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Bipolar Disorder
Effects on Central Nervous System
Various types of neurotransmitter chemicals are present in the human brain that allow the transmission of various nerve impulses across the neurons ADDIN ZOTERO_ITEM CSL_CITATION {"citationID":"aPgwRF5t","properties":{"formattedCitation":"(\\uc0\\u8220{}Gulf Bend MHMR Center,\\uc0\\u8221{} n.d.)","plainCitation":"(“Gulf Bend MHMR Center,” n.d.)","noteIndex":0},"citationItems":[{"id":335,"uris":["http://zotero.org/users/local/CKNkWnK9/items/J9KID6UD"],"uri":["http://zotero.org/users/local/CKNkWnK9/items/J9KID6UD"],"itemData":{"id":335,"type":"webpage","title":"Gulf Bend MHMR Center","URL":"https://www.gulfbend.org/poc/view_doc.php?type=doc&id=11204&cn=5","accessed":{"date-parts":[["2019",11,23]]}}}],"schema":"https://github.com/citation-style-language/schema/raw/master/csl-citation.json"} (“Gulf Bend MHMR Center,” n.d.). Neurotransmitters such as dopamine, norepinephrine, serotonin, GABA (gamma-aminobutyrate), glutamate, and acetylcholine are mainly associated with bipolar disorder. According to another research, neuropeptides that include endorphins, somatostatin, vasopressin, and oxytocin are also suspected to be present in the brains of affected individuals ADDIN ZOTERO_ITEM CSL_CITATION {"citationID":"m9Ed6Dia","properties":{"formattedCitation":"(Maletic & Raison, 2014)","plainCitation":"(Maletic & Raison, 2014)","noteIndex":0},"citationItems":[{"id":332,"uris":["http://zotero.org/users/local/CKNkWnK9/items/9UGR4WVK"],"uri":["http://zotero.org/users/local/CKNkWnK9/items/9UGR4WVK"],"itemData":{"id":332,"type":"article-journal","title":"Integrated Neurobiology of Bipolar Disorder","container-title":"Frontiers in Psychiatry","volume":"5","source":"PubMed Central","abstract":"From a neurobiological perspective there is no such thing as bipolar disorder. Rather, it is almost certainly the case that many somewhat similar, but subtly different, pathological conditions produce a disease state that we currently diagnose as bipolarity. This heterogeneity – reflected in the lack of synergy between our current diagnostic schema and our rapidly advancing scientific understanding of the condition – limits attempts to articulate an integrated perspective on bipolar disorder. However, despite these challenges, scientific findings in recent years are beginning to offer a provisional “unified field theory” of the disease. This theory sees bipolar disorder as a suite of related neurodevelopmental conditions with interconnected functional abnormalities that often appear early in life and worsen over time. In addition to accelerated loss of volume in brain areas known to be essential for mood regulation and cognitive function, consistent findings have emerged at a cellular level, providing evidence that bipolar disorder is reliably associated with dysregulation of glial–neuronal interactions. Among these glial elements are microglia – the brain’s primary immune elements, which appear to be overactive in the context of bipolarity. Multiple studies now indicate that inflammation is also increased in the periphery of the body in both the depressive and manic phases of the illness, with at least some return to normality in the euthymic state. These findings are consistent with changes in the hypothalamic–pituitary–adrenal axis, which are known to drive inflammatory activation. In summary, the very fact that no single gene, pathway, or brain abnormality is likely to ever account for the condition is itself an extremely important first step in better articulating an integrated perspective on both its ontological status and pathogenesis. Whether this perspective will translate into the discovery of innumerable more homogeneous forms of bipolarity is one of the great questions facing the field and one that is likely to have profound treatment implications, given that fact that such a discovery would greatly increase our ability to individualize – and by extension, enhance – treatment.","URL":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4142322/","DOI":"10.3389/fpsyt.2014.00098","ISSN":"1664-0640","note":"PMID: 25202283\nPMCID: PMC4142322","journalAbbreviation":"Front Psychiatry","author":[{"family":"Maletic","given":"Vladimir"},{"family":"Raison","given":"Charles"}],"issued":{"date-parts":[["2014",8,25]]},"accessed":{"date-parts":[["2019",11,23]]}}}],"schema":"https://github.com/citation-style-language/schema/raw/master/csl-citation.json"} (Maletic & Raison, 2014). A wide area of interest in bipolar research is testing neurotransmitters, the chemical changes associated with it, positions, and their impact. This is understood that in an individual with bipolar disorder, certain molecules are somehow uneven in the brain relative to a person without the disease. For instance, it is observed that the blood and spinal fluid of bipolar individuals have a low level of GABA, while oxytocin- active neurons are seen to be present at elevated levels ADDIN ZOTERO_ITEM CSL_CITATION {"citationID":"KGHZMq7Z","properties":{"formattedCitation":"(Maletic & Raison, 2014)","plainCitation":"(Maletic & Raison, 2014)","noteIndex":0},"citationItems":[{"id":332,"uris":["http://zotero.org/users/local/CKNkWnK9/items/9UGR4WVK"],"uri":["http://zotero.org/users/local/CKNkWnK9/items/9UGR4WVK"],"itemData":{"id":332,"type":"article-journal","title":"Integrated Neurobiology of Bipolar Disorder","container-title":"Frontiers in Psychiatry","volume":"5","source":"PubMed Central","abstract":"From a neurobiological perspective there is no such thing as bipolar disorder. Rather, it is almost certainly the case that many somewhat similar, but subtly different, pathological conditions produce a disease state that we currently diagnose as bipolarity. This heterogeneity – reflected in the lack of synergy between our current diagnostic schema and our rapidly advancing scientific understanding of the condition – limits attempts to articulate an integrated perspective on bipolar disorder. However, despite these challenges, scientific findings in recent years are beginning to offer a provisional “unified field theory” of the disease. This theory sees bipolar disorder as a suite of related neurodevelopmental conditions with interconnected functional abnormalities that often appear early in life and worsen over time. In addition to accelerated loss of volume in brain areas known to be essential for mood regulation and cognitive function, consistent findings have emerged at a cellular level, providing evidence that bipolar disorder is reliably associated with dysregulation of glial–neuronal interactions. Among these glial elements are microglia – the brain’s primary immune elements, which appear to be overactive in the context of bipolarity. Multiple studies now indicate that inflammation is also increased in the periphery of the body in both the depressive and manic phases of the illness, with at least some return to normality in the euthymic state. These findings are consistent with changes in the hypothalamic–pituitary–adrenal axis, which are known to drive inflammatory activation. In summary, the very fact that no single gene, pathway, or brain abnormality is likely to ever account for the condition is itself an extremely important first step in better articulating an integrated perspective on both its ontological status and pathogenesis. Whether this perspective will translate into the discovery of innumerable more homogeneous forms of bipolarity is one of the great questions facing the field and one that is likely to have profound treatment implications, given that fact that such a discovery would greatly increase our ability to individualize – and by extension, enhance – treatment.","URL":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4142322/","DOI":"10.3389/fpsyt.2014.00098","ISSN":"1664-0640","note":"PMID: 25202283\nPMCID: PMC4142322","journalAbbreviation":"Front Psychiatry","author":[{"family":"Maletic","given":"Vladimir"},{"family":"Raison","given":"Charles"}],"issued":{"date-parts":[["2014",8,25]]},"accessed":{"date-parts":[["2019",11,23]]}}}],"schema":"https://github.com/citation-style-language/schema/raw/master/csl-citation.json"} (Maletic & Raison, 2014). These are usually structural abnormalities. However, these findings do not contribute to understanding the overall brain functioning in disorder. Some of the changes observed in the bipolar brain are the reduction in size and the Neuroprogression ADDIN ZOTERO_ITEM CSL_CITATION {"citationID":"McdKOZRP","properties":{"formattedCitation":"(Wollenhaupt-Aguiar et al., 2016)","plainCitation":"(Wollenhaupt-Aguiar et al., 2016)","noteIndex":0},"citationItems":[{"id":337,"uris":["http://zotero.org/users/local/CKNkWnK9/items/4EBQ4XQJ"],"uri":["http://zotero.org/users/local/CKNkWnK9/items/4EBQ4XQJ"],"itemData":{"id":337,"type":"article-journal","title":"Reduced Neurite Density in Neuronal Cell Cultures Exposed to Serum of Patients with Bipolar Disorder","container-title":"The International Journal of Neuropsychopharmacology","source":"PubMed","abstract":"BACKGROUND: Increased inflammatory markers and oxidative stress have been reported in serum among patients with bipolar disorder (BD). The aim of this study is to assess whether biochemical changes in the serum of patients induces neurotoxicity in neuronal cell cultures.\nMETHODS: We challenged the retinoic acid-differentiated human neuroblastoma SH-SY5Y cells with the serum of BD patients at early and late stages of illness and assessed neurite density and cell viability as neurotoxic endpoints.\nRESULTS: Decreased neurite density was found in neurons treated with the serum of patients, mostly patients at late stages of illness. Also, neurons challenged with the serum of late-stage patients showed a significant decrease in cell viability.\nCONCLUSIONS: Our findings showed that the serum of patients with bipolar disorder induced a decrease in neurite density and cell viability in neuronal cultures.","DOI":"10.1093/ijnp/pyw051","ISSN":"1469-5111","note":"PMID: 27207915\nPMCID: PMC5091826","journalAbbreviation":"Int. J. Neuropsychopharmacol.","language":"eng","author":[{"family":"Wollenhaupt-Aguiar","given":"Bianca"},{"family":"Pfaffenseller","given":"Bianca"},{"family":"Chagas","given":"Vinicius de Saraiva"},{"family":"Castro","given":"Mauro A. A."},{"family":"Passos","given":"Ives Cavalcante"},{"family":"Kauer-Sant'Anna","given":"Márcia"},{"family":"Kapczinski","given":"Flavio"},{"family":"Klamt","given":"Fábio"}],"issued":{"date-parts":[["2016",5,31]]}}}],"schema":"https://github.com/citation-style-language/schema/raw/master/csl-citation.json"} (Wollenhaupt-Aguiar et al., 2016). Neuroprogression is characterized by the alteration of normal brain functioning, which results in a pathological condition associated with the learning, memory, and repair system. Such changes are mainly the functional abnormalities associated with a disease.
Symptoms
According to the DMS-IV TR, Symptoms of bipolar disorder depend on the type of the bipolar episode. Throughout the manic state, individual experiences the feelings of extreme vitality, inventiveness and ecstasy. Depression phase possibly involves feelings of prickliness, remorse, random temper blows, and agitation. Symptoms involved in the mixed episode are depression shared with feelings of restlessness, prickliness, lack of sleep, anxiety and extreme flow of thoughts ADDIN ZOTERO_ITEM CSL_CITATION {"citationID":"W8bAddjf","properties":{"formattedCitation":"(First, France, & Pincus, 2004)","plainCitation":"(First, France, & Pincus, 2004)","noteIndex":0},"citationItems":[{"id":340,"uris":["http://zotero.org/users/local/CKNkWnK9/items/3EZF57SB"],"uri":["http://zotero.org/users/local/CKNkWnK9/items/3EZF57SB"],"itemData":{"id":340,"type":"book","title":"DSM-IV-TR guidebook","collection-title":"DSM-IV-TR guidebook","publisher":"American Psychiatric Publishing, Inc.","publisher-place":"Arlington, VA, US","number-of-pages":"xi, 501","source":"APA PsycNET","event-place":"Arlington, VA, US","abstract":"This guidebook contains just about everything we know about psychiatric diagnosis. The information was derived from our collective experience with patients, supervision, consulting with colleagues, working on DSM-IV and DSM-IV-TR, developing the Structured Clinical Interview for DSM-IV-TR (SCID), and fielding interesting questions from audiences at talks and workshops. DSM-IV-TR is the product of more than 1,000 individuals. Although we edited the final version of DSM-IV-TR and must bear considerable responsibility for its content, we were attempting to find a voice that best captured the consensus of the entire field. This book provides us with an opportunity to make a much more personal statement that reflects our own perspectives. The views expressed here are our own and do not necessarily reflect those of the DSM-IV Task Force or the American Psychiatric Association. Some of the material included in this guidebook is based on our previous publications, which are listed in the bibliography at the end of this book. This Guidebook was revised and updated in 2004 to correspond with the DSM-IV Text Revision (DSM-IV-TR), which was published in 2000. The main objectives of the text revision were several fold: 1) to review the DSM-IV text to ensure that all of the information is still up-to-date and make changes to reflect information newly available since the close of the initial DSM-IV literature review process; 2) to correct errors and ambiguities that have been identified in DSM-IV; and 3) to update the diagnostic codes to reflect changes in the ICD coding system officially used by the U.S. government for health care reporting. Most of the changes that were intended to update the DSM-IV-TR text had little bearing on the contents of this Guidebook. However, changes that served to correct errors and ambiguities in the DSM-IV diagnostic criteria, subtypes, and specifiers are reflected throughout this Guidebook. Similarly, the diagnostic codes included in this Guidebook have been updated to reflect all coding changes effective as of October 1, 2003. (PsycINFO Database Record (c) 2016 APA, all rights reserved)","ISBN":"978-1-58562-068-5","author":[{"family":"First","given":"Michael B."},{"family":"France","given":"Allen"},{"family":"Pincus","given":"Harold Alan"}],"issued":{"date-parts":[["2004"]]}}}],"schema":"https://github.com/citation-style-language/schema/raw/master/csl-citation.json"} (First, France, & Pincus, 2004).
References
ADDIN ZOTERO_BIBL {"uncited":[],"omitted":[],"custom":[]} CSL_BIBLIOGRAPHY First, M. B., France, A., & Pincus, H. A. (2004). DSM-IV-TR guidebook. Arlington, VA, US: American Psychiatric Publishing, Inc.
Gulf Bend MHMR Center. (n.d.). Retrieved November 23, 2019, from https://www.gulfbend.org/poc/view_doc.php?type=doc&id=11204&cn=5
Maletic, V., & Raison, C. (2014). Integrated Neurobiology of Bipolar Disorder. Frontiers in Psychiatry, 5. https://doi.org/10.3389/fpsyt.2014.00098
Wollenhaupt-Aguiar, B., Pfaffenseller, B., Chagas, V. de S., Castro, M. A. A., Passos, I. C., Kauer-Sant’Anna, M., … Klamt, F. (2016). Reduced Neurite Density in Neuronal Cell Cultures Exposed to Serum of Patients with Bipolar Disorder. The International Journal of Neuropsychopharmacology. https://doi.org/10.1093/ijnp/pyw051
