Transdiagnostic Depression Group Marco Sinai, Ph.D. Mood Disorders - - PowerPoint PPT Presentation

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Transdiagnostic Depression Group Marco Sinai, Ph.D. Mood Disorders - - PowerPoint PPT Presentation

McGill University Health Centre Centre universitaire de sant McGill Transdiagnostic Depression Group Marco Sinai, Ph.D. Mood Disorders Program Outline Brief Introduction to BSD Brief Review of Psychosocial Interventions for BSD


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Transdiagnostic Depression Group

Marco Sinai, Ph.D. Mood Disorders Program

McGill University Health Centre Centre universitaire de santé McGill

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Outline

◼ Brief Introduction to BSD ◼ Brief Review of Psychosocial Interventions for BSD ◼ Description of BSD Group Therapy at the Allan ◼ Description of Results ◼ Discussion

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History of Bipolar Disorder (BSD)

Melancholia Aretaeus (1st Century) Mania Falret (mid-1800s) Melancholia Mania Euthymia Euthymia Kraepelin (Early 1900s) Manic Depressive

Illness Dementia Precox Unipolar Depression Bipolar Depression

Leonhard (1960s)

Bipolar I Bipolar II

DSM-IV (1990s)

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Bipolar Spectrum Disorder (BSD)

Biological illness that causes unusual shifts in:

◼ Mood, level of energy, and

ability to function

◼ Shift between periods of low

mood and lethargy (depression), and periods of high energy and/or irritability (manic)

Manic pole: excessive positive emotions and associated features

◼ Mania (lasting >1 wk), Hypomania (lasting > 4 days) Cyclothymia

(personality trait)

Depressive pole: major depressive episode lasting 2 weeks

◼ Identical dx criteria as unipolar depression ◼ Few clinical differences between unipolar and bipolar depressive episodes

Mixed episode: Predominant symptoms from one polarity, but with features

from opposite polarity.

Euthymic phase: Patient is asymptomatic but remains at risk of relapse.

Comorbid disorders: Anxiety, Substance Use, Personality Disorders, ADHD

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Heterogeneity of BSD

◼ Variable characteristics inherent in definition of mania:

Hallucinations present in 4% to 40% of manic episodes (Rehm and Tyndall, 1993)

excessive positive emotions (happiness; euphoria) excessive negative emotions (anger; irritability)

inflated self- esteem pressured speech

(75% to 100%)

decreased need for sleep

(81%)

excessive involvement in pleasurable activities racing thoughts

(40 % to 100% )

distractibility increased activity/ agitation

(87%)

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BSD Clinical Concepts

◼ Akiskal’s BSD Classification (not DSM)

◼ Bipolar I – Full-Blown Mania ◼ Bipolar I ½ - Depression with protracted Hypomania ◼ Bipolar II – Depression with Hypomania ◼ Bipolar II ½ - Cyclothymic Depressions (often

confused with Borderline Personality Disorder)

◼ Bipolar III – Antidepressant – Associated Hypomania ◼ Bipolar III ½ - Bipolairty masked – and unmasked –

by stimulant use or abuse

◼ Bipolar IV – Hyperthymic Depression

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BSD Clinical Concepts

◼ BSD Temperaments (Akiskal & Pinto, 1999)

◼ The Hypethymic temperament. Cheerful and overoptimistic;

warm, people-seeking, and extroverted; eloquent and jocular; overconfident and self-assured; high energy level, full of plans and improvident activities;

  • ver-involved and meddlesome; uninhibited, stimulus-seeking or

promiscuous; and habitual short sleeper.

◼ The Generalized Anxious temperament. Exaggerated

disposition toward worrying. Evolutionary advantage: “Survival of one’s kin”

◼ The Depressive Temperament. Sensitivity to suffering, a cardinal

feature of the depressive temperament, represents an important attribute in a species like ours, where caring for young and sick individuals is necessary for survival. Self-denying and devoted to others

◼ The Cyclothymic Temperament. Moody–temperamental

individuals, shifting from flamboyant to dysthymic, irritable, capricious, falling in and out of love easily. Evolutionary advantage: “pursuit of lovemaking opportunities”.

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BSD Etiology

◼ Bio-Genetic risk

◼ Concordance studies point to high heritability of Bipolar I disorder

(Edvardsen et al., 2008)

◼ Many candidate genes exerting mild to moderate effects (Kerner, 2014)

Identical Twins 40% concordance Fraternal Twins 5% concordance

VS

◼ Genetic predisposition may underlie physiological abnormalities such

as Circadian Dysregulation and shifts in energy levels. ◼ Psychosocial risk

◼ Despite a strong genetic predisposition, psychosocial risk remains

substantial

◼ Need for psychosocial interventions as part of optimal treatment for

BSD

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Models

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Review of Psychosocial Interventions for BSD

◼ Psychoeducation ◼ Cognitive Behaviour Therapy ◼ Family Interventions ◼ Mindfulness and other Third Wave

approaches

◼ Interpersonal Social Rhythms Therapy

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Psychoeducation

◼ Major Components

◼ Awareness of the disorder ◼ Treatment adherence ◼ Avoiding substance abuse ◼ Early detection of new episodes ◼ Regular habits and stress management

◼ Evidence

◼ Rigorously tested by Colom et al. (2003) ◼ 120 euthymic bipolar patients assigned to 21 sessions of group

psychoeducation or non-specific group meetings.

◼ At 2-year follow up, benefits of psychoeducation with regard to

percentage, number and time to recurrences, and hospitalization per patient. Efficacy maintained over 5 years, and effect sizes did not decrease.

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◼ Major Components

◼ Psychoeducation about bipolar disorder ◼ Identification of triggers and dealing with long-term vulnerabilities ◼ Cognitive behavioral skills to cope with symptoms

◼ Evidence

◼ Improved outcomes compared to treatment as usual (Cochran et

al., 1984; Lam et al., 2005; Ball et al., 2006)

◼ No significant difference compared to individual or group

psychoeducation

◼ Zaretsky et al., 2008 - compared 7 sessions of individual psychoeducation to 20

weeks of individual CBT in 79 patients in full or partial remission. No differences in relapse rates over 12 months.

◼ Parikh et al., 2012 - a Canadian trial compared 6 session of group

psychoeducation to 20 weeks of individual CBT in 204 patients in full or partial

  • remission. No differences in relapse or symptom severity over 18 months.

Cognitive-behavioural therapy

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Family intervention

◼ Major Components

◼ Psychoeducation ◼ Communication enhancement training ◼ Problem solving skills training ◼ Support and self-care for caregivers

◼ Evidence

◼ Miklowitz 2003, 2008, 2013: bipolar I and II patients who received

pharmacotherapy and family focused therapy showed 30-35% lower rates of relapse at 2 years follow-up compared to treatment as usual.

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Third Wave Therapies

◼ Components of DBT, ACT, MBCT

Distress Tolerance tools

Development of a different way (nonjudgmental) of relating to thoughts, feelings and bodily sensations

Ability to switch attention away from negative thoughts and bodily sensations.

Learn to ignore rather than challenge (classical CBT) negative thoughts and emotions

◼ Evidence

Established effectiveness of third wave approaches in depression and anxiety disorders

MCBT showed significantly reduced BDI and BAI scores compared to wait list control in Bipolar adults (Perich et al., 2008)

DBT showed significantly better adherence to treatment, reduced suicidal ideation, and increased weeks being euthymic in adolescents (Goldstein et al., 2015)

ACT showed significant improvement in anxiety, depressive and quality of life measures in uncontrolled study of 26 patients with BAD and comorbid

  • anxiety. (Pankovski et al., 2017)
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Circadian Rhythms

Melatonin signals “darkness” Cortisol signals “activation”

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During mania

higher cortisol levels during the night compared to healthy controls

earlier nadir for plasma cortisol compared to healthy controls

Two hour phase advance when compared with healthy controls

More daytime napping than when euthymic

When euthymic

lower melatonin and later melatonin peak during the night relative to healthy controls

Approximate two hour phase advance of circadian motor activity

relative to healthy controls

Circadian dysregulation is a core feature of BSD

(Salvatore et al., 2008

During mania Euthymic Control Control

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Circadian Rhythms and BSD

◼ Sleep disturbance increases negative mood, irritability,

and affective volatility

◼ At a neural level, affect and sleep circuits interact in bidirectional ways ◼ 35 hour sleep deprivation results in 60% greater amygdala activation to

negative stimuli relative to those who slept normally

◼ Deliberate sleep deprivation is a same-day powerful treatment for bipolar

(and unipolar) depression.

◼ 35 hour sleep deprivation triggers manic episodes in 5% of BSD patients ◼ Therapeutic sleep extension (“dark therapy”) has demonstrated that

stabilizing sleep reduced rapid cycling and decreases manic symptoms relative to treatment as usual group

◼ Lithium

◼ Slows down circadian periodicity and can modify circadian length – may

target circadian dysregulation

◼ In a study of seven rapid-cycling bipolar patients, five had a circadian

rhythm that ran fast, and lithium slowed the rhythm

Murray & Harvey, 2010

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Social Zeitgeber Theory of Mood Episodes

Adapted from: Ehlers et al. 1988

Life Events Change in Social Prompts (Social Zeitgebers = Unobservable Variables) Change in Stability of Social Rhythms Change in Stability of Biological Rhythms Change in Somatic Symptoms Manic and Depressive Episodes = Pathological Entrainment of Biological Rhythms

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Components

◼ Education about bipolar disorder ◼ Management of affective symptoms through adherence to medication

and stabilizing social rhythms

◼ Regulate daily routines ◼ Emphasizes the link between regular routines and moods ◼ Uses Social Rhythm Metric to monitor routines

◼ Resolution of interpersonal problems

◼ unresolved grief, social role transitions, interpersonal role disputes,

interpersonal deficits, grief for the lost healthy self

Evidence:

◼ Frank et al. (2008) 175 patients with Bipolar I in acute phase.

◼ Weekly sessions until measures of depression and mania reached the lower

cutoff scores indicating remission for 4 weeks.

◼ Maintenance = biweekly for 12 weeks, monthly for two years.

◼ Compared to TAU:

◼ survived longer without a new affective episode. ◼ Improvements in occupational functioning.

Interpersonal and social rhythm therapy

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Bipolar Group

◼ Ran 4 groups (19 patients) over 2 years.

◼ Enrolled 19 patients. 16 Treated to completion

◼ 75% of patients closer to depressive pole

◼ Integrative approach with elements of

◼ Psychoeducation ◼ IPSRT

◼ Interpersonal Therapy ◼ Social Rhythm Metric

◼ Third Wave CBT

◼ Mindfulness ◼ Distress Tolerance Skills ◼ Emotion Regulation Skills

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Bipolar Group Results Summary

◼ No group improvement in subjective sleep quality ◼ No evidence of improvement in interpersonal function ◼ No significant improvement in self-reported mood and

anxiety sx

◼ Robust subjective improvement in cognitive function ◼ Self-reported improvements in productivity ◼ Self-reported improvement in self esteem

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Discussion

Increased Distress Tolerance Improved Ability to Work Improved Self Satisfaction

Improved ability to function despite no improvement in mood and anxiety

Emphasis on third wave approaches that:

◼ Targets behavioural avoidance ◼ Allows exploration and tolerance of

negative thoughts and mood

◼ Prioritizes life satisfaction vs

happiness

No change in Mood and Anxiety Sx

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Problems with Bipolar Group

◼ Not enough patients referred to justify running

the group

◼ Most patients (75%) referred to bipolar group

reported majority of symptoms toward depressive pole

◼ Emphasis on Social Rhythms may not be

relevant to most bipolar patients with majority of Sx toward depressive pole.

◼ Program was geared toward manic pole

symptoms and missing Behavioural Activation component.

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TransDiagnostic Group

◼ Does it make sense to run a group that

combines Unipolar and Bipolar depressed patients?

◼ The prevailing model is that unipolar and

bipolar depression are different disorders

◼ Unipolar depression episodes are more

reactive to psychosocial stressors whereas bipolar depression is triggered by endogenous biological factors

◼ But what does the literature say?

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TransDiagnostic Group

◼ The literature says little

◼ Most studies compare unipolar depression

with bipolar disorder as a whole

◼ Studies that compare unipolar and bipolar

depression suggest more similarities than differences (reviewed by Cuellar, Johnson, &

Winters, 2005)

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Inconsistent findings between unipolar and bipolar depression

◼ Well designed studies show inconsistent or no

differences in atypical vegetative sx.

◼ Sleep duration ◼ Psychomotor retardation

◼ Inconsistent findings for

◼ Anger ◼ Melancholia ◼ Cycle Duration

◼ Age at Onset: bipolar 6 years earlier then unipolar (but

for bipolar disorder; first depression episode unspecified; Weissman et al., 1996)

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Differences between unipolar and bipolar depression

◼ Depressed patients with hx of manic episodes

show increased neurotransmitter regulatory deficits

◼ more rapid course changes

◼ Increased number of depressive episodes in bipolar; Roy-

Byrne et al., 1985

◼ Increased puerperal episodes ◼ increased vulnerability to environmental challenges??

◼ In well controlled studies, unipolar depression

associated with increased levels of anxiety, agitation, and appetite loss.

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Similarities between unipolar and bipolar depression

◼ Functional imaging studies suggest similar limbic

activation when exposed to sad stimuli (Yurgelun-Todd et al., 2000)

◼ Similar monoamine levels during episodes. ◼ No difference in episode severity (Ahearn & Carroll,

1996; Dorz et al., 2003)

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Similarities between unipolar and bipolar depression

◼ No diff in psychosocial stressors

◼ life events (Hirschfeld & Cross, 1982) ◼ Stress before suicide (Isometsa et al., 1995) ◼ Low social support

◼ No diff in personality traits

◼ Neuroticism equally associated with unipolar and bipolar

depression but not mania (Lozano & Johnson, 2001)

◼ Cognitive style

◼ Same phenomenology during episode

◼ Negative cognitive style ◼ Low self esteem ◼ Attributions of failure

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TransDiagnostic Group

◼ In sum, literature suggests more

similarities between unipolar and bipolar depression than accepted clinical wisdom

◼ Literature provides firm empirical

justification for transdiagnostic group

◼ Is bipolar disorder the manifestation of two

highly comorbid disorders (i.e., Depression and Mania)?

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Treatment Overview

◼ 12 Weeks Skills-Based Open Group

◼ 12, 2-hour sessions

◼ Led by two psychology interns ◼ 1st hour – week in review ◼ 2nd hour – new skills

◼ 11, mid-week 15-minute coaching calls

◼ Troubleshoot obstacles to skill implementation ◼ Increase motivation and adherence to treatment

◼ 4 modules od 3 sessions each

◼ Module 1 – Behavioural Activation ◼ Module 2 – Thought Defusion and Distress Tolerance ◼ Module 3 – Challenging Thoughts ◼ Module 4 – Interpersonal Skills ◼ Patients can enter the group at the beginning of each module

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Treatment Overview

◼ Measurement Based Treatment

◼ Pre questionnaires:

◼ Personality Inventory MCMI moving to PID-5 (plan is to eventually move to

PID-5 BF)

◼ Treatment Motivation Questionnaire ◼ CUDOS ◼ CUXOS

◼ Weekly measures

◼ CUDOS ◼ CUXOS

◼ Post questionnaires:

◼ PID-5 ◼ CUDOS ◼ CUXOS

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Session 1 – Behavioural Activation Session 2 - Values and Goals Session 3 – Sleep Session 4 – Introduction to Mindfulness Session 5 – Distress Tolerance I Session 6 – Distress Tolerance II Session 7 – Introducing Emotions Session 8 – Emotion Regulation I Session 9 – Emotion Regulation II Session 10 – Assessing Your Interpersonal Universe Session 11 – Interpersonal Relationships I Session 12 – Interpersonal Relationships II

BA TW-Defusion Workbook CBT-Challenge Interpersonal

Treatment Overview

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Participants

7 No Shows 2 Drop Out During First Module 26 Enrolled 18 finished module 1 16 finished module 2 3 Drop Out During Module 3 2 Drop Out During Second Module 13 finished program 2 did not complete post measures

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Patients Demographic

Diagnosis Referral Source Gender Age CUDOS Pre CUXOS Pre 8 Unipolar 7 MDP, 1 DH 5 M, 3 F Range 29-52 AVG 39.6 35.5 33.6 3 Bipolar 3 MDP 1 M, 2 F Range 39-51 Avg: 43.3 28.3 17

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Results – CUDOS

0.00 5.00 10.00 15.00 20.00 25.00 30.00 35.00 40.00 1 2 3 4 5 6 7 8 9 10 11 12 Total CUDOS CUXOS ◼

Cudos: pre post t-test <.001 d = 1.3

Cuxos: pre/post t-test <.01 d = .71