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Norman Bates Case

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Case History The patient presented today is Norman Bates. Bates is a 22-year-old male who was born October 14, 1995. He lives in White Pine, Oregon currently. Bates had moved to White Pine with his mother Norma, when an accident involving Bates had killed his father. Bates has one half-brother, Dylan Bates who has not been present for a majority of Bates childhood. Recently he moved back into the house after his mother and brother moved away from Arizona. The Bates family bought a motel as a family when they moved to White Pine. Bates has decided to seek help after the death of his mother. Bates has expressed concern over the fact that he experiences blackouts. He has had them since he was 16, and in these blackouts, he has no recollection …show more content…

Transmitters for dopamine are over stimulated and because of this, the symptoms of schizophrenia are increased. Drugs such as amphetamines that activate dopamine are proven to worsen some patients with schizophrenia. Due to the fact that certain drugs that increase dopamine cause more symptoms, shows how there is a connection between dopamine and schizophrenia. Furthermore, drugs that block dopamine are shown to help patients with schizophrenia. The other thought with the dopamine hypothesis is that there is another dopamine receptor could be causing it which is dopamine D2. Dopamine D2 is located in the striatum of the brain and these cells control movement, balance, walking, and are reliant on dopamine to function (Barlow & Durand, 2015). The reason this is now a thought in the dopamine hypothesis is because there is a new effective antipsychotic that block all types of dopamine, including dopamine …show more content…

Because of the substantial amount of evidence, the dopamine hypothesis is the best explanation for schizophrenia. Studies have shown that while not all dopamine genes show signals, the DRD2 genes have a significant number of signals (Edwards, A. C., Bacanu, S., Bigdeli, T. B., Moscati, A., & Kendler, K. S. 2016). The DRD2 genes also have low levels of methylation which are trait biomarkers in schizophrenia patients (Yoshino, Y et al. 2016). Patients with schizophrenia who also have depressive symptoms have problems with their dopamine genes and there is also a connection between the reward system to the depressive symptoms (Peitl, V., Štefanović, M., & Karlović, D. 2017; Walter, H., Kammerer, H., Frasch, K., Spitzer, M., & Abler, B. 2009). In addition to these pieces of evidence, elevated dopamine levels are associated with the striatum which would prove that in patients with schizophrenia dopamine is a main cause biologically (Kegeles, L. S. et al. 2010). All of this evidence supports the theory of the dopamine hypothesis and proves how the biological model works best for

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The dopamine hypothesis refers to an excess amount of activity in dopamine synapse in the brain to be the cause of the positive symptoms of schizophrenia. This theory explains why typical antipsychotics only treat the positive symptoms of schizophrenia because the D2 receptors are blocked, leading to less activity in the dopamine synapses. Atypical antipsychotics, also block D2 receptors but also blocks as specific subtype of a serotonin receptor called the 5HT2A receptor. Studies show that the combined blockage at the D2 and 5HT2A receptors treats both the positive and negative symptoms of schizophrenia. Since both the D2 and 5HT2A receptors are blocked, atypical antipsychotics treat both the positive and negative symptoms of schizophrenia.

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There are many different biological speculations as to what causes schizophrenia, but one of the main reasons is that it “involves overactivity if dopamine transmission in the brain (Nevid et al., 431). This hyper-activity can then result in the hallucinations and the other symptoms associated with schizophrenia. Studies have shown though, that it is not necessarily an overage of dopamine in the brain, but rather the brain not being able to properly receive and respond to the dopamine that it receives (Nevid et al., 2018). Strictly, behavioral theorists would claim that people develop schizophrenia from defective learning of what is correct behavior and what is not correct behavior (Nevid et al., 2018). When I was researching and thinking about how behavioral theorists would explain schizophrenia, I was able to grasp how this perspective would explain schizophrenia by realizing that the voices and hallucinations in side the ill person’s head would be the encouraging aspect of the problem.

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With regards to neurochemistry both drug categories target the neurotransmitter Dopamine, specifically the dopamine receptor D2 by blocking the receptor and decreasing the concentration levels of dopamine within the brain (Andreasen et al, 2011). Typical antipsychotics use this receptor blockage as their only method of symptom suppression, which improves positive symptoms. However, this method of symptom suppression has the adverse effect of blocking all D2 receptors within the body, which leads to symptoms such as tremors and muscle spasms, as well as worsening of the negative symptoms associated with the disorder. Atypical antipsychotics have made improvements in this aspect of treatment by not only blocking the D2 dopamine receptors but a subtype of serotonin receptors as well. This treatment approach improves both the positive and negative symptoms (Andreasen et al,

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For example, too much dopamine or oxytocin can cause irrational behavior, binge eating, drug use, adultery, and jealousy (Wu). Oxytocin can also cause outsiders to seem even more different by drawing people closer to their neighbors, leading to xenophobia, and dopamine can cause a love

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Schizophrenia is a psychotic disorder in which personal, social, and occupational functioning deteriorate as a result of unusual perceptions, odd thoughts, disturbed emotions, and motor abnormalities. This disorder is interesting because it’s been found that people who have relatives with schizophrenia are more likely to develop it. Another theory is the Dopamine hypothesis saying that some people develop Schizophrenia from too much activity from the neurotransmitter dopamine. With this being said schizophrenia is not a rare disorder, and it affects many people all over the world. I believe that medication is needed to treat people with Schizophrenia.

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The kind of medication taken can either increase the level of dopamine (neurochemical) or reduce it which influences the possibilities of schizophrenic symptoms to be visible. If the medication does not reduce the symptoms, the individuals might experience according to person 5 agitation, mood swings and fast unorganized thought processes. Argument: Psychological theorists describe schizophrenia similarly as impairment in the cognitive processes; they are described as confused and unaware of reality. These explanations are correct however in my observation while watching a video of a schizophrenic individual especially January Shofield, I viewed that they are aware of reality and their conditions however at a young age of 10 years like January Schofield, they are more vulnerable as they have not yet learnt completely to differentiate between reality and imagination.

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An imbalance of the two neurotransmitters is thought to cause the symptoms of schizophrenia (MHA 3). The “dopamine hypothesis” has been the main theory regarding the cause of the symptoms of schizophrenia. It is known that only an excess amount of dopamine in the brain results in the symptoms. The dopamine hypothesis of schizophrenia generally states that the symptoms of schizophrenia, primarily the hallucinations, delusions, and psychosis is the result of too much dopamine active in the brain. As a result of this, the brain produces an over-stimulation of the cells and the symptoms.

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Schizophrenia is an abnormality in the brain which affects

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Amongst various psychological disorders, schizophrenia effects a relatively low number of people compared to others like major depressive disorder and bipolar disorder. In fact, the lifetime rate of schizophrenia is only .7% whereas substance use disorders have a lifetime rate of 26.6%. Based upon the criteria outlined in the Diagnostic and Statistical Manual of Mental Disorders, to be diagnosed with schizophrenia an individual must display at least two symptoms for one month and one must be a positive symptom. An exception to the time requirement occurs if the person has been receiving treatment that has made their symptoms manifest for less than the month. The positive symptoms include hallucinations that are mostly auditory, delusions, disordered thoughts, or bizarre behaviors.

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According to Mayoclinic, Problems with certain naturally occurring brain chemicals, including neurotransmitters called dopamine and glutamate, may contribute to schizophrenia. Neuroimaging studies show differences in the brain structure and central nervous system of people with schizophrenia. While researchers aren't certain about the significance of these changes, they indicate that schizophrenia is a brain disease. Other important high-risk factors include a family history of schizophrenia, Increased immune system activation, such as from inflammation or autoimmune diseases, certain

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There is a list of reason to confirm this idea. The first is schizophrenia can lead to death, in the form of suicide. The suicide rate will increase to about 5% [2], and 20% - 40% attempt suicide at least once [1]. Second, the cause of this disease is very complex and difficult to diagnose. Actually, although there are some theory try to describe the schizophrenia, but scientists still cannot understand the mechanism of this disease, schizophrenia, completely, just like most mental disorder diseases are difficult for human to understand the reason.

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Introduction Mental illness continues to be a growing problem throughout the world. It can take a toll on one’s mental, physical, and emotional well-being, leaving one feeling lost and alone. During this paper, I will focus on one mental illness that adversely affects one’s life, schizophrenia. I will begin by discussing the history, symptoms, subtypes, causes, and treatments of the disease.

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The environmental model states that either physical or stress factors are the main contributions to schizophrenia. Research has identified high levels of stress as a trigger for schizophrenia by increasing the body’s production of the hormone cortisol. There are several stress-inducing environmental factors that may be involved such as: Physical or sexual abuse in childhood, early parental loss or separation, exposure to a virus during infancy, low oxygen levels during birth (from prolonged labor or premature birth), or prenatal exposure to a viral infection (Jablensky, et al.,

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Another possible cause of schizophrenia is brain chemistry. Certain brain chemicals called dopamine and glutamate, contributes to schizophrenia. Those two neurotransmitters help the brain cells communicate with one another. So if some of those neurotransmitters are not there or destroyed then to can cause schizophrenia. Environment is also another possible cause of schizophrenia.

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A second aspect to this theory is that the dopamine receptors become excessively receptive towards this neurotransmitter. A layman’s interpretation of schizophrenia may be likened to the body producing its own psychedelic drug exploit. A second neurotransmitter under scientific investigation is glutamate, which is altered by stress levels. Glutamate has the function of controlling emotional and sensory information in the brain. It appears that hypo-function of glutamate

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