Bipolar Disorder Research Paper
The Psychopathology and Treatment of Bipolar Disorder
The concept of a drastic shift in mood being classified as an illness was first described by the French psychiatrist Jean-Pierre Farlet in 1851 (Marmol, 2008). Farlet coined the term “Folie Circulaire” to label a disorder characterized by manic and sad episodes separated by symptom-free intervals (Marmol, 2008). As time passed, the description along with the classification changed, altering from an entity on its own to a unified disorder with other mood disorders (Marmol, 2008). As it stands today, bipolar disorder (BD) is a psychiatric disorder characterized by cycling depressive and manic episodes (Federman, 2010). It also encompasses many other cognitive symptoms …show more content…
leading to disruptive daily functioning, deteriorating interpersonal relationships, financial difficulties as well as drawbacks on employment and/or education (Jones & Bentall, 2008). By describing the symptoms, diagnostic criteria, etiology, epidemiology and prognosis of the disorder, it will become clear why certain treatment options are effective while others are not.
Symptoms and Diagnostic Criteria
According to the DSM-IV-TR, bipolar disorder is classified on the Axis I as a mood disorder (Galanter, Hundt, Goyal, Le & Fisher, 2012) and its symptoms can be divided into two subcategories, manic and depressive (Federman, 2010). The criteria for a manic episode constitute a distinct period of abnormally and continuously elevated, or irritable mood, lasting at least 1 week (or any duration if hospitalization is required). Also, during the period of mood disturbance, 3 or more of the following symptoms have been present: inflated self-esteem, decreased need for sleep, more talkative than usual, impulsive behaviour, flight of ideas etc. Furthermore, the mood disturbance is severe enough to cause noticeable impairment in normal functioning and the symptoms are not due to any physiological effect of a substance (Galanter et al., 2012). The criteria for depressive episodes are characterized by the presence of either intense sadness or anhedonia, accompanied by 4 other symptoms such as fatigue, insomnia, psychomotor agitation, feelings of worthlessness and suicidal ideation that last for at least two weeks (Galanter et al., 2012). Bipolar disorder can be divided into Bipolar I disorder and Bipolar II disorder. The first is defined by the presence of at least one manic episode or mixed episodes that include symptoms of both mania and depression (Miklowitz & Johnson, 2006). The second is characterized by at least one hypomanic episode, along with at least one episode of major depression (Miklowitz & Johnson, 2006). Hypomania is defined by the same symptoms as mania but lasts for shorter intervals and does not create a dysfunctional lifestyle (Miklowitz & Johnson, 2006). It is however, more accurate to view hypomania and mania as both existing on a continuum rather than as separate entities (Federman, 2010).
Etiology
Genes play an important role in the etiology of BD with a heritability estimate reaching up to 85% (Miklowitz & Johnson, 2006). The concordance rate amongst identical twins is 57% compared to only 14% in fraternal twins (Miklowitz & Johnson, 2006), and the risk of acquiring the disorder for children of parents with BD is four times greater compared to children of healthy parents (Miklowitz & Johnson, 2006). Also, family studies have shown a 10 to 20-fold increase in the chance of being diagnosed with bipolar disorder amongst first-degree relatives of probands (Marmol, 2008). However, despite the evidence of genetic factors being present, it is still unclear which genes are involved (Marmol, 2008). Nevertheless, it is thought that more than one chromosome is implicated and multiple linkage studies have consistently pointed out markers on the 18th and 22nd chromosome (Marmol, 2008).
Another factor involved in the causation of bipolar disorder is neurotransmitter systems. It was originally believed that low levels of serotonin, dopamine and norepinephrine were causing the depressed state and high levels of dopamine and norepinephrine explained the manic states (Miklowitz & Johnson, 2006). However, the focus has now shifted to a dysregulation in the dopamine and serotonin systems and their neurological effects (Miklowitz & Johnson, 2006). These dysregulations are believed to be causing a change in sensitivity of postsynaptic receptors, malfunctioning of secondary messengers and fluctuation of other neurotransmitters (Miklowitz & Johnson, 2006). Thus, a culmination of these effects may be part of the reason behind the mood related symptoms, rather than the absolute levels of the above-mentioned neurotransmitters (Miklowitz & Johnson, 2006).
Furthermore, with brain imaging techniques such as PET scans and fMRIs, researchers have been able to identify specific brain areas involved in bipolar disorder. When looking into brain functioning, BD seems to be associated with a hyperactive amygdala and hypoactive hippocampus and prefrontal cortex (Miklowitz & Johnson, 2006). In conjunction with the above-mentioned findings, structural studies have found a smaller-than-average neural density in the prefrontal cortex, basal ganglia, hippocampus and an increased volume in the amygdala (Miklowitz & Johnson, 2006). These brain deficits coincide with the limbic-cortical model related to mood disorders. Elevated activity in the amygdala will increase emotional sensitivity and with decreased activity in the cortical areas, there will be difficulty in goal planning, pursuit and emotion regulation (Miklowitz & Johnson, 2006).
Epidemiology
Combined, bipolar I and bipolar II disorders have a lifetime prevalence of 4% (Jones & Bentall, 2008) and the mean age of onset was 25 for males and 26 for females (Mitchell & Malhi, 2006). Also, men and women have an equal chance of developing bipolar I disorder, however, women tend to report more depressive episodes and therefore have a higher number of cases of bipolar II disorder (Miklowitz & Johnson, 2006). In addition, there is a high comorbidity rate between bipolar disorder and psychiatric illnesses such as anxiety disorders and substance abuse (Mitchell & Mahli, 2006). Approximately 50% of individuals also have an anxiety disorder and almost 40% have a substance-use disorder (Mitchell & Mahli, 2006).
Prognosis
Even with proper treatment, BD tends to have a high recurrence rate (Miklowitz & Johnson, 2006). After one year of being in remission and continuing pharmacotherapy, almost 40% of patients have manic or depressed episodes reoccur and after five years, that number increases to almost 75% (Miklowitz & Johnson, 2006). Also, BD patients with high levels of stress and whose families have a high EE (expressed emotion) are at a much higher risk of relapse (Miklowitz & Johnson, 2006). Half of the individuals with BD reported being unable to work and were dysfunctional in daily social and occupational aspects (Miklowitz & Johnson, 2006). Finally, 50% attempt suicide at one point in their lives (Miklowitz & Johnson, 2006)
Treatment
The most effective treatment for the control and prevention of recurring bipolar symptoms is with the use of pharmacotherapy (Miklowitz & Johnson, 2006). Lithium, the drug of choice, is a mood stabilizer with several hypothesized mechanisms (Marmol, 2008). The first begins at the intracellular level. In BD patients, higher intracellular levels of both calcium and sodium have been found. Free calcium inside the cell acts as a secondary messenger and is essential in the presynaptic release of neurotransmitters while elevated sodium levels maintain high cell excitability and increase ion transport (Marmol, 2008). These two occurrences produce an increase in both monoamine and other neurotransmitter release, which are believed to impact the frequency and severity of bipolar symptoms (Marmol, 2008). Long-term lithium treatment has been shown to displace sodium ions by replacing them in the cell and reducing their levels (Marmol, 2008). Furthermore, intracellular calcium levels returned to normal once patients were administered the drug (Marmol, 2008). Another neurological mechanism involves the monoamine hypothesis. It is believed that lithium can both increase and decrease monoamine neurotransmitter concentrations in the brain (Marmol, 2008). In regards to dopamine, studies have shown that long-term lithium treatment reduces presynaptic dopaminergic activity and prevents receptor hypersensitivity on the postsynaptic cells (Marmol, 2008). Also, studies have shown that lithium induces the increase of serotonin release at the synaptic cleft (Marmol, 2008). Although unclear, it is thought that there is an interaction between the receptors itself and the drug molecule. It remains unclear how lithium carries out its effects on the norepinephrine system (Marmol, 2008).
On the other hand, a treatment that would be ineffective in helping bipolar disorder patients is psychodynamic therapy. This Freudian therapy is based on the idea that we are shaped by dynamic processes such as the relationships between child and parent (Maguire, 2012). Also, the development and experience as infants will influence the individual’s unconscious patterns of thought and behaviour. Therefore, when there is internal conflict, certain psychological disorders may arise (Maguire, 2012). The therapy will thus focus on insight: trying to discover within the individual what inner conflicts exists and allow the patient to release them (Maguire, 2012). Therapists will use specific techniques such as free association and hypnosis to allow the patient to enter his unconscious and rediscover past childhood events (Maguire, 2012). Psychodynamic therapy would not benefit bipolar disorder patients because the root of the problem is not based on childhood experience and internal conflicts, but rather on genetically based neurological dysfunctions. The shift from manic states to depressed ones is related to change in neuronal activity and neurotransmitter systems and not a psychological inner conflict (Marmol, 2008).
Bipolar disorder is a complex illness with many aspects that remain to be properly understood. The etiology of BD is based on a genetic predisposition affecting brain functioning, structure and monoamine neurotransmitter systems. These brain abnormalities are thought to lead to a cycling between manic and depressed episodes that the typical patient experiences. With this in mind, the appropriate treatment would then be to try and regulate the neurotransmitter irregularities using pharmacotherapy. The mood stabilizer lithium has proven to be effective in both subsiding bipolar symptoms and decreasing the risk of their recurrence. Psychodynamic therapy has had no significant benefit to bipolar disorder patients, as the treatment does not target the brain abnormalities, but rather unconscious inner conflicts that become disruptive to the individual’s life.
References
Federman, R.
(2010). Treatment of bipolar disorder in the university student population. Journal of College Student Psychotherapy, 25(1), 24-38. doi: 10.1080/87568225.2011.532471
Galanter, C. A., Hundt, S. R., Goyal, P., Le, J., & Fisher, P. W. (2012). Variability among research diagnostic interview instruments in the application of DSM-IV-TR criteria for pediatric bipolar disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 51(6), 605-621. doi: 10.1016/j.jaac.2012.03.010
Jones, S. H., & Bentall, R. P. (2008). A review of potential cognitive and environmental risk markers in children of bipolar parents. Clinical Psychology Review,28(7), 1083-1095. doi: 10.1016/j.cpr.2008.03.002
Maguire, N. (2012). Psychological therapies. Medicine, 40(12), 668-671. doi: 10.1016/j.mpmed.2012.09.003
Marmol, F. (2008). Lithium: Bipolar disorder and neurodegenerative diseases possible cellular mechanisms of the therapeutic effects of lithium. Progress in Neuropsychopharmacology & Biological Psychiatry, 32(8), 1761-1771. doi: 10.1016/j.pnpbp.2008.08.012
Miklowitz, D. J., & Johnson, S. L. (2006). The psychopathology and treatment of bipolar disorder. Annual Review of Clinical Psychology, 2, 199-235. doi:
10.1146/annurev.clinpsy.2.022305.095332
Mitchell, P. B., & Malhi, G. S. (2006). Emerging drugs for bipolar disorder. Expert Opin.Emerging Drugs, 11(4), 621-634. doi: 10.1517/14728214.11.4.621
The concept of a drastic shift in mood being classified as an illness was first described by the French psychiatrist Jean-Pierre Farlet in 1851 (Marmol, 2008). Farlet coined the term “Folie Circulaire” to label a disorder characterized by manic and sad episodes separated by symptom-free intervals (Marmol, 2008). As time passed, the description along with the classification changed, altering from an entity on its own to a unified disorder with other mood disorders (Marmol, 2008). As it stands today, bipolar disorder (BD) is a psychiatric disorder characterized by cycling depressive and manic episodes (Federman, 2010). It also encompasses many other cognitive symptoms …show more content…
leading to disruptive daily functioning, deteriorating interpersonal relationships, financial difficulties as well as drawbacks on employment and/or education (Jones & Bentall, 2008). By describing the symptoms, diagnostic criteria, etiology, epidemiology and prognosis of the disorder, it will become clear why certain treatment options are effective while others are not.
Symptoms and Diagnostic Criteria
According to the DSM-IV-TR, bipolar disorder is classified on the Axis I as a mood disorder (Galanter, Hundt, Goyal, Le & Fisher, 2012) and its symptoms can be divided into two subcategories, manic and depressive (Federman, 2010). The criteria for a manic episode constitute a distinct period of abnormally and continuously elevated, or irritable mood, lasting at least 1 week (or any duration if hospitalization is required). Also, during the period of mood disturbance, 3 or more of the following symptoms have been present: inflated self-esteem, decreased need for sleep, more talkative than usual, impulsive behaviour, flight of ideas etc. Furthermore, the mood disturbance is severe enough to cause noticeable impairment in normal functioning and the symptoms are not due to any physiological effect of a substance (Galanter et al., 2012). The criteria for depressive episodes are characterized by the presence of either intense sadness or anhedonia, accompanied by 4 other symptoms such as fatigue, insomnia, psychomotor agitation, feelings of worthlessness and suicidal ideation that last for at least two weeks (Galanter et al., 2012). Bipolar disorder can be divided into Bipolar I disorder and Bipolar II disorder. The first is defined by the presence of at least one manic episode or mixed episodes that include symptoms of both mania and depression (Miklowitz & Johnson, 2006). The second is characterized by at least one hypomanic episode, along with at least one episode of major depression (Miklowitz & Johnson, 2006). Hypomania is defined by the same symptoms as mania but lasts for shorter intervals and does not create a dysfunctional lifestyle (Miklowitz & Johnson, 2006). It is however, more accurate to view hypomania and mania as both existing on a continuum rather than as separate entities (Federman, 2010).
Etiology
Genes play an important role in the etiology of BD with a heritability estimate reaching up to 85% (Miklowitz & Johnson, 2006). The concordance rate amongst identical twins is 57% compared to only 14% in fraternal twins (Miklowitz & Johnson, 2006), and the risk of acquiring the disorder for children of parents with BD is four times greater compared to children of healthy parents (Miklowitz & Johnson, 2006). Also, family studies have shown a 10 to 20-fold increase in the chance of being diagnosed with bipolar disorder amongst first-degree relatives of probands (Marmol, 2008). However, despite the evidence of genetic factors being present, it is still unclear which genes are involved (Marmol, 2008). Nevertheless, it is thought that more than one chromosome is implicated and multiple linkage studies have consistently pointed out markers on the 18th and 22nd chromosome (Marmol, 2008).
Another factor involved in the causation of bipolar disorder is neurotransmitter systems. It was originally believed that low levels of serotonin, dopamine and norepinephrine were causing the depressed state and high levels of dopamine and norepinephrine explained the manic states (Miklowitz & Johnson, 2006). However, the focus has now shifted to a dysregulation in the dopamine and serotonin systems and their neurological effects (Miklowitz & Johnson, 2006). These dysregulations are believed to be causing a change in sensitivity of postsynaptic receptors, malfunctioning of secondary messengers and fluctuation of other neurotransmitters (Miklowitz & Johnson, 2006). Thus, a culmination of these effects may be part of the reason behind the mood related symptoms, rather than the absolute levels of the above-mentioned neurotransmitters (Miklowitz & Johnson, 2006).
Furthermore, with brain imaging techniques such as PET scans and fMRIs, researchers have been able to identify specific brain areas involved in bipolar disorder. When looking into brain functioning, BD seems to be associated with a hyperactive amygdala and hypoactive hippocampus and prefrontal cortex (Miklowitz & Johnson, 2006). In conjunction with the above-mentioned findings, structural studies have found a smaller-than-average neural density in the prefrontal cortex, basal ganglia, hippocampus and an increased volume in the amygdala (Miklowitz & Johnson, 2006). These brain deficits coincide with the limbic-cortical model related to mood disorders. Elevated activity in the amygdala will increase emotional sensitivity and with decreased activity in the cortical areas, there will be difficulty in goal planning, pursuit and emotion regulation (Miklowitz & Johnson, 2006).
Epidemiology
Combined, bipolar I and bipolar II disorders have a lifetime prevalence of 4% (Jones & Bentall, 2008) and the mean age of onset was 25 for males and 26 for females (Mitchell & Malhi, 2006). Also, men and women have an equal chance of developing bipolar I disorder, however, women tend to report more depressive episodes and therefore have a higher number of cases of bipolar II disorder (Miklowitz & Johnson, 2006). In addition, there is a high comorbidity rate between bipolar disorder and psychiatric illnesses such as anxiety disorders and substance abuse (Mitchell & Mahli, 2006). Approximately 50% of individuals also have an anxiety disorder and almost 40% have a substance-use disorder (Mitchell & Mahli, 2006).
Prognosis
Even with proper treatment, BD tends to have a high recurrence rate (Miklowitz & Johnson, 2006). After one year of being in remission and continuing pharmacotherapy, almost 40% of patients have manic or depressed episodes reoccur and after five years, that number increases to almost 75% (Miklowitz & Johnson, 2006). Also, BD patients with high levels of stress and whose families have a high EE (expressed emotion) are at a much higher risk of relapse (Miklowitz & Johnson, 2006). Half of the individuals with BD reported being unable to work and were dysfunctional in daily social and occupational aspects (Miklowitz & Johnson, 2006). Finally, 50% attempt suicide at one point in their lives (Miklowitz & Johnson, 2006)
Treatment
The most effective treatment for the control and prevention of recurring bipolar symptoms is with the use of pharmacotherapy (Miklowitz & Johnson, 2006). Lithium, the drug of choice, is a mood stabilizer with several hypothesized mechanisms (Marmol, 2008). The first begins at the intracellular level. In BD patients, higher intracellular levels of both calcium and sodium have been found. Free calcium inside the cell acts as a secondary messenger and is essential in the presynaptic release of neurotransmitters while elevated sodium levels maintain high cell excitability and increase ion transport (Marmol, 2008). These two occurrences produce an increase in both monoamine and other neurotransmitter release, which are believed to impact the frequency and severity of bipolar symptoms (Marmol, 2008). Long-term lithium treatment has been shown to displace sodium ions by replacing them in the cell and reducing their levels (Marmol, 2008). Furthermore, intracellular calcium levels returned to normal once patients were administered the drug (Marmol, 2008). Another neurological mechanism involves the monoamine hypothesis. It is believed that lithium can both increase and decrease monoamine neurotransmitter concentrations in the brain (Marmol, 2008). In regards to dopamine, studies have shown that long-term lithium treatment reduces presynaptic dopaminergic activity and prevents receptor hypersensitivity on the postsynaptic cells (Marmol, 2008). Also, studies have shown that lithium induces the increase of serotonin release at the synaptic cleft (Marmol, 2008). Although unclear, it is thought that there is an interaction between the receptors itself and the drug molecule. It remains unclear how lithium carries out its effects on the norepinephrine system (Marmol, 2008).
On the other hand, a treatment that would be ineffective in helping bipolar disorder patients is psychodynamic therapy. This Freudian therapy is based on the idea that we are shaped by dynamic processes such as the relationships between child and parent (Maguire, 2012). Also, the development and experience as infants will influence the individual’s unconscious patterns of thought and behaviour. Therefore, when there is internal conflict, certain psychological disorders may arise (Maguire, 2012). The therapy will thus focus on insight: trying to discover within the individual what inner conflicts exists and allow the patient to release them (Maguire, 2012). Therapists will use specific techniques such as free association and hypnosis to allow the patient to enter his unconscious and rediscover past childhood events (Maguire, 2012). Psychodynamic therapy would not benefit bipolar disorder patients because the root of the problem is not based on childhood experience and internal conflicts, but rather on genetically based neurological dysfunctions. The shift from manic states to depressed ones is related to change in neuronal activity and neurotransmitter systems and not a psychological inner conflict (Marmol, 2008).
Bipolar disorder is a complex illness with many aspects that remain to be properly understood. The etiology of BD is based on a genetic predisposition affecting brain functioning, structure and monoamine neurotransmitter systems. These brain abnormalities are thought to lead to a cycling between manic and depressed episodes that the typical patient experiences. With this in mind, the appropriate treatment would then be to try and regulate the neurotransmitter irregularities using pharmacotherapy. The mood stabilizer lithium has proven to be effective in both subsiding bipolar symptoms and decreasing the risk of their recurrence. Psychodynamic therapy has had no significant benefit to bipolar disorder patients, as the treatment does not target the brain abnormalities, but rather unconscious inner conflicts that become disruptive to the individual’s life.
References
Federman, R.
(2010). Treatment of bipolar disorder in the university student population. Journal of College Student Psychotherapy, 25(1), 24-38. doi: 10.1080/87568225.2011.532471
Galanter, C. A., Hundt, S. R., Goyal, P., Le, J., & Fisher, P. W. (2012). Variability among research diagnostic interview instruments in the application of DSM-IV-TR criteria for pediatric bipolar disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 51(6), 605-621. doi: 10.1016/j.jaac.2012.03.010
Jones, S. H., & Bentall, R. P. (2008). A review of potential cognitive and environmental risk markers in children of bipolar parents. Clinical Psychology Review,28(7), 1083-1095. doi: 10.1016/j.cpr.2008.03.002
Maguire, N. (2012). Psychological therapies. Medicine, 40(12), 668-671. doi: 10.1016/j.mpmed.2012.09.003
Marmol, F. (2008). Lithium: Bipolar disorder and neurodegenerative diseases possible cellular mechanisms of the therapeutic effects of lithium. Progress in Neuropsychopharmacology & Biological Psychiatry, 32(8), 1761-1771. doi: 10.1016/j.pnpbp.2008.08.012
Miklowitz, D. J., & Johnson, S. L. (2006). The psychopathology and treatment of bipolar disorder. Annual Review of Clinical Psychology, 2, 199-235. doi:
10.1146/annurev.clinpsy.2.022305.095332
Mitchell, P. B., & Malhi, G. S. (2006). Emerging drugs for bipolar disorder. Expert Opin.Emerging Drugs, 11(4), 621-634. doi: 10.1517/14728214.11.4.621