Please enable JavaScript.
Coggle requires JavaScript to display documents.
Explanations for schizophrenia - Coggle Diagram
Explanations for schizophrenia
Bio explanation
Neurotransmitters are "fast chemical messengers" that travel between neurons (brain cells) by crossing the synapse.
They bind themselves to receptors on the next neuron and pass in their message in the form of a small electric charge.
The Dopamine Hypothesis
Dopamine is an important neurotransmitter that regulated mood and attention
Proposed by Arvid Carlsson and suggests that schizophrenia is caused by too much dopamine or too many dopamine receptors in key areas of the brain
Dopamine systems in the mesolimbic pathway may contribute to the positive symptoms of schizophrenia (such as hallucinations)
Dopamine function in the mesocortical pathway may be reponsible for the negative symptoms such as avolition (lack of motivation) and alogia (inability to speak)
L-Dopa is a drug used to treat Parkinson's disease by boosting dopamine levels in the brain.
Carlsson discovered that giving L-Dopa o animals reduced their Parkinsons-like symptoms
L-dopa also reduced Parkinsons symptoms in humans but gave them psychotic symptoms that were similar to schizophrenia
Amphetamine is a recreational drug which increases dopamine activity and produces schizophrenia-like symptoms in users (known as 'cocaine psychosis')
Drugs like LSD, which are known to increase dopamine activity, also trigger schizophrenic symptoms in healthy people and exaggerate the positive symptoms of those with the disorder
Antipsychotic drugs like phenothiazines (PTZ) reduce the symptoms of schizophrenia and work by blocking dopamine receptors
Alpert and Friedhoff (1980), for example, found that some patients show no improvement whatsoever after taking dopamine antagonists
Post-mortem (after death) examinations show schizophrenia patients have more dopamine receptors in the left amygdala (Falkai et al., 1988) and the caudate nucleus (Owen et al., 1978).
Genetic explanation
The C4 gene
Sekar et al. (2016) analysed 100,000 human DNA samples from 30 different countries. They identified a gene called complement component 4 (C4), which is part of the immune system.
Genetic analysis of 65,000 people found that those who had particular forms of the C4 gene showed higher risk of developing schizophrenia
The C4 gene plays a role in pruning synapses but excessive pruning could lead to the symptoms seen in schizophrenia
Test mice with increased levels of C4 activity lost more brain cells as they matured
Family members
Risk rates compared to the 1% risk in the general population
Adoption studies show that the risk rises from 1% to 10% if you have a close relative with schizophrenia
Twin studies show that concordance for schizophrenia is 4 times as high in MZ (identical twins) compared to DZ (non-identical) twins
Gottesman (1991) found that if a first degree relative has schizophrenia than the risk increases to between 6 and 17 per cent. However, the biggest risk was between MZ twins which was 48%
Kety et al (1994), 207 offspring of mothers diagnosed with schizophrenia along with a matched control of 104 children with 'healthy' mothers. The children were aged between 10 and 18 years and followed up 12 and 17 years later.
Schizophrenia was diagnosed in 16.2% of the high risk group compared with 1.9% of the low risk group.
Harrison and Owen (2003) reported that recent research has suggested that there is up to 6 different genes that may be involved
Harrison and Weinberger (2004), found that the influence of genes on schizophrenia could be the result of the genes' effect on the functions of synapses and the circutry in the brain
Joseph (2004) found that the concordance rate difference between MZ and DZ twins could be caused by a higher risk of birth complications in twins than others. Further, MZ twins are raised more similarly than DZ twins
Tienari et al (2000) found that almost 7% of adoptees with schizophrenia had a biological mother with the same disorder, compared to only 2% of schizophrenic children born to mothers without schizophrenia
Cognitive
Attention deficit theory
Christopher Frith (1979) argues schizophrenia is the result of a faulty attention system.
Cognitive deficits
Difficulties with following aspects of cognition can make it hard to live a normal life or earn a living: memory, attention, planning and decision making
Preconscious thought contains a huge amount of information that would normally be filtered; however if not, there will be a sensory overload
Frith says this accounts for the positive symptoms of schizophrenia, such as hallucinations, delusions and disorganised speech
McGuigan (1966) identified that immediately before episodes of auditory hallucination were reported, some schizophrenic patients showed activation of the vocal centres, which suggests that they may misinterpret their own 'inner voice' as someone else
McGuire et al (1996) who discovered that during hallucinations, the part of the brain in the temporal love responsible for identifying and monitoring 'inner speech' recorded reduced activity
David Hemsley (1993, 2005) suggests schizophrenia involves a breakdown in the relationship between memory and perception. People with schizophrenia have a disconnect between their schemas and what they actually hear and see
Lack of self-monitoring; throughts and ideas are attributed to external sources (such as hallucinations), or result in delusions because the individual does not realise that they are self-generated
Gold and Harvey (1993) report that people with schizophrenia often score lower on tests of attention, memory and problem solving, than similar people without the disorder.
Corcoran et al (1995) has found that patients with schizophrenia also show deficits in tasks requiring 'theory of mind', which is the cognitive skill associated with the ability to read and interpret the intentions of other people's behaviour
Sitskoom et al (2004) found that the cognitive deficits found in patients with schizophrenia were also found in relatives of the patients who did not have the disorder
Freud's psychodynamic explanation
Abnormality is caused when trauma from unresolved conflict between the id, ego and superego is repressed into the unconscious.
This causes fixation or regression to an earlier stage of psychosexual development
If the ego is not fully developed, the individual may be dominated by the id or the superego, and will lack a sound basis in reality
This might happen to someone who experienced a very harsh childhood, perhaps because their parents were cold and unsupportive.
Schizophrenia is linked to the oral stage, in particular a stage called primary narcissism during which the ego has not seperated from the id.
This explains some of the symptoms of schizophrenia, especially hallucinations, delusions and disorganised thought and speech.
When individuals with schizophrenia find themselves reduced to an infantile state, they try hard to regain contact a degree of ego control
Alternative theory
Social Drift Theory
Evidence has suggested that schizophrenia is more prevalent in lower social classes in society and this has been explained by the social drift hypothesis.
Suggests that symptoms of schizophrenia make it difficult for patients to hold down jobs, achieve well in education and maintain relationships so they often drop down into lower societal and economic classes.
People with schizophrenia also tend to drift towards more urban areas because they gain better access to support services
Social Causation Hypothesis
Members of the lower class experience more stressful lives than other people because of poverty, poorer physical heath etc.
Stress is also more likely to arise through discrimination, because ethnic and racial minorities in many cultures often belong to the lower social classes
A higher level of stress can make people more vulnerable than members of the middle class
The Stress-Diathesis Model
Marcus (1987) found in reported cases of schizophrenia there were poor parenting ratings (hostility, inconsistency and over-involvement)
Schizophrenia is caused by a biological predisposition (diathesis) and an environment trigger (stressor)
Genetic Mutations
Xu et al (2008) compared genetic make-up people (including 152 with schizophrenia) with their parents. 10% of Schizophrenia but only 2% control group had a mutation that distinguished their DNA from that of their parents. This suggests that around 10% of cases of schizophrenia can be explained by mutation. It can also explain why in 89% of cases of schizophrenia, there i no relative with schizophrenia
Brown et al (2002) found the risk of mutation increases with parental age and the risk of a child going on to develop schizophrenia increases with age of the father