Monoamine Dysfunction has been linked to both Affective Disorders and Schizophrenia. Drawing upon Relevant Evidence, Critically Evaluate the role of Monoamines in each of these Disorders. Assessment Number 2
Module Leader ' Dr Rebecca Jenks
Monoamine Dysfunction has been linked to both Affective Disorders and Schizophrenia. Drawing upon Relevant Evidence, Critically Evaluate the role of Monoamines in each of these Disorders.
Schizophrenia is a condition characterised by hallucinations, hearing voices and other dilutions which are known as the positive symptoms. Negative symptoms include social withdraw, flattened emotional response and an inability to experience pleasure. Prevalence is equally split between men and women; however there tends to be an earlier onset for men (20-28) than for women (26-32), Castle et al (1991). Lifetime occurrence is at around 0.55%, Goldner et al (2002) but variations have been found across culture, with urban areas often displaying higher incidence rates even when drugs use and other factors are accounted for, Van Os (2004).
Monoamine dysfunction has been given as a possible explanation of schizophrenia, with plenty of research for support. In particular the Dopamine Hypothesis, which suggests that raised levels of dopamine within the mesolimbic pathway is the cause, and has been noted in schizophrenic patients. Supporting this it was found that amphetamines which raise dopamine levels were found to exacerbate psychotic (positive) symptoms in schizophrenics, Laruelle (1996). In addition all of the early anti-psychotic drugs were chemicals that blocked the function of dopamine in some way, Tollefson and Sanger (1999). Also the ability of these drugs to block dopamine receptors positively correlates with clinical potency, Snyder et al (1978). Furthermore the path of the mesolimbic pathway means it travels firstly through the amygdala, where activation can lead to hallucinations, and secondly through the nucleus accumbens where random activation can lead to disorganised thoughts. Some support for this theory can be found from the effect of the drug PCP. Also known as ‘angel dust’ it causes both the positive and negative symptoms of schizophrenia; and one of its major effects is to increase levels of dopamine within the mesolimbic pathway.
However this hypothesis has been criticized for being overly simplistic with the effect of PCP being evidence against a pure Dopamine Hypothesis. Whilst PCP increases overall levels of dopamine it actually decreases levels in the frontal lobes leading to hypofrontality. In addition it blocks NMDA sensitive glutamatergic transmission; the evidence coming from post-mortem brains of diagnosed schizophrenics, Konradi & Heckers (2003), whilst another glutamate blocking drug (ketamine) has a similar result, Lahti et al (2002), suggesting the effect of other chemicals in the brain. Further evidence against this hypothesis is that newer anti-psychotic medication often called atypical antipsychotic drugs are as or more effective in dealing with the positive symptoms whilst being far more effective against the negative symptoms. These drugs tend to have a lower affinity for dopamine and have an antagonistic effect on serotonin, whilst some even act as dopamine agonists, Jones and Pilowsky (2002). Furthermore the reduction of glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampel activation such as the Wisconsin Sorting Task, where schizophrenics often score poorly on. .
In addition to the glutamate hypothesis there are other theories that aren’t based aren’t monoamine dysfunction. Firstly it has been suggested that there is a genetic link which in part has been strongly supported by evidence. Adoption studies provide evidence for the link, Kety and Ingraham (2000), as do twin studies, Tsuang et al (1991). The genetic link is strengthened by Owen et al (2005), who suggested that several genes interact to cause...
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