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| - | Fig 1: This image is used to outline and explain the major classifications for bipolar disorder. | + | **Figure 1**: This image is used to outline and explain the major classifications for bipolar disorder. |
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| - | Fig 2: This image outlines the main results from the study done by Merikangas et al. | + | **Figure 2**: This image outlines the main results from the study done by Merikangas et al. |
| ===== Societal Impact ===== | ===== Societal Impact ===== | ||
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| ===== Causes/Risk Factors ===== | ===== Causes/Risk Factors ===== | ||
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| + | The root cause of bipolar disorder is unknown, however, various risk factors can trigger the onset of the illness (Mayo Clinic Staff Print, 2017). One cause of bipolar disorder is due to biological differences (Mayo Clinic Staff Print, 2017). Those who are often affected by bipolar disorder have physical changes in their brains (Mayo Clinic Staff Print, 2017). | ||
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| + | The second cause is due to genetics, where individuals who have a first-degree relative affected by bipolar disorder are more susceptible to also suffer from bipolar disorder (Mayo Clinic Staff Print, 2017). Children who have one parent affected by the disorder have a 10-25% chance of developing of the disorder, while children with both parents affected by the disorder have a 10-50% chance of developing the disorder (Bipolar Disorder, n.d.). In the case of identical twins, there is a range of 40-70% chance of the other twin developing the disorder. The range is large due to the fact that genes are not the only contributing factor to the disorder, environment, and one’s lifestyle habits also contribute to the development of the disease (Bipolar Disorder, n.d.). | ||
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| + | In addition, one’s environment can trigger the onset of bipolar disorder. For example, stressful or traumatic events such as a death or loss of a loved one can trigger the onset of bipolar disorder. Research shows that about 50% of individuals suffering from bipolar disorder have a substance use problem (Bipolar Disorder, n.d.). Life style habits such as drug or alcohol abuse and lack of sleep may trigger bipolar disorder. | ||
| ===== Symptoms ===== | ===== Symptoms ===== | ||
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| + | Symptoms of bipolar disorder include high moods (mania) and low moods (depression). Bipolar 1 disorder is characterized by at least one manic episode, while hypomania is characterized by at least one episode of hypomania and a major depressive disorder. Hypomanic episodes are similar to manic episodes except that they do not entail psychosis, hospitalization or severe functional impairment. | ||
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| + | Mania and hypomania include three or more of the following symptoms: “abnormal upbeat, jumpy, or wired; increased activity, energy or agitation; exaggerated sense of well-being and self-confidence (euphoria); decreased need for sleep; unusual talkativeness; racing thoughts; distractibility; poor decision-making (Mayo Clinic Staff Print, 2017).” | ||
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| + | A major depressive episode includes five or more of these symptoms: “depressed mood; marked loss of interest; significant weight changes; insomnia or sleeping too much; restlessness; fatigue; feelings of worthlessness or excessive guilt; decreased ability to concentrate; indecisiveness; planning or attempting suicide (Mayo Clinic Staff Print, 2017). | ||
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| + | General symptoms of bipolar disorder include anxious distress, melancholy, psychosis, sleep dysregulation, increased prevalence of suicidal thoughts among others. However, bipolar disorder is often difficult to identify in children and teens (Mayo Clinic Staff Print, 2017). The most obvious symptom of bipolar disorder evident in children and teenagers may be severe mood swings, which are different from the usual (Mayo Clinic Staff Print, 2017). Some co-occurring conditions include: Anxiety disorders, eating disorders, attention-deficit/hyperactivity disorder (ADHD), alcohol or drug problems and physical health problems (Mayo Clinic Staff Print, 2017). | ||
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| ===== Pathophysiology ===== | ===== Pathophysiology ===== | ||
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| Over the past 40 years, neurobiological studies of mood disorders have primarily focused on abnormalities of the monoaminergic neurotransmitter systems, on characterizing alterations of individual neurotransmitters in disease states, and on assessing response to mood stabilizer and antidepressant medications. The monoaminergic system consists of a network of limbic, striatal and prefrontal cortical neuronal circuits thought to support the behavioral and visceral manifestations of mood disorders (Drevets, 2000). It is hypothesized that BD arises from the complex interaction of multiple susceptibility and protective genes and environmental factors. The phenotypic expression of the disease includes mood disturbance, as well as cognitive, motor, autonomic, endocrine and sleep or wake abnormalities (Schloesser et al., 2008). | Over the past 40 years, neurobiological studies of mood disorders have primarily focused on abnormalities of the monoaminergic neurotransmitter systems, on characterizing alterations of individual neurotransmitters in disease states, and on assessing response to mood stabilizer and antidepressant medications. The monoaminergic system consists of a network of limbic, striatal and prefrontal cortical neuronal circuits thought to support the behavioral and visceral manifestations of mood disorders (Drevets, 2000). It is hypothesized that BD arises from the complex interaction of multiple susceptibility and protective genes and environmental factors. The phenotypic expression of the disease includes mood disturbance, as well as cognitive, motor, autonomic, endocrine and sleep or wake abnormalities (Schloesser et al., 2008). | ||
| - | Figure X shows the pathophysiology of BD from different perspectives, and how these different systems are interlinked. For instance, there are different physiological levels at which the disease manifests: molecular, cellular, and behavioral. In addition, there are environmental factors which also contribute to the onset of BD (Schloesser et al., 2008). Once there is a dysfunction in one physiological level, it has been observed in the literature that there is a cascade of downstream events which are ultimately responsible for primary abnormalities in signaling pathways. | + | Figure 3 shows the pathophysiology of BD from different perspectives, and how these different systems are interlinked. For instance, there are different physiological levels at which the disease manifests: molecular, cellular, and behavioral. In addition, there are environmental factors which also contribute to the onset of BD (Schloesser et al., 2008). Once there is a dysfunction in one physiological level, it has been observed in the literature that there is a cascade of downstream events which are ultimately responsible for primary abnormalities in signaling pathways. |
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| Many signaling pathways play critical roles not only in synaptic plasticity, the cellular process that results in lasting changes in the efficacy of neurotransmission, but also in the long-term atrophic processes. Therefore, plasticity plays a role in the cascading effect for the pathophysiology of the disease (Schloesser et al., 2008). | Many signaling pathways play critical roles not only in synaptic plasticity, the cellular process that results in lasting changes in the efficacy of neurotransmission, but also in the long-term atrophic processes. Therefore, plasticity plays a role in the cascading effect for the pathophysiology of the disease (Schloesser et al., 2008). | ||
| - | In healthy humans, there are numerous biological mechanisms which underlie neuroplasticity, a broader term that encapsulates changes in intracellular signaling cascades and gene regulation, modifications of synaptic number and strength, variations in neurotransmitter release, modeling of axonal and dendritic architecture, and in some areas of the CNS, the generation of new neurons. The remarkable plasticity of neuronal circuits is achieved through different biological means, including alterations in gene transcription and intracellular signaling cascades. These changes thereby modify diverse neuronal properties such as neurotransmitter release, synaptic function and even morphological characteristics of neurons. However, it has been shown that people with BD have abnormalities in cellular signaling cascades that regulate diverse physiologic functions, thereby causing tremendous medical comorbidity associated with BD (Figure Y) (Schloesser et al., 2008). | + | In healthy humans, there are numerous biological mechanisms which underlie neuroplasticity, a broader term that encapsulates changes in intracellular signaling cascades and gene regulation, modifications of synaptic number and strength, variations in neurotransmitter release, modeling of axonal and dendritic architecture, and in some areas of the CNS, the generation of new neurons. The remarkable plasticity of neuronal circuits is achieved through different biological means, including alterations in gene transcription and intracellular signaling cascades. These changes thereby modify diverse neuronal properties such as neurotransmitter release, synaptic function and even morphological characteristics of neurons. However, it has been shown that people with BD have abnormalities in cellular signaling cascades that regulate diverse physiologic functions, thereby causing tremendous medical comorbidity associated with BD (Figure 4) (Schloesser et al., 2008). |
| **Figure 4**: Cellular signaling cascades that regulate diverse physiologic functions have shown to be disrupted in patients with BD. Retrieved from Schloesser et al., 2008. | **Figure 4**: Cellular signaling cascades that regulate diverse physiologic functions have shown to be disrupted in patients with BD. Retrieved from Schloesser et al., 2008. | ||
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| === Structural Neuroimaging Findings === | === Structural Neuroimaging Findings === | ||
| - | Many forms of neural plasticity involve structural changes in the brain. Since neuroplasticity and cellular cascade changes play a role in BD, many studies to date have used neuroimaging and postmortem human brains to investigate the potential alterations in structural plasticity in mood disorders. Studies on people with BD using the aforementioned pathological techniques have revealed several functional and structural abnormalities in brain regions involved in the perception and control of mood states and emotions. These include the prefrontal cortex (PFC), amygdala, insula, hippocampus, anterior cingulate cortex, and ventral striatum (Figure Z). In addition, post-mortem morphometric brain studies in mood disorders have demonstrated that patients with mood disorders undergo cellular atrophy and/or loss (Table A) (Schloesser et al., 2008). | + | Many forms of neural plasticity involve structural changes in the brain. Since neuroplasticity and cellular cascade changes play a role in BD, many studies to date have used neuroimaging and postmortem human brains to investigate the potential alterations in structural plasticity in mood disorders. Studies on people with BD using the aforementioned pathological techniques have revealed several functional and structural abnormalities in brain regions involved in the perception and control of mood states and emotions. These include the prefrontal cortex (PFC), amygdala, insula, hippocampus, anterior cingulate cortex, and ventral striatum (Figure 5). In addition, post-mortem morphometric brain studies in mood disorders have demonstrated that patients with mood disorders undergo cellular atrophy and/or loss (Table 1) (Schloesser et al., 2008). |
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| The prefrontal cortex (PFC) is a key brain region involved in the regulation of emotional behaviour, executive function and fear extinction. This area is sensitive to the remodeling effects of stress. Several studies have shown structural and functional frontal lobe abnormalities (reduction in size) in BD, including the anterior cingulate and subnegual PFC. These are consistent with the cognitive deficits found in BD (Kapczinski et al., 2008). | The prefrontal cortex (PFC) is a key brain region involved in the regulation of emotional behaviour, executive function and fear extinction. This area is sensitive to the remodeling effects of stress. Several studies have shown structural and functional frontal lobe abnormalities (reduction in size) in BD, including the anterior cingulate and subnegual PFC. These are consistent with the cognitive deficits found in BD (Kapczinski et al., 2008). | ||
| - | Figure (?) encapsulates the brain rewiring that happens after recurrent stress and mood episodes in BD patients. Neural substrate reactivity is altered in BD patients, leading to cell endangerment, pro-apoptotic cascades, thereby leading to altered size of brain parts involved in emotional processing and coping. Such brain rewiring is related to increased emotionality and poor coping which render subjects more vulnerable to life stress (Kapczinski et al., 2008). | + | Figure 6 encapsulates the brain rewiring that happens after recurrent stress and mood episodes in BD patients. Neural substrate reactivity is altered in BD patients, leading to cell endangerment, pro-apoptotic cascades, thereby leading to altered size of brain parts involved in emotional processing and coping. Such brain rewiring is related to increased emotionality and poor coping which render subjects more vulnerable to life stress (Kapczinski et al., 2008). |
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| 5. Bipolar and Related Disorders. (n.a). Retrieved March 25, 2017, from http://dsm.psychiatryonline.org/doi/10.1176/appi.books.9780890425596.dsm03 | 5. Bipolar and Related Disorders. (n.a). Retrieved March 25, 2017, from http://dsm.psychiatryonline.org/doi/10.1176/appi.books.9780890425596.dsm03 | ||
| - | 6. CAMH: Antipsychotic Medication. (2017). Camh.ca. Retrieved 24 March 2017, from http://www.camh.ca/en/hospital/health_information/a_z_mental_health_and_addiction_information/antipsychotic_medication/Pages/antipsychotic_medication.aspx | + | 6.Bipolar Disorder: Who's at Risk? (n.d.). Retrieved March 22, 2017, from http://www.webmd.com/bipolar-disorder/guide/bipolar-disorder-whos-at-risk#2 |
| - | 7. Centre for Addiction and Mental Health. (n.d.). Treatments for bipolar disorder. Retrieved March 29, 2017, from http://www.camh.ca/en/education/about/camh_publications/info_guides/bipolar-info-guide/Pages/Treatments-for-bipolar-disorder.aspx#psych | + | 7. CAMH: Antipsychotic Medication. (2017). Camh.ca. Retrieved 24 March 2017, from http://www.camh.ca/en/hospital/health_information/a_z_mental_health_and_addiction_information/antipsychotic_medication/Pages/antipsychotic_medication.aspx |
| - | 8. Colom, F., Vieta. E., Martinez-Aran, A., Reinares, M., Goikolea, JM., Benabarre, A., Torrent, C., Comes, M., Corbella, B., Parramon, G., & Corominas, J. (2003). A randomized trial on the efficacy of group psychoeducation in the prophylaxis of recurrences in bipolar patients whose disease is in remission. Archives of General Psychiatry, 60, (4), 402-4027. http://10.1001/archpsyc.60.4.402 | + | 8. Centre for Addiction and Mental Health. (n.d.). Treatments for bipolar disorder. Retrieved March 29, 2017, from http://www.camh.ca/en/education/about/camh_publications/info_guides/bipolar-info-guide/Pages/Treatments-for-bipolar-disorder.aspx#psych |
| - | 9. Geddes, J., & Miklowitz, D. (2017). Treatment of bipolar disorder. The Lancet. Retrieved 23 March 2017, from http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(13)60857-0/abstract | + | 9. Colom, F., Vieta. E., Martinez-Aran, A., Reinares, M., Goikolea, JM., Benabarre, A., Torrent, C., Comes, M., Corbella, B., Parramon, G., & Corominas, J. (2003). A randomized trial on the efficacy of group psychoeducation in the prophylaxis of recurrences in bipolar patients whose disease is in remission. Archives of General Psychiatry, 60, (4), 402-4027. http://10.1001/archpsyc.60.4.402 |
| - | 10. Kapczinski, F., Vieta, E., Andreazza, A. C., Frey, B. N., Gomes, F. A., Tramontina, J., ... & Post, R. M. (2008). Allostatic load in bipolar disorder: implications for pathophysiology and treatment. Neuroscience & Biobehavioral Reviews, 32(4), 675-692. | + | 10. Geddes, J., & Miklowitz, D. (2017). Treatment of bipolar disorder. The Lancet. Retrieved 23 March 2017, from http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(13)60857-0/abstract |
| - | 11. Mayo Clinic. (2017). Bipolar Disorder. [online] Available at: http://www.mayoclinic.org/diseases-conditions/bipolar-disorder/diagnosis-treatment/treatment/txc-20308001 [Accessed 25 Mar. 2017]. | + | 11. Kapczinski, F., Vieta, E., Andreazza, A. C., Frey, B. N., Gomes, F. A., Tramontina, J., ... & Post, R. M. (2008). Allostatic load in bipolar disorder: implications for pathophysiology and treatment. Neuroscience & Biobehavioral Reviews, 32(4), 675-692. |
| - | 12. National Collaborating Centre for Mental Health (UK). (2006). Bipolar disorder: The management of bipolar disorder in adults, children and adolescents, in primary and secondary care. Leicester, UK: British Psychological Society. | + | 12. Mayo Clinic. (2017). Bipolar Disorder. [online] Available at: http://www.mayoclinic.org/diseases-conditions/bipolar-disorder/diagnosis-treatment/treatment/txc-20308001 [Accessed 25 Mar. 2017]. |
| - | 13. Post, R., Altshuler, L., Leverich, G., Frye, M., Nolen, W., & Kupka, R. et al. (2006). Mood switch in bipolar depression: comparison of adjunctive venlafaxine, bupropion and sertraline. The British Journal Of Psychiatry, 189(2), 124-131. http://dx.doi.org/10.1192/bjp.bp.105.013045 | + | 13. Mayo Clinic Staff Print. (2017, February 15). Symptoms and causes. Retrieved March 21, 2017, from http://www.mayoclinic.org/diseases-conditions/bipolar-disorder/symptoms-causes/dxc-20307970 |
| - | 14. Prevalence of bipolar disorder. (2011, March 07). Retrieved March 25, 2017, from http://www.news-medical.net/news/20110307/Prevalence-of-bipolar-disorder.aspx | + | 14. National Collaborating Centre for Mental Health (UK). (2006). Bipolar disorder: The management of bipolar disorder in adults, children and adolescents, in primary and secondary care. Leicester, UK: British Psychological Society. |
| - | 15. Schloesser, R. J., Huang, J., Klein, P. S., & Manji, H. K. (2008). Cellular plasticity cascades in the pathophysiology and treatment of bipolar disorder. Neuropsychopharmacology, 33(1), 110-133. | + | 15. Post, R., Altshuler, L., Leverich, G., Frye, M., Nolen, W., & Kupka, R. et al. (2006). Mood switch in bipolar depression: comparison of adjunctive venlafaxine, bupropion and sertraline. The British Journal Of Psychiatry, 189(2), 124-131. http://dx.doi.org/10.1192/bjp.bp.105.013045 |
| - | 16. Severus, E., Taylor, M., Sauer, C., Pfennig, A., Ritter, P., Bauer, M., & Geddes, J. (2014). Lithium for prevention of mood episodes in bipolar disorders: systematic review and meta-analysis. International Journal Of Bipolar Disorders, 2(1). http://dx.doi.org/10.1186/s40345-014-0015-8 | + | 16. Prevalence of bipolar disorder. (2011, March 07). Retrieved March 25, 2017, from http://www.news-medical.net/news/20110307/Prevalence-of-bipolar-disorder.aspx |
| - | 17. Smith, D., Jones, I., & Simpson, S. (2010). Psychoeducation for bipolar disorder. Advances in Psychiatric Treatment, 16 (2), 147-154. http://10.1192/apt.bp.108.006403 | + | 17. Schloesser, R. J., Huang, J., Klein, P. S., & Manji, H. K. (2008). Cellular plasticity cascades in the pathophysiology and treatment of bipolar disorder. Neuropsychopharmacology, 33(1), 110-133. |
| - | 18. Tracy, N. (2016, June). Effects of Bipolar Disorder - Bipolar Information - Bipolar Disorder. Retrieved March 26, 2017, from http://www.healthyplace.com/bipolar-disorder/bipolar-information/effects-of-bipolar-disorder/ | + | 18. Severus, E., Taylor, M., Sauer, C., Pfennig, A., Ritter, P., Bauer, M., & Geddes, J. (2014). Lithium for prevention of mood episodes in bipolar disorders: systematic review and meta-analysis. International Journal Of Bipolar Disorders, 2(1). http://dx.doi.org/10.1186/s40345-014-0015-8 |
| + | 19. Smith, D., Jones, I., & Simpson, S. (2010). Psychoeducation for bipolar disorder. Advances in Psychiatric Treatment, 16 (2), 147-154. http://10.1192/apt.bp.108.006403 | ||
| + | 20. Tracy, N. (2016, June). Effects of Bipolar Disorder - Bipolar Information - Bipolar Disorder. Retrieved March 26, 2017, from http://www.healthyplace.com/bipolar-disorder/bipolar-information/effects-of-bipolar-disorder/ | ||
| + | 21.Written by Jaime HerndonMedically Reviewed by. (n.d.). Risk Factors for Bipolar Disorder. Retrieved March 21, 2017, from http://www.healthline.com/health/bipolar-disorder/bipolar-risk-factors#Possibleriskfactors3 | ||
