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Bipolar Disorder

Bipolar Disorder is an affective disorder characterised by mood episodes which can cause considerable impairment in everyday life (Richardson, 2010). It consists of episodes of depression combined with episodes of hypomania or mania. HYPOMANIA episodes are described as elated or irritable mood over 4 days or more. Symptoms include racing thoughts, a reduced need for sleep, increased talkativeness and engaging in impulsive acts such as reckless business investments and sexual promiscuity (APA, 2000). An individual who experiences episodes of both hypomania and mania is diagnosed with Bipolar II disorder. A MANIC episode has similar symptoms but is more severe with disrupted functioning at work or socially, and the possibility of psychotic symptoms and hospitalisation. Those who experience multiple episodes of mania and usually DEPRESSIVE episodes are diagnosed with Bipolar I disorder. Individuals can also be diagnosed with rapid cycling where there is a particular short time between affective episodes (APA, 2000). The impact of Bipolar Disorder: Associated with reduced quality of life, impaired functioning and high rates of martial disruption and an increased risk for suicide attempts (Mitchell et al, 2004). Bipolar disorder is also associated with particularly high levels of co-morbidity (Mitchell et al, 2004). Bipolar disorder is also associated with particularly high levels of drug and alcohol use, especially those with co-morbidity anxiety disorders (Richardson, 2010). Coryell et al. (1993) found that the effects of manic episodes on work, social, and family disturbance could be observed for as many as five years after an episode BD patients experience on-going functional impairment even between episodes, especially if they have sub-syndromal depressive symptoms (Fagiolini et al. 2005). In a 12-month followup of BDI patients hospitalised for a manic or mixed episode, 48% recovered from their initial syndrome by 12 months but only 24% achieved functional recovery (Keck et al. 1998). Conversely, several studies indicate above-average accomplishment among the family members of those with the disorder (Johnson, 2005). BD is believed to be associated with elevated creativity and productivity: many famous artists, musicians, writers, and politicians appear to have had the disorder (Jamison, 1993). There are also temperamental commonalities between BD patients and highly creative persons without psychiatric disorder, including openness to new experiences and novelty seeking (Nowakowska et al., 2005). The family members of BD persons often show high creativity (Richards et al., 1988). AETIOLOGY Three neurotransmitters have received the most attention in studies of mood disorders: norepinephrine, dopamine, and serotonin (Miklowitz & Johnson, 2006). Some studies suggest that a low or high level of a specific neurotransmitter such as serotonin, norepinephrine or dopamine is the cause.

The original neurotransmitter models suggested: Depression was tied to low levels of norepinephrine and dopamine Mania was tied to high levels of norepinephrine and dopamine. Mania and depression were both posited to be tied to low levels of serotonin, a neurotransmitter that helps regulate norepinephrine and dopamine. Indirect evidence for the role of neurotransmitters comes from among people without BD where several different dopaminergic drugs have been found to trigger manic symptoms such as increased mood, energy, and talkativeness (Willner, 1995). Other studies have found evidence that a change in the sensitivity of the receptors on nerve cells may be the issue. Neuroimaging studies indicate mood disorders are generally associated with decreased sensitivity of the serotonin receptors (Stockmeier, 2003). Furthermore, serotonin systems can be challenged by manipulating levels of tryptophan, the precursor to serotonin (Staley et al., 1998). Consistent with the idea that decreased sensitivity of serotonin receptors is involved in BD, people with a positive family history of BD developed more cognitive deficits after a serotonin depletion procedure than people without a family history (Sobczak et al., 2002). In one study, however, a procedure used to increase serotonin levels, tryptophan loading, produced similar cognitive deficits in family historypositive participants compared with family historynegative participants (Sobcazk et al. 2003). Such effects are consistent with dysregulation in serotonergic systems, but the nature of that dysregulation remains undefined. In short, researchers are quite certain that the neurotransmitter system is at least part of the cause of bipolar disorder, but further research is still needed to define its exact role. Psychosocial Predictors Ellicott et al. (1990) found that BD patients with high life eventsstress scores were at greater risk for relapse in a two-year follow-up than patients with medium or low life eventsstress scores. Miklowitz et al. (1988) found that BD I manic patients who returned after a hospitalization to families rated high on expressed emotion (EE) attitudes (criticism, hostility, or emotional over involvement) or who showed high levels of caregiver-topatient affective negativity (criticism, hostility, or guilt-induction) during face-to-face interactions were at high risk for relapse. Those whose families had high EE or high affective negativity were highly likely to relapse within nine months (94%), whereas those whose families rated low on both attributes were unlikely to relapse (17%). Two prospective studies of BD found that neuroticism was associated with increasing depressive symptoms but was unrelated to manic symptoms (Heerlein et al. 1998, Lozano & Johnson 2001). Similarly, low social support is a predictor of BD depression but not mania (Johnson et al. 1999). Although negative cognitive styles (negative biased cognitions) are often documented in BD disorder, they are most likely to be found during depression compared with well periods (Johnson & Kizer 2002), they more consistently predict depression than

mania (Johnson & Fingerhut 2004), and they can be explained by the presence of depressive history rather than manic history (Alloy et al. 1999). Furthermore, negative cognitive styles and low self-esteem predict increases in depression over time (Johnson & Fingerhut 2004, Johnson et al. 2000)

Predictors of Mania Compared with BD depression, less is known about the psychosocial variables influencing mania. Available models highlight three types of predictors of mania: negative threats (the manic-defence model), goal engagement, and life events involving sleep deprivation. Manic Defence Model Psychodynamic models have long conceptualised mania as a defence against loss experiences and painful awareness of negative feelings about the self (Adler 1964). The manic-defence theory suggests that mania unfolds as part of a defensive process. In support of this idea, two studies found that people with remitted BD tend to endorse positive views of the self when asked directly but display more negative cognitive styles on subtler cognitive measures than healthy controls, including measures of attributions for negative life events or attention to negative words (Lyon et al. 1999,Winters & Neale 1985). Other research suggests that in the context of a threat (writing an essay about their own mortality), people with high vulnerability to hypomania demonstrate more defensive responses than people with low vulnerability to mania (Johnson et al. 2005). They are also more likely to pursue highly stimulating, sensation-seeking activities (Thomas & Bentall 2002). Hence, people with BD may show certain types of defensiveness, but there is a lack of evidence to show that this defensiveness spirals into mania in the context of negative life events.

Goal Dysregulation This model suggests that mania may result from excess goal engagement secondary to increased sensitivity of the dopaminergic reward pathways (Johnson 2005). Johnson et al. (2000) hypothesize that excess reward sensitivity may heighten reactivity to success, such that manic symptoms would be more likely to occur after life events involving goal attainment. Results of a longitudinal study supported this hypothesis: goal-attainment life events predicted increases in manic symptoms but not depressive symptoms. Such effects were apparent even after controlling for baseline levels of manic symptoms and excluding life events that could have been caused by the patients symptoms. In studies of responses to standardised (false) success feedback, people vulnerable to BD demonstrate more robust increases in confidence than non-vulnerable people (Johnson et al., 2005, Stern & Berrenberg 1979). With increases in manic symptoms, people with D remember more positive than negative memories (Eich et al. 1997), pay less attention to negative stimuli (Murphy et al. 1999), and become unable to accurately detect negative facial expressions (Lembke & Ketter 2002).

Impulsivity, or the tendency to pursue rewards without awareness of potential negative consequences, also becomes elevated as people become manic (Swann et al. 2004).

In sum, goal attainments and success feedback may trigger increased goal engagement, and this excess goal engagement may contribute to a positive feedback loop that accelerates the development of manic symptoms (Johnson 2005). Schedule Disruption Sleep is incredibly important in dopamine regulation. In approximately 10% of people with a history of mania, one full night of sleep deprivation will trigger manic symptoms by the next morning (Barbini et al. 1998). Sleep deprivation may interfere with normalising the sensitivity of dopamine receptors (Ebert et al. 1994). Malkoff-Schwartz et al. (1998) conducted interviews with BD patients to assess the life events preceding their most recent illness episode. They found that patients reported more life events involving social-rhythm disruption (events that affect sleep or wake times, patterns of social stimulation, or daily routines) in the eight weeks preceding the onset of mania than in the eight weeks preceding depression. They replicated these results in a second study (Malkoff-Schwartz et al. 2000). Such findings provide one more potential mechanism for understanding how life events affect the onset of mania. Psychological Treatment/Interventions Due to negative outcomes associated with bipolar disorder, it is important for clinicians to consider effective treatments. There are number of pharmacological treatments are available, however these are associated with a number of side effects (Malhi et al, 2010). Therefore it is prudent to consider the effectiveness of psychological interventions for bipolar disorder. The Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) represents the largest prospective examination of bipolar disorder outcomes conducted to date (Sachs et al, 2003). STEP-BD explicitly allows for the inclusion of patients with medical and psychiatric comorbidity and those who require complex treatment regimens. It uses a common disease management model in which clinicians use evidence-based treatment guidelines (Sachs et al, 2003) that encourage the use of core psychosocial interventions (in addition to medications) in all patients. As such, STEP-BD allows for the assessment of longitudinal illness course and outcomes in a generalizable cohort of patients who receive best practice therapeutic regimens with modern pharmacotherapies. Participants in STEP-BD received evidence-based care from specialised clinicians with training in the use of standardised assessments, combination pharmacotherapy, and psychosocial treatments where appropriate. In addition, participants received at minimum a core psycho-educational intervention. The finding that nearly half of the study participants nonetheless suffered at least one recurrence during follow-up highlights the need for development of new interventions in bipolar disorder (Perlis et al, 2006).

Interpersonal and Social Rhythm Therapy (IPSRT) This is based on theory and research suggesting that relapse in BD is often caused by disrupted social routines or rhythms and stressful major life events (Shen et al, 2008). IPSRT combines behavioural techniques with elements of interpersonal therapy in an attempt to improve medication adherence and assist development of regular routines and sleep pattern, thereby reducing risk of relapse (Frank et al, 2000). Frank et al (2005) found that those who received IPSRT during an acute affective episode had longer in between episodes. IPSRT also led to more stable social rhythms, which in turn reduced the risk of relapse (Frank et al, 2005) Swartz et al (2009) found reduced depression and mania, with 29% achieving a full remission (reduction) IPSRT also appears to improve occupational functioning (Frank et al, 2008) Limitations = effects on functioning were NOT maintained 2 years later and that it was more effective for women than for men (Frank et al, 2008)

CBT It includes a number of elements such as developing treatment goals and using C-B techniques to address dysfunctional thoughts and beliefs, and the development of emotional management and relapse prevention techniques (Scott et al, 2010) Lam et al (2003) reported that patients receiving group CBT had significantly fewer episodes, fewer hospitalisations, higher social functioning, and better medication adherence. A total of 44% of patients in the CBT group experienced a relapse over 1 year, compared with 75% in the control group. However, the same group of investigators showed that although over 30-month followup, the CBT group had significantly better outcomes in terms of time to relapse, the effect on relapse prevention was mostly limited to the first year. This could mean that as therapy became more distant, the beneficial effects became weaker. Further investigations should explore the possibility of booster sessions or maintenance therapy (Lam et al, 2005) CBT has also led to fewer hospitalisations, reduced fluctuation between mood states (Lam et al, 2003) and improve affective symptoms (Ball et al, 2006) CBT may be effective for those with rapid-cycling BD (Reilly-Harrington et al, 2007). It can reduce hopelessness (Lam et al, 2000), improves compliance with medication (Lam et al, 2000, 2005) and reduce the amount of medication needed (Zaretsky et al, 2008). Although cognitive interventions may be costly to implement, they appear to save money in LT due to reduce service use (Lam et al, 2005).

Limitations of CBT Lam et al (2005) observed that the effects of CBT only reduce relapse rates in the first year after treatment, with no LT benefit. It is also unclear which specific type of affective episode is reduced by CBT. Lam et al (2003) found an impact on depressive and manic episodes, but not hypomanic episodes. In contrast, Lam et al (2000) found improvements in hypomanic episodes, but not manic and depressive episodes.

There may be subtle characteristics that determine the effectiveness of CBT. For example, Lam et al (2005) found that cognitive therapy was less effective for those who believed that they had personal attributes similar to hypomania. They did not see hypomanic symptoms as part of their illness and thus these symptoms were resistant to change. Family-focused Therapy this intervention has been developed which more actively involve the family members. In addition to psycho-education, these interventions include elements such as communication and problem skill training for families (Reinares et al, 2008). Family focused interventions appear to be more effective than individually administered interventions. Rea et al (2003) found that 28% in family intervention relapsed compared to 60% in individual intervention. Plus, only 12% were hospitalised compared to 60% who had individual work. Solomon et al (2008) similarly found that actively involving all members of the patients family reduced rates of hospitalisation. However, there is evidence to suggest that the effect on relapse rates is seen for hypomanic or manic episodes, BUT not for depressive or mixed episodes (Reinares et al, 2008). Additional work has documented that family-focused therapy also reduce affective symptom severity (Miklowitz et al, 2003), but mainly with depressive symptoms and not manic or hypomanic symptoms (Miklowitz et al, 2000).

Limitations Some research has failed to find a benefit of family-focused treatments e.g. Miller et al (2004) found it did not improve recovery more than medication alone. It may reduce relapse rate but they have no impact on recovery from an acute affective episode (Solomon et al, 2008) It is possible that only certain families will benefit from such interventions e.g. Miller et al (2008) found that those with Bipolar I disorder only led to some improvements in patients who were part of a dysfunctional family. Similarly, Miklowitz et al (2000) showed that improvements were more pronounced when there were high levels of expressed emotions. Eisner and Johnson (2008) found that a family intervention improved knowledge about BD, but families still have high levels of blame, criticism and anger. Psycho-education (PE) PE goes beyond mere delivery of information, as information alone has no therapeutic effect (Miklowitz, 2008). It is rather an information-based behavioural training aimed at providing BD patients with a theoretical and practical approach to understanding and coping with the consequences of their illness, which thus allows them to change their attitudes toward and beliefs about the illness, and provides specific coping strategies. Evidence suggests that structured group PE is more effective than unstructured group support (Colom et al, 2003). PE has been found to lead to reduced relapse rates, increase the time between episodes, and reduce the time spent in affective episodes (Colom et al, 2009).

It also appears to reduce the number and duration of hospital admissions (Colom et al, 2009). Group PE may also improve quality of life at least in terms of physical functioning and general satisfaction (Mischalak et al, 2005). The effectiveness appears to be for hypomanic, manic and depressive episodes, and benefits are maintained up to 5 years later (Colom et al, 2009). Also group PE appears to be cost-effective, although it costs money to implement in ST however, saves money in the long-run due to fewer inpatients stays (Scott et al, 2001) To increase accessibility, a number of research groups have begun to adapt PE interventions for an online format (Smith, 2010) and recovery road (Barnes et al, 2007). However there is no evidence on the clinical effectiveness of these as of yet.

Limitation of PE Illness severity affects outcomes those with more episodes before intervention have poorer outcomes (Colom et al, 2010) An analysis of 5-year outcomes found that those with more than 7 episodes prior to treatment had no benefit in terms of duration between episodes; and those who had experienced more than 14 episodes did not have a reduced time spent in an affective episodes (Colom et al, 2010) Even et al (2007) found that inpatients were more likely to take part if they were younger, more educated and had been ill for less time. Those with an external locus of control i.e. they believed they could not control what happened to them, were less likely to take part in PE The majority of interventions have been developed for the use with both Bipolar I and II patients together. Whilst PE appears to benefit Bipolar II specifically, it has been suggested that Bipolar II patients need specifically designed interventions (Colom et al, 2009)