McGill University Health Centre Centre universitaire de santé McGill Transdiagnostic Depression Group Marco Sinai, Ph.D. Mood Disorders Program
Outline ◼ Brief Introduction to BSD ◼ Brief Review of Psychosocial Interventions for BSD ◼ Description of BSD Group Therapy at the Allan ◼ Description of Results ◼ Discussion
History of Bipolar Disorder (BSD) Aretaeus (1 st Century) Melancholia Mania Euthymia Falret (mid-1800s) Melancholia Mania Euthymia Kraepelin (Early 1900s) Manic Depressive Dementia Illness Precox Unipolar Bipolar Leonhard (1960s) Depression Depression DSM-IV (1990s) Bipolar I Bipolar II
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 ◼
Heterogeneity of BSD ◼ Variable characteristics inherent in definition of mania: excessive positive emotions excessive negative emotions (happiness; euphoria) (anger; irritability) inflated self- distractibility esteem excessive involvement in increased decreased need pleasurable activity/ agitation for sleep activities (87%) (81%) racing thoughts pressured speech (40 % to 100% ) (75% to 100%) Hallucinations present in 4% to 40% of manic episodes (Rehm and Tyndall, 1993) ◼
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
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; over-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 ”.
BSD Etiology ◼ Bio-Genetic risk ◼ Concordance studies point to high heritability of Bipolar I disorder (Edvardsen et al., 2008) Identical Twins Fraternal Twins VS 40% concordance 5% concordance ◼ Many candidate genes exerting mild to moderate effects (Kerner, 2014) ◼ 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
Models
Review of Psychosocial Interventions for BSD ◼ Psychoeducation ◼ Cognitive Behaviour Therapy ◼ Family Interventions ◼ Mindfulness and other Third Wave approaches ◼ Interpersonal Social Rhythms Therapy
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.
Cognitive-behavioural therapy ◼ 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.
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.
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)
Circadian Rhythms Melatonin signals “darkness” Cortisol signals “activation”
Circadian dysregulation is a core feature of BSD 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 During Euthymic mania Control Control (Salvatore et al., 2008
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
Social Zeitgeber Theory of Mood Episodes 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 Adapted from: Ehlers et al. 1988
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