NURS 63200 Week 6 Discussion Board

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1. Identify the brain regions and neurotransmitters associated with each symptom of schizophrenia. Explain why someone with depression or bipolar disorder may have psychotic symptoms. Explain the mesolimbic and mesocortical hypotheses symptoms, and the NMDA receptor hypofunction hypothesis. Schizophrenia is characterized by positive symptoms such as delusions and hallucinations, negative symptoms like amotivation, anhedonia, and social withdrawal, and cognitive symptoms that involve deficits in memory and executive functioning. These symptoms are associated with specific neurotransmitters in distinct regions of the brain, particularly dopamine in the mesolimbic pathway and dorsal striatum, serotonin in the cerebral cortex, and glutamate in the prefrontal cortex (McCutcheon et al., 2020). The positive symptoms of schizophrenia are thought to be caused by dopamine hyperactivity at D2 receptors in the mesolimbic pathway, with paranoid delusions and auditory hallucinations specifically linked to excessive excitation in the ventral striatum. Newer theories have emerged, however, suggesting that this hyperactivity is a downstream consequence of glutamate dysfunction in the prefrontal cortex and that enhanced subcortical serotonergic transmission may contribute to positive symptoms (Stahl, 2018). The negative and cognitive symptoms of schizophrenia are believed to arise from hypodopaminergic activity in the frontal lobe, as well as decreased serotonergic action in the prefrontal cortex (Stahl, 2018). An individual with major depressive disorder (MDD) or bipolar disorder (BD) may have psychotic symptoms because these conditions are also characterized by the dysfunction of various neurotransmitters including dopamine, serotonin, glutamate, and GABA. Furthermore, hormonal imbalances and abnormalities in the hypothalamus- pituitary-adrenal axis (HPA) and hypothalamus-pituitary-thyroid axis (HPT) have consistently been found in individuals who have experienced symptoms of psychosis (Rutigliano et al., 2020). The mesolimbic hypothesis of schizophrenia theorizes that positive symptoms are associated with overactivity in the mesolimbic dopamine pathway that innervates numerous areas of the forebrain, including the nucleus accumbens. Conversely, the mesocortical hypothesis posits that negative and cognitive symptoms are related to hypofunction of dopaminergic neurons in the mesocortical pathway that project from the ventral tegmental area to the prefrontal cortex (Guzman, n.d.). The N-methyl-D-aspartate (NMDA) receptor hypofunction hypothesis suggests that hypofunction of NMDA receptors on gamma-aminobutyric acid (GABA) interneurons in the prefrontal cortex triggers overactive glutamate signaling and excessive stimulation of the mesolimbic dopamine pathway, leading to the positive symptoms of schizophrenia (Stahl, 2018). 2. What is the reason that someone who you believe to be schizophrenic is more likely to be diagnosed with schizophreniform or schizoaffective disorder upon their first hospitalization?

Schizophreniform disorder is characterized by the presence of schizophrenia symptoms, including delusions, hallucinations, disorganized thoughts or behaviors, anhedonia, and amotivation, for a duration of at least 1 month but less than 6 months (Drake, 2022). Schizoaffective disorder is also associated with the presence of at least 2 of these symptoms, in addition to symptoms of a major manic or depressive mood episode that persist throughout the active and residual portions of the illness (Wy & Saadabadi, 2022). These similarities in presentation may explain why someone with schizophrenia is more likely to be diagnosed with schizophreniform or schizoaffective disorder upon their first hospitalization. In such instances, the individual is likely experiencing a psychotic episode and may therefore be a poor historian who is incapable of articulating the character or duration of their symptoms. This would warrant further evaluation on the part of the provider to ensure an appropriate diagnosis and treatment course. 3. Why might a 40-year-old female with schizophrenia fare better than a 40-year-old male with schizophrenia? Schizophrenia is associated with several sex differences that include a later age of onset, less severe disease course, and superior treatment response among females with the disorder. Males, on the other hand, tend to experience a greater incidence of disease, increased hospitalizations, more negative symptoms and cognitive deficits, decreased social functioning, and poorer long-term outcomes (Goncalves et al., 2019). Proposed hypotheses for these disparities encompass biological, psychological, and social paradigms, with biological models emphasizing the influence of genetics and hormones like estrogen on the presentation and progression of the disease. Estrogen has specifically been shown to produce neuroprotective effects via increased dopamine sensitivity in the ventral tegmental area, synaptic plasticity promotion, and decreased neuroinflammation, which could explain why a 40-year-old female with schizophrenia might fare better than a 40-year-old male with the same illness (Brand et al., 2021). 4. What is the relationship between a history of trauma and the development of a psychotic disorder? Childhood trauma, which involves exposure to physical, sexual, and emotional abuse or neglect in children under the age of 18, has been implicated as a risk factor for the development of psychotic disorders. More specifically, trauma involving interpersonal violence or intense neglect is associated with a 2- to 3- fold increased risk of a psychotic experience by early adulthood (Croft et al., 2019). The neurobiological mechanisms that underly this correlation are thought to be related to a decreased expression of brain-derived neurotrophic factor (BDNF), which can lead to dysregulation of the HPA axis and subsequent abnormalities in dopaminergic activity. Furthermore, prolonged sympathetic nervous system activation and stress hormone exposure can cause

damage to the amygdala, hippocampus, and orbitofrontal cortex and exacerbate psychotic symptoms, emotional dysregulation, and cognitive impairments (Giotakos, 2020). 5. Are auditory hallucinations in children always reflective of a psychotic disorder? Childhood auditory hallucinations are associated with a prevalence rate of up to 17% in children between the ages of 7 and 12 and 12.4% among adolescents ages 13 to 18. They are typically linked to psychiatric conditions like BD, MDD, anxiety disorders, personality disorders, and post-traumatic stress disorder (PTSD), but can also be a symptom of nervous system disorders (Parkinson’s disease, epilepsy, etc.), tumors or lesions of the temporal lobe, brainstem, or thalamus, or drug and alcohol intoxication (Maijer et al., 2018). The primary neurobiological explanation for auditory hallucinations in psychotic disorders involves dopaminergic hyperactivity in the striatum, however contemporary evidence has elucidated the role of glutamatergic and serotonergic neurotransmitter systems as alternative mediating pathways, which suggests a potentially heterogenous etiology. Additionally, environmental and psychosocial factors such as exposure to psychological trauma and extreme social isolation or withdrawal are known to precipitate auditory hallucinations in the absence of psychotic disorders (Waters et al., 2018). 6. How would you recognize childhood schizophrenia? Childhood-onset schizophrenia (COS) is a rare disorder that is associated with an earlier onset, more severe disease course, and poorer prognosis than adult-onset schizophrenia (AOS). It can be difficult to diagnose because it shares overlapping symptoms with numerous mental disorders (BD, PTSD, anxiety disorders) and medical illnesses (encephalitis, epilepsy, autoimmune and metabolic disorders) and these conditions must be ruled out before a definitive diagnosis of COS can be given. In general, however, COS is characterized by both positive and negative symptoms that begin between the ages of 7 and 13 and disrupt normal development and daily functioning. Individuals with COS typically experience more auditory, visual, and tactile hallucinations than delusions, and can present with neuromotor, receptive, language, and cognitive impairments as well (Adhikari et al., 2022). References Adhikari, S., Ghane, N., Ascencio, M., Abrego, T., & Aedma, K. (2022). Differentiating childhood-onset schizophrenia from other childhood disorders. Cureus, 14 (2), 1-8. https://doi.org/10.7759/cureus.22594

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Brand, B.A., de Boer, J.N., & Sommer, I.E. (2021). Estrogens in schizophrenia: Progress, current challenges, and opportunities. Current Opinion in Psychiatry, 34 (3), 228-237. https://doi.org/10.1097/YCO.0000000000000699 Croft, J., Heron, J., Teufel, C., Cannon, M., Wolke, D., Thompson, A., Houtepen, L., & Zammit, S. (2019). Association with psychotic experiences in early adulthood. Archives of General Psychiatry, 76 (1), 79-86. https://doi.org/10.1001/jamapsychiatry.2018.3155 Drake, M.E. (2022). Schizophreniform disorder: DSM-5 295.40 (F20.81) . Theravive. https://www.theravive.com/therapedia/schizophreniform-disorder-dsm--5-295.40- (f20.81)#:~:text=.%2C%201991).,Diagnostic%20Criteria,above%20may%20also%20be %20present. Giotakos, Q. (2020). Neurobiology of emotional trauma. Psychiatriki, 31 (2), 162-171. https://doi.org/10.3120/EN000000000000-2020-064-2 Goncalves, V.F., Cuperfain, A.B., & Kennedy, J.L. (2019). Sex differences in schizophrenia: Estrogen and mitochondria. Neuropsychopharmacology, 44 (1), 216-217. https://doi.org/10.1038/s41386-018-0228-0 Guzman, F. (n.d.). The four dopamine pathways relevant to psychopharmacology . Psychopharmacology Institute. https://psychopharmacologyinstitute.com/publication/the- four-dopamine-pathways-relevant-to-antipsychotics-pharmacology-2096 Maijer, K., Begemann, M.J.H., Palmen, S.J.M., Leucht, S., & Sommer, I.E. (2018). Auditory hallucinations across the lifespan: A systematic review and meta-analysis. Psychological Medicine, 48 (6), 879-888. https://doi.org/10.1017/S0033291717002367 McCutcheon, R.A., Krystal, J.H., & Howes, O.D. (2020). Dopamine and glutamate in schizophrenia: Biology, symptoms, and treatment. World Psychiatry, 19 (1), 15-33. https://doi.org/10.1002/wps.20693 Rutigliano, G., Cahumette, B., & Seeman, M.V. (2020). Editorial: Psychoneuroendocrinology of psychosis disorders. Frontiers in Psychiatry, 14 (9), 1-13. https://doi.org/10.3389./fpsyt.2020.607590 Stahl, S. (2018). Beyond the dopamine hypothesis of schizophrenia to three neural networks of psychosis: Dopamine, serotonin, and glutamate. CNS Spectrums, 23 (3), 187-191. https://doi/.org/10.1017/S1092852918001013 Waters, F., Blom, J.D., Jardri, R., Hugdahl, K., & Sommer, I.E. (2018). Auditory hallucinations, not necessarily a hallmark of psychotic disorder. Psychological Medicine, 48 (4), 529- 536. https://doi.org/10.1017/S0033291717002203 Wy, T.J.P., & Saadabadi, A. (2022). Schizoaffective disorder. StatPearls . StatPearls Publishing. Retrieved October 1, 2022 from https://www.ncbi.nlm.nih.gov/books/NBK541012/

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