SZ - Biological Explanations + Treatments

What are the key explanations for SZ?

• genetics

• dopamine

• neural correlates

A genetic basis for SZ…..

• song evidence to suggest people have a predisposition to develop the problems that lead to a diagnosis of SZ

• disorder is in someway genetically inherited

• this evidence comes in two strands - relatives and specific genes

Relatives explanation

• evidence (Gottesman) indicates that people who have relatives diagnosed as SZ have a greater risk of developing the disorder themselves -closer the biological relationship, the greater the risk

• also derived from research which indicates that SZ in universal, prevalent in all cultures and groups of people

• this supports a genetic argument as it indicates that SZ is still prevalent even when the environment changes

Specific genes explanations …

some researchers have attempted to identify specific genetic abnormalities which lead to the disorder….

• Kelly and Murray 2000: argue that people need to inherit a number of defective genes in order to develop SZ, as its a complex disorder with a range of symptoms

• Curling 1989: identified chromosome 5 as being linked to SZ as he found that many SZ’s had abnormalities on this chromosome, however this chromosome holds over 1000 genes, so it does not identify specific genes which are responsible for the disorder

then Ripke 2014, identified that SZ is what and how?

• polygenic - multiple genes play a part on the offset

• conducted one of the largest genome wide association studies ever done, analysing over 37000 patents with SZ

• they identified 108 separate genetic loci associated with increased risk of SZ

limitation of genetic explanation: clear evidence of environmental factors, making the explanation incomplete and too simplistic (tienari Finnish adoptees)

• clear evidence to show that environmental factors also increase the risk of developing SZ making the explanation incomplete and too simplistic

• SZ only developed at high rights when the adoptive family environment was dysfunctional;, children with the same genetic risk places in healthy families were less likely to develop SZ

• this shows that SZ cannot be explained by genes alone because environmental experiences play a major role in whether the disorder actually develops. gene if someone has a genetic vulnerability, they may never show symptoms unless certain environmental triggers occur

strength of genetic explanation - twin studies (Cardno 2002)

• Cardno conducted a Twin study of SZ where he used the Maudsley TWIN REGISTER (used strict diagnostic criteria increases validity of conclusions)

• found a concordance rate of 26.5% across MZ and 0% across DZ twins

• here DZ twins serve as a control groups, if SZ was caused by nurture factors, we would expect the concordance rates between MZ and DZ twins to be the same

• however the concordance rates between MZ twins is significantly higher so this is strong evidence that SZ has genetic basis

The Dopamine Hypothesis

• assumption that SZ is caused by neurological abnormalities

• in particular the way synapses communicate with each other and with the electrical messages/impulses which are produced in the brain and which influence behaviour

• Dopamine is thought to have many roles, including the initiation and control pf movements and regulating high order cognitive functions like perception, motivation ad behaviour

what ddi the original dopamine hypothesis argue that SZ may be a result of

high levels of dopamine activity in the sub cortex

what are these high levels known as

hyperdopaminergia

what can this explain (high levels) -brocas

• positive symptoms like hallucinations

• also explains speech problems due to excess receptors in the Broca’s area

function of dopamine - regulation of brocas area, symptoms when in excess…

• overstimulates neural lining

• causing disorganised speech

• too much dopamine causes a person to produce multiple speech streams at once

function of dopamine - perception (interpretation of sensory info), symptoms when in excess…

• overperception

• leads to hallucinations as we are unable to accurately perceive info in our environment

function of dopamine - perception of pain, symptoms when in excess…

• the brain may generate false pain sensations - tactile hallucinations

• due to increase of transmission of nerve cells

function of dopamine - cognition and reasoning, symptoms when in excess…

• causes overthinking - not effectively reasoning leading to delusions and paranoia

• misinterpretation of reality

• difficulty filtering irrelevant info

function of dopamine - initiation of movement, symptoms when in excess…

• excessive or abnormal movement

• leading to CATATONIA symptoms - agitation of complete immobility

what is hypodopaminergia?

low levels of dopamine in the pre-frontal cortex

function of dopamine - supports decision making, functioning, problem solving, symptoms when in lack…

• avolition: lack of motivation because the PFC cannot initiate goal directed behaviour

function of dopamine - regulates working memory, symptoms when in lack…

• alogla: poverty of speech due to impaired cognitive processes

function of dopamine - enables cognitive flexibility, switching tasks, adapting behaviour, symptoms when in lack…

• flat affect

• reduced emotional expression due to PFC not being able to regulate emotional output

function of dopamine - maintains attention, symptoms when in lack…

• anhedonia

• reduced ability to experience pleasure linked to disrupted reward processing

strength of dopamine hypotheses: supporting evidence - amphetamines

• P : Research supports the dopamine hypothesis because increased dopamine activity is associated with schizophrenia-like symptoms.

• E: Amphetamines increase dopamine activity and can produce hallucinations and delusions in healthy people. They can also worsen symptoms in people with schizophrenia.

• E: This suggests that excessive dopamine activity may contribute to the development of positive symptoms, supporting the dopamine hypothesis.

• L: Therefore, this provides evidence for the role of dopamine in schizophrenia

more supporting evidence for DH - antipsychotic drugs

• P: The effectiveness of antipsychotic drugs supports the dopamine hypothesis.

• E: Many antipsychotic drugs, such as chlorpromazine, block dopamine receptors (D2receptors), reducing dopamine activity.

• E: These drugs often reduce positive symptoms, such as hallucinations and delusions.This suggests that dopamine activity is involved in these symptoms because reducing its effects can improve them.

• L: Therefore, this supports the dopamine hypothesis by providing evidence that dopamine is involved in schizophrenia.

limitation of DH: confuses cause and effect - too much dopamine may not be the cause

• P: The dopamine hypothesis may confuse cause and effect.

• E: Antipsychotic drugs can reduce dopamine activity, but they may take several weeks to have their full therapeutic effect.

• E: This suggests that schizophrenia may involve other processes besides dopamine activity, as blocking dopamine receptors does not immediately remove symptoms. Therefore, dopamine abnormalities may not be the sole cause of schizophrenia.

• L: This weakens the hypothesis because it suggests that dopamine alone cannot fully explain schizophrenia.

limitation of DH - ignores other neurotransmitters

• P: The dopamine hypothesis may be an oversimplification because it ignores the role of other neurotransmitters.

• E: Research suggests that glutamate, another neurotransmitter, may also be involved in schizophrenia.

• E: This suggests that schizophrenia may result from abnormalities in several neurotransmitters systems rather than dopamine alone. Therefore, focusing only on dopamine cannot provide a complete explanation of the disorder.

• L: This reduces the explanatory power of the dopamine hypothesis because it cannot account for all the factors involved in schizophrenia.

Neural Correlates - what are they?

• patterns if structure or activity in the brain that occur in conjunction with an experience

• may be implicated in the origins of that experience - could tell us what causes the activity

• there are neural correlates for both positive and negative symptoms

Neural correlates of negative symptoms are….

Ventral Striatum

Neural Correlates for positive symptoms are

• Superior Temporal Gyrus

• Anterior Cingulate Gyrus

Role of Ventral Striatum

• part of the reward system

• involved in motivation, anticipating rewards and goal directed behaviour

what happens if there is reduced activity in the Ventral Striatum (symptoms)

• abolition: no motivation , rewards don’t register properly

• flat effect: emotional blunting

• anhedonia: reduced ability to feel pleasure

role of Superior Temporal Gyrus and Anterior Cingulate Gyrus

• processes auditory information

• involved in language perception

what goes wrong to trigger positive symptoms in this areas?

• structural abnormalities

• reduced grey matter

• leads to misprocessing

what happens if there a structural abnormalities and reduced grey matter in the STG and ACG (symptoms)

• auditory hallucinations

• hearing voices because brain misinterprets internal speech as external sound

limitation of neural correlates: other factors could explain findings

P: Neural correlates may not be the only explanation for schizophrenic symptoms.

E: Psychological factors, such as stress, may influence the onset or severity of symptoms.

E: This suggests that brain activity may interact with environmental experiences, rather than being the sole cause of schizophrenia.

L: Therefore, the explanation may be reductionist because it focuses on biological factors and overlooks the possible role of psychological and environmental influences.

strength for neural correlates: practical application

P: Research into neural correlates can lead to effective treatments.

E: Antipsychotic medication can affect neurotransmitter activity, particularly dopamine, which is linked to some symptoms of schizophrenia.

E: If abnormal neural activity contributes to symptoms, treatments targeting the relevant biological processes may help reduce them.

L: Therefore, neural correlates research has practical value because it can inform biological treatments and improve our understanding of how symptoms may be managed.

limitation of neural correlates: cause and effect cannot be established

P: A weakness is that neural correlates research cannot establish cause and effect.

E: Researchers identify differences in brain activity between people with schizophrenia and people without the disorder.

E: It is unclear whether abnormal brain activity causes schizophrenia or whether having schizophrenia leads to changes in brain activity.

L: Therefore, the explanation may not fully explain the development of schizophrenia because it only establishes an association, not a causal relationship.

Biological therapies for SZ: DRUG THERAPY

• developed in 1950s - antipsychotics

• rooted in the assumptions of the biochemical theory of SZ

• biochemical theories which argue that AZ is a result of biochemical imbalances

• SZ drugs focus on the action of the NT Dopamine - aiming to reduce the action/activity at dopamine receptor sites

Typical Antipsychotics such as Chlorpromazine work by…

• blocking the receptors in the synapse that absorb dopamine

• reducing positive symptoms of the disorders - auditory hallucinations and delusions

Atypical Antipsychotics such as Clozapine work by….

• acts on serotonin as well as dopamine systems

• affects negative symptoms of the disorder like reduced motivation

About typical antipsychotics - side effects and origin

• first antipsychotic developed, in 50s

• however are now seen to affect other NTs which lead to a number off side effects

• much worse side effects than atypical

• key side affect is tardive dyskinesia: uncontrollable muscle movements, twitches without realising you are doing it

• main reason for atypicals being produce

atypical

• side effects seen as less severe - still quite bad

• Weight gain, High fever, Sweating Unstable blood pressure\muscle rigidity, Blood clots Diabetes, Muscle tremors

• Reduces likelihood of developing tardive dyskinesia compared to typical antipsychotics

  

strength of drug treatments: cost effective

• P: Drug therapy can be cost-effective.

• E: Antipsychotics are relatively inexpensive and can reduce the need for long hospital stays by helping patients manage their symptoms.

• E: This means healthcare services may spend less money on long-term inpatient care.

• L: Therefore, drug therapy is a practical treatment that can benefit both patients and healthcare services.

limitation of drug treatments: treats symptoms rather than underlying symptoms

• P: Drug therapy may not address the underlying causes of schizophrenia.

• E: Antipsychotics mainly reduce symptoms by affecting neurotransmitter activity, particularly dopamine.

• E: However, schizophrenia may involve several factors, including genetic, psychological and environmental influences.

• L: Therefore, medication may manage symptoms without resolving all the difficulties associated with schizophrenia.

strength for drug treatments: research support (placebo)

• P: Drug therapy is effective in treating schizophrenia.

• E: Thornley et al. reviewed studies comparing chlorpromazine with a placebo and found that chlorpromazine was more effective at reducing symptoms.

• E: This suggests antipsychotics can reduce symptoms such as hallucinations and delusions.

• L: Therefore, this supports the effectiveness of drug therapy as a treatment for schizophrenia.

limitation of drug therapies: side effects

• P: A weakness of drug therapy is that it can cause unpleasant side effects.

• E: Typical antipsychotics, such as chlorpromazine, can cause sedation and movemen tdisorders, including tardive dyskinesia.

• E: These side effects may make patients reluctant to continue taking their medication.

• L): Therefore, drug therapy may be less effective in the long term if patients stop taking their medication.

additional limitation - dopamine hypothesis suggests…

• that SZ is primarily caused by dopamine activities

• drug effectiveness is heavily tied to the dopamine hypothesis

• creates a theoretical problem as it means that the antipsychotics only work if dopamine is the cause - again only reducing symptoms not underlying cause

• SZ is not purely dopaminergic

• if the dopamine hypothesis his incomplete or partially wrong then frug treatments are limited