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Bipolar disorder - a psychological perspective (talk 1)
This document provides an overview of bipolar disorder from multiple perspectives including the brain, cognition, circadian rhythms, life events, and dysfunctional beliefs. Key points include: 1) Brain imaging and studies show differences in brain structures and activity in areas related to mood regulation like the prefrontal cortex and limbic system between those with bipolar disorder and healthy controls. 2) Disruptions to circadian rhythms and sleep patterns are implicated in bipolar disorder through their effects on mood regulation. 3) Stressful life events and lack of social support are associated with increased risk of bipolar episodes, while positive social support predicts a better illness course. 4) Cognitive models suggest dysfunctional beliefs and information processing styles may
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Bipolar disorder - a psychological perspective (talk 1)
- 1. BIPOLAR A psychologicalperspective Dr. Nick Stafford
- 2. WHAT HAPPENS INTHE BRAIN IN BIPOLAR?
- 3. AETIOLOGY MECHANISMS SYNDROMES THE BLACK BOX OF PATHOPHYSIOLOGY Life events Early environment SCHIZOPHRENIA BIPOLAR DEPRESSIVE DISORDER
- 4. With thanks ProfM Berk
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- 7. Mitochondrial dysfunction & oxidative stress in bipolar disorder Yatham et al 2010. p249, figure 1.
- 8. Andreassan et al2010
- 9. Cortex Hippocampus Hypothalamus Cortex Hippocampus Hypothalamus Cortex Hippocampus Hypothalamus Respiratory control ration Oxygen consumption ST4 Oxygen consumption ST3 Gong 2011
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- 16. Berk et al2011
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- 18. Structural brain differences Contrast Differences Depressed cases vs. Normal controls • LV enlargement • Larger CSF volume • Smaller volumes of BG, thalamus, hippocampus, frontal lobe, orbitofrontal cortex, gyrus recytus Depressed UPs vs. Remitted UPs • Smaller hippocampal volume Depressed vs. Bipolar • Reduced rates of deep white matter hyperintensities • Increased corpus callosum cross-sectional area • Smaller hippocampus and basal ganglia Bipolars and Depressed vs. Normal controls • Increased lateral ventricle volume • Increased rates of subcortical gray matter hyperintensities compared with healthy controls Prefrontal cortical areas (SGPFC), striatum and amygdala exist early in the course of BP illness and, therefore, potentially, predate illness onset. Kempton et al 2011 (Meta-analysis 143 studies since 1980)
- 19. Functional imaging furthermore… • Magnetic resonance spectroscopy investigations – membrane and second messenger metabolism, as well as bioenergetics, in striatum and prefrontal cortex. • Functional imaging studies report activation differences between bipolar and healthy controls in these same anterior limbic regions. • Together, these studies support a model of bipolar disorder that involves dysfunction within – subcortical (striatal–thalamic)–prefrontal networks and – the associated limbic modulating regions (amygdala, midline cerebellum). • There may be diminished prefrontal modulation of subcortical and medial temporal structures within the anterior limbic network (eg, amygdala, anterior striatum and thalamus) that results in dysregulation of mood. • Future prospective and longitudinal studies focusing on these specific relationships are necessary to clarify the functional neuroanatomy of bipolar disorder &: – Are there brain changes that occur in time with repeated episodes – Are these changes are associated with decrement in social or neuropsychological functioning
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- 21. Creativity Speed ofthinking Range of emotions experienced Associations and between ideas and emotions • Evidence – Studies focusing on well known sufferers – Controlled studies • Higher levels of people in creative occupations • Higher IQ in children who later develop bipolar Jameson 1996 Tihonen et al 2005 Tremblay et al 2010 McCabe et al 2010
- 22. MacCabe et al2010
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- 24. Cognitive deficits ineuthymic BP • Robinson et al 2006 – Marked deficits in executive functioning – Verbal memory • Kurtz et al 2009: Myths? – Methodological flaws? – Consequence of medication? – Just a function of motivation? – A function of other symptoms (e.g. sleep)? – Large number of studies of BP in remission (50+) & 5 meta-analyses Robinson et al 2006 Kurtz et al 2009
- 25. Cognitive deficits ineuthymic BP Kurtz et al 2009
- 26. Multiple or singlecognitive deficits? Baddeley et al 2000
- 27. Janusz et al2009
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- 30. Instability Model ofBD Vulnerability to Bipolar Disorder (Genetic- Biological) Medication adherence Disrupted social (circadian) rhythms Sleep disruption RELAPSE Life events Goodwin & Jameson 2007
- 31. Circadian rhythms inthe general population • 24.18 hours under controlled lighting conditions – Sleep – Melatonin – Core body temperature control – Cortisol – Consistent across all ages of adults • Circadian rhythms seem in cellular activity, body temperature, alertness, fluctuations in hormone secretion
- 32. Circadian rhythms •Driven by oscillators • Oscillators entrained by external zeitgebers (light-dark; social) • At least these 2 types of oscillator found through studies of free runners • Under normal conditions these cycles are synchronized together – under free running conditions they move in and out of phase with each other
- 33. Oscillators • Weak& Strong oscillators • Strong – drives cycles which are less sensitive to environmental manipulations, including REM sleep, body temperature, cortisol secretion, urinary potassium secretion • Weak – rest/activity cycle, sleep/wake cycle, sleep associated neuroendocrine activity • Phase advance of the strong oscillator is implicated in depression • SCN function in synchronizing the oscillators
- 34. Circadian rhythms inmania & depression • Peripheral & core body temperature • Cortisol, prolactin, growth hormone, dopamine beta-hydroxylase, 3-methoxy-4- hydroxyphenylglycol • Body temperature rhythms in manic and depressed patients do not fit the sinusoidal patterns of normals (Tsujimoto) – Difference in rhythmic stability
- 35. Sleep in thediagnostic criteria of BP • Importance of sleep and behavioural disturbances as symptoms in both types of episode • Depression – insomnia & hypersomnia, withdrawal from activities and agitation or retardation • Mania – decreased need for sleep and increased goal-directed and pleasurable ( but high risk activities)
- 36. Circadian genes associatedwith BP • BmaL1 • TIMELESS • PERIOD3 • ARNTL2 • CLOCK • DBP • CSNK1E Mansour et al 2005; Mansour 2009; Milhiet et al 2011; Shi et al 2008
- 37. Bidirectional relationship betweensleep, circadian functioning and mood regulation in bipolar
- 38. Sleep and amygdalaactivation • Healthy participants who are sleep deprived show increased amygdala activation to negative emotional images – 60% more amygdala activation cf. controls – Associated with loss of activity in the medial-prefrontal cortex • Does sleep contribute to maintaining the circuit between the amygdala and PFC? • Effect of enforced darkness on mania Refs
- 39. Problems with sleep/wake • Changes in cycle with illness • Sensitivity to alterations to cycle – Sleep wake cycle – Jet lag – Shift work • Regular sleep cycle important – Part of treatment plan • Sleep disturbance is the ‘final-common pathway’ for mania • Lithium lengthens primary circadian rhythm • Antidepressant effects on sleep – Sleep phase advance or deprivation for bipolar depressives
- 40. Inter-episode sleep •Resembles sleep pattern of an insomnia group • More fragmentation of sleep/wake rhythm • Longer sleep onset latency • More night-to-night variability • Higher REM density during first REM episode • More shifts to stage I and more awake or movement time Jones 2006
- 41. Circadian system •IPSRT – clinical effectiveness based on regularity • Shifted / arrhythmic circadian systems • Zeitgebers / Zeitstorers / Entrainment • Suprachiasmatic nucleus (SCN) • Peripheral clocks across organs and cells – SCN and periphery can become desynchronized • SCN sensitive to light • Liver sensitive to food • Muscle sensitive to exercise
- 42. Implications of anintegrative multilevel model of bipolar disorder • Circadian instability outside of episodes • Importance of early intervention • Development of internal attribution measures • Learning to reattribute fluctuations to external causes
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- 44. Illness Life events Current environment Early environment
- 45. Extensions of thecognitive models of unipolar depression ‘Manic defence’ hypothesis – psychodynamic model Dysfunctional cognitive style Information processing Onset Course Expression Above and beyond genetic predisposition Life events Current environment (supportive, non-supportive social) Early environment (parenting and maltreatment histories) Jones et al 2006
- 46. Life events &social support • Stressful life events – Prior to the onset of first episode – Hypomanic/Manic relapses – Depressive relapses • Positive social support – more positive course • Negative support – high EE – worse course • Much research since 1970s Jones et al 2006
- 47. Life events associatedwith relapse • Destabilizing effects on sleep, circadian rhythms and social rhythms • Goal attainment or goal striving (hypersensitive BAS) • Kindling model Jones et al 2006
- 48. Social support &bipolar • Bipolar individuals experience less support than controls • Poor social support predicts greater relapses and longer time to recover • EE studies – ↑symptoms ↑perception of negative family environment – F31 make more supportive comments than F20 • High EE is predictive of a worse outcome Jones et al 2006
- 49. Parenting & maltreatment • Coverdale & Turbott 2002 – Compared physical and sexual abuse <16yrs – Patients = bipolar (15.6%) & schizophrenia – PA + SA – no difference Patients & Controls • Abramson 2005 – Childhood stress and maltreatment (PA & SA) – Bipolar spectrum vs. Matched controls – Attempted to rule out reporting biases – PA & SA combined and “achievement failure events” were the only category events assoc. with bipolar onset Jones et al 2006
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- 51. Manic defence hypothesis • Psychodynamic model • Little empirical evidence • The grandiosity of mania is a defence or counter-reaction to underlying depressive tendencies • Recent cognitive reconceptualization of this ‘manic defence’ hypothesis are consistent with the potential relevance of negative, depressive cognitive styles to mania • Mania is thus cognitively akin to and not the opposite of depression Abraham 1911/1927; Dooley 1921; Freeman 1971; Klein 1994; Rado 1928
- 52. Manic defence psychodynamicprocess Life event perceived to be a threat Underlying fragile self-esteem Underlying depressive cognitions Grandiose thoughts prevent cognitions entering consciousness
- 53. Cognitive styles indepressed states • 5 studies compared UP vs. BP • 4/5 found no difference in cognitive styles Hill et al 1989; Hollon et al 1986; Reilly-Harrington et al 1999 • 1/5 found that BP had – higher ego strength and – lower social introversion cf. UP Donnelly & Murphy 1973
- 54. Depressive cognitive style • Equal in UP & BP – Negative dysfunctional attitudes – Automatic negative thoughts – Attributional styles – Self-referent information processing – More negative than normal comparisons – Unstable self-esteem Hill et al 1989; Hollon et al 1986; Reilly-Harrington et al 1999
- 55. Cognitive styles inmania/hypomania • Three studies – Hypomania associated with global attributions for both positive and negative events – Emotional Stroop test, high hypomanics took longer to name the colour of the depression but not the euphoria words Thompson & Bentall 1990; Bentall & Thompson 1990
- 56. Cognitive styles ineuthymic states • Eleven studies – Mostly using a mixture of implicit and explicit measures of cognition – No differences in a range of cognitive styles between BP, UP and controls • Six studies – Mostly explicit measures of cognition – Negative cognitive styles BP cf. controls – Set of cognitive styles consistent with high drive/incentive motivation associated with high BAS sensitivity Jones et al 2006
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- 58. There is ClinicalEvidence for … CBT FFT IPSRT PE
- 59. Mania & MixedStates • There is no evidence yet for psychotherapy to work in treating acute manic episodes • No studies have looked at the efficacy of psychosocial interventions for treating mixed episodes • For subsyndromal and hypomanic symptoms there is: – positive (Lam et al. (2000, 2003); Scott et al. (2001)) and – negative evidence (Miklowitz et al. (2003))
- 60. Prodromes in bipolar • Inherent problems in defining prodromes in mental health • Methodological issues • Empirical findings – Can bipolar patients report prodromes? – Common prodromes – Length of prodromal period
- 61. Coping in bipolardisorder • Importance of coping • Primary and secondary appraisal • Functions of coping • Coping with prodromes
- 62. Coping strategies forprodromes of mania Ten most frequently endorsed strategies Good coping group (N=21) (%) Poor coping group (N=15) (%) Modifying excessive behaviour 62 0 Engaging in calming activities 48 13 Take extra time to rest 43 0 See a doctor 29 7 Take extra medication as 19 7 previously agreed Enjoy the feeling of a high 5 20 Continued to move about 0 27 Did nothing 0 27 Spend more money 0 20 Find more to do 0 20 Lam & Wong 1997
- 63. Coping strategies forprodromes of depression The seven most frequently endorsed strategies Good coping group (N=17) (%) Poor coping group (N=12) (%) Get oneself and keep busy 53 0 Get social support and 29 0 meet people Distract myself from negative thoughts 24 8 Recognize and evaluate unrealistic thoughts 24 0 Stay in be and hope it will go away 6 53 Take extra medication without prescription 6 17 Do nothing 0 25 Lam & Wong 1997
- 64. Intervention studies thatincorporate coping with bipolar prodromes as a therapy component Study Subjects Therapy Control Duration Outcome Identify prodromes and seek help early: Perry et al 1999 N=69. I = 63; II=6 Relapsed in previous 12 months Training to identify prodromes. Rehearse action plan when recognized. TAU – drugs, monitoring, support from key worker 7-12 individual sessions Over 18months: - Significantly longer time to relapse - No beneficial effects on depression Schmitz et al 2002 N=46 with comorbid substance misuse Psychoeducation about BD and substance dependence. Identification of prodromes. Coping skills training. Four brief clinic visits for medication monitoring, discuss compliance, SEs, substance use and mood symptoms 16 individual sessions of 60 minute cognitive therapy Over 3 months: - No difference in substance misuse - Improvement in mood symptoms (significant) - Better attendance & compliance (trend only) FFT. Miklowitz et al 2000, 2003 N=101 type I Episode previous 3 months Radom allocation: 1/3 FFT 2/3 Rx & crisis management Psychoeducation Identify prodromal signs Relapse prevention plans Problem solving Communication training Medications 2 sessions of family education Crisis management 9 months of FFT Over 24 months FFT: - Fewer relapses - Longer time to relapse - Better medication compliance - Greater reduction in mood symptoms Cognitive therapy. Lam et al 2005 N=103 type I At risk of relapse 12-20 sessions CT with psychoeducation Psychiatric outpatients on mood stabilizers 6 months therapy with 2 booster sessions Over 30 months: Fewer bipolar relapses Fewer days in episode Lower depression scores & less fluctuation of manic symptoms Better coping strategies FFT 2. Rea et al 2003 N=53 type I recently hospitalized 21 group sessions: psychoeducation, prodromal signs, relapse prevention, problem-solving, communication training Individual sessions over 9 months. (12 weekly, 6 fortnightly, 3 monthly) General psychoeducation. 9 months Over 24 months: Fewer hospitalizations Fewer relapses No differences in time to relapses Psychoeducation. Colom et al 2003. N=100 stable euthymic I N=20 type II YMRS<6 HAM-D <8 Group psychoeducation Weekly 21 sessions Medication in OPC 20x 90 minute non-structured group sessions 21x 90-minute group sessions weekly of 9-12 patients Over 24 months: Fewer relapses Increased time to episode Fewer hospitalizations Shorter length of hospitalizations
- 65. Medication adherence •Use of antidepressants • Medication is usually necessary & effective • 20-62% relapse despite medication • 23-52% stop taking their medication – Complexities of medication treatments – Monitoring of long term medication – Adjusting to taking medication chronically – Dealing with side effects – Reduce dysfunctional attitudes
- 66. Subsyndromal symptoms •Early identification of prodromal symptoms • Preventing the symptoms • Managing the symptoms • Managing comorbidity – Anxiety disorders – Alcohol & Drug misuse – Personality disorder – Medical disorders – Psychosocial problems
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- 70. CBT model forbipolar Medication Individual deficits Stress Individual resources Basco & Rush, 1996; Meyer & Hautzinger, 2004 Instability of biological rhythms Hypomanic / manic, mixed or depressive Thoughts Prodromal symptoms symptoms Emotions Behaviour
- 71. SYSTEM POSITIVE REINFORCEMENT THREAT / NEGATIVE REINFORCEMENT Controlling stimuli External & internal cues for reinforcement / reward Cues for missing reward or punishment Specific systems Goal directed: • Social • Achievement • Sexual Irritability / active avoidance General systems Behavioural Activation System (BAS) • Motor activation • Incentive motivation Depue & Iacono (1989); Depue & Zald (1993)
- 72. BAS Core processof mania Depue & Zald, 1993; Alloy et al., 2006; Johnson 2005 Expecting reward / success Task done
- 73. CBT Evidence •Administered in euthymic state, works better – Than waiting for treatment – Sometimes better than treatment-as-usual – Than brief psychoeducation • However – It depends on the outcome – If CBT has lasting effects
- 74. CBT Euthymic: Anew German RCT Randomisation THERAPY For 9 months 20 sessions N=38 CBT N=38 ST FOLLOW UPS (every 3/6 months) B A S E L I N t0 t1 t2 t3 t4 t5 Blind ratings Meyer & Hautzinger, in press, Psycholog Medicine
- 75. CBT Euthymic: AGerman RCT Cognitive Behavioural Therapy Supportive Therapy 20 sessions (each 50 minutes) 20 sessions (each 50 minutes) 9 months 9 months Psychoeducation Psychoeducation Mood diary Mood diary Relapse analysis and individual early warning plan Focus on current problems Behavioural strategies Client-centered perspective Cognitive strategies Problem solving and communication skills Meyer & Hautzinger 2011
- 76. CBT Euthymic vs.ST • Shorter time to relapse: – a higher number of prior episodes – a lower number of therapy sessions – a diagnosis of bipolar II disorder Log Rank (Mantel-Cox) χ2 = 0.004, n.s. Meyer & Hautzinger 2011
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- 78. PE: Elemental mechanisms Awareness of the disorder Adherence with treatment Early detection Secondary mechanisms & Desirable objectives
- 79. PE: Secondary mechanisms Controlling stress & psychosocial factors Avoiding substance use and misuse Achieving regularity in lifestyle Role of individual psychological Preventing suicidal behaviour factors
- 80. PE: Desirable objectives Increasing knowledge and facing the psychosocial consequences of past and future episodes Improving social and interpersonal activity between episodes Sub-syndromal symptoms and impairment Increasing well-being and improving the quality of life
- 81. Psychoeducation Evidence Colomet al. 2009
- 82. Elements of psychologicaltherapy • Sufficiently long psychoeducation group – CBT – FFT – IPSRT • Relapse prevention is the main goal
- 83. IPSRT • Developedfrom IPT for depression • Influenced by the instability model of bipolar • Self-monitoring programme • Maintain life characterized by zietgebers • Increase awareness of, minimize zeitstorers Stages of IPSRT 1. Psychoeducation & interpersonal inventory 2. Initiation of the Social Rhythm Metric (SRM) 3. SRM used to identify & work on imbalances Swartz et al 2001
- 84. Acknowledgments • Dr.Thomas Meyer. Newcastle University • Prof. Steven H Jones. Lancaster University • Prof. Michael Berk. Melbourne University
Editor's Notes
- #30 Response to prophylactic lithium in bipolar disorder may be associated with a preservation of executive cognitive functions Janusz K. Rybakowski, Agnieszka Permoda-Osip, Alina Borkowska We assessed performance on the Wisconsin Card Sorting Test (WCST), measuring executive functions, in 30 patients showing different prophylactic effect of lithium (excellent lithium responders—ER, partial responders—PR and non-responders—NR), and in fifty persons of their offspring (12 of ER, 26 of PR, and 12 of NR). Age- and gender head-to-head matched population consisted of 30 subjects for lithium group and 50 subjects for the offspring of lithium patients. In lithium patients, NR had significantly worse results compared to the remaining groups and to control subjects on perseverative errors (WCST-P) and conceptual responses (WCST-%conc). No differences were observed in the offspring of patients with different effect of lithium, however, they showed an impairment on WCST-P and WCST-%conc compared to matched healthy controls. Therefore, the favorable effect of lithium prophylaxis may be associated with a preservation of executive cognitive functions and the offspring of bipolar patients shows an impairment of such functions.