Final Project: Biopsychological Analysis of a Neuropsychological Disorder

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Final Project: Biopsychological Analysis of a Neuropsychological Disorder

In your Final Project, you will synthesize an overview of the major theories relating to the pathology of a disorder as well as provide a detailed discussion of the etiology (causes) and clinical interventions, using research to support your analysis.  Your topic will be the neuropsychological disorder that was selected and approved by the instructor in your Week One assignment, and for which you provided an outline in the Week Two assignment.  

In keeping with the focus of this class, the emphasis of your paper will be on the neuroscience aspects of the disorder, to include:

  • Theories of etiology (causes)
  • Associated factors in development of the disorder (genetic, environmental, familial, lifestyle)
  • Pathology (abnormalities of physical structure and function, including genetic and biochemical aspects)
  • Treatment options (pharmacologic and nonpharmacologic, with rationales for use based on current understanding of the disorder)
  • Diagnostic and research technologies employed in clinical diagnosis, care, and basic science research  


Your research will include a minimum of six to eight peer-reviewed sources, which provide evidence-based information regarding the biological and psychological features of the disorder and were published within the last five years. At least four of your references should be peer-reviewed publications of original research studies. To justify your assertions, provide in-text citations for all factual statements taken from your research, with corresponding references drawn from scholarly sources.  All citations and sources are to be documented according to APA style, as outlined in the Ashford Writing Center, and should support and enhance your analysis of the selected disorder. Sources may include review articles, original research articles, information from government agencies (e.g., National Institutes of Health, Centers for Disease Control, Food and Drug Administration, Drug Enforcement Administration) or professional societies (e.g., professional society position papers or clinical practice guidelines).   

Final Project- Components

Section I:  Introduction


This section should provide a general introduction to the topic as well as an overview of the background and history of the disorder. Further, it should provide a succinct thesis statement of the purpose and overall direction of the paper.  For instance, if your paper will have a large focus on the role of particular neurotransmitters in the etiology of the disorder as a rationale for treatment options, you should indicate this in the introduction. Finally, this section should provide demographic data that indicates the prevalence of the disorder in both general and specific populations.  

Specific required components of the Introduction:   

  1. Succinct thesis statement (one or more sentences detailing the focus of your Final Project and informing the reader about your topic and the scope of your paper)
  2. Define the type of disorder
    1. Neurological
    2. Psychological
    3. Neuropsychological
  3. Diagnostic criteria
    1. What components must be present for the disorder to be diagnosed?
    2. Include physical and psychological signs and symptoms.  
  4. Reason(s) why you chose this topic
    1. Personal experience
    2. Professional experience
    3. Other reason
  5. Epidemiology
    1. Who is affected?
    2. Are they young/old?
    3. Male/female
    4. Rural/urban
    5. Ethnicities


Section II: Discussion

This section should make up the majority of the Final Project in terms of size. Here, you will expand upon the main aspects of the disorder and provide details relating to the disorder and its management. This section should provide specific and detailed information (Reminder: All statements of fact require an in-text citation).  Cited/referenced sources should be used to support your analysis of the components of the discussion.  

Specific required components of the Discussion section:   

  1. Detailed description of the disorder
    1. Signs and symptoms
    2. Epidemiology
    3. Any subtypes of the disorder
  2. Detailed description of the natural history of the disorder
    1. How the disorder develops over time with treatment
    2. How the disorder develops over time without treatment
  3. Methods used to diagnose, evaluate, and manage the disorder
    1. Initial diagnosis (e.g., physical exam, imaging and/or laboratory testing, special studies, psychological evaluation, psychometric testing)  
    2. Ongoing management (e.g., physical exam, imaging and/or laboratory testing, special studies, psychological evaluation, psychometric testing)
  4. Risk factors
    1. Genetics
    2. Lifestyle
    3. Environmental factors
  5. Other causative factors
    1. Known
    2. Theorized
  6. Nervous system structures and/or pathways involved in the disorder (detailed information regarding the underlying pathology as it applies to these structures and functional pathways)
  7. Neurotransmitter(s) and receptor system(s) involved in the pathology of the disorder
  8. Current treatment options
    1. Drug (pharmacologic) therapies
    2. Nonpharmacologic therapies (including psychological and other therapeutic services)
    3. Type of care providers (e.g., medical, nursing, therapists)
    4. Type of healthcare setting (e.g., hospital, home, outpatient, nursing facility)
  9. Future areas of research
    1. Treatment options
    2. Evaluation and diagnostic methods for initial diagnosis
    3. Increasing knowledge relating to etiology and pathologic processes


Section III: Conclusion

Provide a concluding summary of your findings regarding your selected disorder. The conclusion is a summarization of information that has already been presented.  Typically, if you mention something in the conclusion section of an academic paper, you should have already mentioned this aspect of the topic earlier in the paper.

Specific required components of the Conclusion section:   

  1. The conclusion reaffirms your initial thesis statement.
  2. The conclusion may be one or more paragraphs. Use the material you have discussed in the paper to support the validity of your synthesis and elaborate on the theme of your paper.


Writing the Final Project
The Final Project:

  1. Must be 10 to 12 double-spaced pages in length, and formatted according to APA style as outlined in the Ashford Writing Center.
  2. Must include a title page with the following:
    1. Title of paper
    2. Student’s name
    3. Course name and number
    4. Instructor’s name
    5. Date submitted
  3. Must begin with an introductory paragraph that has a succinct thesis statement.
  4. Must address the topic of the paper with critical thought.
  5. Must include section headings, formatted according to APA style, to organize your paper. Each paragraph must have a minimum of three full sentences.  
  6. Must include in-text citations for all statements of facts obtained through your research.
    1. Remember that direct quotes (identical phrases or sentences taken from a source) require in-text citations with appropriate formatting.
    2. Statements of opinion should be clearly stated as such, and include a rationale to support why you hold this opinion (e.g., personal or professional experience, your research findings).
  7. Must end with a conclusion that reaffirms your thesis.
  8. Must use at least six to eight scholarly sources that were published within the last five years, including a minimum of four peer-reviewed original research studies.
    1. In general, dictionaries and encyclopedias are not considered appropriate resources for academic writing.
  9. Must document all sources in APA style as outlined in the Ashford Writing Center.
  10. Must include a separate reference page, formatted according to APA style as outlined in the Ashford Writing Center.
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Running head: PHYSIOLOGICAL PSYCHOLOGY Bipolar Disorder Type-II 1 PHYSIOLOGICAL PSYCHOLOGY 2 Bipolar Disorder Type-II Bipolar II disorder is one of the mood disorders in the bipolar spectra. Bipolar II disorder is characterized by at least one episode of hypomania and at least one episode of depression (Berk, M., Dodd, S., 2005). Unlike bipolar I disorder, patients with bipolar II disorder do not experience episodes of mania, unless it is caused by the use of antidepressant drugs. According to DSM-5 classification, the hypomania must last for most of the day and for at least four days. In addition, three or more of the following have to be present: grandiosity, decreased need for sleep, being talkative, experiencing racing of ideas, distractibility, excessive involvement in pleasurable activity, not to have experienced a manic or mixed episode or psychomotor agitation (American Journal of Psychiatry, 2013). Etiology The causes of bipolar II disorder are not elaborate and several theories have been used to explain the etiology of this condition. Some of the causes that are thought to cause bipolar II disorder are attributed to biological factors, genetic factors, and the psychosocial factors. The biological factors implicated in bipolar II disorder are altered biochemistry and the two neurotransmitters in the central nervous system. The two neurotransmitters are norepinephrine and serotonin. Both serotonin and norepinephrine are excitatory neurotransmitters. Too low levels of norepinephrine cause depression, a major characteristic of bipolar II disorder. Postmortem studies have shown an increased NE turnover in the cortical and thalamic areas of bipolar II disorder subjects. Serotonin is involved in brain activities such as wakefulness, regulation of sleep, moods, learning and memory (Barrett, K. E., Barman, S. M., & Boitano, S., 2010). In the brain, PHYSIOLOGICAL PSYCHOLOGY 3 serotonin acts through its receptors. There are several receptors involved in the action of serotonin, known as the 5-hydroxytryptamine receptors and abbreviated 5-HT. Alterations in brain circuits using serotonin have been implicated in mood disorders and in depression. Positron emission tomography (PET) scans have shown reduced binding of serotonin to 5-HTIA receptors in the raphe and amygdala-hippocampus of patients with bipolar II disorder (Manji, H. K., Quiroz, J. A., Payne, J. L., Singh, J., Lopes, B. P., Viegas, J. S., Zarate, C. A., 2003). Post mortem results of suicide completers suffering from bipolar II disorder have demonstrated low levels of serotonin and 5-hydroxyindoleacetic acid, a major metabolite of serotonin(Novick, D. M., Swartz, H. A., Frank, E., 2010). The cerebral spinal fluid of those with suicide impulse and those who have attempted suicide has also demonstrated low levels of the 5-hydroxyindoleacetic acid. Other biological factors that have been implicated in bipolar II disorder are hormonal imbalances and electrolytes imbalances. The receptor potential for serotonin receptors can be reduced by increased levels of serum cortisol. Hypothyroidism is also associated with depression and hypomania. Calcium is useful in brain electrochemistry and low serum calcium levels have been implicated in bipolar II disorder. Psychosocial factors that cause a lot of stress have been implicated in causing bipolar disorder type-2. Such stressors include loss of a spouse and loss of a job or loss of a close relative such as losing a parent. For example, losing a parent before the age of 11 years is associated with an increased risk of developing bipolar II disorder later in life. The theory behind this is that long lasting stress can cause changes in the brain biology including neurotransmitter and brain signaling pathways. Stress is also associated with loss of synaptic contact between PHYSIOLOGICAL PSYCHOLOGY 4 neurons. Therefore, a person may have a repeated episode of bipolar II disorder even when the primary stressor has been removed. Other factors that are thought to cause bipolar II disorder include genetic factors. Monozygotic twins have a concordance rate of 70-90% for developing mood disorders, while siblings of different sex have concordance rates of only 8%. Familial factors are also implicated in development of bipolar II disorders. Family data indicate that a child whose parent has a bipolar II disorder has a risk of 20-25% of developing the same. Personality and lifestyle may also contribute to bipolar II disorder. People who feel insecure and have a rigid, strict and uncompromising lifestyle are likely to suffer from a bipolar disorder. Use of drugs and substance abuse can also cause bipolar II disorder. Pathophysiology of Bipolar II Disorder Depletion of excitatory neurotransmitters in the brain causes an increase in the inhibitory response of the brain to the inhibitory neurotransmitters such as gamma amino-butyric acid (GABA). This leads to inhibition of neuronal activities in brain areas that control mood, memory, learning and emotions such as the amygdala and the hippocampus. In bipolar II disorder, there is a reduced level of neurotransmitter serotonin at the synaptic connections for the neurons. There is reduced neuronal activity and this results in the mood depression that is typical of the bipolar II disorder. Norepinephrine is a stress hormone and affects areas of the brain in which attention and response to actions are controlled. When norepinephrine levels are reduced, there is persistent inhibition of neurons, causing slowed brain neuronal activity which results in the hypomania that is seen in subjects of bipolar II disorder. Treatment of Bipolar II Disorder PHYSIOLOGICAL PSYCHOLOGY 5 During treatment, the safety of the patient should be considered. A complete evaluation is also very important. Stressful life events have to be addressed so as to avoid relapse. Treatment of bipolar II disorder is both pharmacological and non-pharmacological. Pharmacological treatment involves the use of antidepressant drugs and mood stabilizing drugs. The mood stabilizing drugs that can be used in treatment of bipolar II disorder include valproic acid, carbamazepine and lithium bicarbonate. Newer antipsychotic agents such as olanzapine can also be used. There are various categories of antidepressant drugs that are used in treatment of bipolar II disorder. These drugs are classified according to the neurotransmitters they affect and receptor selectivity. Selective serotonin reuptake inhibitors prevent the reuptake of serotonin from the neuronal synapses, allowing more time for its action. These drugs include fluoxetine. Selective serotonin norepinephrine reuptake inhibitors block the reuptake of both serotonin and norepinephrine. These drugs include venlafaxine and desvenlafaxine. Monoamine oxidase inhibitors reduce the breakdown of monoamine neurotransmitters. They include phenyzine and resegeline. Non pharmacological treatment for bipolar II disorder includes use of the electroconvulsive therapy (ECT). Family therapy and counseling are also useful in reducing stress and ensuring compliance to treatment. Diagnostic and research technologies employed in clinical diagnosis, care, and basic science research Clinical diagnosis of bipolar II disorder is through a detailed clinical history and mental examination, and diagnosis made using the DSM-5 guidelines. Diagnostic technologies help in the process of making a clinical diagnosis and in further evaluation of the patient. Positron emission tomography (PET) scans can be used to measure the receptor activity and the levels of PHYSIOLOGICAL PSYCHOLOGY 6 serotonin in the brain. PET scans can also be used in the evaluation for the destruction of the neuronal synapses by checking for the degree of uptake of radionuclide labeled monoamines such as serotonin and norepinephrine. This can also be used in researching about the etiology of bipolar II disorder. Magnetic resonance imaging and electroencephalograms are used in imaging of the brain in checking for organic causes of mental illness. Electroencephalogram can be used in distinguishing bipolar II disorder from other forms of bipolar disorders by monitoring brain activity. Functional magnetic resonance imaging and spectrum photo emission tomography (SPECT) are used in researching for structural brain abnormalities as the basis for bipolar disorders, including bipolar II disorder (Heng, S., Song, A. W., & Sim, K., 2010). Thyroid function tests are used in establishing whether the condition is caused by hypothyroidism. Cortisol levels and dexamethasone suppression test can be used in detecting hormonal imbalances that can cause or aggravate bipolar II disorder. PHYSIOLOGICAL PSYCHOLOGY 7 References American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing. Berk, M., Dodd, S. (2005). Bipolar II disorder: a review. Bipolar Disorder. Barrett, K. E., Barman, S. M., & Boitano, S. (2010). Ganong's review of medical physiology. New Delhi: McGraw Hill, 2010 Heng, S., Song, A. W., & Sim, K. (2010). White matter abnormalities in bipolar disorder: insights from diffusion tensor imaging studies. Journal of neural transmission, MacQueen, G. M.,Young, L. T. (2014). Bipolar II disorder: symptoms, course, and response to treatment. Psychiatric Services. Manji, H. K., Quiroz, J. A., Payne, J. L., Singh, J., Lopes, B. P., Viegas, J. S., Zarate, C. A. (2003). The underlying neurobiology of bipolar disorder. World Psychiatry, Novick, D. M., Swartz, H. A., Frank, E. (2010). Suicide attempts in bipolar I and bipolar II disorder: a review and meta‐analysis of the evidence. Bipolar disorders Running head: PHYSIOLOGICAL PSYCHOLOGY Bipolar Disorder Type-II 1 PHYSIOLOGICAL PSYCHOLOGY 2 Bipolar Disorder Type-II Introduction Bipolar II disorder is one of two mood disorders in the bipolar spectra. It is a disorder characterized by at least one episode of hypomania and at least one episode of depression (Berk, Dodd, 2005). Unlike bipolar I disorder, patients with bipolar II disorder do not experience episodes of mania. According to DSM-5 classification, the hypomania must last for most of the day and for at least four days. In addition, three or more of the following have to be present: grandiosity, decreased need for sleep, being talkative, experiencing racing of ideas, distractibility, excessive involvement in pleasurable activity, not to have experienced a manic or mixed episode or psychomotor agitation (Black, Grant, 2014). Etiology The causes of bipolar II disorder are not elaborate and several theories have been used to explain the etiology of this condition. Some of the causes that are thought to cause bipolar II disorder are attributed to biological factors, genetic factors, and the psychosocial factors. The biological factors implicated in bipolar II disorder are altered biochemistry and the two neurotransmitters in the central nervous system. The two neurotransmitters are norepinephrine and serotonin. Both serotonin and norepinephrine are excitatory neurotransmitters. Having too low levels of norepinephrine causes depression which is a major characteristic of bipolar II disorder. Postmortem studies have shown an increased NE turnover in the cortical and thalamic areas of bipolar II disorder subjects (Kupfer, Regier, 2014). PHYSIOLOGICAL PSYCHOLOGY 3 Serotonin is involved in brain activities such as wakefulness, regulation of sleep, moods, learning and memory (Barrett, Barman, Boitano, 2010). In the brain, serotonin acts through its receptors. There are several receptors involved in the action of serotonin, known as the 5hydroxytryptamine receptors and abbreviated 5-HT. Alterations in brain circuits using serotonin have been implicated in mood disorders and in depression. Positron emission tomography (PET) scans have shown reduced binding of serotonin to 5-HTIA receptors in the raphe and amygdalahippocampus of patients with bipolar II disorder (Sullivan, Ogden, Oquendo, Kumar, Simpson, N., Huang, Parsey, 2009). Post mortem results of suicide completers suffering from bipolar II disorder have demonstrated low levels of serotonin and 5-hydroxyindoleacetic acid, a major metabolite of serotonin (Novick, Swartz, Frank, 2010). The cerebral spinal fluid of those with suicide impulse and those who have attempted suicide has also demonstrated low levels of the 5hydroxyindoleacetic acid. Other biological factors that have been implicated in bipolar II disorder are hormonal imbalances and electrolyte imbalances. The receptor potential for serotonin receptors can be reduced by increased levels of serum cortisol. Hypothyroidism is also associated with depression and hypomania. Thyroid hormone facilitates mental processes and low levels are associated with slowed mental function (Koeppen, Stanton, 2012). Psychosocial factors that cause a lot of stress have been implicated in causing bipolar disorder type-2. Such stressors include loss of a spouse, loss of a job, or loss of a close relative such as losing a parent. For example, losing a parent before the age of 11 years is associated with an increased risk of developing bipolar II disorder later in life. The theory behind this is that long lasting stress can cause changes in the brain biology including neurotransmitter and brain signaling pathways. Stress is also associated with loss of synaptic contact between neurons. PHYSIOLOGICAL PSYCHOLOGY 4 Therefore, a person may have a repeated episode of bipolar II disorder even when the primary stressor has been removed. Other factors that are thought to cause bipolar II disorder include genetic factors. Monozygotic twins have a concordance rate of 70-90% for developing mood disorders, while siblings of different sex have concordance rates of only 8%. Familial factors are also implicated in development of bipolar II disorders. Family data indicate that a child whose parent has a bipolar II disorder has a risk of 20-25% of developing the same. Personality and lifestyle may also contribute to bipolar II disorder. People who feel insecure and have a rigid, strict and uncompromising lifestyle are likely to suffer from a bipolar disorder. Pathophysiology of Bipolar II Disorder Depletion of excitatory neurotransmitters in the brain causes an increase in the inhibitory response of the brain to the inhibitory neurotransmitters such as gamma amino-butyric acid (GABA). This leads to inhibition of neuronal activities in brain areas that control mood, memory, learning and emotions such as the amygdala and the hippocampus. In bipolar II disorder, there is a reduced level of neurotransmitter serotonin at the synaptic connections for the neurons. There is reduced neuronal activity and this results in the mood depression that is typical of the bipolar II disorder. Norepinephrine is a stress hormone and affects areas of the brain in which attention and response to actions are controlled. When norepinephrine levels are reduced, there is persistent inhibition of neurons, causing slowed brain neuronal activity which results in the hypomania that is seen in subjects of bipolar II disorder (Salvadore, Quiroz, Machado-Vieira, HenterManji, Zarate Jr, 2010). Treatment of Bipolar II Disorder PHYSIOLOGICAL PSYCHOLOGY 5 During treatment, the safety of the patient should be considered. A complete evaluation is also very important. Stressful life events have to be addressed so as to avoid relapse. Treatment of bipolar II disorder is both pharmacological and non-pharmacological. Pharmacological treatment involves the use of antidepressant drugs and mood stabilizing drugs. The mood stabilizing drugs that can be used in treatment of bipolar II disorder include valproic acid, carbamazepine and lithium bicarbonate. Newer antipsychotic agents such as olanzapine can also be used. There are various categories of antidepressant drugs that are used in treatment of bipolar II disorder. These drugs are classified according to the neurotransmitters they affect and receptor selectivity. Selective serotonin reuptake inhibitors prevent the reuptake of serotonin from the neuronal synapses, allowing more time for its action. These drugs include fluoxetine. Selective serotonin norepinephrine reuptake inhibitors block the reuptake of both serotonin and norepinephrine. These drugs include venlafaxine and desvenlafaxine. Monoamine oxidase inhibitors reduce the breakdown of monoamine neurotransmitters. They include phenyzine and resegeline. Non pharmacological treatment for bipolar II disorder includes use of the electroconvulsive therapy (ECT). Family therapy and counseling are also useful in reducing stress and ensuring compliance to treatment. Diagnostic and research technologies employed in clinical diagnosis, care, and basic science research Clinical diagnosis of bipolar II disorder is established through a detailed clinical history and mental examination, and diagnosis made using the DSM-5 guidelines. Diagnostic technologies help in the process of making a clinical diagnosis and in further evaluation of the patient. Positron emission tomography (PET) scans can be used to measure the receptor activity PHYSIOLOGICAL PSYCHOLOGY 6 and the levels of serotonin in the brain. PET scans are also used to evaluate the destruction of neuronal synapses by checking the degree of uptake of radionuclide labeled monoamines such as serotonin and norepinephrine. This can also be used in researching about the etiology of bipolar II disorder. Magnetic resonance imaging and electroencephalograms are used in imaging of the brain in checking for organic causes of mental illness. Electroencephalogram can be used in distinguishing bipolar II disorder from other forms of bipolar disorders by monitoring brain activity. Functional magnetic resonance imaging and spectrum photo emission tomography (SPECT) are used in researching for structural brain abnormalities as the basis for bipolar disorders, including bipolar II disorder (Heng, Song, Sim, 2010). Thyroid function tests are used in establishing whether the condition is caused by hypothyroidism. Cortisol levels and dexamethasone suppression test can be used in detecting hormonal imbalances that can cause or aggravate bipolar II disorder. Conclusion Bipolar II disorder is a mood disorder in the bipolar spectrum and is characterized by episodes of hypomania and depression. The exact cause of this condition is not known. However, there are various theories that explain the possible cause of bipolar II disorder. Notably, the biological theory explains that the condition could be due to abnormalities in the brain circuits that use neurotransmitters such as serotonin and norepinephrine. Genetic factors are also thought to play a role in the development of the condition as explained above under the etiology of bipolar II disorder. Bipolar II disorder is difficult to diagnose and differentiate it from other types of bipolar disorders. A good history and complete evaluation of the patient is important in diagnosing the condition. Once the patient has been diagnosed with bipolar II disorder, they are PHYSIOLOGICAL PSYCHOLOGY 7 put on both pharmacological and non-pharmacological treatment. Pharmacological treatment involves use of mood stabilizing drugs and antidepressant drugs. Non-pharmacological treatment includes use of electroconvulsive therapy, counseling of the patient and family therapy. Diagnostic technologies used in the clinical diagnosis and in research about bipolar II disorder include brain imaging modalities such as positron emission tomography, computed tomography scans, functional magnetic resonance imaging, and physiological tests such thyroid function test, and assessment of levels of cortisol in the body. PHYSIOLOGICAL PSYCHOLOGY 8 References Berk, M., Dodd, S. (2005). Bipolar II disorder: a review. Bipolar Disorder. 7.1 (2005): 11-21. Barrett, K. E., Barman, S. M., & Boitano, S. (2010). Ganong's review of medical physiology. New Delhi: McGraw Hill, 2010 Black, D. W., & Grant, J. E. (2014). DSM-5® Guidebook: The Essential Companion to the Diagnostic and Statistical Manual of Mental Disorders. American Psychiatric Publishers. Heng, S., Song, A. W., & Sim, K. (2010). White matter abnormalities in bipolar disorder: insights from diffusion tensor imaging studies. Journal of neural transmission, 117(5), 634-659. Koeppen, B. M., & Stanton, B. A. (2012). Berne and Levy Physiology. Elsevier. Kupfer, D. J., Regier, D. A. (2014). Neuroscience, clinical evidence, and the future of psychiatric classification in DSM-5. American Journal of Psychiatry. American Psychiatric Publishers MacQueen, G. M.,Young, L. T. (2014). Bipolar II disorder: symptoms, course, and response to treatment. Psychiatric Services. Novick, D. M., Swartz, H. A., Frank, E. (2010). Suicide attempts in bipolar I and bipolar II disorder: a review and meta‐analysis of the evidence. Bipolar disorders 12(1), 1-9 Salvadore, G., Quiroz, J. A., Machado-Vieira, R., Henter, I. D., Manji, H. K., & Zarate Jr, C. A. (2010). The neurobiology of the switch process in bipolar disorder: a review. The Journal of clinical psychiatry, 71(11). Sullivan, G. M., Ogden, R. T., Oquendo, M. A., Kumar, J. D., Simpson, N., Huang, Y. Y., ... & Parsey, R. V. (2009). Positron emission tomography quantification of serotonin-1A PHYSIOLOGICAL PSYCHOLOGY 9 receptor binding in medication-free bipolar depression. Biological psychiatry, 66(3), 223230.
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