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Carlsson et al. (2000) Network interactions in schizophrenia – therapeutic…
Carlsson et al. (2000) Network interactions in schizophrenia – therapeutic implications (CLINICAL CONTEMPORARY STUDY - SCHIZOPHRENIA)
Conclusion
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There may be different types of schizophrenia that are caused by different neurotransmitters and different levels too' it's not all caused by dopamine.
Increased levels of serotonin also contribute to the positive and negative symptoms of schizophrenia, posing good implications for future treatments.
Future research should look into other neurotransmitters such as GABA and acetylcholine, as well as explore how the disorder evolves.
Method
A literature review was undertaken by compiling lots of different research regarding neurochemical levels in patients diagnosed with schizophrenia, (recreational) drugs known to induce symptoms of psychosis (amphetamines and PCP), brain scans (for example, Abi-Darghan et al (1998) and Breier et al (1997)) and the effectiveness of antipsychotic drugs.
Results
There's lots of evidence supporting the role of low levels of glutamate in the development of psychotic symptoms. For example, PCP acts as an antagonist on NMDA glutamate receptors by blocking them and increasing dopamine.
Some research has found a relationship between levels of glutamate and dopamine production, such as low levels of glutamate are associated with both high and low levels of dopamine.
Serotonin seems to be implicated in schizophrenia as well as dopamine, as various monoamine agonists work together with NMDA antagonists.
Evidence revealed that glutamate failure in the cerebral cortex may lead to negative symptoms, whereas glutamate failure in the basal ganglia may lead to positive symptoms.
Evidence from studies into antipsychotic effectiveness found that clozapine is a highly effective drug treatment for schizophrenia, with fewer reported negative side effects.
Aim
To review studies into the relationship between levels of neurotransmitters, especially dopamine and glutamate, on the symptoms of schizophrenia, as well as explore the theory of glutaminergic deficiency (hypoglutamatergia).
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Evaluation
✓ Application - The findings of this research can be used to develop more effective treatments for schizophrenia for patients who find current antipsychotics ineffective. A large percentage of patients don't respond to current antipsychotics quickly and later it can take a while to develop an effective treatment regimen. This research evidence suggests other neurotransmitters as well as dopamine can cause psychotic symptoms, so newer compounds of antipsychotics can be developed to target these imbalances.
✗ Ethics - There were no direct ethical issues with the literature review, however some of the secondary studies reviewed did. Many of the studies involved animals like lab mice who had been injected with antipsychotic drugs. Other studies involved humans with or without schizophrenia being given amphetamines or PCP to increase psychotic symptoms, making these participants 'drug naïve' in a single-blind trial - they didn't know if they were being given a real drug or a placebo. So deception and risks were involved.
✓/✗ Generalisability - Carlsson used 33 studies (including 14 of which he was a part of) making these representative selections of the happenings of schizophrenia research at that time in 2000. However, this could be considered a 'time-locked' study as the understanding of schizophrenia has advanced since then.
✓ Reliability - All the studies used in the literature review were lab experiments, many on animals and objective PET and SPECT brain scanning techniques too. These methods are controlled, standardised and replicable to find consistent findings. This makes the study highly reliable. Sendt et al. (2012) agreed that drugs focusing on dopamine don’t work for many schizophrenia patients and that they need to focus on glutamate deficiency. She also agreed that positive and negative symptoms were a result of glutamate dysfunction, giving Carlsson's findings inter-rater reliability.
✗ Validity - Some of the studies reviewed may have had validity issues that impacted Carlsson's findings. Glutamate and serotonin are more difficult to study in the living brain than dopamine. This is because they are involved in numerous processes within the brain, making it difficult to separate their functions and effects, impacting the validity of what is being measured.
✓ The secondary data used in this literature review is useful. Large volumes of information from studies was complied quickly, providing an overview to core fidnings about schizophrenia. This would have been a cheaper method than if Carlsson carried out primary research himself. By using a mass of data that used reliable methods such as PET and SPECT scans, more valid conlcusions were drawn.