Schizophrenia Term Paper

Schizophrenia is classified as a mental disorder that shows profound disruption of cognition and emotion which affects a person’s language, perception, thought and sense of self. The dopamine hypothesis states that schizophrenic’s neurones transmitting dopamine release the neurotransmitter too easily, leading to the characteristic symptoms of schizophrenia. This hypothesis claims that schizophrenics have abnormally high amounts of D2 receptors; receptors that receive dopamine, therefore resulting in a higher amount of D2 receptors binding to the receptors causing more impulses. Dopamine neurotransmitters play a

Expert’s reason that unevenness in the complicated interconnected chemical responses of the brain connecting the neurotransmitters dopamine and glutamate, and maybe others, performs a part in schizophrenia. Neurotransmitters are elements that permit brain cells to interconnect with each other. Experts are acquiring more about brain chemistry and its connection to schizophrenia. Similarly, in small methods the brains of people with schizophrenia appear diverse than those of healthful people. For instance, fluid-filled holes at the middle of the brain, called ventricles, are greater in certain people with schizophrenia. The brains of people with the disorder similarly manage to have less grey matter, and certain

Physiological Changes Due to Risperdal Hallucinations, delusions, paranoia, psychosis and thought disorder are all symptoms of Schizophrenia and people who suffer from these symptoms seek the treatment of atypical anti-psychotic medications. Those medicines include Risperidone (Risperdal), Clozapine (Clozaril) , Ziprasidone (Geodon) and Quetiapine(Seroquel). The purpose of these medications is to alleviate symptoms of Schizophrenia and lessen the chances of a recurrence. The basic function of Atypical Antipsychotics is to reduce the effects of blockage in the dopamine receptors and serotonin and allow communication between nerve cells. Dopamine is thought to be relevant in Schizophrenic symptoms and

Genetics can cause differences in brain chemistry and biochemistry may be important in the development and maintenance of schizophrenia. The dopamine

Research by Johnstone in 1994, explained the biological approach of interventions, explanation and treating of schizophrenia patients (Hansell & Damour, 2005). In studies of Fisher in 2001, discoveries that the brain had more dopamine receptors know as B_2 receptors in a person suffering from schizophrenia, than a non-suffer (Hansell & Damour, 2005). Biological findings of schizophrenia suggest that a genetic factor was hereditary, but not conclusive because the element of environment does make a difference (Hansell & Damour, 2005).

For the past fifty years treatment of schizophrenia has been marked by its basis on the dopamine hypothesis for schizophrenia. However, this model for the disease and its subsequent treatment have left many patients without relief or help in dealing with this disease which has lead to a search for a better model. The dopamine model lacks the recognition of a whole range of symptoms associated with the disease and therefore can not be an accurate basis for treatment. More recently, there has been a shift to the glutamate hypothesis which has been shown to more accurately characterize the wide range of symptoms experienced by patients living with this disorder as well as the possibility in improvements for drug treatments.

Schizophrenia is a complex and highly debilitating mental illness that we are currently unable to treat in any way that guarantees success or return to previous function. It affects around 1% of the population and is associated with a thirteen-fold increase in the likelihood of suicide, so its effective control is paramount (Gogos et al., 2015). There have been several hypotheses as to the cause of schizophrenia. Many link genetic and environmental factors, and dysregulations of neurotransmitters dopamine, glutamate, and serotonin (Egbujo, Sinclair, & Hahn, 2016). The dopamine hypothesis currently suggests that hyperactive dopamine transmission in the basal ganglia leads to psychosis and underactive dopamine transmission in the prefrontal

The major support and refutation of the dopamine hypothesis has come from the examination of dopamine receptors in these regions of the brain. There are two main types of dopamine receptors, D1 and D2. However, within the category of D2 receptors, there are three subtypes, D2, D3, and D4. (5) Through PET scan analysis of dopamine usage in the brain and post-mordum molecular analysis of brain tissue, researcher were able to determine relative levels of dopamine receptors in patients with schizophrenia compared to non-schizophrenics. Overall analysis of dopamine

Currently there are no cures for schizophrenia, but the symptoms are helped by taking antipsychotic medication. The symptoms experienced by those with schizophrenia are grouped in to three categories: negative symptoms, positive symptoms, and cognitive symptoms (Regier 1993, p.92). The positive symptoms include, hallucinations, delusions, unusual or dysfunctional ways of thinking, agitated body movements. Negative symptoms include, flat affect, reduced pleasure in everyday life, difficulty sustaining tasks, and reduced speech. Cognitive symptoms include, disruption in executive functioning and working memory, as well as reduced ability to concentrate. The etiology of schizophrenia is still debated by psychologists and neuroscientists, but factors such as neuroanatomy, and environmental influences are believed to play a key role. A genetic predisposition to schizophrenia has been established by researchers, but it remains unclear what causes the phenotype to be expressed. The most agreed upon cause of schizophrenia refers to the diathesis-stress model, which explains schizophrenia as a response to an individual’s allostatic load becoming too much for the brain to cope with. Another popular explanation amongst neuroscientists is the dopamine

Researchers think that overly responsive dopamine systems might magnify brain activity in some way, perhaps creating hallucinations and other so-called positive symptoms as the brain loses its capacity to tell the difference between internal and external stimuli. For this reason, dopamine blocking drugs are often used as anti-psychotic medications in treatment. Modern neuroimaging studies show that some people with schizophrenia have abnormal brain activity in the thalamus,when patients were hallucinating for example, which is involved in filtering incoming sensory signals. Patients with paranoid symptoms showed over-activity in the fear processing amygdala. Schizophrenia seems to involve not just problems with one part of the brain, but abnormalities in several areas and their interconnections. What might be causing these abnormalities under the “iathesis-stress” model? This way of thinking involves a combination of biological and genetic vulnerabilities -diathesis- and environmental stressors -stress- that both contribute to the onset of schizophrenia. This model helps explain why some people with genetic vulnerability might not always develop schizophrenia and why the rates of schizophrenia tend to be higher with some degree of poverty or socioeconomic stress. It seems too that there is some kind of genetic predisposition for the

Dopamine is a neurotransmitter associated with attention. Schizophrenics seem to have an increased number of D2 dopamine receptors on receiving neurons. This theory is support by the fact that Phenothiazines bind with D2 receptors and reduce positive symptoms. Another piece of supporting evidence is that Parkinson’s disease drug L-dopa, increase the level of dopamine and causes schizophrenic like symptoms in some people. However excess dopamine can only explain some types of schizophrenia, usually positive rather than negative.

Over the years, experiments have produced evidence to suggest that dopamine plays a role in the development of Schizophrenia (Howes, McCutcheon, & Stone, 2015). Dopamine is a neurotransmitter that is produced in the substantia nigra and ventral tegmental regions of the brain. The belief that dopamine was involved in Schizophrenia arose after multiple studies performed with compounds produced an increase in extracellular concentrations of dopamine (Lieberman, Kane, & Alvir, 1987). The patients that were administered these compounds had similar symptoms to those observed from patients who were diagnosed with Schizophrenia (Lieberman et al., 1987).

Another major problem with the dopamine theory is that it only takes into consideration a single neurotransmitter and neglect the roles of other neurotransmitters in schizophrenia. The findings are inconsistent where some findings proposed that the abnormality causes the availability of dopamine transporters changed, and effect to the increased or decreased of dopamine level (Fusar-Poli, and Meyer-Lindenberg, 2012), while some other findings suggested that there are other neurotransmitter such as glutamine which involved in excitatory response in the brain has played a role in resulting cognitive deficits of schizophrenia (Stone, Howes, Egerton, Kambeitz, Allen, Lythgoe, et al, 2010). These assumptions have allowed researchers to implicate schizophrenia by using another pathway or biochemical mechanism other than dopamine hypothesis or dopaminergic

Treatment of schizophrenia may vary according to what clinicians believe to be its causes. For example, some believe (and this is backed by evidence) that the condition is caused by over activity of the dopamine system, so that the person experiences too much stimulation. Dopamine is a neurotransmitter, so that in effect too much activity is occurring in the brain. Clinicians who believe this is the case are likely to use drug therapies to correct this over activity, and will use antipsychotic drugs.

The Dopamine Hypothesis theorizes that the symptoms portrayed in Schizophrenia is can be explained by abnormal function of dopamine in the brain. There have been three versions of the Dopamine Hypothesis. The first version of the hypothesis focuses on the dopamine receptors. Antipsychotic drugs that impact the metabolization and reabsorption of dopamine where found to be effective in treating the symptoms. It was theorized that if the symptoms of a Schizophrenic episode can be treated by the use of dopamine