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• Inconsistencies in diagnosis, treatment and research design -> true epidemiological picture unclear (Power et al. 2002)

• Narrow or broad BPD criteria: unipolar/bipolar vs. manic hypomanic, rapidcycling and mixed mania

• Goodwin & Johnson (1990): underestimation more likely than overestimation-life time risk in industrialized countries 0.6-0.9% (BPD I & II)-annual incidence rate for men: 0.009-0.015% / women: 0.007-0.013%

• Conservative criteria estimated BPD 0.3-1.5% of population and only 10-15% of mood disorders (Weissman et al. 1996)

• Newer studies show prevalence rates due to broadening of the concept of BPD 1-8% (Power et al. 2002)

• Using clinical significance criteria rather than broadening the concept of BPD reduced prevalence rates ( Narrow et al. 2002)

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What causes BPD?

• Complex interactions of environmental and inherited factors create vulnerabilityfor BPD -> however processes mostly unknown (Blackwood & Muir, 2009)

• Among the biological factors observed in bipolar disorder:

- Over secretion of cortisol, a stress hormone.

- Excessive influx of calcium into brain cells.

- Abnormal hyperactivity in parts of the brain associated with emotion and movement coordination and low activity in parts of the brain associated with concentration, attention, inhibition, and judgment. (Well Connected, 2002)

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What causes BD? The biological view

Genetic factors

• Family, twin and adoption studies: heritability factor of between 63% and 79% for BD (Smoller& Finn, 2003)

• family history of mood disorder: earlier age of onset, more mood episodes, increased likelihood of hospitalization (Mradet al. 2007)

• Clearly genetic basis, but exact mechanisms remain uncertain (Bienvenu, Davydow, & Kendler, 2011)

• no single gene is completely responsible(Patel & DeUgiannidis, 2010)•Gene mutation coupled with stress and environmental factors increase risk for BD


• Because serotonin activity often parallels norepinephrine activity in unipolar depression, theorists expectedthat mania would also be related to high serotonin activity -> wrong

• This apparent contradiction is addressed by the “permissive theory” (Newberg et al., 2008)about mood disorders:low serotonin may open the door to a mood disorder and permit norepinephrine activity to define the particular form the disorder will take:Low serotonin + low norepinephrine = DepressionLow serotonin + high norepinephrine = Manianot sufficient proofs

• Dopamine hypothesis: faulty homoeostasis between DA transporter and receptors underly depressiveand manic phases of the illness-elevated D2/D3 receptor availability and hyperresponsive reward system in mania-increased DA transporter availability in bipolar depressionImplication for treatment: reduction of DA synthesis, selective DAT blockage-> partially true

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Reward hypersensitivity model

• Hypersensitive reward system in BP

• Reward system (behavioral activation system, BAS) regulates approach motivation, goal-directed behavior to attain rewards (Gray, 1994)

• Linked to a dopaminergic fronto-striatal neural circuit sensitive to reward stimuli (Haber & Knutson, 2010)

• BAS activation associated with increased motor behavior, incentive motivation and positive goal striving emotions (Gray, 1994)

• But also with anger when goal striving is blocked (Carver, 2004)

• Vulnerability to BD is result of overly sensitive reward system that ishyperactive to goal-and reward relevant cues

• Leading to hyperactivation to goal-and reward related cues

• Excessive reward motivation and approach related affect in responseto life events that involve rewards or goals -> hypomanic / manic symptoms•BAS/reward activation leads to hypo/manic activation symptoms

• Decrease in behavioral approach in response to nonattainment->depressivesymptoms

• Support from fMRI studies showing excessive increase in fronto-striatal-reward related neural activation (Hassel et al. 2008)

• Abnormal elevation during remission suggests fronto-striatal hyperactivity trait-like profile -> however only neuroimaging evidence so far

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Social / circadian rhythm disruption model

• Circadian rhythms = biological processes that repeat about every 24 hours (Czeisler & Gooley, 2007)

• Regulated by suprachiasmatic nucleus (SCN) in hypothalamus

• Under normal conditions entrained by external Zeitgebers (light)

• Circadian rhythm disruption is key neurobiological vulnerability for BD (Mc Clung, 2007)

• Life events that disrupt social zeitgebers precipitate BPD symptomse.g. change in bedtime -> increased light exposure->melatonin-> disruptcircadian rhythm

• Decreased need for sleep is prodromal feature of hypo/mania in 80% of individuals with BP (Jackson, 2003)

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Integrated model

• In individuals with hypersensitive reward system, BAS-activating/deactivatingevents lead to states of excessive reward (de) activation which disruptsocial and circadian rhythms

• Excessive reward activation -> excessively high appetitive motivation-> incongruent with maintaining regular social rhythms -> disruptioncircadian rhythms and trigger mood symptoms (Nusslock et al. 2009)

• Failure leads to excessive reward deactivation -> decreased response initiation and disregard of social routines

• Integrated model predicted the first onset of BPD better than just rewardhypersensitivity (Alloy, 2010)

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Cognitive model of BPD

General assumption:

• Thoughts feelings and behavior are strongly connected

• Changes in mood and changes in cognitive processes influence behavior

• The behavioral response reinforce the process of affective states that haveprompted behavior

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Cognitive model of BPDHow serious is BPD?

• Relapse rates high as 40% in 1 year, 60% in 2 years, 73% in 5 or moreyears (Gitlin et al. 1995) despite use of mood stabilizing agents

• Poor medication adherence in one half to two-thirds of patients within 12 months of treatment (Keck et al. 1998)

• Negative life events are associated with threefold increase in time to recovery(Alloy et al. 1999)

• Prophylaxis with mood-stabilizers protects fewer than 50% of individuals withBPD agains further episodes (Dickson and Kendell, 1994)

Risk for Suicide: An estimated 15-20% of patients who suffer from bipolar disorder and do not receive medical attention commit suicide.

• In a 2001 study of Bipolar I disorder, more than 50% of patients attempted suicide; the risk was highest during depressive episodes.

• Patients with mixed mania, and possible when it is marked by irritability and paranoia, are also at particular risk.

• Many young children with bipolar disorder are more severely ill than are adults with the disorder. According to a study in 2001, 25% of children with the disorder are seriously suicidal.