What is Schizophrenia?
Topic: Schizophrenia
Respond to two classmates
Classmate 1:
The dopamine hypothesis of schizophrenia assumes that overactive dopamine D2 receptor neurotransmission in the cortex and limbic brain regions contributes to the positive symptoms of schizophrenia (Howes, 2015). In contrast, the disease’s negative and cognitive symptoms can be attributed to dopamine in the prefrontal cortex D1 receptors that have poor neurotransmission.
The dopamine hypothesis of schizophrenia has always been one of the most enduring ideas in psychiatry (Yang, 2017). Initially, the focus was on high dopamine pain in the etiology of schizophrenia but later conceptualized to designate subcortical high dopamine pain and prefrontal low dopamine pain (Yang, 2017). However, these hypotheses are too narrowly focused on dopamine itself, a mixture of psychosis and schizophrenia, and predate the development of genetics, molecular biology, and imaging studies of schizophrenia. Since the second edition, there have been more than 6,700 articles on dopamine and schizophrenia. Expert selectively reviewed these data to outline 5 critical new evidence: neurochemical imaging studies, genetic evidence, the discovery of environmental risk factors, extended phenotypic studies, and animal studies (Howes, 2015). Expert combined this evidence into a new dopamine hypothesis for schizophrenia-version III: the ultimate universal approach (Yang, 2017). This hypothesis aims to provide a framework that links risk factors, including pregnancy and obstetric complications, stress and trauma, drug use, and genes, to enhance presynaptic striatal dopaminergic function to achieve a broad goal (Howes, 2015). It explains how a series of complex pathologies, positron emission tomography, magnetic resonance imaging, and other discoveries such as frontotemporal structural and functional abnormalities and cognitive impairment can aggregate neurochemicals and cause psychosis through abnormalities (Howes, 2015). Lead to the diagnosis of schizophrenia, and this hypothesis has important implications for treatment methods. Current treatments are working downstream of severe neurotransmitter abnormalities. Future drug development and research on etiology should focus on identifying and manipulating upstream factors that converge to the dopaminergic funnel point (Yang, 2017).
References:
Howes, O. D., & Kapur, S. (2015). The dopamine hypothesis of schizophrenia: version III–the final common pathway. Schizophrenia bulletin, 35(3), 549–562. https://doi.org/10.1093/schbul/sbp006 (Links to an external site.)
Yang, A. C., & Tsai, S. J. (2017). New Targets for Schizophrenia Treatment beyond the Dopamine Hypothesis. International journal of molecular sciences, 18(8), 1689. https://doi.org/10.3390/ijms18081689
Classmate 2:
Schizophrenia
Schizophrenia is one of the more common and severe mental disorders (Howes et al., 2015). The onset of Schizophrenia typically happens by early twenties for men, and shortly after for women (Howes et al., 2015). Schizophrenia symptoms usually are hallucinations, social withdrawal, and cognitive impairments (Howes et al., 2015). Typically Schizophrenia treatment involves the use of antipsychotic drugs (Howes et al., 2015). Although initially, the Dopamin hypothesis was developed through post-mortem studies, more recently, studies have been done in vivo (Howes et al., 2015).
Dopamine Hypothesis of Schizophrenia
They were initially discovered in studies that administered amphetamines that resulted in psychotic episodes similar to that of Schizophrenia (Howes et al., 2015). Dopamine studies in the 1970s further showed that an abnormality in dopamine receptors was involved in the development of Schizophrenia (Howes et al., 2015). As a result of these studies, the treatment of Schizophrenia relies on Dopamine antagonists (Kim et al., 2017). In about a third of the patients, they do not respond to antipsychotics as a treatment even though they have abnormalities in their dopamine receptors (Howes et al., 2015). Some psychologists believe that patients whose negative symptoms (social withdrawal or cognitive impairments) are not treated by the dopamine antagonists, which would explain why some patients that line of treatment does not work (Kim et al., 2017).
Kim et al. (2017) suggest that new scientific findings should be included in treatment consideration. Treatment choices should also include glutamate and GABA systems in the decision making process. Kim et al. (2017) propose that a bio-psychosocial-behavioral model be developed for the treatment of Schizophrenia and included consideration of non-dopaminergic systems. This model should focus on prevention, reducing stigma, and should be personalized to the patient versus the dopamine hypothesis that only prescribes dopamine antagonists even if it doesn’t see success Kim et al., 2017)
Reference
Howes, O., McCutcheon, R., & Stone, J. (2015). Glutamate and dopamine in schizophrenia: An update for the 21st century. Journal of Psychopharmacology, 29(2), 97.
Kim, Y., Choi, J., & Park, S. (2017). A Novel Bio-Psychosocial-Behavioral Treatment Model in Schizophrenia. International Journal of Molecular Sciences, 18(4), 734. https://doi.org/10.3390/ijms18040734 (Links to an external site.)
Topic: Stress
There is significant evidence that stress causes a number of changes in the brain and body. The changes are significantly different between acute and chronic stress. Discuss the difference between acute and chronic stress, and discuss whether or not either of these conditions are beneficial in humans. Respond to at least two of your classmates’ posts no later than Monday, Day 7.
Respond to classmate 1:
Acute stressis short-term stress. An acute stress response occurs when symptoms appear due to
a particularly stressful event. The term “acute” means that symptoms develop quickly, but
usually do not last long. These events are usually severe, and an acute stress response usually
occurs after an unexpected life crisis. For example, this could be a severe accident, sudden
bereavement, or other traumatic events (Meiser, 2017). Road traffic accidents cause many
casualties each year, and the person may be directly or indirectly affected by such abnormal
stress events. Sexual assault or domestic violence can also cause acute stress reactions
Chronic stressis long-term stress. Chronic stress is a response to long-term emotional stress, during which the individual feels that he cannot control or cannot control at all. When stress starts to interfere with the individual ability to maintain a healthy life for a long time, it becomes even more dangerous (Mental health diseases and conditions, 2019). The longer the stress lasts, the more harmful it is to the individual body and mind. For example, the person may feel tired, unable to concentrate, or irritable for no reason. However, chronic stress can also cause visible wear. Some pressure is good for you. Too little stress can cause boredom and depression, while too much stress can cause anxiety and ill health. However, the right amount of acute stress can regulate the brain and improve performance and health.References:
Meiser-Stedman, R., McKinnon, A., Dixon, C., Boyle, A., Smith, P., & Dalgleish, T. (2017). Acute stress disorder and the transition to posttraumatic stress disorder in children and adolescents: Prevalence, course, prognosis, diagnostic suitability, and risk markers. Depression and anxiety, 34(4), 348–355. https://doi.org/10.1002/da.22602
Mental health diseases and conditions – chronic variable stress; reports from university of cincinnati advance knowledge in chronic variable stress (lasting impact of chronic adolescent stress and glucocorticoid receptor selective modulation in male and female rats). (2019, Dec 16). Mental Health Weekly Digest Retrieved from https://search-proquest-com.proxy-library.ashford.edu/docview/2328021680?accountid=32521
Respond to classmate 2:
The dopamine theory on Schizophrenia runs on the basis that the disorder is caused by the neurotransmitters related to dopamine. The fire too often or transmit too many messages, creating an excess of dopamine and its activity. It is one of the most supported biological theories, and there have been many studies and lots of research focused on it. Research relating to Parkinson’s patients was one of the most significant breakthroughs (MacDonald & Schulz, 2009). Patients diagnosed with Schizophrenia who were treated with antipsychotics would sometimes develop Parkinson’s like uncontrollable tremors and movements from the medication. It was then also noticed that Parkinson patients treated with a drug high in dopamine were shown to experience some psychosis schizophrenia symptoms after copious amounts of the drug. The drug, known as L-dopa, rose dopamine levels so high that it pushed patients into a psychosis (Martin Brüne, 2005). So, the drug that eliminated the psychosis but caused tremors was one that limited dopamine and the one that limited shaking but caused psychosis was one that stimulated extra dopamine. It thus suggests the secure connection between dopamine and Schizophrenia.
Other studies surrounding amphetamines also support this theory. These are drugs that stimulate the central nervous system by adding dopamine to the brain. When high levels are taken, amphetamine psychosis can occur (MacDonald & Schulz, 2009). This result is very similar to the psychosis and symptoms of Schizophrenia, thus suggesting a dopamine link. Further studies of the brain of people with Schizophrenia after death shows that some do have more significant amounts of dopamine receptors than non-schizophrenic people (Martin Brüne, 2005). However, this is not concrete evidence, as the medications they were on throughout their lives could have had an influence. Some of the most concrete evidence is simply in the fact that patients have shown improvement in taking the medications that act on dopamine levels and receptors (Leigh et al., 2005). Although the dopamine theory doesn’t account for all reasoning behind Schizophrenia, it most likely is a factor and has a definite role in the big picture.
Reference
Leigh Harrington, Richard Siegert & John McClure (2005) Theory of mind in schizophrenia: A critical review, Cognitive Neuropsychiatry, 10:4, 249-286, DOI: 10.1080/13546800444000056Links to an external site.
MacDonald, A. W., & Schulz, S. C. (2009). What we know: findings that every theory of schizophrenia should explain. Schizophrenia bulletin, 35(3), 493–508. https://doi.org/10.1093/schbul/sbp017Links to an external site.
Martin Brüne, M.D., “Theory of Mind” in Schizophrenia: A Review of the Literature, Schizophrenia Bulletin, Volume 31, Issue 1, January 2005, Pages 21–42, https://doi.org/10.1093/schbul/sbi002Links to an external site.
