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The Involvement of The Brain Neurotransmitters Serotonin in The Psychological Diseases

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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 disorder, this essay will evidence 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 treatments are important as well and needed to have a lasting sustainability from the disorder. This is because there’s underlining factors that need to be addressed and the use of medical drugs only treats the surface.

The psychological disorder, schizophrenia, is a result of overactivity of the neurotransmitter, dopamine, in the system pathways. Dopamine pathways are specialized and may influence the different type of behavior or thinking. High levels of dopamine in parts of the brain may experience psychotic symptoms or paranoid thinking, symptoms described as schizophrenia. There are two types of symptoms for recognizing schizophrenia; positive and negative. The positive symptoms consisted of delusions and hallucinations (auditory and visual), which are described as engaging behavior. Whereas the negative symptoms were catatonic behaviour or flat/ inappropriate performance, this was described as a lack of activities. However, it’s hard to diagnose schizophrenia as no one symptom is 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 clinicians to diagnose mental health disorders, a person needs to display these behaviors for at least a week, and have a continuous sign of disturbance for six months, before they’re characterized as having schizophrenia. Studies suggest that dopamine systems in the mesolimbic pathway may have a connection to the positive symptoms of schizophrenia. Underactivity in the mesocortical pathway is said to be related to the negative symptoms of schizophrenia, whereas overactivity in the mesolimbic pathway is suggested to be the mediator of the positive symptoms (Meltzer and Stahl, 1976). There is no concrete evidence as to the cause of schizophrenia, with evidence suggesting that there might be abnormalities in the brain with schizophrenics, which shows changes in grey matter density in the frontal and temporal lobes (Seeman et al, 2005). This suggests that there are multiple causes for schizophrenia, including gene mutation and anatomical lesions. In 1976, Johnstone et al found that schizophrenic brains had an enlarged ventricle-brain ratio compared to non-schizophrenic brains and were said to be related to cognitive impairments.

However, it is believed that these size differences are much smaller than previously thought and aren’t significant in diagnosing schizophrenia in the brain (Van Horn and McManus, 1992). There are various treatments for schizophrenia, the most common is drug therapy. Beforehand, schizophrenic patients had psychosurgery, which is a rare procedure that consisted of a frontal lobotomy. The effectiveness was doubtful and there was a lack of consent. However, this made patients easier to manage. Later, Cognitive Behavioural Therapy (CBT) was introduced. Sarin et al (2011), did a meta-analysis of random controlled trials and found that changes were able with CBT over months with longer treatment, at least 20 sessions or so. 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 combing with dopamine receptors and blocking them. This prevented dopamine receptors to absorb too much of the neurotransmitter and limited the amount that went into the neighboring neuron which would create normal activity flow. This was said to be effective in reducing positive symptoms. However, this would later generate Parkinson-like symptoms in the patient.

Further experiments, challenged the view that the blocking of receptors by drugs weren’t effective. Studies show that patients had over 90% of their receptors blocked by antipsychotic drugs, but hardly showed changes in their psychosis. This was dominant in patients who had their symptoms for ten to thirty years. However, 90-95% of first episode patients responded to the drugs. Harding et al (1987), reviewed 5 long-term studies, with patients being treated between 22 and 37 years. The sample sizes were 118. They found that there was an improvement in patients who suffered from the disorder, by being able to control their symptoms. Between ½ to 1/3 did achieve an improvement or recovered. Kissling (1992), conducted a similar study when he reviewed 7 studies of patients on drugs and in remission between 6 months and 5 years.

The findings suggested that there was a relapse rate between 53% and 100%, with a mean of 73%. Which suggests that antipsychotic drugs aren’t as effective as they should be. Following up with patients between 6 months and 2 years, they later found that ¼ of the patients don’t relapse when taken off the drugs. Further studies suggest that there is at least a 20% relapse when it comes to schizophrenia (Weiden and Olfson, 1995). Which suggest that the effectiveness of drug therapy in removing or reducing these symptoms are very low. The neurotransmitter, serotonin, is mainly associated with the psychological disorder, depression, although it plays a key role in many body functions. This can occur when there isn’t enough serotonin being released into the brain. The neurotransmitter is created by a biochemical conversion process, which begins with the building block, tryptophan (Richard et al, 2009). Cells then use tryptophan hydroxylase, a chemical reactor which creates serotonin, when combined with tryptophan.

Depression is stated to occur when there is a reuptake process in the brain, where the neurotransmitters are naturally reabsorbed back into the nerve cells after they are released to send messages. Reuptake inhibitors, such as Selective Serotonin Reuptake Inhibitors (SSRI’s), which are antidepressants, prevents this from happening. Instead of being reabsorbed, the neurotransmitter stays, temporarily, in the synaptic gap. These are indirect agonists as they make more neurotransmitters available.

Symptoms related to unipolar depression is a loss of pleasure in things, sleeping problems, appetite changes or loss of energy. Five symptoms are needed for at least two weeks before a diagnosis is possible. It remains unsure whether decreased levels of serotonin contribute to depression, or id depression causes a decrease in serotonin. According to genetics, there is a 53% and 28% concordance rate between MZ and DZ twins (McGuffin et al, 1991). However, in 1992, it leveled out with MZ twins having a 48% concordance rate and DZ twins having a 42% concordance rate (Kendler, 1992). Antidepressant drugs were introduced and believed to increase serotonin activity in the brain by increasing the release of serotonin or blocking the reuptake process. These drugs, however, showed major side effects which were liable to depressive individuals to overdose. The drugs had a delayed action time of 2-3 weeks, which caused individuals to be too impatient and stop taking them. SSRI’s, such as Prozac and Seroxat, had fewer side effects and overdoses. But, there was an increase in aggression and suicidal thoughts.

Clinical trials also found that the antidepressants were effective in 30% of participants, which shows that it isn’t effective in more than 60% of participants (Khan and Brown, 2015). Which suggests that a reduction in symptoms is possible, but it may not be effective for more people. Other studies found that 30 to 40% of patients failed to respond to antidepressants, and 60 to 70% were unable to achieve remission of their symptoms (Amsterdam, 1998). Davidson et al (2004), conducted a placebo study and found that there was a 19% response rate. Their results suggest that there was no superiority of treatment, even though almost 50% of the participants didn’t respond to the treatment. Throughout the year’s various methods have been used to ‘cure’ depression and schizophrenia, with the use of drugs one of the most common.

However, this is only effective in a small proportion of psychological disorders, 30% for depression according to Khan and Brown (2015) and a 20% relapse rate in schizophrenia, according to Weiden and Olfson (1995), as therapy and the use of drugs is said to be more effective, than drugs alone, as we need to find out the underlining cause of the disorder.

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The Involvement of the Brain Neurotransmitters Serotonin in the Psychological Diseases. (2018, Jun 10). GradesFixer. Retrieved May 19, 2022, from https://gradesfixer.com/free-essay-examples/the-involvement-of-the-brain-neurotransmitters-serotonin-in-the-psychological-diseases/
“The Involvement of the Brain Neurotransmitters Serotonin in the Psychological Diseases.” GradesFixer, 10 Jun. 2018, gradesfixer.com/free-essay-examples/the-involvement-of-the-brain-neurotransmitters-serotonin-in-the-psychological-diseases/
The Involvement of the Brain Neurotransmitters Serotonin in the Psychological Diseases. [online]. Available at: <https://gradesfixer.com/free-essay-examples/the-involvement-of-the-brain-neurotransmitters-serotonin-in-the-psychological-diseases/> [Accessed 19 May 2022].
The Involvement of the Brain Neurotransmitters Serotonin in the Psychological Diseases [Internet]. GradesFixer. 2018 Jun 10 [cited 2022 May 19]. Available from: https://gradesfixer.com/free-essay-examples/the-involvement-of-the-brain-neurotransmitters-serotonin-in-the-psychological-diseases/
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