Physiology of Manic Depression

Physiology of Manic DepressionBre WilsonManic Depression, or more commonly cognize as bipolar disorder, is a disorder that causes the patient affected to bike through periods of imprint and dementia (NIMH n.d.). There are three ordinary types of Bipolar throw out of kilter and then a fourth category for those who do not fall at bottom any of the previous categories. Bipolar I Disorder is defined by frenetic contingencys that last at least(prenominal) 7 days and then a depressive episode lasting at least two weeks. Symptoms may be severe enough to explore immediate medical care. Bipolar II Disorder is defined by recurring depressive, and hypo wild episodes, exclusively not to the extent of Bipolar I. Cyclothymic Disorder is defined by numerous periods of hypomania and falloff that lasts longer than two old age in adults, (for one year for children), except the symptoms evinceed do not correspond the within the categories of a open hypomanic episode or a simple depr essive episode. The final category is Other Specified and Unspecified Bipolar and connect Disorders which is defined as bipolar tendencies, and symptoms, that do not meet the requirements within the previous three categories (NIMH n.d.). The true cause of Bipolar Disorder is enigmatical but scientists believe that it could be due to many another(prenominal) environmental and patrimonial factors, as considerably as chemical imbalances within the wizardry- such(prenominal) as GABA, serotonin, dopamine and norepinephrine (Bressert 2016). Some people experience rapid pass of episodes while others experience a prolonged period of time betwixt cycles of episodes. The exact cause behind the rapid cycling is unclear but researchers believe that its due to the consistent misfiring of receptors causing mayhem within the aboriginal Nervous System. These neurotransmitters play a huge role in a persons circadian rhythm, their emotional expression and regulation, their port and how wel l they respond to stress. by and by years of study, Manic Depression is now thought to be a outlet of serotonin, norepinephrine and dopamine imbalance, as well as a GABA defect within the hippocampus (Frey 2007). GABA, a relative of Glutamate, is a primary inhibitory neurotransmitter which means that it mediates other neurotransmitters to prevent over exertion. Glutamate is the near abundant neurotransmitter present within the Central Nervous System. Its hypothesized that erratic misfiring of the Glutamate receptors within the brain could possibly be the cause of GABA fluctuations (Frey 2007). This causes the neurotransmitters that GABA mediates, (norepinephrine, dopamine and serotonin), to fluctuate unpredictably as well causing the mood swings, sleeplessness, depression and self-destructive behavior expressed by patients diagnosed with Manic Depression. Dopamine, which acts on the D receptors in the brain, is the neurotransmitter that regulates a persons feelings of pleasure and emotional reward. Norepinephrine, which acts on alpha and genus Beta adrenergic receptors, is the terminal neurotransmitter of the Sympathetic Nervous System. Norepinephrine is the fight or flight molecule. serotonin, which acts on the 5-HT receptors within the brain, is the neurotransmitter that fosters feelings of happiness and well-being. Modifying the effectiveness, or quantity, of these three neurotransmitters is what leads mania, hypomania, and depression exhibited in patients with Manic Depression.People who are experiencing a manic episode a good deal engage in unfit behaviors, (binge drinking or promiscuity), exhibit restlessness, and experience disruptions in their sleep patterns. Manic episodes can be triggered chemically within the brain, or they can be triggered by external factors such as excessive stress, a change in diet or exercise, excessive caffeine intake, antidepressant medicine, and certain other medicinal drugs as well (Bressert 2016). Dopamine plays a r ole in the behaviors exhibited by patients in manic episodes. Dopamine acts on the D receptors within the brain and cause a person to be emotionally satisfied. When the receptors cannot receive dopamine due to a blockage, or antagonist, emotional satisfaction is dramatically lowered- causing patients to engage is risky behavior to try to fulfill their emotional needs. Rapid firing of norepinephrine receptors cause unpredictable, behavior due to the influence on the sympathetic nauseated dust. Some studies suggest that mania is due to certain circadian cues and asseve footstep that treatment for manic depression be scheduled around a persons circadian rhythm (Roybal et al 2007). Serotonin plays a role in mania because patients surrender decreased binding affinity at 5-HT receptors during a manic episode (Yatham 2010). Serotonin and norepinephrine play a study role in mania but has also been linked to the depressive episodes as well.Depressive episodes almost always follow manic episodes which is most likely the result of neurotransmitter reuptake and are the result of neurotransmitter imbalance within the brain. Many times, manic depression is often misdiagnosed as depression since depressive episodes are easier to diagnose than manic episodes, and thence an antidepressant is prescribed. However, when a patient takes an antidepressant, such as a serotonin reuptake inhibitor, it doesnt allow the active reuptake of serotonin which often leads to a manic episode because of the reduced binding (Yatham 2010). In stock with manic episodes, brain serotonin 5-HT receptor binding is increased during bipolar depressive episodes. Treating manic depression is often very complex and combines a edge of finding just the right regime of medication, as well as psychotherapy.Although manic depression is a life-long illness that cannot be totally eradicated, many patients can lead a semi-normal, productive life if properly medicated. distinctive treatments for bipolar dis order include psychotherapy, mood stabilizers, antipsychotics, and some Selective Serotonin Reuptake Inhibitors (NIMH n.d.). In some cases, doctors will prescribe a medication to invade the depression, a medication to combat the mania, and then medication to combat any side effects caused by the other medications. Patients who exhibit a higher rate of serotonin 5-HT binding prior to starting medication had a higher chance of recurring episodes, even while fetching medication, than did those who had a lower rate of serotonin 5-HT binding prior to medication (Parsey 2013). Lithium was a drug that works within the nervous system to strengthen the neural connections between cells to increase cell signaling therefore limiting the frequency and intensity of manic-depressive episodes. Lithium was anticipated to have success rates as high as 70%-80% but studies now indicate that Lithium really has a success rate of approximately 40% and comes with a plethora of side effects (Surgeon usua l Report for affable Health). Modafinil is an alpha-adrenergic agonist and directly stimulated the receptors within the brain (modafinil.com n.d.). The reuptake of noradrenaline by the noradrenergic is decreased and increase excitatory glutamatergic transmittance is increased. This decreases GABAergic transmission, resulting in the elimination of GABA receptor signaling which could combat symptoms of bipolar depression by limiting the abundance of GABA receptor misfiring (modafinil.com n.d.). Studies argue a significant improvement in depressive symptoms in the patients who received the data-based drug (Modafinil) by the second week with maintained improvement passim the remainder of the experiment (Frye 2007). The drug did not seem to affect mania however, because during the experimental period, there was no significant difference between the matter of mania or in hospitalizations due to mania (one per group) (Frye 2007).Works CitedBressert, S. (2016). Causes of Bipolar Disord er. Psych Central. Frey B. N., Andreazza A. C., Nery F. G., Martins M. R., Quevedo J., Soares J. C., Kapczinski F. (2007). The role of hippocampus in the pathophysiology of bipolar disorder. Behavioral Pharmacology, 18(5-6)419-30Frye, M. A., Grunze, H., Suppes, T., Mcelroy, S. L., Keck, P. E., Walden, J., . . . Post, R. M. (2007). A Placebo-Controlled valuation of Adjunctive Modafinil in the discussion of Bipolar Depression. American Journal of Psychiatry, 164(8), 1242-1249.Modafinil (Provigil). (n.d.). Retrieved edge 29, 2017, from https//www.modafinil.com/National Institute of Mental Health. (n.d.). Retrieved March 28, 2017, from https//www.nimh.nih.gov/health/topics/bipolar-disorder/index.shtmlpart_145402Parsey RV, Olvet DM, Oquendo MA, Huang YY, Ogden RT, Mann JJ. (2013). Higher 5-HT(1A) sense organ Binding Potential During a Major Depressive Episode Predicts Poor Treatment Response Preliminary Data from a Naturalistic Study. Neuropsychopharmacology.Roybal, K., Theobold D., G raham A., DiNieri, J. A., Russo, S. J., Krishnan, V., Chakravarty, S., Peevey, J., Oehrlein N., Birnbaum S., Vitaterna, M. H., Orsulak, P., Takahashi J. S., Nestler, E. J., Carlezon Jr., W.A., and McClung C. A. (2007). Mania-like behavior induced by disruption of CLOCK. PNAS.Surgeon General Report for Mental Health. (n.d.). Accessed March 28, 2017.Yatham, L. N., Liddle, P F., Erez, J., Kauer-SantAnna, M., Lam, R. W., Imperial M., Sossi, V., and Ruth, T. J. (2010). Brain serotonin-2 receptors in acute mania. The British Journal of Psychiatry, 47-51