Schizophrenia

Biological Explanations

Dopamine Hypothesis

Started with the research in the ==1950s== in the role of ==dopamine== in ==Parkinson’s disease==. They developed ==L-DOPA== to treat Parkinson’s, but those given it then ==displayed symptoms== of ==schizophrenia.==

The Original Hypothesis - Those with schizophrenia had ==too much dopamine==. Supported by ==J.J. Griffith== ==et al== who induced psychosis in non-schizophrenic volunteers using dextro-amphetamine. Too simple, research showed that dopamine reducing meds had ==no impact== on those who suffered with ==neg symptoms==.

Dopamine Receptor Sites - ==Seeman and Lee== discovered ==receptor sites== D1-D5. ==D2 Receptor== became the main focus, it is found in the ==limbic system==.

Upgraded/Revised dopamine hypothesis

Focus on ==dopamine in the limbic system, mainly D2==. Limbic system is engaged in many functions like ==emotions, memory, formation and arousal==. Nerve pathways go from limbic system to ==subcortical pathways== and the cerebral cortex. Two main pathways are ==mesolimbic== and ==mesocortical.==

==Mesolimbic pathway== - Carries signals from ==ventral tegmental== area to ==nucleus accumbens==. Too much dopamine causes positive symptoms. Antipsychotics reduce dopamine neurotransmission here, lowering dopamine activity and reducing positive symptoms.

==Mesocortical Pathway== - Carries signals from ==ventral tegmental area== to ==frontal lobe==. Pathway is vital in ==emotional responses==, ==motivation== and ==cognition.== Davis et al note that too little dopamine is shown in D1 receptors of those with negative symptoms of schizophrenia.

Evaluation points:

What causes dopamine imbalance? ==Gottesman, 1991,== studies incidence of schizophrenia within families. Found that the closer the genetic similarity, the increased probability of both having schizophrenia. - Despite this, it has been difficult to try and identify a ‘schizophrenic’ gene.
How to measure dopamine? To assess neurotransmitters, we must also assess metabolite levels (which is what neurotransmitters get broken down into.) It is measured via cerebral spinal fluid, which is obtained via lumbar puncture. - can be difficult and very intrusive. Metabolites are also effected by diet and substance use.
Does serotonin have a role? ==Atypical antipsychotics== block the ==serotonin receptor 5-HT2A==, suggesting serotonin has a role. These are considered ‘more effective.’
Cause or effect? Is high dopamine a result of having schizophrenia or does it cause the individual to have schizophrenia.

Structural abnormalities

Enlarged Ventricles - Ventricles ==produce== and ==transport cerebrospinal fluid==. The brain has ==4 ventricles;==

Left and right lateral ventricles (in L+R frontal, occipital and temporal lobes)
Third ventricle (between left and right thalamus)
Fourth ventricle (between pons and medulla oblongata)

Some with schizophrenia seem to have ==larger ventricles==. Weinberger et al used CAT scans to reported ventricles to be bigger in 58 schizophrenics than in 56 from the control. Andreasen, MRI scans, those with schizophrenia had ventricles that were 20-50% larger than control groups.

Cortical Atrophy

Means the ==loss of neurons== in the cerebral cortex, makes it look like the brain has shrunk. Affects the function of the area it occurs in. Results in ==widening of grooves== covering the cerebral cortex. This damage occurs on ==20-35%== of people with ==chronic schizophrenia==. Vita et al found that ==33%== of 124 individuals with schizophrenia had ==moderate== to ==severe atrophy.==

Reversed Cerebral asymmetry

Most non-schizophrenics have a slightly ==larger left hemisphere==. In some individuals with schizophrenia, the ==right hemisphere== is noticeably ==bigger==. Left hemisphere is associated with language so damage to this could result in speech poverty (alogia) which is often seen in schizophrenia.

Evaluation points:

Other factors? ==McCarley== suggests that other factors, such as ==age, sex and the severity of symptoms== can effect the pattern of observed brain abnormalities in research.
==Cause or effect?== Environmental influences are capable of impacting brain tissue, so how can we establish if brain differences are the cause or effect of schizophrenia. The antipsychotic medication may also cause structural abnormalities.
Other conditions also have links to structural abnormalities. ==Roy, 1998,== those with ==bipolar has enlarges ventricles.== There are overlapping symptoms between schizophrenia and bipolar, which may be the cause of abnormalities. Classification and causation of these conditions should be reviewed.

Individual Differences Explanations

Psychodynamic approach

Fixation

During ==oral stage==, the ==libido== finds satisfaction in ==oral stimulation==. Too much or too little oral stimulation causes a ==fixation== of libidinal energy.

Regression

If an individual experiences ==lots of stress== they may ==regress== back to the ==oral stage==. This is an ego defence mechanism.

Losing touch with reality

The ==ego== is ==not well developed== in the oral stage. The ego controls the id’s impulses and balances the id and superego. When you regress to a stage when the ego is not developed, the ==id acts unimpeded.== ==Hallucinations== and ==delusions== represent the ==id’s unchecked activities.== They cannot distinguish between ==fantasy== and ==reality.==

Schizophrenogenic Mother

Huge emphasis on mother-child relationships. The mothers of individuals who develop schizophrenia are ==overprotective== and ==controlling==, but also ==rejecting== and ==distant.== The child is prevented from emotionally developing (overprotective), and they are deprived of personal security (emotional distance). They are now very vulnerable when faced with stress.

Evaluation Points:

==Out of date==, the ideas are unfalsifiable and not capable of describing complex disorders.
==No effective treatment==, psychoanalytic techniques can show harm to and distress to patients.
==Kasanin, 1934==, 33/45 cases of schizophrenia had maternal overprotection. Almost a third didn’t, so it cannot even explain all cases of schizophrenia.
==Overlooks role of genetics==, adoption studies are capable of explaining a sight correlation for relation and schizophrenia. Suggests that mother and child genetic similarity is the main cause.

Cognitive Approach

Explaining Hallucination

2.5-4% of individuals have experiences hallucinations, a lot of which are not diagnosed with a psychiatric problem. Morrison said that ==triggers==, like sleep deprivation, can cause one to ==hear ‘voices’ in a maladaptive way==. They then ==appraise the voices inappropriately==, which then ==elicits behaviours== like ==social withdrawal== or ==self-harm==. These behaviours produce negative emotions which then reinforce the messages, making it a circle.

Explaining negative symptoms

Beck et al used the ==cognitive triad==. The individual endorses ==negative beliefs== about their ability to experience pleasure and their performance, and they hold a ==negative view== of the ==future==. Their mental filters only allow messages that support their negative views. These lead to the negative symptoms of schizophrenia.

Lack of preconscious filters

Frith said that core positive symptoms are explained by difficulties in restricting preconscious content. Normally we receive information from our environment, and we interpret it. We get the ‘best fit’ of the information and that gets propelled into our consciousness, so we can understand the information. He suggested that those with schizophrenia have ==faulty attentional filters== that inhibit most of the sensory information from leaving the preconscious. They become aware of ==multiple interpretations== of events and their environment and are unable to understand the authentic reality of the information they are interpreting.

Evaluation Points:

==Barch, 1999==, used ==stroop== test. Schizophrenics did significantly worse, suggesting that they can’t filter information effectively.
==Reductionist==, as it reduces a complex disorder down to a lack of function in brain circuits.
==Not comprehensive==, the origin of the deficits is not explained so regardless of the fact that can explain positive and negative symptoms it cannot show how they develop lacking preconscious filters.

Social psychological explanation

Dysfunctional families

Double bind theory

==Bateson (1956)== proposed that schizophrenic symptoms are a result of ==communication difficulties== between parent and child.

Conflicting messages - A child is repeatedly exposed to social interactions in which there are ==two conflicting messages== and the child cannot ignore them or accurately respond to them both. The child’s ==ability to respond== is ==incapacitated== by the verbal and non verbal messages cancelling each other out. Due to the child’s reliance on the parent they are ==unable to metacommunicate== (cannot comment on that contradictory messages have been used.)

Link to symptoms of schizophrenia

Bateson claimed that long term exposure to this communication means that the child ==perceives the world== in terms of ==contradictory input== from their ==environment==, so they cannot discriminate between the messages given to them as they have ==internalised the double bind.==

Expressed Emotion (EE)

Brown investigated 156 men with schizophrenia after they had been discharged. Relapse was strongly connected to the home they returned to. Those staying with ==parents== or ==wives== were ==more likely to relapse== than those staying with siblings or in lodgings. There was a relationship between the amount of EE and the likelihood of relapse.

Components of EE;

==Critical comments== about the individuals behaviour. Comments like ‘so lazy’ and ‘don’t help around the house’ were made more by high EE caregivers. Low EE caregivers acknowledge these behaviours are because of their illness.
==Hostility== was present in high EE caregivers in interviews. It was the result of irritation, anger and rejection of the patient.
==Emotional over involvement== is shown in both high happiness and sadness, overprotective behaviour and self-sacrifice towards the individual. Very evident in the parents of the individuals as they feel guilty.
==Warmth== was measured by the vocal qualities, smiling and empathy shown by the caregiver when discussing the individual. More evident in low EE caregivers.
==Positive regard== is the number of reinforcing statements showing support and appreciation. This was lacking in low EE caregivers.

Evaluation Points:

==Cause or effect?== ==Liem, 1974,== the parents of 11 schizophrenic boys had no less disordered communication than those who did not have schizophrenic children (also 11 boys). Parents may have to adapt their communication in order to suit their schizophrenic child.
==Where== does a ==double bind come from==? ==Koopmans== suggests that incidental variations in family interactions which would normally have no effect, at times of family disruption, can lead to a double bind. ==Little evidence== to support this. Could be a ==result of parents pathology.==
Support of EE. ==Vaughn and Leff,== ==53%== of individuals with schizophrenia who had a ==high EE== relative relapsed in 12 months, but only ==12% no EE relatives== relapsed.
Shared environment could be the cause but so could the shared genes. Potential for a diathesis-stress model, as family relationships may trigger a genetic basis.

Sociocultural factors - Brown

Urbanicity

==Higher prevalence== of ==schizophrenic== people in ==urban areas.== This is likely due to ==specific environmental features== of urban life. Krabbendam and Os identified factors such as greater socioeconomic adversity, pollution, overcrowding, drug abuse and exposure to toxins and infectious agents. There is also greater social stress from living in a densely populated area.

Social Isolation

==Urbanicity== and ==overcrowding== can lead to ==social isolation==, as they find contact with others stressful. This ==self isolation== cuts the ==individual off== from ==feedback== about what are ==inappropriate behaviours== and thoughts so they start behaving strangely. It is suggested that the isolation starts very early, around 4-6 (Jones et al).

Ethnicity and discrimination

Since the 1970s, there have been higher than expected levels of individuals of Afro-Caribbean descent being diagnosed with schizophrenia. They are more likely to be ==compulsory admitted== to psychiatric hospitals. It is not genetic, as the pattern is not the same in studies conducted in the Caribbean. It is suggested that this is as a ==result of discrimination in society .==

Evaluation Points:

==Healthcare== is normally seen as ==better in urban areas==, as there is more access.
There is ==more social capital== in urban areas. McKenzie proposed higher social capital actually ==protects us from stress==. This means that it is ==unclear== how the mechanisms underlying ==urbanicity works==.
Does living in an urban area cause schizophrenia, or are people more willing to move to urban areas once they start experiencing schizophrenic symptoms? ==Pedersen and Mortensen== reported people with high risk of developing psychotic disorders reduced the likelihood of developing schizophrenia if they move to a rural area. Suggests link.
==Social isolation== could be a ==cause== or an ==effect==.
Ethnicity and discrimination. We cannot tell is ethnicity is cause and effect until we remove racism and prejudice from psychiatry.