Biopsychological Analysis of a Neuropsychological Disorder

Biopsychological Analysis of a Neuropsychological Disorder

Ashford University

PSY 350

Biopsychological Analysis of a Neuropsychological Disorder

The disorder that I will be discussing for this analysis is Generalized Anxiety Disorder (GAD). Generalized anxiety disorder is a psychological disorder characterized by excessive worry. As I move through this paper I will examine the causes of GAD from both the neurobiological perspective as well as from the genetic, environmental, familial, and lifestyle aspects associated with the development of GAD. I will also discuss the pathology of GAD and how it affects the nervous system, specific areas, and different brain structures; I will provide treatment options for GAD from both a pharmacological aspect as well as non-pharmacological therapies, and finally, I will discuss diagnostic and research technologies involved in the diagnosis of GAD. In our society, today over 6.8 million people suffer from GAD, and it is among the most common anxiety disorder in the United States (Anxiety and Depression Association of America [ADAA], 2018).

In the diagnosis of generalized anxiety disorder (GAD), according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), a person must display chronic worry and anxiety occurring more often than not for at least 6 months, as well as displaying at least 3 of the 6 symptoms associated with this disorder (APA, 2013) As per the DSM-5, the six symptoms that are associated with GAD include restlessness or feeling on edge, becoming tires easily, difficulty concentrating, irritability, muscle tension, and sleep disturbances. GAD is also associated with continuous worry and anxiety (APA, 2013). individuals who suffer from GAD may also experience other symptoms such as “trembling, twitching, feeling shaky, and muscle aches or soreness” (APA). There are also somatic symptoms along with autonomic symptoms. The somatic symptoms associated with GAD are “sweating, nausea, diarrhea”, and the autonomic symptoms include “accelerated heart rate, shortness of breath, dizziness”, while some individuals will also experience symptoms such as digestive problems like “irritable bowel syndrome”, and “headaches” (APA). (Locke, Kirst, & Shultz, 2015).

In relation to some of the theories associated with generalized anxiety disorder, the causes relating to GAD can include; heritability, environmental stressors, and biological vulnerability (Arul, 2016), also, prolonged exposure to stressful situations during one’s life, as well as, a family history of mental illness. Many of the neurobiological causes for GAD have been thought to have a strong genetic foundation, suggesting the possibility that GAD is an inherited condition in some cases (Bandelow et al., 2016). Another neurobiological factor associated with individuals affected by GAD is that they show increased activity in the limbic system, specifically the amygdala (Martin, Ressler, Binder, & Nemeroff, 2013).

There are many different types of anxiety disorders, such as social anxiety disorder (SAD) may contain some similar symptoms of GAD such as worry and anxiety, however, SAD is brought on by anticipating social situations or events whereas GAD is always present. Obsessive-compulsive disorder (OCD) is also an anxiety disorder that has some similar components to GAD, however, while GAD and OCD share the symptom of excessive worry, the focus of the worry is different. In GAD excessive worry is focused on future problems, while the excessive worry in OCD is associated with intrusive thoughts. Post-traumatic stress disorder (PTSD) and adjustment disorders also have symptoms associated with GAD, yet because they are triggered by other factors such as traumatic events or specific stress-related factors they do not meet the criteria for GAD (APA, 2013).

While negative environmental factors such as abuse and low socioeconomic status play a significant role in the development of GAD, life events are also a contributing factor in the development of GAD; due to the unpredictable nature of certain life situations this may often spark anxiety especially if the situation does not end with a desirable outcome (Arul, 2016). As previously mentioned GAD is thought to have a strong genetic connection in its hereditability, however, in twin studies, only 32% of participants showed genetic inheritability, that is only a small portion showed signs of inheriting GAD from a parent or relative affected by this disorder, although first generation relatives of those affected by GAD are thought to be at a higher risk of developing the disorder than those of future generations. The remaining percentage is believed to be contributions from other factors such as an individual’s personal environment and lifestyle (Martin et al., 2013).

Individuals who suffer from GAD tend to experience more stressful life events than those who are not affected by this disorder (Arul, 2016). Among individuals who suffer from GAD, women are more likely to suffer from the disorder than men (APA, 2013). Individuals from low socioeconomic status are more likely to experience symptoms of GAD than those of high socioeconomic status because they have less financial security. While approximately 33.7% of the population suffers from some form of anxiety related disorder, the majority of individuals range from 18-64 years of age, however, GAD seems to get worse in the early ’30s and then begins to level out (Bandelow & Michaelis, 2015).

In recent MRI studies, researchers have found that individuals with GAD display more grey matter in the amygdala and dorsomedial prefrontal cortex (PFC), and less grey matter in the hippocampus than those who do not suffer from the disorder. While in teens it has been noted that there is more grey matter in the superior temporal gyrus and less in the medial and superior frontal gyri. Yet the main area of the brain that is subject to increases in grey matter is the right cerebral hemisphere (Bandelow et al., 2016). The amygdala, prefrontal cortex (PFC) is the main areas of the brain that are responsible for the symptoms that are associated with GAD. In the amygdala’s bilateral regions electrical stimulation is what causes the fear and anxiousness associated with anxiety, while the PFC is responsible for sending messages to and from the “excitatory glutamatergic projections” which activate stimuli, and also regulates anxiety via the basolateral amygdala (Nuss, 2015).

The neurotransmitter gamma-aminobutyric acid (GABA) plays a key role in GAD. The dysregulation of GABA and prevention of neurotransmission is responsible for the anxiousness in many anxiety disorders. A decrease in the number of GABA receptors has been seen in individuals with GAD and is thought to be one of the causes for onset (Martin, Ressler, Binder, & Nemeroff, 2013). When GABA receptors are introduced into the amygdala this helps to reduce fear and anxiousness (Nuss,2015). However, it is important to note that GABA is not the only neurotransmitter that has an influence on anxiety, other neurotransmitters such as “serotonin, opioid peptides, endocannabinoids, neuropeptide Y, oxytocin, and corticotropin-releasing hormone” (Nuss). It has also been thought that GABA is used in nearly 33% of the GABA used is in the central nervous system making it the main source of neurotransmission (Nuss).

As mentioned earlier, the neurotransmitter serotonin is also thought to be important in the regulation of anxiety symptoms associated with GAD. Serotonin (5-HT) is found in large quantities in the “ventromedial prefrontal cortex (vmPFC)”and has also been found to be a controlling influence on anxiety-related behaviors (Yamashita, Rosa, Lowry, & Zangrossi Jr, 2018). The release of serotonin in the prelimbic cortex (PL) may prevent anxious behaviors like those seen in individuals with GAD (Yamashita, Rosa, Lowry, & Zangrossi Jr).

One treatment option is that of medication. There are many medications available for those who suffer from GAD. Some of the medications available are Benzodiazepines such as Xanax, Ativan, Valium, and Klonopin (Locke, Kirst, & Shultz, 2015, table 4). Benzodiazepines target neurotransmitters in the brain and increase Gamma-aminobutyric acid (GABA) which is responsible for sending messages in the brain and throughout the nervous system this aids in producing the calming feeling one might receive from taking these types of medications, Benzodiazepines also affect the central nervous system (CNS) by binding to GABA receptor sites in the brain. The macromolecular complex is thought to be important to the way that benzodiazepines work. Benzodiazepines make the process of GABA transmission easier by increasing the response of GABA receptor sites in the CNS (Barchas & Altemus, 1999).

Other medications that are used in the reduction of symptoms associated with GAD are selective serotonin reuptake inhibitors (SSRI’s) such as Prozac, Celexa, Lexapro, Zoloft, and Paxil are also helpful in reducing the symptoms associated with GAD. SSRI’s also affected the brains neurotransmitters, however, SSRI’s block the reabsorption of serotonin in the brain so that it is more available, this also helps to produce a calm relaxed feeling for individuals who take this medication to reduce anxiety symptoms related to GAD (Locke, Kirst, & Shultz, 2015, table 4). These medications are the most effective in the treatment of symptoms associated with GAD; however, I have learned through personal experience that while the pharmacological approach can provide significant symptom relief some of the medications that are available for individuals with GAD are highly habit-forming (mostly the benzodiazepines), so it is important to do your research before taking medication.

Another form of treatment available for GAD is that of cognitive behavioral therapy (CBT). CBT is one of the most effective ways to treat GAD. CBT is a form of psychotherapy that helps individuals with GAD to shift their thinking in a more positive direction. The purpose of CBT is to reprogram the way that an individual thinks about things in order to produce a more positive outlook on circumstances pertaining to future events (Kaczkurkin & Foa, 2015). Individuals who are treated with CBT are able to make better evaluations of otherwise stressful issues, which allow them to make better choices.

Some methods of ongoing management for GAD involve relaxation therapy such as yoga, a regular exercise regimen, and regular sleep/wake schedule (Stein & Sareen, 2015), along with CBT and or medication. Individuals who suffer from GAD will usually be seen regularly by a therapist for CBT and sometimes depending on the type of treatment that an individual receives a psychiatrist or medical Dr. to prescribe medication.

There is a lot of promising research in the diagnosis of GAD using current technologies such as functional magnetic reconnaissance imaging (fMRI). fMRI allows researchers to identify certain aspects of brain activity that is associated with this disorder so that more effective treatments can be developed. This also allows for Drs. to more accurately diagnose individuals who suffer from this disorder. Positron emissions tomography (PET) and single- photon emission computerized tomography (SPECT) have also proven useful in research regarding the treatment and diagnosis of GAD.

While there are many aspects associated with the development of GAD, the major contributors are environment and lifestyle. There are many treatment options available for those who suffer from GAD, as more than 6 million people in the United States suffer each year from, and less than half are receiving treatment. GAD can be debilitating and life-changing if left untreated, and yet many who are affected suffer daily. While there are no specific lab tests available at this time to directly diagnose GAD, through the development of technology imaging tests such as fMRI, PET and SPECT can assist with diagnosis and treatment options.

References

American Psychiatric Association. (2013). Section II: Anxiety Disorders. In Diagnostic and statistical manual of mental disorders (5th). https://doi.org/https://doi-org.proxy-library.ashford.edu/10.1176/appi.books.9780890425596

Anxiety and Depression Association of America. (2018). Facts & Statistics. Retrieved from https://adaa.org/about-adaa/press-room/facts-statistics

Arul, A. J. (2016, April 1, 2016). Study of Life Events andPersonality Dimensions generalized Anxiety Disorder [Journal]. Journal of Clinical & Diagnostic Research, 10(4), 5-9. https://doi.org/ 10.7860/JCDR/2016/18123.7652

Bandelow, B., & Michaelis, S. (2015). Epidemiology of anxiety disorders in the 21st century [Journal article]. Dialogues in clinical neuroscience, 17(3), 327-335. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4610617/

Barchas, J. D., & Altemus, M. (1999). Biochemical Aspects of Anxiety. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK28190/

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Locke, A. B., Kirst, N., & Shultz, C. G. (2015, May 1, 2015). Diagnosis and Management of Generalized Anxiety Disorder and Panic Disorder in Adults [Journal article]. American Family Physician, 91(9), 617-624. Retrieved from (Locke, Kirst, & Shultz, 2015)https://www.shastahealth.org/sites/default/files/residency/Diagnosis-and-Management-of-Generalized-Anxiety-Disorder-and-Panic-Disorder-in-Adults.pdf

Martin, E. I., Ressler, K. J., Binder, E., & Nemeroff, C. B. (2013). The Neurobiology of Anxiety Disorders: Brain Imaging, Genetics, and Psychoneuroendocrinology. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684250/

Nuss, P. (2015, January 17, 2015). Anxiety disorders and GABA neurotransmission: a disturbance of modulation [Journal article]. Neuropsychiatric Disease and Treatment, 2015, 165-175. https://doi.org/10.2147/NDT.S58841

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Yamashita, P. S., Rosa, D. S., Lowry, C. A., & Zangrossi Jr, H. (2018). Serotonin actions within the prelimbic cortex induce anxiolysis mediated by serotonin 1a receptors. Journal of Psychopharmacology, 33(1), 3-11. https://doi.org/10.1177/0269881118817384