Build a Better DSM: Support PDF

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Essay supporting inclusion biological pathophysiology in the diagnosis of disorders in the DSM....

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Andrew Wei Dr. Treadway PSYC 210 31 March 2020 Prompt 1: Support Since its creation in 1952, the Diagnostic and Statistical Manual for Mental Disorders (DSM) has not contained empirically tested information about the neurobiology of mental disorders. Rather it only contains symptomatic information based on what clinicians have collectively observed about the disorders. In the past, researchers did not have a strong understanding of the pathophysiology of mental disorders to include in the DSM (Jabr, 2013). However, this is no longer true for the modern DSM-5, as the field now has achieved a great degree of knowledge about the neurobiology of many of mental disorders (abr, 2013). Some topics that have seen great advances include understanding of individual genes, altered brain regions, neurotransmitter and hormone functioning, immune system abnormalities, and as well as other neurobiological risk factors that contribute to mental disorders. Scientists now understand much more about the specific neurological hardware that controls emotion, memory, and attention in mental disorders (Jabr, 2013). However, the DSM has failed to keep up with everything the field now knows. It has maintained an antiquated, purely symptomatic approach to classifying and diagnosing mental disorders. While understanding the phenomenological symptoms is incredibly important for identifying and diagnosing mental disorders, symptoms are only half of the battle. The DSM serves the dual purpose of guiding the field of Psychology as a model of scientific truth, as well as providing a clinical model for diagnosing and treating patients. However, by only addressing the symptoms of these disorders, the DSM is falling short

on both counts. Through including more information on the neurobiological effects and causes of disorders into its diagnostic framework, the DSM can better serve as foundation for progress in scientific research, improve diagnostic methods by distinguishing subtypes and distinctions between disorders, and provide better treatment options for different individuals. Recent literature on the neurobiology of Depression has revealed the immune system’s prevalence in the pathophysiology of psychiatric disorders. Particularly in Major Depressive Disorder (MDD), the “Cytokine Hypothesis of Depression” proposes that pro-inflammatory cytokines serve as a central mediator of the behavioral, neuroendocrine, and neurochemical features of depressive disorders (Schiepers, 2005). Evidence of this hypothesis comes from studies revealing that administration of pro-inflammatory cytokines, such as IFN-alpha, has been associated with the behavioral effect of “sickness behavior,” which encapsulates many of the key symptoms of Depression, including anhedonia, dysphoria, lost appetite, fatigue, sleep changes, appetite changes, and decreased appetite (Schiepers, 2005). The introduction of cytokines has been associated with decreased inhibition of the HPA axis for stress, reduction in gray matter in multiple areas of the brain, and deficiencies in monoamine transmission, especially serotonin and dopamine. These features are key factors in the pathophysiology of Depression, and it is clear that they are related to increased cytokine levels (Schiepers, 2005). In addition, higher levels of inflammation have been associated with depressed patients that are resistant to traditional methods of psychotherapy and antidepressant medications. This all indicates that incorporating inflammatory biomarkers into the DSM measure of Depressive Disorders can help diagnose an “Inflammatory Subtype” of Depression (Schiepers, 2005). In regards to medication treatment, although there hasn’t been enough research to establish antiinflammatories as effective anti-depressant drugs, it us not unreasonable to assume, based on the

evidence of inflammation’s link to Depression, that with further research, anti-inflammatories can offer strong anti-depressant effects. Ideally, clinicians can use inflammatory biomarkers to know when to prescribe these anti-inflammatory drugs. This neurobiological information provides a powerful tool to identify treatment-resistant patients and offer novel treatments of anti-inflammatory medications (Strawbridge, 2015). If the DSM incorporates this knowledge into its diagnostic criteria, it can use high inflammatory bio markers to identify high risk, treatment-resistant depressive patients and provide them with the treatment they need.

Furthermore, existing literature also offers measurable neurobiological differences between Unipolar Depression and Bipolar Disorder (Chen, 2019). When looking at a patient in a depressive episode, it can be difficult to distinguish between the depressive symptoms of Unipolar Depression vs Bipolar Disorder (LeBano, 2013). If a patient is expressing their first depressive episode, it is often impossible to distinguish between the two, as the depressive phase of Bipolar Disorder can manifest identically to a depressive episode in Unipolar Depression (LeBano, 2013). As a result, Bipolar Disorder is frequently misdiagnosed as MDD (LeBano, 2013). Tragically, the antidepressant treatment commonly prescribed for MDD can increase suicide risk for Bipolar Disorder (LeBano, 2013). However, research has revealed multiple important biomarkers that can help distinguish between the two. As previously discussed, Depression is associated with higher levels of inflammation and inflammatory cytokines. In fact, Bipolar Disorder is also associated with higher levels of inflammation and cytokines, but to a significantly greater degree than Unipolar Depression. In addition, although both MDD and Bipolar Disorder are associated with Gray Matter (GM) reductions in the brain, particularly in the frontal cortex, the GM reduction is much greater and more pervasive in Bipolar Disorder than

in Unipolar Depression (Chen, 2019). Using fMRI, it is possible to see the degree of GM reduction in key brain areas like the frontal cortex and distinguish between Unipolar Depression and Bipolar Disorder (Chen, 2019). By including these markers for degree of inflammation and GM in the DSM, clinicians can have a neurobiological criterion available to properly diagnose between MDD and Bipolar Disorders, thus allowing them to properly treat the patient. By including this type of neurobiological information in the DSM, the DSM can much more effectively serve as a catalogue of scientific information. It allows the field of Clinical Psychology to further progress as there is a central consensus of the neurobiology of mental disorders that researchers can build upon. If this key information was included in the DSM, it would further legitimize and progress the development of novel treatments like the antiinflammatory drugs for cytokine-induced Depression. Overall, the field of Clinical Psychology has greatly evolved to understand the neurobiology of mental disorders to a much greater degree. For example, clinicians can use biomarkers of increased inflammation and decreased GM in the frontal cortex to more effectively identify treatment-resistant Depression and Bipolar Disorder, respectively. However, our current DSM does not reflect this knowledge, and still only focuses on the symptoms of these disorders. Due to this lack of information, clinicians are limiting their diagnostic and treatment tools for patients. Therefore, this lack of neurobiological information is preventing numerous patients from receiving the best treatment possible. Ultimately, to ensure that patients with mental disorder are accessing the best treatment based on modern science, the primary diagnostic mechanism of the DSM should utilize modern science.

Chen, M.-H., Chang, W.-C., Hsu, J.-W., Huang, K.-L., Tu, P.-C., Su, T.-P., … Bai, Y.-M. (2019). Correlation of proinflammatory cytokines levels and reduced gray matter volumes between patients with bipolar disorder and unipolar depression. Journal of Affective Disorders, 245, 8–15. doi: 10.1016/j.jad.2018.10.106 Jabr, F. (2013, May 1). New DSM-5 Ignores Biology of Mental Illness. Retrieved from https://www.scientificamerican.com/article/new-dsm5-ignores-biology-mental-illness/ LeBano, L. (2013, July 8). How to Differentiate Bipolar Disorder from Unipolar Depression. Retrieved from https://www.psychcongress.com/article/how-differentiate-bipolar-disorderunipolar-depression Schiepers, O. J., Wichers, M. C., & Maes, M. (2005). Cytokines and major depression. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 29(2), 201–217. doi: 10.1016/j.pnpbp.2004.11.003 Strawbridge, R., Arnone, D., Danese, A., Papadopoulos, A., Vives, A. H., & Cleare, A. (2015). Inflammation and clinical response to treatment in depression: A meta-analysis. European Neuropsychopharmacology, 25(10), 1532–1543. doi: 10.1016/j.euroneuro.2015.06.007...