How Bill Has Changed Our Lives

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.

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

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

Schizophrenia is a complex and puzzling illness. Even the experts in the field are not exactly sure what causes it. Some doctors think that the brain may not

Biological theorists believe that individuals may have a genetic predisposition for the schizophrenia if a close family member has been diagnosed with the disorder. Stress during adolescent years seems to provoke the disorder among individuals who have a family history of the disorder. In addition, this theory suggests biochemical abnormalities related to the dopamine neurotransmitters may also contribute to the illness as the brains neurotransmission of the dopamine is too frequent in occurrence (Comer, 2005). CAT and MRI scans have also indicated that abnormal brain structuring may also play a role in the development of schizophrenia due to a common occurrence of enlarged ventricles within schizophrenia sufferers (Comer, 2005). Various parts of the brain may not develop for function properly which seems lead to Type II schizophrenia. Studies have also pointed towards the idea that exposure to certain viruses before birth may lead to the eventual development of schizophrenia (Comer, 2005).

On the other hand there are problems with the dopamine hypothesis, as it suggests that schizophrenics have an excess of dopamine in their brains. Deakin, 1988, as cites in Wickens, 2005, found little evidence for this following post-mortems of schizophrenics. However a number of studies have found that schizophrenics have an increase of dopamine D-2 receptors (Jaskiw and Kleinman, 1988 as cited in Wickens, 2005) therefore it may be that increased uptake by receptors is responsible rather than an excess of dopamine. This gives rise to cause and effect, as is the schizophrenia caused by an increased number of receptors or is the increased number of receptors a result of antipsychotic drugs.

Some researchers think some of these symptoms of schizophrenia (delusions, hallucinations, and confusion) may be caused by too much dopamine the brain (or very sensitive dopamine receptors). “Dopamine regulates many normal body functions, including movement, emotions, behavior, and appetite” (http://www.mhsource.com/narsad/schiz.html)

Schizophrenia has been defined as a mental disorder characterized by a breakdown in mental thinking and a poor emotional response. This disorganization hasn’t till now acquired a clear understanding of the mechanisms that lie behind (Harrison 1999) but researchers suggest an increase in the dopaminergic transmission in the prefrontal cortex coupled to an inhibition of the glutamatergic pathways, majorly at the level of NMDA receptors (Wen-Jun Gao). For more than 50 years, the dopamine hypothesis had been considered the mother of the theories of schizophrenia. Van Rossum first proposed it in 1966 suggesting that a hyperactivity occurring at the level of the mesolimbic dopamine pathway is the mediator of positive symptoms of schizophrenia

Data collected over the years has begun to show more and more evidence as to why researchers consider schizophrenia a brain disorder. First of all, schizophrenia is genetically inherited shares a lot of similarities with Alzheimer's and Bipolar disorder. Schizophrenia has also demonstrated severe structural difference when compared to a normal human brain and often shows severe gray tissue deterioration. The final reason researchers consider schizophrenia a brain disorder is due to the dopamine hypothesis. This hypothesis states that schizophrenia is caused due to high amounts of dopamine in the brain. Something

Schizophrenia is a chronic neurological disease that results in a combination of positive, negative, and cognitive symptoms. Positive symptoms of Schizophrenia include hallucinations and delusions. Negative symptoms of Schizophrenia most commonly consist of avolition, anhedonia, and alogia. Cognitive symptoms affect the person’s cognition. Patients with the disorder have disorganized speech and behavior, deficits in learning and memory, as well as deficiencies in abstract thinking and problem solving. Positive symptoms of Schizophrenia are commonly attributed to the abnormally high levels of dopamine (Konradsson-Geuken, slide 25). While there is no current cure for Schizophrenia there are different treatments that prove to help certain aspects of the disorder.

Roy is currently receiving intensive outpatient services in a psychiatric hospital setting. Roy has been diagnosed with Schizoaffective disorder. Patient has a history of non-compliance with medication and send medicating with alcohol and drugs. The patients lack of medication compliance and self medicating has exasperated his symptoms. Patient is currently presenting with auditory and visual hallucinations. Patient frequently experiences suicidal ideations stemming from voices telling him, “I am the devil.” Patient denies current or past homicidal ideations. Roy reports the following: Mood swings, disorganized

Antipsychotics are the most common form of medication that is used to help with the symptoms of schizophrenia. There are two main types of antipsychotic, traditional and new (http://www.nimh.nih.gov/health/publications/mental-health-medications/index.shtml#pub9). Traditional antipsychotics are used mainly to control hallucinations, delusions, and confusion of schizophrenia. These medications, for example chlorpromazine and haloperidol, primarily block the dopamine receptors and are very effective in treating the “positive” symptoms of schizophrenia. The newer antipsychotic medications, for example Risperdal and Zyprexa, work on both serotonin and dopamine, meaning that it can treat the “positive” and the “negative” symptoms of schizophrenia. There are many side effects that can come with taking antipsychotic medications. Mild side effects include a dry mouth, blurred vision, constipation, drowsiness and dizziness. These side effects will usually disappear after a period of time (http://www.nimh.nih.gov/health/publications/schizophrenia/index.shtml). More serious side effects of antipsychotics include trouble with muscle control, muscle spasms or cramps, fidgeting or pacing, tremors and shuffling of the feet. These symptoms mimic

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

To further compare the dopamine hypothesis, the Neurological substrates including errors in neurotransmitter levels. Some studies have suggested that negative, disorganized, and some positive symptoms may possibly could result from damage occurring to the neural system itself (Basso et al. 1998). The most frequently found findings in brain scans of those diagnosed with schizophrenia have included enlarged cerebral ventricles and reduced cortical volume especially in the temporal and frontal lobes in comparison to scans from non-schizophrenics. Post-mortem examinations have revealed a reduction of neuron density and size in the limbic, temporal and frontal regions of the brain and the connections between the neurons are noticeably disorganized.

Another route towards treating schizophrenia is the medication route. The main drugs used to treat schizophrenia are antipsychotic drugs (Schizophrenia, Mayo Clinic). The drug’s main goal is to try and maintain a healthy level of dopamine in the brain (Some examples include: Asenapine, Brexpiprazole, Paliperidone, etc.) (Schizophrenia, Mayo Clinic). Research has shown that the use of antipsychotic drugs seems to be working effectively for some patients but not for others (Schizophrenia, Web MD). However, one major problem that can come up after using prescription medications to treat schizophrenia can be relapsed once the patient stops using their medication (Schizophrenia, Web MD). Another negative aspect of medications are the potential side