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| ====== History ====== | ====== History ====== | ||
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| During the age of enlightenment (18th and 19th century) depression was thought be inheritable and untreatable weakness in temperament. Thus, depressed individuals were locked up in mental institutions and were subject to homelessness and poverty. <sup>[14]</sup> | During the age of enlightenment (18th and 19th century) depression was thought be inheritable and untreatable weakness in temperament. Thus, depressed individuals were locked up in mental institutions and were subject to homelessness and poverty. <sup>[14]</sup> | ||
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| ====== Types and Symptoms ====== | ====== Types and Symptoms ====== | ||
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| **Cyclothymic disorder**: mild, chronic form of Bipolar disorder. A person with cyclothymic disorder experiences both hypomanic episodes and milder symptoms of major depressive disorder for most days for at least two years, with the symptoms being absent for no more than two months at once during that period <sup>[6]</sup>. | **Cyclothymic disorder**: mild, chronic form of Bipolar disorder. A person with cyclothymic disorder experiences both hypomanic episodes and milder symptoms of major depressive disorder for most days for at least two years, with the symptoms being absent for no more than two months at once during that period <sup>[6]</sup>. | ||
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| ====== Risk Factors ====== | ====== Risk Factors ====== | ||
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| * Certain prescription drugs | * Certain prescription drugs | ||
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| ====== Pathophysiology ====== | ====== Pathophysiology ====== | ||
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| Abnormalities in the cortisol response to stress may underlie depression. The black arrows in Figure 2 show that in response to stress, which is perceived by the brain cortex and the amygdala and transmitted to the hypothalamus, corticotropin-releasing hormone (CRH) is released. This induces the anterior pituitary gland to secrete corticotropin into the bloodstream. Corticotropin stimulates the adrenal cortexes to secrete the glucocorticoid hormone cortisol. The red line in Figure 2 shows that cortisol, in turn, induces feedback inhibition in the hypothalamus and the pituitary, suppressing the production of CRH and corticotropin, respectively. Activation of hippocampal glucocorticoid receptors by cortisol normally leads to feedback inhibition of the HPA axis. In depressed patients this feedback is disrupted thus leading to the hyperactivation of HPA. A molecular basis for the diminished hippocampal response to cortisol is a decreased number of glucocorticoid receptors. The number of receptors is regulated by genes, monoamines and early childhood experiences. Findings in patients with depression that support the hypothalamic–pituitary–cortisol hypothesis include the following: cortisol levels are sometimes increased in severe depression, the size of the anterior pituitary and adrenal cortex is increased, and CRH levels in the cerebrospinal fluid and CRH expression in the limbic brain regions are increased. Furthermore, hippocampal size and the numbers of neurons and glia are decreased, possibly reflecting reduced neurogenesis due to elevated cortisol levels or due to reduced brain-derived neurotrophic factor. <sup>[7]</sup> | Abnormalities in the cortisol response to stress may underlie depression. The black arrows in Figure 2 show that in response to stress, which is perceived by the brain cortex and the amygdala and transmitted to the hypothalamus, corticotropin-releasing hormone (CRH) is released. This induces the anterior pituitary gland to secrete corticotropin into the bloodstream. Corticotropin stimulates the adrenal cortexes to secrete the glucocorticoid hormone cortisol. The red line in Figure 2 shows that cortisol, in turn, induces feedback inhibition in the hypothalamus and the pituitary, suppressing the production of CRH and corticotropin, respectively. Activation of hippocampal glucocorticoid receptors by cortisol normally leads to feedback inhibition of the HPA axis. In depressed patients this feedback is disrupted thus leading to the hyperactivation of HPA. A molecular basis for the diminished hippocampal response to cortisol is a decreased number of glucocorticoid receptors. The number of receptors is regulated by genes, monoamines and early childhood experiences. Findings in patients with depression that support the hypothalamic–pituitary–cortisol hypothesis include the following: cortisol levels are sometimes increased in severe depression, the size of the anterior pituitary and adrenal cortex is increased, and CRH levels in the cerebrospinal fluid and CRH expression in the limbic brain regions are increased. Furthermore, hippocampal size and the numbers of neurons and glia are decreased, possibly reflecting reduced neurogenesis due to elevated cortisol levels or due to reduced brain-derived neurotrophic factor. <sup>[7]</sup> | ||
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| ====== Conclusion ====== | ====== Conclusion ====== | ||
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| Overall, depression is a heterogenous, burdensome disorder that exhibits a highly variable course, an inconsistent response to treatment and an incomplete understanding of the underlying neurobiology. Its onset is gradual and it can manifest itself not only in psychological symptoms but physical symptoms as well. Future initiatives are focusing on novel treatments that can start to take effect quicker than the 4-5 weeks required for antidepressants. Research is beginning to look at the use of theta-burst stimulation which involves delivering magnetic pulses to the brain. It is a fast acting, simple, non invasive form of treatment. These magnetic pulses stimulate electric current in the brain and the hope is that repeated treatment can capitalize on the brain's neuroplasticity by changing the way in which the brain's neurons fire. However, this is a very new field and much more research needs to be done surrounding the efficacy and safety of this treatment. | Overall, depression is a heterogenous, burdensome disorder that exhibits a highly variable course, an inconsistent response to treatment and an incomplete understanding of the underlying neurobiology. Its onset is gradual and it can manifest itself not only in psychological symptoms but physical symptoms as well. Future initiatives are focusing on novel treatments that can start to take effect quicker than the 4-5 weeks required for antidepressants. Research is beginning to look at the use of theta-burst stimulation which involves delivering magnetic pulses to the brain. It is a fast acting, simple, non invasive form of treatment. These magnetic pulses stimulate electric current in the brain and the hope is that repeated treatment can capitalize on the brain's neuroplasticity by changing the way in which the brain's neurons fire. However, this is a very new field and much more research needs to be done surrounding the efficacy and safety of this treatment. | ||
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| ====== References ====== | ====== References ====== | ||
