Topic > The involvement of brain neurotransmitters, serotonin, in psychological diseases

This essay will focus on the involvement of the brain neurotransmitters serotonin in the psychological disorder, depression, and dopamine in the psychological disorder, schizophrenia. With evidence from various studies relating to the effectiveness of drug treatments in both disorders, this essay will highlight the treatments of psychological disorders and that drugs are only effective in less than 60% of people with these disorders as therapy, or another form of treatment is equally important and necessary to achieve lasting sustainability from the disorder. This is because there are obvious factors that need to be addressed and the use of medications only treats the surface. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an Original Essay The psychological disorder, schizophrenia, is the result of overactivity of the neurotransmitter, dopamine, in the system's pathways. Dopamine pathways are specialized and can influence different type of behavior or thinking. High levels of dopamine in some parts of the brain can manifest psychotic symptoms or paranoid thinking, symptoms described as schizophrenia. There are two types of symptoms to recognize schizophrenia; positive and negative. Positive symptoms consisted of delusions and hallucinations (auditory and visual), which are described as addictive behaviors. While negative symptoms were catatonic behavior or flat/inappropriate performance, this was described as a lack of activity. However, it is difficult to diagnose schizophrenia because no symptoms are specific to the disorder and no two patients have the same symptoms in common. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM), a manual used by doctors to diagnose mental health disorders, a person must exhibit these behaviors for at least one week and have continuous signs of disorder for six months, before they are characterized as suffering from schizophrenia. Studies suggest that dopamine systems in the mesolimbic pathway may have a connection to the positive symptoms of schizophrenia. Hypoactivity of the mesocortical pathway is believed to be related to the negative symptoms of schizophrenia, whereas hyperactivity of the mesolimbic pathway is considered to mediate positive symptoms (Meltzer and Stahl, 1976). There is no hard evidence about the cause of schizophrenia, with evidence suggesting that there may be abnormalities in the brains of schizophrenics, showing changes in gray matter density in the frontal and temporal lobes (Seeman et al, 2005). This suggests that there are multiple causes for schizophrenia, including genetic mutation and anatomical lesions. In 1976, Johnstone and colleagues found that schizophrenic brains had an enlarged ventricle-to-brain ratio compared to non-schizophrenic brains and were said to be related to cognitive impairments. However, these size differences are believed to be much smaller than previously thought and are not significant in the diagnosis of schizophrenia in the brain (Van Horn and McManus, 1992). There are various treatments for schizophrenia, the most common being drug therapy. Previously, schizophrenic patients underwent psychosurgery, a rare procedure that consisted of a frontal lobotomy. The efficacy was doubtful and consensus was lacking. However, this made patients easier to manage. Cognitive behavioral therapy (CBT) was later introduced. Sarin et al (2011), performed a meta-analysis of randomized controlled trials and found that changes were possible with CBT over the course of months with alonger treatment, at least approximately 20 sessions. This suggests that CBT is effective in reducing schizophrenic symptoms. In 1952, drugs called antagonists were introduced to treat schizophrenia, a common one was called chlorpromazine. This worked by combining with dopamine receptors and blocking them. This prevented the dopamine receptors from taking up too much of the neurotransmitter and limited the amount that entered the nearby neuron creating a normal flow of activity. This was said to be effective in reducing positive symptoms. However, this would later generate Parkinson's-like symptoms in the patient. Further experiments challenged the idea that blocking the receptors by drugs was not effective. Studies show that patients had more than 90% of their receptors blocked by antipsychotic drugs, but hardly showed any changes in their psychosis. This was dominant in patients who had symptoms for ten to thirty years. However, 90-95% of first-episode patients responded to medications. Harding et al (1987), examined 5 long-term studies, with patients treated between 22 and 37 years of age. The sample size was 118. They found that there was an improvement in patients suffering from the disorder, being able to control their symptoms. Between ½ and 1/3 achieved improvement or recovery. Kissling (1992), conducted a similar study examining 7 studies of patients treated with drugs and in remission between 6 months and 5 years. The results suggested there was a relapse rate of between 53% and 100%, with an average of 73%. This suggests that antipsychotic drugs are not as effective as they should. Following the patients for 6 months to 2 years, they subsequently found that ¼ of the patients did not relapse after stopping the drugs. Further studies suggest that at least 20% relapse occurs when it comes to schizophrenia (Weiden and Olfson, 1995). Which suggests that the effectiveness of drug therapy in removing or reducing these symptoms is very low. The neurotransmitter serotonin is primarily associated with the psychological disorder depression, although it plays a key role in many body functions. This can occur when there is not enough serotonin released in the brain. The neurotransmitter is created by a biochemical conversion process, which begins with the building block, tryptophan (Richard et al, 2009). The cells then use tryptophan hydroxylase, a chemical reactor that creates serotonin, when combined with tryptophan. Depression is believed to occur when a reuptake process occurs in the brain, where neurotransmitters are naturally reabsorbed into nerve cells after being released to send messages. Reuptake inhibitors, such as selective serotonin reuptake inhibitors (SSRIs), which are antidepressants, prevent this from happening. Instead of being reabsorbed, the neurotransmitter temporarily remains in the synaptic cleft. These are indirect agonists as they make more neurotransmitters available. Symptoms related to unipolar depression are loss of pleasure in things, sleep problems, changes in appetite, or loss of energy. Five symptoms are needed for at least two weeks before a diagnosis is possible. It is not yet clear whether decreased serotonin levels contribute to depression or whether depression causes a decrease in serotonin. According to genetics, there is a concordance rate of 53% and 28% between MZ and DZ twins (McGuffin et al, 1991). However, by 1992, the concordance rate stabilized with MZ twins having a 48% concordance rate and DZ twins having a 42% concordance rate.