavioural therapy with additional meditation components. (Segal, Williams, & Teasdale, 2002) Both MBCT and CBT include didactic elements, which provides the participants with information about depression to facilitate them in recognising and dealing with their relapse signatures. Is it effective? • NICE recommends MBCT for depressive relapse: http://www.nice.org.uk/cg90 • In individuals who had > 3 episodes of depression relapse was reduced when compared to TAU. (Ma & Teasdale, 2000, 2004) • MBCT shown to be more effective than m-ADM at preventing relapse. (Kuyken, 2008) • MBCT has shown promise for those still currently depressed or experiencing chronic depression. (Kenny & Williams, 2007; Kingston et al., 2007) Summary • A range of cognitive approaches are available in the UK • CBT has one of the largest evidence bases Both cognitive and behavioural techniques help the individual to develop strategies for managing problems and guide the development of more adaptive perspective on the world. • MBCT has been developed to break the cycle of relapse common to depression Techniques teach individuals to be present, in the moment, to recognise negative thinking and decentre from it. Compassion and kindness to the self are fostered. Interpersonal Psychotherapy Historical Influences of IPT • • • • Psychoanalysis Harry Stack Sullivan Object Relations Therapy Interpersonal Theory (Leary, Kiesler) IPT: Roots in Psychodynamic Theory • Primary instincts of sex and aggression involve relating to others • Relationships with others contribute to personality development • Psychological Problems due to deficits in early relations Transference and counter-transference are interpersonal Outline of IPT Intervention Initial Sessions (Overview) • Assess Depressive symptoms • Complete Interpersonal Assessment • Identify Major Interpersonal Problem Area • Explain IPT and make treatment contract Prominent Features of IPT • IPT designed for symptom reduction and improved interpersonal relationships • Focus on current disputes, frustrations, anxieties in the interpersonal context which impact mood and self esteem IPT Compared to CBT • Focus on affect and expression of emotions • Explores avoidance and resistance behavior • Identification of patterns in client’s behavior, thinking, feeling and relationships • Attention to past experiences • Focus on interpersonal experience • Emphasis on the therapeutic relationship • Exploration of client’s wishes, dreams, fantasies Blagys & Hilsenroth, 2000 Role of IPT Therapist • Therapist is patient advocate, not neutral • Expresses unconditional positive regard • Intentionally cultivates positive expectations of treatment – Optimistic, positive, reassuring • Therapist is active in keeping interpersonal problem areas to focus Setting Treatment Contract • Set 2 –3 treatment goals with client related to problem area focus • Ask client what would be the: – Best possible outcome – Most expectable outcome – Worst possible outcome • Describe expected Duration and Frequency of treatment (12-16 weeks) Relate Depression to Interpersonal Context What interpersonal events related to depression? Review current & past interpersonal relationships • Who does client interact with? • Frequency of contact, activities shared? • Assess quality and themes of relationships • Assess expectations of client (and other) in relationships • Assess satisfying and unsatisfying aspects of relationships • Discuss changes client wants in relationships Identification of Major Problem Area Assess interpersonal experience and depression to identify of one of Four Problem Areas: • Interpersonal Role Dispute: with spouse, lover, family member, friends, co-worker • Role Transition: e.g. new job, relocation, divorce • Interpersonal Deficits: evidenced by social impoverishment, loneliness, isolation • Grief: following death if abnormally severe, protracted or impairing Evidence for IPT Efficacy • • • • • • Boston-New Haven Study (1979) 4 Tx Groups (16 wks & 1yr follow-up): IPT, amitriptyline, both combined, control IPT and amitriptyline equally effective Combination IPT & amitrip. most effective IPT grp. Sustained improved psychosocial functioning 1 yr later (not amitrip. Grp) NIMH Tx Depression Research (1989) • 4 Tx grps (16 wks, multi-site, N=250) • IPT, CBT, Imipramine & clinical management (CM), placebo & CM • IPT comparable to Imipramine & CM • CBT showed somewhat less improvement • IPT grp. had lowest attrition rate • Results for mod.-severe depression Brain Activity Changes with either IPT or Antidepressant Tx • PET scans showed higher prefrontal and less temporal activity in depressed vs controls • Both IPT and Paroxetine resulted in normalized PET scan activity and improved Depressive symptoms. Brody (2001); Martin (2001) References • NICE guideline CG 90-2009(Review March 2015) • Rush AJ, Trivedi MH, Wisniewski SR, et al. Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression. N Engl J Med. Mar 23 2006;354(12):1231-1242. • Trivedi MH, Fava M, Wisniewski SR, et al. Medication augmentation after the failure of SSRIs for depression. N Engl J Med. Mar 23 2006;354(12):1243-1252. • Fava M, Rush AJ, Wisniewski SR, et al. A Comparison of Mirtazapine and Nortriptyline Following Two Consecutive Failed Medication Treatments for Depressed Outpatients: A STAR*D Report. Am J Psychiatry 2006; 163:1161-1172. • Nierenberg AA, Fava M, Trivedi MH, et al. A Comparison of Lithium and T3 Augmentation Following Two Failed Medication Treatments for Depression: A STAR*D Report. Am J Psychiatry 2006; 163:1519-1530. • www.ids-qids.org References CBT • • • • • • • • • • • • • Bennett-Levy, J., Butler, G., Fennell, M., Hackmann, A., Mueller, M. & Westbrook, D. (2004) The Oxford guide to behavioural experiments in cognitive therapy. Oxford: Oxford University Press. Butler, A. C. Chapman, J. E. Forman, E. M. & Beck, A. T. (2006). The empirical status of cognitive-behavioral therapy: a review of metaanalyses. Clinical Psychology Review, 26, 17-31). Cuijpers P, Clignet F, van Meijel B, van Straten A, et al. (2011). Psychological treatment of depression in inpatients: a systematic review and meta-analysis. Clinical Psychology Review 31(3):353-60. DeRubeis, R. J., Hollon, S. D., Amsterdam, J.D., Shelton, R. C., Young, P. R., Salomon, R. M., et al. (2005). Cognitive therapy vs. medications in the treatment of moderate to severe depression. Archives of General Psychiatry, 62, 409-416. Dozois, D.J.A. & Beck, A.T. (2008). Cognitive schemas, beliefs, and assumptions. In K.S. Dobson & D.J.A. Dozois (Eds.), Risk factors in depression. London Academic Press. (Available online via ScienceDirect).(Nice explanations of main factors of cognitive model of depression) Rachman S, Wilson GT. (2008). Expansion in the provision of psychological treatment in the United Kingdom. Behaviour Research & Therapy, 46(3), 293-5. Westbrook, D. Kennerley, H. & Kirk, J. (2007). An introduction to Cognitive Behaviour Therapy: Skills and application. Sage. London MBCT Kenny, M. A., & Williams, J. M. G. (2007). Treatment-resistant depressed patients show a good response to mindfulness-based Cognitive Therapy. Behaviour Research and Therapy, 45, 617-625. Kingston, T., Dooley, B., Bates, A., Lawlor, E., & Malone, K. (2007). Mindfulness-based cognitive therapy for residual depressive symptoms. Psychology and Psychotherapy, 80 (2), 193- 203. Kuyken, W., Byford, S., Taylor, R.S., Watkins, E.R., Holden, E.R., White, K., Barrett, B., Byng, R., Evans, A., Mullan, E. & Teasdale, J.D. (2008). Mindfulness-based cognitive therapy to prevent relapse in recurrent depression. Journal of Consulting and Clinical Psychology 76(6), 966-978. Ma, S.H., & Teasdale, J.D. (2004). Mindfulness-based cognitive therapy for depression: Replication and exploration of differential relapse. Journal of Consulting and Clinical Psychology, 72, 31-40. Manicavasgar, V. Parker, G. & Perich, T. (2011). Mindfulness-based cognitive therapy vs cognitive behaviour therapy as a treatment for non-melancholic depression. Journal of Affective Disorders, 130, 138–144. Segal, Z.V., Williams, J.M.G., & Teasdale, J.D. (2002). Mindfulness-based cognitive therapy for depression: A New Approach to Preventing Relapse. New York: Guilford. • Thanks for your attention!!