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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