(please retain and use the 4 articles being referenced for intext and reference citations along with any of your own scholorly references) The purpose of this assignment is to COMPLETE a paper that w

(please retain and use the 4 articles being referenced for intext and reference citations along with any of your own scholorly references) The purpose of this assignment is to COMPLETE a paper that w
Running Head: THE BIOLOGY OF BIPOLAR DISORDER 0 The Biology of Bipolar Disorder A Former Student PSYC 301 Abstract Bipolar disorder is a devastating mental health condition caused by a dysfunction of the nervous system. Symptoms of this condition are episodes of mania followed by episodes of depression. Research has been conducted to investigate the causes of this condition and have identified several hormones and structures of the brain that are involved in the bipolar disorder. Researchers have identified that hormones included in the hypothalamus, pituitary gland, and gonads has an impact on these patients. It has also been observed that the frontal lobe is affected in patients with bipolar disorder. Patients with bipolar disorder have been classified based on their cognitive profiles, and these profiles have been compared to their brain activity. Existing and continued research will help to gain a greater understanding of these patients in order to create more effective treatment plans. The Biology of Bipolar Disorder Bipolar disorder is a spectrum of mood disorders that affects 60 million people globally (Gooding et al., 2019). The effects of bipolar disorder can be devastating for the individual and those around them due to the symptoms of this disorder (Ritchie & Roser, 2018). Symptoms include episodes of mania, or a “high” and elated mood, followed by episodes of depression (Moore, 2013). These episodes can last for weeks or months without intervention or treatment. Bipolar disorder is a destructive disease caused by the disfunction of the nervous system, several different parts of the brain, and multiple different hormones. During the manic episodes of bipolar disorder, individuals may experience an increase in mood, self-esteem, and irritability. They may experience grandiosity or believing they can accomplish anything. They may also experience psychotic symptoms including paranoia and hallucinations. These episodes are followed by episodes of a low or depressed mood, feelings of worthlessness, reduction in motivation or energy, and suicidal thoughts (Moore, 2013). Bipolar disorder has different classifications that are divided by severity. Bipolar I disorder is the most severe and is classified by the frequency of hospitalizations and the impairment in functioning caused by the symptoms. Bipolar II disorder is a milder form of the disorder and individuals with this classification experience “hypomania”, which is a less severe form of mania (Moore, 2013). Both classifications of bipolar disorder are associated with the highest rate of suicide of all psychiatric disorders (Gooding et al., 2019). Several studies have been conducted to explore the biological causes of bipolar disorder. Research supports that this disorder is caused by an impairment in hormonal function and the disfunction of electrical impulses as identified by EEG, and activity in different parts of the brain as identified by MRI. This research provides valuable data allowing insight to the bipolar brain, equipping practitioners to more successfully treat and understand bipolar patients. In the study of neuroendocrine hormones in patients with major depressive disorder, Feng et al. (2019) tested the hypothesis that there is a negative correlation between the hypothalamic-pituitary-thyroid (HPT) axis and the hypothalamic-pituitary-gonadal (HPG) axis in patients with major depressive disorder, but there is no correlation in patients with bipolar disorder. This study also sought to evaluate the differences between the hypothalamic-pituitary-adrenal (HPA), HPT, and HPG axes in patients with major depressive disorder and bipolar disorder (Feng et al., 2019). Ultimately, the study sought to evaluate how the three neuroendocrine pathways are related to each other in patients with affective disorders. The study was conducted on two groups: a group with major depressive disorder and a group with bipolar disorder. Both groups were evaluated for the following hormone levels in their blood: thyroid stimulating hormone (TSH), triiodothyronine (T3), free triiodothyronine (FT3), thyroxine (T4), free thyroxine (FT4), cortisol (COR), adrenocorticotropic hormone (ACTH), estradiol (E2), and testosterone (T). Only female patients were evaluated for E2 levels, and only male patients were evaluated for T levels (Feng et al., 2019). The participants of this study were 679 patients with major depressive disorder and 83 patients with bipolar disorder, composed of 263 male participants and 416 female participants with major depressive disorder, and 39 male participants and 44 female participants with bipolar disorder. The mean age for participants with major depression was 31.4 years and the mean age for participants with bipolar disorder was 24.8 years. The illness duration for participants with major depression was 1.56 and 3.87 for participants with bipolar disorder (Feng et al., 2019). Participants were evaluated for current mood state using the 17-item Hamilton Rating Scale for Depression, Hamilton Rating Scale for Anxiety, and Young Mania Rating Scale. All participants were hospitalized overnight, and blood collection was performed the following morning between 8 a.m. and 9 p.m. Alprazolam was the only medication administered to the patients to treat insomnia from hospitalization (Feng et al., 2019). The results of this study demonstrated that participants with major depression had a hyperactivity of the HPA axis and lower activity of the HPT axis when compared to participants with bipolar disorder. Participants with bipolar disorder were found to have reduced testosterone secretion, indicating lower activity of the HPG axis. This study also discovered that ACTH, FT3 and FT4 may potentially mark severity and symptoms of untreated major depression. This study did not support the hypothesis that there is a negative correlation between the HPG and HPT axes (Feng et al., 2019). This study provided important information about the interaction of hormones within the brain of the bipolar patient. It also displayed the differences between two closely related but psychologically different affective disorders. This research clarified the parts of the endocrine system that are associated with this disorder and provided insight about the parts of the brain that these hormones affect in individuals with affective disorders. Other studies have performed more in depth research regarding the function of the parts of the brain that are affected by bipolar disorder. In a study of alpha and gamma activity in patients with affective disorders, Kim, Oh, Jeon, Hong and Baek (2019) investigated the differences in the neurobiological characteristics of the ADHD symptoms that are often displayed in patients with major depression and bipolar disorder. This study sought to measure the neurological activity of these patients in order to gain greater understanding of the relation of these symptoms. There were four groups of participants being evaluated, separated into groups of individuals with major depressive disorder, bipolar disorder type I, bipolar disorder type II, and bipolar disorder not otherwise specified (Kim et al., 2019). These conditions were being compared against each other and evaluated based on their ADHD symptoms. As the study sought to evaluate dimensional characteristics of ADHD rather than those clinically diagnosed with ADHD, participants who met full DSM criteria for ADHD were excluded. All participants were aged between 18 and 45 and were currently in a depressive episode based on DSM criteria. Participants who were currently in a manic or mixed state were excluded. A total of 67 subjects were evaluated: 48 with major depression, 8 with bipolar disorder type I, 13 with bipolar disorder type II, and 8 with bipolar disorder not otherwise specified. 9 participants had psychotic features (Kim et al., 2019). The methods used to evaluate symptoms and mood state were Mini International Neuropsychiatric Interview, Adult ADHD self-report scales, Hamilton rating scale for depression, Hamilton rating scale for anxiety, and mood disorder questionnaire. All participants underwent EEG following evaluation (Kim et al., 2019). This study demonstrated that participants with major depression and ADHD symptoms had greater powers of alpha waves in both frontal regions, while ADHD symptoms in bipolar disorder showed association with right frontal gamma power. The patterns of correlation between ADHD symptoms and frontal qEEG measures were different between participants with major depression and bipolar disorder. The study was also able to determine a weak association with hyperactivity and right frontal gamma activity in participants with bipolar disorder (Kim et al., 2019). This research is important because it demonstrates the difference between two related conditions, major depression and bipolar disorder, and how the electrical energy in the brain differs between these two conditions. It also demonstrates how the symptoms of ADHD can overlap these conditions and can make differentiating between the two difficult. This research provided useful information about the affected parts of the brain that can be used in conjunction with other research in order to produce a greater understanding of the bipolar brain. Subsequent research has been able to further identify the parts of the brain impacted by bipolar disorder and classify these individuals on cognition and associated brain activity. In a study of patients with bipolar disorder type I, Kollmann, Yuen, Scholz and Wessa (2019) investigated the different cognitive profiles of these patients and evaluated the underlying neuronal network changes. This study hypothesized that patients with bipolar disorder type I often display cognitive profiles that can be divided into different categories, rather than grouped and applied widespread to all patients with bipolar disorder. This study compared a group of participants with bipolar disorder type I and compared these participants to a control group. The study aimed to compare the cognitive and behavioral abilities and deficits in these two groups, in order to separate them into three categories of cognitive profiles. Each cognitive profile would then undergo FMRI to evaluate the activity of the brain correlating with these characteristics (Kollmann, et al., 2019). The study evaluated 54 participants with bipolar disorder type I and compared with 54 control participants matched for gender, age and IQ. Control participants were excluded if they had any psychiatric or neurological disorders, if they had a first degree relative with bipolar disorder, or substance abuse for 3 months prior to testing. Bipolar participants were required to have a stable mood on day of testing and on medication for 2 months prior to testing. All participants were aged between 18 and 60 years (Kollmann, et al., 2019). The Cambridge Neuropsychological Test Automated Battery, Cambridge Gambling Task, Stop Signal Task, Intra-Extra Dimensional Set Shift, Stockings of Cambridge, Multiple-Choice Word Vocabulary Test, structured clinical interview and questionnaire related to general functioning was used to evaluate mood states and cognitive capabilities of participants. All patients underwent FMRI after evaluation (Kollmann, et al., 2019). After testing, this study was able to group participants into three different cluster categories relating to their cognitive functions. Cluster 1 was defined by difficulty with adaptation to changing demands, Cluster 2 was defined by impulsivity and Cluster 3 was characterized by superior ability to strategize and excellent visuospatial planning skills. These differences in cognitive abilities and deficits were reflected by activity recorded by FMRI. This study was also able to demonstrate that cognitive differences observed in individuals with bipolar disorder are not always negative and can be beneficial to the bipolar individual (Kollmann, et al., 2019). This research is important because it demonstrates how different brain activity causes bipolar disorder to be a multi-dimensional affective disorder. It demonstrates the importance in slight brain changes in the symptomology of the patient and explains what parts of the brain are affected in individuals with bipolar disorder. In conclusion, it can be observed that bipolar disorder is a multi-dimensional disorder, affecting many parts of the brain and endocrine system. Bipolar disorder varies from patient to patient depending on what parts of the brain are being affected, but research supports that this variation is consistent among groups. As research is continually conducted on this disorder, greater understanding is gained on how this devastating mental illness can be most effectively treated, and how these patients can find relief. References Feng, G., Kang, C., Yuan, J., Zhang, Y., Wei, Y., Xu, L., … Yang, J. (2019). Neuroendocrine abnormalities associated with untreated first episode patients with major depressive disorder and bipolar disorder. Psychoneuroendocrinology, 107, 119–123. Gooding, D. C., Wolford, K., & Gooding, D. C. (2019). Bipolar disorder. Salem Press Encyclopedia of Health. Kim, J. S., Oh, S., Jeon, H. J., Hong, K. S., & Baek, J. H. (2019). Resting-state alpha and gamma activity in affective disorder with ADHD symptoms: Comparison between bipolar disorder and major depressive disorder. International Journal of Psychophysiology, 143, 57–63. Kollmann, B., Yuen, K., Scholz, V., & Wessa, M. (2019). Cognitive variability in bipolar I disorder: A cluster-analytic approach informed by resting-state data. Neuropharmacology, 156, 1–14. Moore, N. B. (2013). Bipolar Disorder : Symptoms, Management and Risk Factors. Hauppauge, New York: Nova Science Publishers, Inc. Ritchie, H. and Roser, M. (2018, April). Mental health. Our World in Data. Retrieved from https://ourworldindata.org/mental-health
(please retain and use the 4 articles being referenced for intext and reference citations along with any of your own scholorly references) The purpose of this assignment is to COMPLETE a paper that w
Running head: RESEARCH SUMMARIES 0 Research Summaries PSYCH 495 Abnormal Emotional Processing and Emotional Experience in Patients with Peripheral Facial Nerve Paralysis: A MEG Study In a review analysis of this article, “Abnormal Emotional Processing and Emotional Experience in Patients with Peripheral Facial Nerve Paralysis: A MEG Study,” several conclusions were made. The study by Kheirkhah et al. (2020) aimed to examine how the brain reacts abnormally to situations in clients with facial nerve paralysis. The research question for this study was investigating patients with facial nerve paralysis based on their brains’ unusual emotional responses. The hypothesis for the study was to evaluate an emotion grading task to determine variations in such patients. Through this, it would be easier to discover the brain’s abnormal emotional reactions for patients living with facial nerve paralysis syndrome.  The author’s used 33 subjects, both male and female. However, 17 of the subjects in this study were healthy, and 16 were identified patients with facial nerve paralysis condition. The female subjects were 25, and the remaining number were male. The method used to test the research question and hypothesis was a logistic regression machine learning technique with LASSO regularization. The patients’ diagnosis was made using spectrums of brain frequency bands to test the differences in emotional reaction. According to Kheirkhah et al. (2020), healthy subjects have less emotional reactions or responses than patients with facial nerve paralysis. All the tests were based on unpleasant, pleasant, and neutral stimuli for both subjects for the study. These results established that there is a classification accuracy of brain-neutral responses for healthy people and facial nerve paralysis patients. It was because patients didn’t want to experiment. This study showcased that there is a difference in emotional brain processing for facial nerve paralysis patients as compared to healthy people. Emotional Factors Contributing to Facial Paralysis Goldberg and Harte have shared quick facts facial paralysis in this article, “Emotional Factors Contributing to Facial Paralysis,” which was published initially in 1972. As the title of the topic suggests, the authors focused on investigating emotional aspects that contributed to facial paralysis. The research question for this study was to examine the emotional factors that majorly resulted in facial paralysis among patients with this related syndrome. The hypothesis was to identify the historical reviews of emotions for the subjects of the study. Also, to ascertain facial nerve variations from different physiological blocks that completed the degeneration of paralysis. The subjects used in this study were that patients affected with facial paralysis since the main objective was to ascertain the emotional factors that could lead to paralysis degeneration. According to Goldberg & Harte (1972), determining psychological factors effects requires examining marital backgrounds, vocational aspects, and pre-morbid personalities. The methodology used for this study based on data generated from healthcare organizations with facial paralysis patients. The examination of the emotional status based on a psychiatric method assessment to ascertain the levels of emotional trauma if available for each patient. More than 100 patients were examined to outline the rate number of emotional trauma experienced. The finding of this research was that emotional trauma preceded the onset of facial paralysis patients. Every seven patients out of forty-four experienced psychological trauma that caused their facial paralysis; thus, the research question was attested. This study is significant because it has stated some of the etiological factors of facial paralysis, which is emotional trauma. It has contributed an understanding of what’s required to control patients with facial paralysis conditions. This study has also demonstrated that emotional crisis and severe anxiety should be avoided because it can lead to facial paralysis in the long run. Bell’s Palsy and Autoimmunity In this article, “Bell’s Palsy and Autoimmunity,” the authors focused on a discussion about disease etiopathogenesis and pharmacotherapy of Bell’s palsy. It is a syndrome that affects the idiopathic peripheral facial nerve. In a review analysis of this study, the author’s articulated all unilateral facial nerve palsy to outline the prevalence of the Bell’s palsy nerve condition and autoimmunity. The research questions that were being tested included reviewing the current knowledge of Bell’s palsy etiopathogenesis, the viral infection frequency, and autoimmunity. The hypothesis for the research study was to discuss the pathogenesis of this nerve syndrome basing on pharmacotherapy. As a result, to understand the etiology of Bell’s palsy and its autoimmunity. The subjects used to develop this research based on relevant publications on Bell’s palsy condition using clinical presentation, histopathology, etiopathogenesis, and diagnosis of this condition. All the research publications used in this study were from 1975-2012 to ascertain the frequency of this syndrome in patients. The number of these publications was 82. The method used to establish Bell’s palsy frequency was built from the 82 relevant publications. The etiology, diagnosis, treatment, autoimmunity, and clinical presentation of this syndrome in patients were outlined and discussed. According to Greco, Marinelli, Marci, & De Vincentiis, (2012), Bell’s palsy accounts for 60-75% of unilateral facial nerve diseases, and the annual occurrence is 15-30 people per 100,000 persons. Also, it was found that it caused by the reactivation of latent herpes viruses from cranial nerve ganglia. However, it was concluded that Bell’s palsy is an autoimmune condition. As a result, the hypothesis and research questions were both tested and discussed. This study’s importance is that the diagnosis, occurrence, treatment, and the history of Bell’s palsy are given. Disrupted Functional Connectivity of Striatal Sub-Regions in Bell’s Palsy Patients Striatal functional connectivity in people with a motor disorder such as Parkinson’s disease have limited research studies. In this article, “Disrupted Functional Connectivity of Striatal Sub-Regions in Bell’s Palsy Patients,” numerous facts have been made regarding motor disorders. The purpose of the study was to investigate how striatum controls motor functions in people and how its degeneration can cause severe disorders. The research question was to examine how functional connectivity is affected by peripheral nerve injury between the motor cortex and the striatum. This study focused on Bell’s palsy (BP) clients and healthy people to ascertain the difference. The subjects used to carry out this study were 25 Chinese right-handed patients with left/right-sided BP syndrome. Out of the 25 subjects, 15 were male, and ten were female without psychiatric disorders. The methodology used was MRI data processing, with each subjects’ eyes scanned and a seed-based approach applied to eliminate correlations. According to Song et al. (2017), BP patients had disrupted striatal because the striatum and the putamen were affected. The condition was regardless of gender. Contrarily, the healthy people had stronger functional connectivity because of the strong sensorimotor area. The disruptive functional connectivity was all factored by nerve injury of the caudate and putamen. This study has helped lay out a comprehensive understanding of striatal functional connectivity in patients with BP syndrome. Through this, it is easier to identify what causes BP syndrome condition, and it can help in identifying recovery solutions for such patients. Still, more studies must be developed to examine disruptive functional connectivity for BP patients in acute, late, and recovery stages. This study has shared the vital role that striatum plays in motor functions in the human body system. References Goldberg, J. M., & Harte, S. (1972). Emotional factors contributing to facial paralysis. Journal Of Geriatrics Sociology. Vol 7, p.324-329. Wiley Online Library. Greco, A., Gallo, M., Marinelli, C., Macri, G. F., & De Vincentiis, M. (2012). Bell’s Palsy and autoimmunity. Autoimmunity Reviews, 12(2), 323-328. Retrieved from https://www.sciencedirect.com/science/article/pii/S1568997212001152 Kheirkhah, M., Brodoehl, S., Leistritz, L., Götz, T., Baumbach, P., Huonker, R., Witte, O. W., Volk, G. F., Guntinas-Lichius, O., & Klingner, C. M. (2020). Abnormal emotional processing and emotional experience in patients with peripheral facial nerve paralysis: A MEG study. Brain Sciences (2076-3425), 10(3), 147. Retrieved from https://doi-org.ezproxy.umgc.edu/10.3390/brainsci1… Song, W., Cao, Z., Lang, C., Dai, M., Xuan, L., Lv, K., Cui, F., Jorgenson, K., Xu, M., &Kong, J. (2017). Disrupted functional connectivity of striatal sub-regions in Bell’s Palsy patients. Neuroimage: Clinical,14©, 122-129. Retrieved from https://www.sciencedirect.com/science/article/pii/S2213158217300086
(please retain and use the 4 articles being referenced for intext and reference citations along with any of your own scholorly references) The purpose of this assignment is to COMPLETE a paper that w
Step 1: Selecting a Research Paper Topic PSYC 301 1. The Topic: I’ve decided to write about Bell’s Palsy Bells palsy is a type of facial paralysis the result of either trauma or damage to one or two of a persons facial nerves. 2. Summarize Symptoms: Rapid onset of mild weakness to total paralysis on one side of your face — occurring within hours to days Facial droop and difficulty making facial expressions, such as closing your eye or smiling Drooling Pain around the jaw or in or behind your ear on the affected side Increased sensitivity to sound on the affected side Headache A loss of taste Changes in the amount of tears and saliva you produce  3. Nervous System Changes: Identify one or more nervous system changes. List key types of changes in nervous system associated with the disease or disorder. The cause of Bell’s palsy is not known. It is thought that it may be due to inflammation that is directed by the body’s immune system against the nerve controlling movement of the face. This condition results from damage to the facial nerve (the 7th cranial nerve). Pain and discomfort usually occur on one side of the face or head. Symptoms are usually temporary but few may experience the effects for life.  References Song, W., Cao, Z., Lang, C., Dai, M., Xuan, L., Lv, K., Cui, F., Jorgenson, K., Xu, M., & Kong, J. (2017). Disrupted functional connectivity of striatal sub-regions in Bell’s Palsy patients. NeuroImage: Clinical,14©, 122-129. Doi: 10.1016/j.nicl.2017.01.008 Murthy, J., & Saxena, A. (2011). Bell’s Palsy: Treatment guidelines. Annals of Indian Academy of Neuorlogy, 14(5). DOI: 10.4103/0972-2327.83092 McCaul, J. A., Cascarini, L., Godden, D., Coombes, D., Brennan, P. A., & Kerawala, C. J. (2014). Evidence based management of Bell’s palsy. British Journal of Oral & Maxillofacial Surgery, 52(5), 387. Greco, A., Gallo, M., Marinelli, C., Macri, G. F., & de Vincentiis, M. (2012). Bell’s Palsy and autoimmunity. Autoimmunity Reviews, 12(2), 323-328. Retrieved from https://www.sciencedirect.com/science/article/pii/S1568997212001152 Kheirkhah, M., Brodoehl, S., Leistritz, L., Götz, T., Baumbach, P., Huonker, R., Witte, O. W., Volk, G. F., Guntinas-Lichius, O., & Klingner, C. M. (2020). Abnormal Emotional processing and emotional experience in patients with peripheral facial nerve paralysis: An MEG study. Brain Sciences (2076-3425), 10(3), 147. https://doi-org.ezproxy.umgc.edu/10.3390/brainsci10030147 Li, Y., Li, J., Mao, Y., Li, X., Liu, W., Xu, L., Han, Y., & Wang, H. (2015). The alteration of SHARPIN expression in the mouse brainstem during herpes simplex virus 1-induced facial palsy. Neuroscience Letters, 586, 50–54. https://doi-org.ezproxy.umgc.edu/10.1016/j.neulet.2014.12.008 Goldberg MJ, Harte S. Emotional factors contributing to facial paralysis. J Am Geriatr Soc. 1972;20(7):324-329. doi:10.1111/j.1532-5415.1972.tb00821.x SIOL, T., HUBER, M., & BUCHNER H. (2001). Post traumatic Bell’s Palsy. Am J Psychiatry 158:2. https://ajp.psychiatryonline.org/doi/pdf/10.1176/appi.ajp.158.2.322