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Bipolar Disorder

Overview

Bipolar disorder (formerly known as manic-depressive disorder) is a mood disorder characterized by fluctuations between intense mood states (mania and depression or “highs” and “lows”). In addition to mood symptoms, bipolar disorder is associated with cognitive dysfunction in attention, processing speed, executive functions, and memory. These deficits may be related to structural and functional changes in the brains of individuals with bipolar disorder relative to healthy controls. Bipolar disorder is primarily treated with medications. However, psychotherapy may be an ideal complementary intervention after the mood states are better controlled.

 

Typology

Bipolar disorder-I is comprised of fluctuations between episodes of depression and mania (highly euphoric/energized states). Bipolar disorder-II consists of depressive and hypomanic (milder than mania) episodes. If symptoms are mild (for at least two years) and do not fully meet criteria for bipolar disorder, it is termed Cyclothymic Disorder (1).

 

Symptoms

Bipolar disorder is a disorder of emotion dysregulation. Individuals may experience intense episodes of highs (mania) and lows (depression). During manic states, a person with bipolar disorder may be highly energized (talking fast, needing little sleep) and engage in impulsive behaviors, such as gambling and shopping excessively. During depressive states, the person may feel very sad and low in energy, even to the point of considering suicide. Sometimes an episode may be mixed with both manic and depressive features. Insight is often lacking during manic/hypomanic episodes, while individuals are usually aware during depressive states. Without treatment, an individual with hypomania may develop mania. In addition, some people with bipolar disorder may present with psychotic symptoms, such as delusions and hallucinations (1).

 

Bipolar disorder is associated with cognitive difficulties with attention, processing speed, executive functions (high-order abilities such as cognitive flexibility and inhibition), and memory (particularly for verbal materials), even during euthymic (not manic or depressed) states (2-4). The severity of cognitive symptoms are correlated with disease duration as well as numbers of past manic episodes, hospitalizations, and suicide attempts (2).

 

Neuroimaging

Several neural circuits may be disrupted in individuals with bipolar disorder, including networks underlying emotion processing and regulation (bilateral prefrontal-hippocampal-amygdala) and reward processing (left ventrostriatal-ventrolateral and orbitofrontal). There is also evidence for decreased volume for the prefrontal and temporal cortices (including the amygdala and hippocampus) and reduced integrity in the connections between prefrontal and subcortical areas (5).

 

Prevalence

According to the National Comorbidity Survey Replication (NCS-R), the lifetime prevalence rate is estimated to be 1% for BP-I, 1.1% for BP-II, and 2.4% for cyclothymia in the U.S. The average age of onset is 18.2 years for BP-I, 20.3 years for BP-II, and 22.2 years for cyclothymia. Bipolar disorder status is not related to sex or race/ethnicity (6). The presence of bipolar disorder in the family history puts one at risk for the development of bipolar disorder, although the exact genetic mechanism for bipolar disorder is unknown (1).

 

Treatments

The most common treatment for bipolar disorder is drug therapy, such as mood stabilizers (e.g., lithium). However, the use of antidepressants (usually in combination with another antimanic agent to avoid induction of mania) and atypical antipsychotics may also be utilized to address symptoms. Non-pharmacological interventions, such as psychotherapy, may complement the drug treatment. They are most effective once the mood states are well stabilized (7).

 

In addition, neurofeedback can help bipolar disorder in that it can help balance and enhance the frontal lobe functions. Additionally, LORETA neurofeedback (three-dimensional training) of subcortical areas can address the dysregulated networks of the frontal areas of the brain.

 

By Michelle Chen

References

1.  National Institute of Mental Health. Bipolar Disorder. Retrieved from https://www.nimh.nih.gov/health/topics/bipolar-disorder/index.shtml

2.  Martínez-Arán, A, Vieta, E, Reinares, M, Colom, F, Torrent, C, Sánchez-Moreno, J & Salamero, M (2004). Cognitive function across manic or hypomanic, depressed, and euthymic states in bipolar disorder. American Journal of Psychiatry161(2), 262-270.

3.  Torres, I, Boudreau, V & Yatham, L (2007). Neuropsychological functioning in euthymic bipolar disorder: a meta‐analysis. Acta Psychiatrica Scandinavica116(s434), 17-26.

4.  Robinson, L, Thompson, J, Gallagher, P, Goswami, U, Young, A, Ferrier, I & Moore, P (2006). A meta-analysis of cognitive deficits in euthymic patients with bipolar disorder. Journal of affective disorders93(1), 105-115.

5.  Phillips, M & Swartz, H (2014). A critical appraisal of neuroimaging studies of bipolar disorder: toward a new conceptualization of underlying neural circuitry and a road map for future research. American Journal of Psychiatry171(8), 829-843.

6.  Merikangas, K, Akiskal, H, Angst, J, Greenberg, P, Hirschfeld, R, Petukhova, M & Kessler, R (2007). Lifetime and 12-month prevalence of bipolar spectrum disorder in the National Comorbidity Survey replication. Archives of general psychiatry64(5), 543-552.

7.  Fountoulakis, K, Vieta, E, Sanchez-Moreno, J, Kaprinis, S, Goikolea, J & Kaprinis, G (2005). Treatment guidelines for bipolar disorder: a critical review. Journal of affective disorders86(1), 1-10.

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