Biopsychosocial Model of Analysis of Bipolar Disorder

Introduction

The World Health Organization (WHO) has consistently ranked bipolar disorder (BD) as a main causes of disability world-wide, effecting approximately 2.9% of people in the United States (Muneer, 2016; National Institute of Mental Health, 2017). BD is a condition involving contrasting periods of depression and elevated moods, causing significant impairment in regards to employment, relationships, and academic performance. First identified in Ancient Greece, BD has undergone substantial review since its rediscovery in modern medicine in the 1800s. Despite the prevalence of medical literature, researchers can’t pinpoint the exact etiology of BD or identify a specific gene marker. Well- substantiated theories suggest abnormal neurotransmitter activity and brain structure differences as possible explanations. Due to its complex etiology and symptoms, BD requires complex treatments involving cognitive behavioral therapy (CBT) and drug combinations.

Evolution of the Disorder

BD was first recognized by Aretaeus of Cappadocia in 100 AD as a relationship between melancholy and mania, an observation which didn’t gain traction until the modern era (Yutzy, Woofter, Abbott, Melhem, & Parish, 2012; Angst & Marneros, 2001). The modern  concept of BD originated in the 1800s when Jean-Pierre Falret identified cyclical intervals between depressed and elevated moods and attributed a genetic link  (Falret, 1854; Angst & Marneros, 2001). Similarly, French psychiatrist Jules Baillarger used “folie à double forme” to describe manic-depression and differentiate it from schizophrenia (Yutsy et al., 2012, Angst & Marneros, 2001). In 1875, “manic-depressive psychosis” was classified a psychiatric illness, and Emil Kraepelin conducted further studies on the prognosis of depression and mania in 1913. An early study between 1875 to 1924 found mania to be extremely rare at 3.6 admissions per 100,000 people per year (Yutsy et al., 2012, Angst & Marneros, 2001).

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 The first edition of the DSM-I was based on psychoanalysis, with little distinction between abnormal and normal behavior (Angst & Marneros, 2001; Solimano & Manfredi, 2006). BD was initially classified as manic-depression under psychotic disorders, and required presences of a stressor causing distress to person’s inner psyche (Angst & Marneros, 2001; Solimano & Manfredi, 2006). The classification detailed symptoms of mania similar to the criteria today; however, the cyclical nature of the disorder was not given full recognition in the primary diagnostic criteria until the DSM-II (Angst & Marneros, 2001). Furthermore, psychosis was initially listed as an essential symptom, but the criteria was later modified to omit that requirement (Yutsy et al., 2012; Solimano & Manfredi, 2006). With the publication of DSM-II in 1968, manic depression was now classified under affective disorders (Solimano & Manfredi, 2006). The disorder was further divided into three major subtypes: manic, depressed, and circular, with the circular type referring to at least one episode of both mania and depression (Feighner et al., 1972). Around the introduction of the DSM, a preliminary review completed between 1938 and 1973 found prevalence rates for manic-depression ranging between 0.07% and 1.88% among the general population (Yutsy et al., 2012).

A valid and reliable criterion for BD wasn’t developed until the DSM-III in 1980 (Cassidy, Murry, Forest, & Carroll, 1997; Vieta & Phillips, 2007). At this time, the definition of schizophrenia and manic-depressive insanity were more distinct (Cassidy et al., 1997; Feighner et al., 1972).  The term “bipolar disorder” was also introduced to better reflect the presence of mood polarity, and specific time-frames were included to further identify the disorder’s course (Angst & Marneros, 2001). The possibility of mixed episodes was included, and the term hypomania was introduced, referring to a less severe mania that still exhibited cyclical activity (Cassidy et al., 1997; Angst & Marneros, 2001). Reviews in 1980 determined the prevalence of BD at 0.4% to 1.6%, indicating an underdiagnosis of the disorder (Yutsy et al., 2012). Reasons for this may include lack of awareness by clinicians, and aggressive marketing of antidepressants (Yutsy et al., 2012).

In 1994, the DSM IV was introduced and BD’s diagnosis further evolved to a nuanced subtype system, where Bipolar I, II, Cyclothymia, and “Bipolar Not Otherwise Specified were introduced” (Vieta & Phillips, 2007). Two of these forms were distinguished primarily by the type of mania experienced by individuals; with Bipolar I Disorder featuring mania as opposed to Bipolar II Disorder featuring hypomania (Yutsy et al., 2012; Amero et al., 2015; Angst & Marneros, 2001). A mixed bipolar episode was also an added feature to the DSM IV diagnosis. The DSM IV lacked validity due to unspecific criteria for mania. Poor validity and a broader definition of hypomania, may have lead to a dramatic increase in prevalence, resulting in a 5-7% prevalence rate among the general population, indicating a potential over-diagnosis (Yutsy et al., 2012, Amero et al., 2015; Kessing, Willer, Andersen, & Bukh 2017).

In the DSM 5, the four episodes of BD were reduced to three, with mixed episode changing to a “mixed feature” specifier present during the other episodes (Blanco et al., 2017). The episodes were all operationally specified, with the mood criteria for a manic episode now requires both mood disturbance and increased goal-directed activity/energy (Blanco et al., 2017). The prevalence rates today stand at around 2.9%, which could indicate a misdiagnosis of the disorder surrounding poor recognition of depression onset following elevated mood states. (National Institute of Mental Health, 2017). During the last 15 years, various reports have identified the error of assigning a diagnosis of major depression when one of BD would have been appropriate (Katzow et al., 2003; Amero et al., 2015).

Biopsychosocial Model of the Disorder

BD is a complex psychiatric disorder whose etiology involves genetic factors acting alongside psychosocial stresses, causing differing clinical manifestations (Muneer, 2016). Despite the research available, exact integration of neurobiological elements remains unclear (Muneer, 2015; Manji et al., 2003). Evidence points to numerous causes such as brain structure impairments, molecular abnormalities, and hormone cycling issues (Muneer, 2015; Manji et al., 2003). BD genetic indicators are primarily linked to a hyperactive hypothalamic-pituitary-adrenal (HPA) axis and sympo-adrenal medullary axis, resulting in an over production of cortisol, epinephrine and norepinephrine (Muneer, 2016; Bender & Alloy, 2011). Some studies also link genetic indicators to an overactive dopaminergic system stimulated by stress, based on evidence linking dopamine agonists to mania; Hence the efficacy of mood stabilizers in modulating intracellular signalling (Manji et al., 2003).

In recent years, a large body of evidence suggests that HPA-induced inflammation also plays a role in the pathological processes underlying BD (Manji et al., 2003; Muneer, 2016; Muneer, 2015; Ziogas et al., 2014; Nassar & Azab, 2014). In this theory, the constant release of stress receptors releases cytokines that trigger microglia to have an inflammatory response in neuro circuits (Muneer, 2016). Microglia are functionally intended to contain neuron damage; however, in repeated mood episodes, microglia activated chronically by the HPA axis can disrupt homeostasis and cause and damaging inflammatory environment (Muneer, 2016; Ziogas et al., 2014). Unbalanced types of pro-inflammatory cytokine triggers result in a manic and depressive expression of the disorder (Muneer, 2016, Ziogas et al., 2014). An over-active HPA and neuro-inflammation can be attributed to the lower cognition and higher comorbidity rates among people with BD (Muneer, 2016; Nassar & Azab, 2014).

 Biological indicators of stress are activated by psychosocial influence. In fact, 30-50% of patients attribute trauma to the onset and recurrence of bipolar mood episodes (Geddes & Miklowitz, 2013; Brietzke et al., 2012). Minor events such as changing shifts and international travel can even take a toll, by disrupting circadian rhythms (Bender & Alloy, 2011; Ziogas et al., 2014; Muneer, 2015).  In the case of decreased light absorption, the release of melanin, an immunomodulator, is inhibited (Lee, Son, & Geum, 2013; Ziogas et al., 2014; Muneer, 2015). Depleted levels of immunomodulators leads to a deregulation of inflammatory cytokines acting on the brain, resulting in unbalanced moods; hence circadian rhythm maintenance is a key component of CBT (Lee et al., 2013; Morriss, 2015).

Treatment

While there is no cure for BD, combined pharmaceutical and CBT treatment options have proved beneficial in managing expressions of the disorder. The complexity of BD treatment stems from the need to target different drugs for individual symptoms. Commonly prescribed combination treatments include mood stabilizers, atypical antipsychotics, and antidepressants, presented with CBT coping mechanisms. Treatment of BD involves the acute treatment of a manic or depressive episode, an improvement phase, and the maintenance phase (Geddes & Miklowitz, 2013; Vieta & Sanchez-Moreno, 2008).

Treatment of an acute episode focuses on diagnosis and initiation of pharmacological intervention (Geddes & Miklowitz, 2013; Vieta & Sanchez-Moreno, 2008). Antipsychotics are indicated for bipolar depression refractory to treatment with mood stabilizers, as they are more effective than lithium and anticonvulsants during acute onset. Lithium was first introduced to psychiatry in 1949 as the sole treatment for BD both in the acute stages and throughout maintenance due to their effectiveness in treating manic episodes, preventing relapses and mitigating depression (Vieta & Sanchez-Moreno, 2008; Nassar & Azab, 2014). However, lithium is slow-acting and is an unsuccessful antagonist during acute onset, so modern research suggests including adjunctive anticonvulsants like valproate, carbamazepine or lamotrigine, which reduce manic symptoms within 1-2 weeks (Geddes & Miklowitz, 2013; Vieta & Sanchez-Moreno, 2008). All these drugs function as modulators in intracellular signaling, with lithium inhibiting overactive pro-inflammatory enzymes, thus stimulating healthy neuronal repair, (Nassar & Azab, 2014; Manji et al., 2013). The exact effect of anticonvulsants remains unclear, though carbamazepine stabilizes the circadian rhythm in hamsters, and is thus indicated for inhibiting manic symptoms (Klemfuss & Kripke, 1995; Geddes & Miklowitz, 2013; Manji et al., 2013). Once used as the first line of treatment in the 90s’, antidepressants have been recently contraindicated as a treatment for BD due to significant non-discrimination from placebos and the risk of inducing mania (Post, 2016; Johnson & Leahy, 2004; Geddes & Miklowitz, 2013). Potentially, MAO inhibitors appear to more effective than SSRIs in bipolar depression, though the conflicted view toward antidepressants as a viable drug reflects inconsistencies in available research, with many guidelines still recommending antidepressants for acute bipolar depression (Geddes & Miklowitz, 2013; Post, 2016). As an alternative, ECT is used to help ease severe depression, psychosis, or intractable symptoms (Geddes & Miklowitz, 2013). Under an intensive pharmacological treatment plan, patients achieve remission in around four to eight weeks (Vieta & Sanchez-Moreno, 2008).

During the improvement phase of treatment, which lasts six months on average, the patient remains in volatile condition (Vieta & Sanchez-Moreno, 2008). Treatment during this phase consists of frequent clinic visits, medication adjustments based on response and side effects, and CBT (Nusslock, Abramson, Harmon-Jones, Alloy, & Coan, 2009).. Relapse is most likely to occur during the improvement stage of recovery and particularly in the absence of CBT (Vázquez, Holtzman, Lolich, Ketter, & Baldessarini, 2015). CBT is aimed at alleviating mood symptoms and equipping patients with cognitive and behavioral skills to recognize episode triggers and work toward maintenance of remission (Nusslock et al., 2009). If patients do not relapse during the improvement phase of treatment, they have recovered from the episode and enter the maintenance phase of treatment.

Lithium takes months to take affect and reports a 30-50% success rate as a monotherapy, with many patients needing to continue with adjunctive treatments (Vázquez et al., 2015; Geddes & Miklowitz, 2013). Evidence supports anticonvulsants as long-term mood stabilizers, with lamotrigine having a strong effect in symptomatic depression (Bowden & Singh, 2008; Geddes & Miklowitz, 2013). During maintenance, CBT focuses on education about the disorder triggers, lifestyle changes regarding stress management and circadian rhythm stabilization, and medication adherence. Despite the treatments available today, the course of BD is characterized by a high relapse rate (75-90%) and a low rate of remission, in part due to medication non-adherence (Vázquez et al., 2015; Post, 2016).

Conclusion

Bipolar disorder has been in medical literature for several millennia, and its’ diagnostic criteria has been significantly modified over the last 50 years. Despite the magnitude of available research concerning BD’s etiology, there is no single genetic factor contributing to the onset of the disorder. For this reason, the biopsychosocial model of analysis is critical in evaluating the onset of this disorder, as well as recognizing environmental triggers that can turn genetic switches. Although there is no specified cause of the disorder, there are many medication and CBT options available to help people manage the illness and reduce risk of relapse. BD is a well established mental illness and is a leading cause of disability in the world today,

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