Biological Bases: Bipolar Disorder

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According to the National Institute of Mental Health, approximately 4.4% of adults in the United States experience bipolar disorder in their lives (Bipolar Disorder, 2016). Bipolar disorder is characterized by unusual changes in mood, energy, and activity levels. There are four types of bipolar disorder: Bipolar I Disorder, Bipolar II Disorder, Cyclothymia, and other related disorders (Bipolar Disorder, 2016). Bipolar I Disorder involves manic episodes that last about a week long and can include depressive episodes that last approximately two weeks long. Bipolar II Disorder involves a pattern of depressive episodes and hypomanic episodes that are less severe than the manic episodes of Bipolar I. Cyclothymia is characterized by the expression of depressive and hypomanic symptoms but not to the extent of being labeled an episode as in Bipolar II (Bipolar Disorder, 2016). Other disorders include symptoms of bipolar that cannot be matched with the previously mentioned categories. Bipolar disorder is a disorder of the brain.

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The amygdala is a structure in the limbic system involved in our experience of emotion and tying emotional meaning to our memories (Spielman, 2014, p. 103). It has been determined that the amygdala is often altered and affecting in regards to bipolar disorder. Increased function of the amygdala is associated with not only manic states of bipolar disorder but also with basic cognitive processes and actions (Brian Problems, 2013). Additionally, the size of the amygdala is altered in the brains of those affected with bipolar disorder. In the early stages of the disorder, the amygdala is smaller than average, but inversely, as age increases the amygdala appears larger than average size. (Brian Problems, 2013). An article discussing homeless individuals in Salem, Oregon mentioned that while someone is homeless their amygdala begins to work overtime and hyper-analyze situations. Many of the homeless individuals showed signs of bipolar disorder among other mental conditions, as they began misinterpreting different incoming signals (Pate, 2018).

The prefrontal cortex is the area in the frontal lobe responsible for higher-level cognitive functioning (Spielman, 2014, p. 104). It is related to one’s ability to plan, organize, and make decisions. Additionally, the prefrontal cortex has been found to regulate certain emotional reflexes through its linkage to the amygdala. Where the amygdala had an increase in function in association with bipolar disorder, the prefrontal cortex shows a decrease in activation. Especially during emotional situations, the prefrontal cortex does not adequately regulate the amygdala, thus emphasizing the effects of the over-productive system. In the same article about homeless in Salem, Oregon, it was determined that because of the constant awareness and over-activity of fight-or-flight responses, many individuals experienced damage to their prefrontal cortex and were, thus unable to logically comprehend situations they were in. Because the prefrontal cortex was damaged, the individuals were not able to regulate the hyperactive amygdala and the severity of their mental illnesses and disorders increased (Pate, 2018).

A neurotransmitter is a chemical messenger of the nervous system (Spielman, 2014, p. 104). Different neurotransmitters can cause different signals to get sent to the brain, and thus alter processes of the brain. Altered brain functioning resulting from these neurotransmitters can contribute to disorders such as bipolar disorder. A few, but not all, of the neurotransmitters connected to bipolar disorder include dopamine, serotonin, and norepinephrine. Dopamine is associated with mood, sleep, and learning; serotonin with mood and sleep. Norepinephrine is connected with alertness and functions of one’s heart and intestines. Individuals who express bipolar disorder are known to have an imbalance of neurotransmitters, such as those mentioned, compared to that of someone without the disorder (Nemade & Dombeck).

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Biological Bases: Bipolar Disorder. (2019, Dec 04). Retrieved October 1, 2022 , from
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