Schizophrenia - Paper 3

What is Schizophrenia?

Psychotic disorder - individual has severe mental health issues that causes them to lose touch with reality.

Can not distinguish their own thoughts and ideas from reality.

First identified by Kraeplin (1886) - Dementia Praecox.

Bleuler (1911) - Schizophrenia.

Schizo = split.

Phrenia = mind.

Better understood as a split between cognition and emotion.

Prevalence of Schizophrenia

How common in the population.

Affects around 1% of population. 

1 in every 100.

Equally common in males and females.

Males - diagnosed in late teens to mid 20’s.

Females - diagnosed in early 30’s.

Prognosis of Schizophrenia

Expected outcome of mental health in terms of recovery.

Bleuler (1978) - longitudinal study of 2000 schizophrenics.

Found:

• Symptoms most severe in early adulthood (first 5 years after onset).

• 40% recover from positive symptoms.

• 20% full recover if diagnosed early.

• 40% continue to suffer symptoms for the rest of their lives.

Symptoms of Schizophrenia 

• hallucinations – hearing or seeing things that do not exist outside of the mind. They are faulty sensory input.

• delusions – unusual beliefs not based on reality

• muddled thoughts and speech based on hallucinations or delusions

• losing interest in everyday activities

• not wanting to look after yourself and your needs, such as not caring about your personal hygiene

• wanting to avoid people, including friends

• feeling disconnected from your feelings or emotions

Positive symptoms

Delusions.

Hallucinations.

Disorganised speech.

Negative symptoms

Flattened affect.

Reduced speech.

Lack of initiative.

What is classification?

Identifying groups or patterns of behavioural, emotional, physical or motivational symptoms that happens to form a mental disorder.

Syndrome - groups of symptoms happen together.

Important:

• helps in treatment.

• helps identify cause of their disorder.

• helps with prognosis - predicting the future course of disorder.

Diagnostic criteria

Set of signs, symptoms, and tests developed for use in routine clinical care to guide the care of individual patients.

The diagnosis typically guides treatment. 

Classification criteria

Standardised definitions grouping health issues into categories based on similar properties.

These categories may be grouped by type of disease, body system or anatomy.

Classification criteria have no treatment implications for patients

What is the DSM classification system?

First published in 1952.

Used by American Psychiatric Association.

Has had a number of revisions.

Current edition - DSM-5-TR published in 2022.

Has over 300 mental disorders arranged in several categories.

Each disorder - lists specific diagnostic criteria that must be met for diagnosis to be given.

Includes details on symptoms that have to be present and for how long (inclusion criteria) and details on symptoms that must not be met (exclusion criteria).

Reliability of diagnosis

Consistency of diagnosis.

2 or more practitioners make the same diagnosis of SZ of the same person.

Inter-rater reliability = clinicians make identical diagnosis of the same patient.

But does not always happen as shown:

Beck et al 1963 - reviewed 153 patients who had been diagnosed by multiple doctors found only 54% concordance rate between the doctors assessments, suggests there is low inter-rater reliability in the diagnosis of SZ. 

Could mean many people have been diagnosed incorrectly , potentially having inappropriate treatment.

Test re-test reliability (external reliability) - making the same diagnosis of the patient on separate occasions based on the same information.

Weakness of reliability of SZ diagnosis

Research study - Copeland (1970).

Shows how the culture of the clinician can damage inter-rater reliability.

Found - with the same description of a patient was given to British psychiatrists and US Psychiatrists 69% of US psychiatrists diagnosed the patient with SCH compared to just 2% of British Psychiatrists.

US clinicians are more likely to diagnose SCH than their UK counterparts.

Questions the reliability of the diagnosis of schizophrenia.

Patients may display the same symptoms but have different diagnoses due to the clinicians ethnic background

(With standard criteria) Inter- rater reliability cannot be guaranteed.

Potential influence of cultural bias.

Weakness of reliability of SZ diagnosis

Research study - Read (2004).

Test re-test analysis is as low as 37%.

Considering possible false positives and false negatives this could create. 

Patients without - diagnosed as having SZ.

Patients with - diagnosed as not having SZ.

People who need treatment may not get it or get the wrong treatment.

Strength of reliability of SZ diagnosis

Tool used in diagnosis. 

Farmer (1988) - standardised interview techniques known as Present state examination (PSE) focuses on frequency and severity of symptoms.

Increases reliability of diagnosing SZ.

Mental status test assessing a patient's current psychiatric condition.

Contains 140 items each scored on a 3-point or 4-point scale.

Can be learned by American-trained clinicians with inter-rater reliability comparable to that of British and European clinicians.

Using the right standardised tools - leads to reassurance for patients that the outcome and treatments they receive are based on diagnosis that would be consistent amongst practitioners.

Strength of reliability of SZ diagnosis

DSM improved the reliability.

DSM V - stripped the criteria out that was difficult to differentiate.

For example, deciding between bizarre (an impossible) delusion and non-bizarre (possible) delusions.

Mojtabi & Nicholson (1995) - 50 psychiatrists failed to differentiate between bizarre and non bizarre delusions.

May receive the wrong diagnosis.

Bizarre - belief of FBI putting a microchip inside you to track you.

Non-bizarre - belief of being followed by FBI.

Has helped to increase the reliability of diagnosis.

Adapts and changes certain specific criteria to make categorising more consistent.

Validity of SZ diagnosis

Accuracy of diagnosis.

Co-morbidity - when one or more disorders exists alongside a primary diagnosis, two different conditions co-exist in the same patient at the same time, questions validity of their classification (many people have multiple problems rather single problems), SZ with substance abuse or OCD.

Mental health = complex area not a simple one, challenges validity of diagnosis.

Overlapping symptoms - SZ shares symptoms with other conditions, leads to invalid diagnosis.

Symptoms of SZ = not pathognomic.

Bipolar disorder, OCD  and autism = overlapping symptoms.

Read et al (2011) - estimated 13 % of population hear voices but only 1% are diagnosed with SZ.

SZ and bipolar disorder = positive symptoms like delusions and negative symptoms like avolition.

This might lead to problems with diagnosis/classification as shared symptoms could lead to an incorrect diagnosis, show a symptom typical of SZ but could instead have another condition.

Weakness of validity of SZ diagnosis

Research evidence.

Rosenhan (1973) - investigated the reliability and validity of staff diagnosis in psychiatric hospitals, pseudo-patients with no mental illness pose as mentally ill to see if staff in hospitals could accurately diagnose them, 8 ‘sane’ people complain of hearing unclear voices saying ‘thud, hollow, empty’, all admitted to hospital and all but one was diagnosed with SZ, the other with manic-depressive psychosis.

Upon admission, all pseudo-patients stopped showing any ‘symptoms’ and took part in ward activities.

Average length of stay was 19 days.

Release = pseudo-patients were given the diagnosis of SZ  ‘in remission’.

2nd follow up study = one hospital was told that one or more pseudo-patients would try to be admitted, hospital staff were asked to rate the patients on the likelihood of them being a pseudo-patient.

44% were judged by at least one member of staff to be a pseudo patient.

No pseudo patients were ever sent.

Real patients with mental illness symptoms were turned away.

Psychiatrists could not reliably tell the difference between an insane or sane person.

Questions the reliability of a SZ diagnosis.

Normal behaviour was assumed as abnormal.  

Psychiatric diagnoses using the DSM-2 at the time was flawed.

Weakness of validity of SZ diagnosis

Research evidence - comorbidity reduces the validity of diagnosis.

Buckley et al (2009) - 50% of patients with a diagnosis of schizophrenia also have a diagnosis of depression (50%) or substance abuse (47%), post-traumatic stress occurred in 29% of cases and OCD in 23%.

Shows that schizophrenia commonly occurs alongside other mental illnesses and the disorders are co-morbid.

Hard to judge which part of the disorder is just SZ and which belongs to another disorder.

Meaning the wrong focus of treatment may be provided to the patient.

Weakness of validity of SZ diagnosis

Research evidence - overlapping symptoms can decrease the validity of diagnosis. 

Konstantareas and Hewitt (2001) - investigated the symptoms of autistic patients and patients of SZ.

Compared 14 autistic patients and 14 with SZ (all were male).

Found not all of the SZ patients had autism symptoms but 50% of autistic patients had the negative symptoms of SZ.

Symptom overlaps makes it difficult to come to a valid diagnosis.

Leads to treatments that are not directly targeting the SZ symptoms.

Strength of validity of SZ diagnosis

Classification systems like DSM - patients have to meet more than one criteria to be diagnosed with SZ.

One criteria for SZ is the characteristic symptoms.

Another criteria is social/occupational malfunction.

Both must be met as part of the diagnosis.

Symptoms must be present for a certain time frame. 

Diagnostic criteria that covers a variety of categories - helps to make accurate diagnoses.

Especially where symptoms are not physical.

Cultural bias and SZ diagnosis

DSM-V-TR and other manuals are culturally biased as they only consider individualistic western concepts.

Hallucinations - more acceptable in African cultures because of cultural beliefs in communication with ancestors, seen as bizarre and irrational, psychiatrists are culturally biased towards what is ‘normal’ in their culture, ethnocentric.

Hearing voices - in Maori culture matakites are visionaries (prophets) who hear voices, highly respected voices are not regarded as auditory hallucinations (Lakeman 2001).

USA - Whaley (2004) says that cultural bias is responsible for the over-diagnosis of African Americans with SZ, incidence of diagnosed SZ is 2.1 %, while Americans of European origin it is 1.4 %. 

Cochrane and Sashidaran (1996) - poverty and racism experienced by immigrants and refugees is likely to lead to poor mental health.

African Americans and English people of Afro-Caribbean origin are several times more likely than white people to be diagnosed with SZ.

Cochrane (1977) - reported that the incidence of SZ in the West Indies and Britain to be similar at around 1%.

 

Evaluation - culture bias has affected diagnosis

Research evidence.

Copeland - US psychiatrists diagnosed patients with SZ 69% compared to 2% in British psychiatrists, when given the same description of symptoms. 

Shows that the background of the clinician and their own cultural biases can impact diagnosis.

Leads to patients either getting the wrong treatment or no treatment at all.

Evaluation - culture bias affects SZ diagnosis.

Research evidence.

Malgady’s - demonstrated that in traditional Costrican culture hearing voices is interpreted as spirits talking to the individual, whereas in the USA this is interpreted as a core symptoms of SZ.

Clinicians have to be mindful of the cultures and beliefs people come from.

Ensures they are not imposing their own cultural bias when diagnosing people.

Evaluations - positive from culture bias in SZ diagnosis

Practical applications.

Finding cultural biases allows for training for psychologists into the differences in interpretation of symptoms in cultures.

Improves diagnosis - by being aware of the biases they can consciously try to avoid them.

More objective in their diagnosis process.

Highlights the problems.

Leads to a reduction in these biases and to more valid diagnosis for people from different cultural backgrounds.

Evaluation - positive of culture bias in SZ diagnosis

Come up with a ‘symptom pool’ (certain symptoms for each culture).  

For example - patients from different cultures may choose to describe only physical symptoms, only emotional symptoms, or both.

Very beneficial for the validity of diagnosis of SZ - helps understand differences in symptoms in different cultures.

Means that cultural norms can be taken into consideration when a diagnosis is made.

Gender bias and SZ diagnosis

Gender of the patient (and clinician) can impact accurate diagnosis of SZ.

Men are far more likely to be diagnosed.

Women are able to cope better with the symptoms.

The tendency for diagnostic criteria to be applied differently to males and females.

Research - shows males get diagnosed with SZ more than females.

Clinicians - ignore that there are different predisposing/risk factors between males and females.

Gives them different vulnerability levels at different points in life.

May be used to explain the gender difference in the onset of schizophrenia.

Women are under-diagnosed - validity of the diagnosis of SZ is poor.

The procedures for diagnosis works well only on patients of one gender. 

Clinicians fail to consider that males tend to suffer more negative symptoms than women and have higher levels of substance abuse, or that females have better recovery rates and lower relapse rates.

Misconceptions - affect the validity of a diagnosis as clinicians are not considering all symptoms.

Evaluation - gender bias affect diagnosis of SZ.

Research evidence - Beta bias.

Cotton (2009) - women recover more and suffer less relapse than their male counterparts.

Ignoring these facts would result in gender bias (a beta bias) in clinicians not considering important factors in the diagnosis and recovery from schizophrenia.

Means that key differences that may help treatment to be tailored to help the different genders could be ignored.

Diagnosis of SZ may not be valid.

Gender differences are not considered.

Limits full understanding of the unique experiences of SZ for the different genders.

Can impact treatment plans.

Evaluation - gender bias affects SZ diagnosis

Research evidence.

Nasser (2002) - early research on SZ was conducted on men only. 

Means lots of research findings concerning treatments and explanations of the disorder may be inappropriate for women (Alpha bias).

Androcentric.

Limits our ability to generalise the finding to both males and females.

Detrimental to valid diagnosis and treatment.

Evaluation - gender bias affects SZ diagnosis.

Research evidence.

Loring and Powell (1988) - conducted a study where 290 male and female psychiatrists read 2 cases, asked to judge the condition, using standardised diagnostic criteria.

Male or no gender information - 56% were diagnosed as having SZ.

Female only 20 % were diagnosed with SZ  (but gender bias was less prominent with female psychiatrists). 

Gender of the patient impacts diagnosis as well as the gender of the clinician.

Women are more likely to be misdiagnosed with depression and anxiety.

These disorders are more commonly identified in females.

Leads to incorrect treatment.

Prolonging the illness.

Evaluation - positive of gender bias in SZ diagnosis

Practical application.

Research - used to help train psychologists to not misdiagnose females who have SZ symptoms with other disorders associated with females.

Should result in more women receiving the correct diagnosis of SZ. 

Means that male patients should not be over diagnosed and should not receive a diagnosis of SZ that is incorrect.  

Findings from studies like Loring and Powell can help to show there are biases when diagnoses are made.

Help improves the validity of the process moving forwards.

The right diagnosis leads to the right treatment offered to the patients.

Biological explanation of schizophrenia

Received the greatest empirical support.

Sees mental disorders as having physical causes.

Genetic vulnerability.

Neural correlates: the role of the neurotransmitter dopamine.

Further Neural correlates: the structure of the brain.

Genetic explanation for schizophrenia

Genetic component to schizophrenia which predisposes some individuals to the illness. 

Development of SZ at least partly due to their genes. 

Explains why patients often have other family members with schizophrenia.

Could be inherited through faulty genes.

Candidate genes = been implicated in the development of schizophrenia from research.

C4 gene variations in chromosome 8 & 11.

Polygenic = not determined by a single gene but many.

Ripke et al 2014 found 108 genetic variants.

Little predictive power from this explanation.

Genes associated with SZ include those coded for the functioning of a number of neurotransmitters including dopamine.

Increases SZ by inheriting biochemical imbalances or brain structure abnormalities.

Sekar (2016) - C4 gene is involved in immune function and synaptic pruning.

Increased C4 activity = higher chance of developing SZ.

Increased C4 activity is a genetic mutation (survival value = helps the brain to adapt, learn and prune synapses that are no longer needed) but too much of this synaptic pruning can ‘backfire’.

In adolescents = synaptic pruning occurs in the brain to help the brain prune ‘under used’ or ‘damaged’ synaptic connections making space for new ones.

C4 = excessive pruning can lead to cognitive symptoms seen in SZ.

Explains why SZ emerges after adolescence/early adulthood .

Explains why the brains of SZ patients have a thinner cerebral cortex with fewer synapses.

Family studies = find individuals who have SZ and determine whether their biological relatives are also affected more often than non-biological relatives.

Gottesman & Shields (1991) = if both parents suffer from SZ then there is a 46% chance of also developing the disorder (compared to a 1% chance for the general population).

Findings = greater the degree of genetic relatedness, the greater the risk of developing SZ.

Gottesman’s study - genes do play a role but if only cause then it would be 100%.

Seen as deterministic - just because we are ‘predisposed’ cannot mean we necessarily get SZ. 

Many researchers accept that SZ concordance rates in families may be more to do with common rearing patterns or other environmental factors.

Tienari et al (2000) = adoption study in Finland, 164 adopted kids whose biological mothers had SZ, matched with kids whose biological mothers did not have SZ.

Found = 11 whose mum’s had SZ had also been diagnosed with SZ compared to just 4 from the control group. 

Validates the idea that SZ has a genetic component as the adopted children do not share environmental influences with their biological mothers.

Twin studies - help researchers to work out whether nature or nurture has the greatest influence.

Joseph (2004) = found how genetic similarity can increase risks of developing SZ, from pooled data carried out before 2001, 40% concordance rate in SZ for MZ twins (who share 100% genetic similarity) and a 7% concordance rate for DZ twins (who share 50% genetic similarity).

The higher concordance rate for MZ twins (when the environmental influences on both groups were assumed to be the same) suggests genes have some influence on the development of the disorder.

Neural correlates (dopamine hypothesis) explanation for SZ

Biochemical explanations - argues SZ is caused by elevated levels of dopamine (DA) at key synaptic sites within the subcortical regions of the brain like the mesolimbic pathway and limbic system (brain area governing emotion).

Excess of dopamine = shown in the symptoms of schizophrenia.  

Dopamine neurons - regulate attention.

Process is disturbed - leads to problems with attention, perception and thought.

Neurons that use ‘dopamine’ fire too often and transmit too many messages.

Certain D2 receptors = play a key role in guiding attention and perception.

Lowering DA activity helps remove the symptoms of schizophrenia.

Main Dopamine hypothesis = have high numbers of D2 receptors on receiving neurons, more dopamine binding and more neurons firing.

Theory claims = excessive amounts of dopamine or an oversensitivity of the brain to dopamine is the cause of SZ. (hyperdopaminergia).

States that messages from neurons that transmit dopamine fire too easily or too often - leads to positive symptoms of SZ.

Evidence from drugs = antipsychotic drugs (dopamine antagonists) which block the activity of dopamine in the brain, reduces stimulation of the dopamine system, eliminates hallucinations and delusions.

Revised Dopamine Hypothesis = Davis et al (1991) suggests that negative symptoms of SZ like avolition can be explained by lower levels of dopamine in the prefrontal cortex where there is no D2 receptors (hypodopaminergia).

Hyperdopaminergia in the subcortex = focuses on the possible role of high levels of dopamine in the subcortex (central areas of the brain).

Broca’s area (speech production) and the experience of auditory hallucinations linked to positive symptoms of SZ.

Hypodopaminergia in the cortex =  focuses on abnormal dopamine systems in the brain’s cortex.

Goldman-Rakic et al.(2004) = identified a role for low levels of dopamine in the prefrontal cortex (responsible for thinking and decision making) in the negative symptoms of SZ.

Evidence for DA Hypothesis includes:

Amphetamines (speed - methamphetamine) = dopamine agonist stimulates nerve cells containing dopamine causing the synapse to be ‘flooded’ – large doses can cause hallucinations and delusions.

Cocaine = increases the levels of dopamine in the brain, causes the positive symptoms of SZ exaggerating them.

Antipsychotic drugs (dopamine antagonists) = blocks the activity of dopamine in the brain, reduces the stimulation of the dopamine system, eliminates hallucinations and delusions.

Antipsychotic drugs strengthen the case for dopamine being a significant contributory factor.

Further neural correlates explanation for schizophrenia

Neural correlates = measurements of the structure or function of the brain that occur in conjunction with or are correlated with SZ.

SZ is linked to structural abnormalities in the brain  and biochemistry.

Brain scanning techniques have made it possible to investigate living brain images. 

Both positive and negative symptoms have correlates (brain structure changes correlate with symptoms of SZ).

Enlarged ventricles = ventricles are cerebrospinal fluid filled cavities, brains are lighter than normal, grey matter volume shrinks in SZ patients as ventricles enlarge, consequence of nearby parts of the brain not developing properly or being damaged, links to active loss of grey matter in early stages of SZ which is consistent with onset of SZ in late teens or early 20’s, loss of grey matter leads to cognitive decline linked to negative symptoms.

Ventral striatum = involvement in SZ is multifaceted, underactivity in response to potential rewards contributes significantly to the debilitating negative symptoms such as apathy that strip individuals of their drive and capacity for pleasure, overactivity driven by a dysregulated dopamine system, fuels the positive symptoms.

Superior Temporal Gyrus = part of a larger network of brain regions involved in language and auditory processing, connections between the STG and other areas, such as the prefrontal cortex, are disrupted, failure to correctly identify the source of inner speech, perceived as an external voice (auditory hallucinations - a positive symptom).

Anterior Cingulate Gyrus = brain's limbic system, heavily involved in a wide range of functions, emotional regulation, decision-making, error detection, and attention, reduced activity (hypoactivation) in the ACG, particularly in response to emotional stimuli, contributes to negative symptoms such as the flat effect.

Strength of genetic explanation of SZ

Research evidence.

Joseph (2004) - found that genetic similarity can increase risks of developing the condition.

40% concordance rate in schizophrenia for MZ twins (who share 100% genetic similarity).

7% concordance rate for DZ twins (who share 50% genetic similarity).

The higher concordance rate for MZ twins suggests genes have a significant influence on the development of the disorder. 

Heredity must have a key part to play in causing SZ as there is such a high concordance rate for SZ in MZ twins.

Adds credibility.

Strength of genetic explanation of SZ

Research evidence using objective measures.

Ripke et al (2014) - carried out a study combining all previous data from genome-wide studies of SZ.

The genetic makeup of 37000 patients was compared to that of 113000 controls.

108 separate genetic variations were associated with increased risk of SZ.

Heredity has a key part to play in SZ has been supported by scientific data.

Adds further credibility.

Weakness of genetic explanation of SZ

Reductionist explanation.

Focus of this explanation is only biological, at the genetic level of explanation.

Ignores the role of psychological and environmental factors.

For example, people who suffer economic deprivation and are poorer are considered to be much more at risk from SZ at a societal level of explanation or at the Psychological level of explanation.

SZ can be due to faulty information processing in the cognitive explanation.

Should consider more than one level of explanation to understand a complex disorder.

Means the biological explanation alone is too simplistic.

Weakness of genetic explanation of SZ

Considered incomplete as other alternative explanations.

For example, genetics cannot be the sole cause of SZ, because if this was the case MZ twins would have a concordance rate of 100% (as they have 100% shared genes).

However as this is not the case, nurturing (environmental) influences must play a role.

Some environmental factors linked to SZ could be family dysfunction and dysfunction in cognitive processes of external stimuli. 

Need to look wider than just genetics to fully understand the cause of SZ as this could mean help with a variety of treatments based on different explanations that would help SZ patients have a better chance of recovery.

Strength of neural correlates explanations of SZ

Research evidence.

Randrup & Munkvad = created SZ like behaviour in a sample of rats by giving them DA agonists (amphetamine- AMP).

The rats were given AMP to raise the DA levels.

Showed long lasting abnormalities inducing behaviour such as being unable to filter out irrelevant sounds.

This was reversed by using antipsychotic drugs that reduced DA levels.

Dopamine may be implicated in humans who experience SZ.

Adds credibility.

However, this outcome was seen in rats so results from animal research may be limited to some extent in explaining human behaviour linked to excess DA.

Strength of neural correlates explanations of SZ

Practical application. 

Identifying DA as a possible cause of SZ it has allowed clinicians to formulate drugs to target this problem and be able to prescribe antipsychotic drugs which reduce levels of DA and help patients go into remission.

This implies that by targeting dopamine as the cause, this has helped guide the most common and popular form of medical treatment of anti-psychotics that has helped many patients to overcome this debilitating disorder and get back to living more productive lives in society again.

Weakness of neural correlates explanations of SZ

Reductionist 

Focus of this explanation is only biological, at the neurochemical level of explanation.

Ignores the role of psychological and environmental factors.

For example, people who suffer economic deprivation and are poorer are considered to be much more at risk from SZ at a societal level or the idea that dysfunctional families may create an environment that can initiate the onset of SZ at a psychological level of explanation.

Should consider more than one level of explanation to understand a complex disorder such as SZ.

Biological explanation of DA alone is too simplistic for a full understanding of the development of SZ.

Weakness of neural correlates explanations of SZ

Alternative explanations.

For example, antipsychotics have been shown to be effective in up to 85% of patients with SZ, which poses the question of why decreasing the dopamine activity for the remaining 15% of patients isn’t decreasing their symptoms as they do not respond to medication targeting dopamine levels.

The DA explanation cannot explain SZ in all patients.

This implies that there must explanations other than just this biological reason for example genetic predispositions or psychological explanations like dysfunctional cognitive processing could help explain the onset of SZ for those who do not respond to medication that only targets excess DA levels.

Strength of further neural correlates explanation

Research evidence.

McEwen (2007) argues that nurturing influences could actually instigate structural changes in the brain. 

Children and adolescent brains are far more sensitive to chronic stressors (such as prenatal stressors or physical abuse) which can reshape the structure and organisation of cortical regions, contributing to symptoms of SZ.

This suggests that the structural changes may actually be caused by nurture/environment having an interplay with biology to develop the symptoms of SZ.

Weakness of further neural correlates explanation

Reductionist. 

Focus of this explanation is only biological, at the anatomical level.

Ignores the role of psychological and environmental factors.

For example, people who suffer economic deprivation and are poorer are considered to be much more at risk from SZ at a societal level or the idea that dysfunctional families may create an environment that can initiate the onset of SZ at a psychological level of explanation.

This implies that psychologists should consider more than one level of explanation to understand a complex disorder such as SZ.

The biological explanation alone is too simplistic for a full understanding of the development of SZ.

Weakness of further neural correlates explanation

Methodological issues as research studies in this area are correlational.

Cannot establish that neural correlates is the definitive cause of SZ.

For example, it is still uncertain whether structural abnormalities lead people to acquire SZ or whether the onset of SZ causes these structural changes or in fact if other factors completely have a key part to play in the acquisition of SZ i.e. high dopamine levels or genetics. 

This implies that a true causal relationship cannot be reliably established for SZ and structural abnormalities.

More research needs to continue to be done to fully understand the reasons for the development of SZ.

Weakness of further neural correlates explanation

Alternative explanations.

For example, structural abnormalities cannot be the sole cause of SZ, as of this were the case, all SZ patients would have some structural abnormalities that could be identified.

This is not the case and many have no signs of structural abnormalities but do suffer from the disorder.

This suggests we need to look beyond structural abnormalities to fully understand the cause of SZ as this could mean patients can be offered a variety of different treatments based on other explanations like DA hypothesis (antipsychotic drugs).

Which could help a wider range of SZ patients to have a better chance of recovery.