Issues affecting the reliability and validity of Schizophrenia diagnosis

Hello everyone, sorry it's been a while! Thought I'd finally finish off the last schizophrenia post - diagnostic criteria, and issues affecting diagnostic validity. As usual:

Black: AO1 - Description
Blue: AO2 - Evaluation - studies
Red: AO2 - Evaluation - evaluative points/IDAs

Diagnostic Criteria

The diagnostic criteria for schizophrenia were separated by Schneider into two sets: "First-rank" and "Second-rank" symptoms, and it was suggested that having one of the 1st rank symptoms means that you are likely to have schizophrenia. The ICD (International Classification of Diseases) still focuses on 1st-rank symptoms, but the DSM (Diagnostic and Statistical Manual of mental disorders) has moved away from them.

First-rank symptoms include delusions (e.g of control, or persecution), auditory hallucinations, and thought disturbances (the belief that either your thoughts are being broadcast for others to hear, or that others are inserting thoughts into your head.)

Second-rank symptoms include disturbances of speech such as fragmentation, interruption, and incoherency, catatonic symptoms such as stupor, mutism and repeated movements, and "negative" symptoms such as apathy, avolition, a flattened range of emotional expression, and a lack of communication.

However, an issue with the concept of first-rank symptoms is that many other conditions such as bipolar disorder share these symptoms, threatening validity of diagnosis - the presence of just one first-rank symptom without any second-ranks to help make a more specific diagnosis could lead to a bipolar patient being incorrectly diagnosed with schizophrenia instead, under the ICD's diagnostic criteria.

Diagnostic Issues

Due to the two different classifications for diagnosis, criterion validity is an issue - the extent to which two different diagnostic systems agree. If schizophrenia can be diagnosed using one but not the other, either could be a potentially invalid diagnosis - one must be incorrect.

The DSM-V diagnoses schizophrenia on 5 axis: 1 and 2 for symptoms, 3 for medical conditions, 4 for social conditions, 5 for state of function. It no longer differentiates between subtypes of schizophrenia, as these are unreliable due to symptom overlap between subtypes and prominent symptom changes. To be diagnosed, a patient must have two of the criteria, one of which must be first-rank. The symptoms must be present for the last 6 months, and active for at least one.

The ICD-10 differentiates between 7 subtypes of schizophrenia, such as catatonic, paranoid, residual and undifferentiated, based on most prominent symptoms. To be diagnosed under the ICD, the patient must display one first-rank symptom, or two second-rank symptoms. It places much more emphasis on first-rank symptoms by allowing a patient to be diagnosed based on the presence of just one of them.

Comorbidity is another potential problem with schizophrenia diagnosis - the presence of one or more additional disorders occurring alongside schizophrenia makes it difficult to identify which disorder is the cause of a specific symptom, making it harder to diagnoses the correct disorders and treat them accordingly and reducing diagnostic validity.

Buckley et al (2009) analysed medical records of their schizophrenic patients, and found that 50% had depression, 47% had substance abuse disorders, 29% had PTSD, and 15% had panic or anxiety disorders. Bottes (2009) carried out a similar analysis for the Psychiatric Times, and found that 26% of schizophrenic patients had OCD, 52% had obsessive compulsive symptoms. These studies suggest that many schizophrenics have multiple disorders, and this should be taken into consideration when diagnosing patients in order to avoid an invalid diagnosis.

Contrastingly, symptom overlap can also invalidate diagnosis - many disorders share symptoms with schizophrenia, meaning that the wrong disorder could be diagnosed based on a specific, shared symptom.

Zorumski and Rubin (2013) found that bipolar disorder's most prominent symptom, severe episodes of mania, often includes delusions, hallucinations and catatonia - all symptoms that could lead to a bipolar sufferer being incorrectly diagnosed with schizophrenia.

Marsha et al (1995) found that 32% of bipolar sufferers showed 1st-rank symptoms of schizophrenia, and Carpenter (1974) found that 16% of depression sufferers showed them, suggesting that there is a clear symptom overlap between the conditions that could affect validity of diagnosis. 

Ross (1998) found that the more 1st-rank symptoms a patient displays, the more likely they are to be diagnosed with multiple personality disorder rather than schizophrenia, suggesting that 1st-rank symptoms are an indicator of MPD rather than schizophrenia specifically.

Reliability

Reliability is the consistency of diagnosis, measured by inter-rater reliability, internal consistency (if multiple patients with the same symptoms will be diagnosed in the same way) and test-retest consistency.

Several factors can reduce reliability of schizophrenia diagnosis. The main diagnostic method is the clinical interview, and individual differences between clinicians will mean different responses according to the age, personality, aptitude of the rater, as well as the bond of trust between the psychologist and the patient. These all reduce inter-rater reliability. The severity of symptoms at the time of diagnosis can affect the test-retest consistency, and deception can affect general reliability, as evidenced by Rosenhan's 1973 study.

In Rosenhan's 1973 study, 8 psychologists turned up at mental hospitals claiming to have experienced auditory hallucinations. Upon admission for schizophrenia, they stopped presenting symptoms, and were kept in for 7-52 days despite no further schizophrenic symptoms, and were given over 2000 doses of antipsychotic drugs between them. A followup on this told a mental hospital to expect pseudopatients over the next 3 months - 83 out of 193 patients were suspected of being pseudopatients by at least 1 medical professional, but they were all actually genuine.

Although based on the DSM-II criteria at the time of at least 1 auditory hallucination, the diagnoses were both reliable and valid, the admissions only showing an inability to recognise a lie, Rosenhan claimed from these results that psychiatrists could not make a consistent and accurate diagnosis. He suggested that patients' behaviour was viewed through their label of mental illness - the original set of pseudopatient psychologists' behaviour was pathologised, with note-taking observations being pathologised as "writing behaviour".

Rosenhan's conclusions lack temporal validity - the modern version of the DSM has been revised to have more stringent diagnostic criteria. Symptoms must now be present for 6 months and active for 1 month in order for schizophrenia to be diagnosed.

Once institutionalised, the participants were passive, not normal - passively keeping up the deception rather than admitting to their lie, and the relative speed of release in light of this could actually have suggested competent and efficient mental health staff.

Rosenhan's suggestion that psychiatrists cannot reliably and accurately diagnose has been challenged by: 

Jakobsen (2005) who tested 100 Danish schizophrenic patients and assessed them based on their case notes, coming to a correct diagnosis for 98% of them.

Hollis (2000) who used the DSM-IV and case notes to correctly assess and diagnose 100% of a sample of schizophrenic patients. 

These results suggest that mental health professionals are much better at diagnosing schizophrenia nowadays, and this part of Rosenhan's conclusion lacks temporal validity.

Cultural bias in diagnosis

Emic constructs are behaviours or norms that only apply to a certain number of cultures, whereas etic constructs apply globally. When an etic construct is considered to be a universal norm, this is imposing an etic. Eurocentrism leads to imposed etics in the diagnosis of schizophrenia, as the imposed etic of the DSM is used to apply a western, subjective idea of perfect mental health to non-western cultures. If people from one culture are assessing people from another, behaviour can be misconstrued, leading to an invalid diagnosis.


Cultural difference could help to explain the higher rates of schizophrenia diagnosis in some ethnic minorities. If someone is uneasy talking to a psychologist of a different ethnicity to them, they may show withdrawal, alogia, and a lack of eye contact - all of which could be interpreted as symptoms of schizophrenia, reducing diagnostic validity.

Cochrane (1977) found that schizophrenia rates in the UK and in the West Indies are very similar, and close to 1%, but people in the UK of Afro-Caribbean origin are 7 times more likely to be diagnosed with schizophrenia than those of white European ethnicity. Migration stress and socioeconomic factors were ruled out, as other ethnic groups such as South Asian that migrated at a similar time are no more likely to be diagnosed, suggesting that there is a bias that leads to racial overdiagnosis of Afro-Caribbean people.

Harrison (1997) supports the temporal validity of Cochrane's earlier research, finding that 20 years later, the gap in racial diagnosis rates had widened - Afro-Caribbean patients were now 8 times more likely to be diagnosed with schizophrenia. 

Stowell-Smith and McKeown (1999) carried out a discourse analysis of psychiatrists' reports on 18 white and 18 black psychopaths, and found that with black psychopaths there was more emphasis on aggression and potential threat to society, compared to a greater emphasis on trauma and emotional state with white psychopaths. This suggests a racial bias in the area of psychopathology that leads to biased reporting of symptoms, calling diagnostic reliability into question. 

Read (1970) gave 194 UK and 134 US psychiatrists a case report and asked them to come to a diagnosis from it. 69% of US and 2% of UK psychiatrists diagnosed schizophrenia from it, suggesting large cultural differences in behaviour interpretation and diagnostic criteria. 

Neki (1973) studied the prevalence of catatonic schizophrenia among schizophrenics in the UK and India, and found the rate was 44% in India but only 4% in the UK, again suggesting large cultural variations in behaviour interpretation and classification.

Schizophrenia - cognitive therapies

One more schizophrenia post after this one - diagnosis, reliability & validity. This post will cover Cognitive Behavioural Therapy and Cognitive Behavioural Family therapy, two psychological treatments for schizophrenia. There's probably more here than you can expect to write in half an hour, so pick your favourite studies and relevant evaluative points and use those. The only one I would recommend to definitely use would be be Falloon et al (1985), as it is some strong supporting evidence for the efficiency of CBFT compared to CBT.

Black: AO1 - Description
Blue: AO2 - Evaluation - studies
Red: AO2 - Evaluation - evaluative points

Cognitive Behavioural Therapy

CBT is not a "cure" for schizophrenia, as the cognitive distortions and disorganised thinking associated with schizophrenia are a result of biological processes that will not right themselves when the correct interpretation of reality is explained to the patient. The patient is not in control of their thought processes. The goal of CBT is to help the patient use information from the world to make adaptive coping decisions - improving their ability to manage problems, to function independently and to be free of extreme distress and other psychological symptoms. CBT teaches them the social skills that they never learned, as well as how to learn from experience and better assess cause and effect. Skills taught often address negative symptoms, such as alogia, social withdrawal and avolition, and can include social communication skills, the importance of taking antipsychotics routinely, and managing paranoia and delusions of persecution by challenging the evidence for these irrational beliefs.

Cognitive Behavioural Family Therapy (CBFT) is designed to delay relapse by helping the family of the schizophrenic to support the patient, by methods such as stress management training, relaxation techniques, communication and social skills, emphasis on the importance of antipsychotic drugs, and assessment of expressed emotion. High levels of expressed emotion on scales of hostility, emotional over-involvement and critical comments have been linked to rehospitalisation, so CBFT uses cognitive and behavioural methods to lower the emotional intensity of the patient’s home life. It has two general goals: To educate family members about schizophrenia, and to restructure family relationships to facilitate a healthier emotional environment.

Laing suggested the most important factor in the progression of schizophrenia is the family and how they treat the patient. A study by Brown (1972) supports this - he studied family communication patterns in schizophrenics returning home after hospitalisation.  Results showed that communication was a critical variable in whether patients would relapse into a psychotic state – patients returning to homes with a high level of expressed emotion were much more likely to relapse than those returning to homes with a low level. This supports the role of expressed emotion in determining long-term outcomes for schizophrenics.

Vaughn + Leff (1976) studied 128 schizophrenics discharged from hospital and returned to their families. Communication patterns between family members were rated for EE. The crucial finding was that families showing high levels of negative expressed emotion (Hostility, over-involvement, criticism) were more likely to have their patient relapse than families showing low levels of negative EE. Relatives with high levels of negative EE responded fearfully to the patient, characterised by lacking insight into and understanding of the condition. 

Leff + Vaughn (1985) found that a high level of positive EE with communication patterns showing warmth and positive comments is associated with prevention of relapse. They concluded that not all expressed emotion is detrimental to the relapse prospects of the patient. 

Sarason + Sarason (1998) summarised key findings from research into EE and schizophrenia: 

• Rates of EE in a family may change over time – during periods of lower symptom severity, rates of negative EE drop and vice versa. High rates of EE may only reflect periods of high symptoms severity, and not be an overall reflection of the family dynamic. 
• Cultural factors may play a role in EE. The association between high EE rates and relapse has been replicated in many cultures, but cultural factors may influence rate of EE and the way it is communicated. Cross-cultural studies have shown that Indian and Mexican-American families show lower levels of negative EE than Anglo-American families. 
• EE is not limited to families. The association between EE and relapse has been demonstrated with patients living in community care - the significant factor could be communication patterns between patient and those they live with, rather than with family. 

Falloon et al (1985) found a markedly lower relapse rate among schizophrenic patients receiving CBFT than in those just receiving individual CBT. FT sessions took place in the patients’ homes, with family and patient participating. Importance of medication was emphasised, and the family was instructed in ways in which to express both positive and negative emotions in a constructive, empathetic manner. Symptoms were explained to the family, and both family and patient were instructed in adaptive coping mechanisms. Large differences in effectiveness were found - 50% of those in the individual-therapy group returned to hospital over the course of the study compared with only 11% of those in the family-therapy group. 

However, investigators were mindful that patients undergoing CBFT may have improved more than the controls due to taking their medication more routinely – family therapy subjects complied better with their with their medication regimens.

However, these results were challenged by a study by the University of Hertfordshire, carrying out a meta-analysis of over 50 studies on the use of CBT from around the world. They only found a small therapeutic effect on schizophrenic symptoms such as delusions and hallucinations, which disappeared when blind studies were used, suggesting that CBT has a negligible effect in treating schizophrenia, if any at all.

Jauhar et al (2014) conducted a systematic review and meta-analysis of the effectiveness of CBT for schizophrenia, examining potential sources of bias. They found that overall, CBT has a small therapeutic effect on schizophrenic symptoms in the "small" range, but this effect reduces further when sources of bias are controlled for.

Sarason and Sarason suggested two ways in which findings have been misinterpreted. “Expressed emotion” has been misinterpreted to mean that the expression of any emotion is harmful, rather than just negative emotions – in fact, the expression of warmth and positive emotions can play a role in reducing relapse rates.

Secondly, some family members feel guilty for their emotional expression – it is important to emphasise to them that it does not play a direct causal role, but rather, is a factor that may influence relapse. Allowing them to feel guilt can actually increase the family's levels of negative expressed emotion, harming the patient's long-term prospects.

Global cultural differences mean that in some cultures, high levels of expressed emotion is not a social norm. Results from research suggest that cultures with lower levels of expressed emotion should have lower schizophrenia rates, but they do not, challenging the role of EE in the development and maintenance of schizophrenia.

There are ethical issues with comparing a therapy group with a control. If the therapy group improves and the control group doesn't, the researcher has knowingly denied the control group an effective method of treatment.

Schizophrenics do tend to lack social skills, and many of the negative symptoms (disorganised speech, speaking very little, lack of emotion) do help isolate them socially, so therapy that emphasises social functioning is appropriate and important in helping treat this specific aspect of the disorder.

Research into CBFT has not shown a causal role for the family in schizophrenia development, as Bateson once thought, but has shown that the family can be a powerful factor in determining the patient’s risk of relapsing to a psychotic state. CBFT used to restructure family relationships and reduce levels of negative EE is a crucial tool in both increasing the patient’s quality of life, and helping the family detect early warning signs of a relapse.

Studies that compare effectiveness between different therapies often do not measure outcomes in the same way - some look at attrition rates, some look at symptom severity before and after, and some look at relapse rates. Also, the "hello-goodbye effect" refers to the bias caused by patients who tend to exaggerate their symptoms before therapy, and exaggerate their progress after therapy, leading to inaccurate conclusions being drawn. This makes holistic comparisons of effectiveness between therapies difficult, and results must be handled with care.

CBT/CBFT does significantly improve functioning and reducing the suffering of schizophrenic patient, but it is not a cure, and is unlikely to work on its own. When used in conjunction with appropriate drugs, it tackles symptoms such as poor social skills, alogia and avolition, but is often unsuccessful at treating the more serious positive symptoms. Even when social function is the focus of therapy, it is not possible to increase social functioning to the level of non-schizophrenics.

Schizophrenia - the psychological explanation

I think this topic will follow on well from the biological approach to schizophrenia - it's a little more complex, bringing together the social, psychodynamic and cognitive approaches. Psychological treatments should follow on from this shortly - CBT and CBFT should be coming up soon. In the exam, it's highly unlikely that a question will ask about a specific explanation - questions into this area are much more likely to be "discuss 1/2/2+ psychological explanations for schizophrenia" rather than "discuss the psychodynamic/cognitive/social approach to schizophrenia."

Black: AO1 - Description
Blue: AO2 - Evaluation - studies
Red: AO2 - Evaluation - evaluative points

Psychodynamic explanations of schizophrenia

The psychodynamic approach rose to popularity in the mid-20th century as an environmental explanation, emphasising the causal role of the family in the development of schizophrenia. It explains schizophrenia as a regression to the Id-dominated oral stage, with little awareness of the outside world. "Primary narcissism" develops - delusions arise from the child feeling threatened and persecuted by the  outside world, but also feeling omnipotent over their internal world.

The schizophrenogenic mother

Fromm-Reichman and Kasanin were key psychologists in pioneering the concept of a "schizophrenogenic" mother, who was not schizophrenic herself, but would cause the development of schizophrenia in her children due to her treatment of them. The two central traits of the schizophrenogenic mother are being domineering (maternal overprotection) yet cold and uninvested (maternal rejection.)

Kasanin (1934) studied the parents of 45 schizophrenics and found maternal rejection in 2 patients, and maternal overprotection in 33. These results suggest that overprotection is the most significant quality of the archetypal schizophrenogenic mother, supporting the hypothesis of certain maternal behaviours inducing the development of schizophrenia in their children. 

Kasanin gathered data through interviews and case-report studies, prone to methodological problems such as researcher bias and subjectivity that reduce internal and external validity. The case reports were retrospective, so detail may have been recalled incorrectly, biased towards reporting maternal overprotection due to leading questions, or carrying the risk of false information due to social desirability bias. Also, the significant mental disturbances, possible substance abuse, and chronic use of antipsychotic medications all contribute towards a mental state where information from early life may not be recalled correctly.

Schofield and Balian also studied the early lives of schizophrenic patients. The only significant distance they found between schizophrenics and non-schizophrenics was the quality of the maternal relationships - schizophrenics were more likely to have had less affectionate mothers.

Schofield and Balian's study was a retrospective, in-depth interview on the profoundly mentally ill, many of whom had histories of substance abuse and chronic use of antipsychotic medications, meaning that information was likely to be unreliable.

Mischler (1968) carried out an observation of mothers with schizophrenic children and found the mothers to be aloof, unresponsive and emotionally distant - but only towards their schizophrenic children, behaving normally towards their non-schizophrenic children. This raises an important issue of cause and effect - the coldness and distance attributed to the schizophrenogenic mother may be her response to psychological disturbances in the child.

Parker criticised this theory by suggesting that there is no archetypal schizophrenogenic mother- there is a parental type distinguised by hostility, criticism and intrusiveness, but this type is not particularly overrepresented by the parents of schizophrenics.

Hinsie and Cambell criticised this hypothesis for ignoring the fact that many mothers fulfill Kasanin's criteria for schizophrenogenesis, but very few of them have children who develop schizophrenia, and not all schizophrenics have the archetypal schizophrenogenic mother, so the hypothesis is reductionist to suggest that the disorder is only a result of maternal relationships. The hypothesis is also reductionist in its failure to take evidence for a biological basis into account, such as the evidence for a significant genetic component.

Marital schism, marital skew and double bind

Lidz proposed the concept of "marital skew" and "marital schism" being traits found in the relationship between the parents of a schizophrenic. Marital schism refers to the open hostility and criticism that occurs when the parents are unable to adopt role reciprocity (the ability to understand each other's goals, roles and motivations.) Marital skew refers to the tendency of one parent to dominate interaction - usually an intrusive and domineering mother and a distant, passive father.

A problem with this theory is the inability to isolate the direction of the cause and effect relationship between marital skew and schizophrenia. The early symptoms of schizophrenia in childhood and the resultant psychological vulnerability in the child could cause one parent to be more involved than the other.

However, Lidz did find supporting evidence for the role of the family in the development of schizophrenia - he found that 90% of schizophrenics have a family background that is disturbed in some way, while 60% have parents who either one or both suffer from a serious personality disorder.

Bateson proposed the idea of "double bind" scenarios being responsible for schizophrenia formation - receiving conflicting emotional messages from the parents in early childhood, for example, emotional warmth one day, withdrawal and hostility the next, leads to the child losing their grip on reality and seeing their own feelings as unreliable - contributing towards schizophrenia development.

Kennedy analysed letters sent between schizophrenics and their parents, and compared the results to a control group. The results showed evidence of double bind scenarios, but, like Parker's criticism of the schizophrenogenic mother hypothesis, double bind scenarios were not particularly over-represented by schizophrenic patients. Double bind scenarios were observed in the analysis of letters between non-schizophrenics and their parents too - he concluded that the majority of people get mixed messages, but most don't develop schizophrenia, so double bind theory cannot exclusively explain the illness. 

Overall evaluation of psychodynamic explanations

The causal role of the family lacks reliable and objective empirical evidence, and established relationship so far is only correlational.

However, lots of research suggests an unstable family background may increase the risk of schizophrenia in children who already have a biological predisposition - Sorri et al's study of Swedish adoptive children of schizophrenics found that the quality of adoptive parenting was the most important factor in determining whether the children grew up to develop schizophrenia. Wahlberg (2000) examined earlier data and concluded that environmental factors such as family communication can strongly affect the chance of schizophrenia development in children with a genetic predisposition to the disorder.

Neil suggested that political and cultural conditions post-WWII influenced psychodynamic theories into schizophrenia, as psychologists such as Bowlby placed greater emphasis on the role of the mother in the early development of the child. It is possible that the sudden focus on maternal roles led to the scientific popularity of the schizophrenogenic mother hypothesis, rather than the theory having any specific credibility.

Cause and effect is difficult to determine when carrying out research in this area - early schizophrenic symptoms in a child can put significant levels of stress upon a family, causing potential instability and disturbance.

Cognitive explanations of schizophrenia

The cognitive approach seeks to explain schizophrenia as the result of faulty information processing. Frith explains it as a result of faulty "metarepresentation" the cognitive process that allows us to reflect on our thoughts and behaviour, generate thoughts, ideas and intentions, and to reflect on the thoughts and behaviour of others. 

Metarepresentation takes place through the action of two systems - the "supervisory attention system" that is responsible for self-generated actions, and the "central monitoring system", that is responsible for recognising our thoughts as our own, and external voices as belonging to others. Problems with the supervisory attention system lead to the negative symptoms such as alogia, catatonia and apathy, while problems with the central monitoring system lead to the positive symptoms such as hallucinations, delusions and thought disturbances.

Frith (1980) carried out a card guessing game with groups of both schizophrenics and non-schizophrenics, guessing whether a drawn card would be black or red. Non-schizophrenics made logical choices, taking into account probabilities and cards already drawn. Schizophrenics made very rigid decisions, finding it difficult to take self-generated cognitive actions and ideas into account, as well as probabilities.

Frith and Done (1986) carried out a verbal fluency assessment of schizophrenics and non-schizophrenics, where they were given a category and asked to generate lists. Schizophrenics performed very poorly in this task compared to the control group. In a similar visual fluency task involving categorisation, they performed equally poorly.

Bentall (1991) had schizophrenics either generate words for a list, or read off the list. A week later, they were read the words used in the initial test, and asked if they'd generated them or read them a week ago. Compared to a control group, schizophrenics performed very poorly.

Lots of empirical evidence supports the cognitive explanation - the above studies support the concept of some very definite cognitive impairment in schizophrenics, such as an inability to recognise self-generated thoughts. However, the patients' history of strong antipsychotic medication could account for the cognitive impairment in these tests.

The cognitive explanation manages to explain the both positive and negative symptoms of schizophrenia, as opposed to the dopamine hypothesis which only manages to explain the positive symptoms. However, it only explains the symptoms of schizophrenia, not the causes - what causes the metarepresentative faults in the first place?

Hemsley (1993) explained schizophrenic symptoms as a result of an inability to activate schemas. Schemas develop in early childhood as a way to categorise and process information from the outside world - if these fail to activate correctly, self-generated sensory information could be interpreted as external, causing an auditory hallucination.

This theory manages to explain the origins of auditory hallucinations, but has little empirical evidence to support it.

Social explanations of schizophrenia

Social causation theory seeks to explain the overrepresentation of schizophrenics in poor and deprived urban populations as a result of factors such as poor education, diet, healthcare, access to drugs, unemployment, overcrowding and stress.

Social drift theory suggests that schizophrenia development is not a consequence of deprivation, but a cause of it - schizophrenia symptoms lead to economic and social hardship due to being unable to hold down jobs, mortgages, relationships, which leads to moving into poor urban areas.

Castle (1993) studied Camberwell, a deprived area of  London, and found that the majority of schizophrenics were born locally, as opposed to having moved there after developing schizophrenia, supporting the causation theory and challenging drift.

However, potential effects of drift cannot be ruled out - it is possible that the schizophrenics born there also had schizophrenic parents who moved there due to socioeconomic hardship - and evidence suggests a definite genetic basis to schizophrenia.

Overcrowding is a common issue affecting wellbeing in deprived areas, leading to greater exposure to viruses - if the viral explanation is true, that could explain how socioeconomic hardship increases the risk of schizophrenia development. Malnutrition is also a problem - poverty leads to malnutrition, which leads to illness and possibly abnormalities in the development of brain anatomy, another theorised explanation of schizophrenia.

Schizophrenia - drug therapies

This topic follows along nicely from the last one, and again, is relatively straightforward. AO1 is fairly simple here, and AO2 evaluation works with reference to effectiveness (using research evidence) and appropriateness, (using more specific IDA-style evaluative points.) As with all my posts, if I come across any useful new information at any point, I will update this.

Black: AO1 - Description
Blue: AO2 - Evaluation - studies
Red: AO2 - Evaluation - evaluative points

Typical antipsychotics

First developed in the 1950s, this class includes chlorpromazine, haloperidol and fluphenazine. They act as dopamine antagonists, reducing the neurotransmitter levels by blocking D2 receptors in the brain's dopamine pathways. Generally, they are administered either as a course of tablets, or as a "depot injection", a single injection every 2-4 weeks which releases the medication slowly over time. Both classes of antipsychotics work on the dopamine hypothesis - the idea that abnormally high levels of the dopamine neurotransmitter due to oversensitive receptors cause schizophrenia, and, due to this, only really function to treat the positive symptoms such as hallucinations, delusions and thought disturbances.

There are several potentially harmful side effects than can result from the use of typical antipsychotics. Side effects vary between specific chemicals, but are likely to include muscle stiffness, cramp, tremors, and extrapyramidal symptoms (drug-induced movement disorders) such as muscle spasms, rigidity, involuntary muscle movement and restlessness.

Chronic use of atypical antipsychotics carries the risk of causing development of tardive dyskinesia, a serious degenerative disorder characterised by repetitive and involuntary muscle movements such as excessive blinking, grimacing and limb twitches.

Atypical antipsychotics

Atypical antipsychotics such as clozapine, risperidone and olanzapine also act dopamine antagonists, interfering with post-synaptic D2 dopamine receptors to prevent the transmission of dopamine across the synapse. They can also reduce serotonin levels by blocking receptors.

Compared to the most common typical antipsychotics such as haloperidol, they are less likely to cause extrapyramidal motor impairment, as well as the development of the serious motor disorder tardive dyskinesia. 

However, they have been found to carry an increased risk of stroke, blood clots and sudden cardiac arrest. They can also cause agranulocytosis – low white blood cell count, resulting in immune weakness and increased susceptibility to infection.

Compared to many antipsychotics, atypicals carry a very low risk of withdrawal symptoms – possibly on account of the drugs being absorbed into adipose tissue and slowly released. 

Effectiveness of drug therapies

Stargardt et al (2008) - investigated cost effectiveness of typical and atypical antipsychotics by comparing drug costs to rehospitalisation rates after a course of treatment. Studying 321 patients, they found no statistically significant differences in the effectiveness of either class – Atypical antipsychotics were often more useful in the most severe cases, whereas typical antipsychotics were often more useful in less severe cases. Atypical antipsychotics also have a much smaller risk of harmful side effects – but they are also more expensive. They concluded that in terms of efficiency balanced between cost and effectiveness, there is no great difference between either class of antipsychotic.   

Correll + Schenk (2008) – 28000 participants stratified by age across 12 trials, assessing incidence of tardive dyskinesia in patients treated with typical or atypical antipsychotics. Across all the trials, TD risk is 3.9% for atypical, 5.5% for typical, with significant variations in incidence between trials. Four adult trials even suggest that compared to unmedicated schizophrenics, atypical antipsychotics actually reduce the risk of TD development: 13.1% incidence for atypicals, 15.6% for unmedicated, 32.4% for typicals. Overall, results suggest a lower risk of tardive dyskinesia in patients medicated by atypical antipsychotics than those medicated by typical antipsychotics.

Bagnall et al (2003) – Meta-analysis of studies into attrition across 2000 schizophrenic participants for 2 years of antipsychotic medication. A higher attrition rate was assumed to indicate lower satisfaction with the treatment, resulting from more side effects and less effective relief of symptoms. Generally, fewer participants left trials early from atypical drug groups than from typical drug groups, suggesting that patients found atypical antipsychotics more acceptable. Individuals with schizophrenia may have found atypical antipsychotics more acceptable than typical counterparts – even if they are no more effective in the relief of symptoms, they have fewer negative side effects.

Davis (1980) - analysed the results of 29 studies (3519 people), they found that relapse occurred in 55% of the patients whose drugs were replaced by a placebo compared to 19% in those patients who remained on the real drug. Suggests significant effectiveness of the drug – however, challenged by Ross + Read (2004) – 45% of patients given a placebo did not relapse. The effectiveness of drug treatments is challenged as 45% of patients did well on the placebo therapy. However, the fact that 45% of patients did not relapse when antipsychotics were replaced by a placebo challenges the actual effectiveness of drug treatments.

Overall evaluation of drug therapies

Antipsychotic drugs are a relatively cheap, effective treatment, reducing symptoms in the majority (roughly 70%) of patients and allowing them to live comparatively normal lives.

However, like all drug therapies for mental illness, they treat symptoms, not underlying causes. This means that the underlying disorder is not treated – and relapse is likely when the course of drugs is discontinued. This can lead to “revolving door syndrome” – where patients are readmitted and given a new course of antipsychotics very soon after completing a prescribed course of treatment – remaining on a cycle of rehospitalisation and medication for potentially many years.

Antipsychotics are generally better at treating positive symptoms such as hallucinations and delusions rather than negative symptoms such as apathy and alogia, suggesting that factors other than an excess of dopamine may be responsible for negative symptoms.

Ethical issues can result not only from the often severe side-effects, but also from the use of drugs as a “chemical straitjacket.” There are potential ethical concerns with compulsory medication for schizophrenics – forcing patients to take drugs against their will as a form of social control.

Schizophrenia - the biological explanation

Thought I'd start with this topic as it's quite straightforward. I probably won't be posting these in any particular order - diagnosis and classification, treatments of schizophrenia etc. will all follow in due time. As with all my posts, if I come across any useful new information at any point, I will update this.

Black: AO1 - Description
Blue: AO2 - Evaluation - studies
Red: AO2 - Evaluation - evaluative points

The Dopamine hypothesis 

The hypothesis that underpins most biological explanations and drug therapies for schizophrenia, this suggests schizophrenia is simply a result of heightened levels of the neurotransmitter dopamine, caused by oversensitive D2 dopamine receptors.

This can be measured by:

• MRI scans measuring activity/density of post-synaptic dopamine receptors and levels.
• Comparison of dopamine levels between schizophrenics and a control group.
• Studies where schizophrenics are given dopamine agonists, resulting in an increase in symptom severity.

Amphetamines

Amphetamines are a class of CNS stimulant that act as agonists (increasing activity) for the neurotransmitters adrenaline and dopamine. Addicts can develop amphetamine psychosis - giving hallucinations and delusions in a similar form to those that result from schizophrenia, suggesting that heightened dopamine levels may explain some of the positive symptoms.

Homovanillic acid, produced as the body metabolises (breaks down) dopamine, is found in increased concentrations in the urine of schizophrenics. This supports the dopamine hypothesis - increased dopamine levels in schizophrenics, but correlation does not mean causation - another biological mechanism responsible for schizophrenia could also lead to these increased levels as a secondary effect.

Brain scans have found a greater density of dopamine receptors in schizophrenics - suggesting that the condition may well be a result of greater dopamine sensitivity. However, the patients studied already had schizophrenia, so cause and effect cannot be established - it may be the case that increased D2 density might be a response to either the condition itself, or the dopamine antagonists commonly prescribed as antipsychotic medication.

Some studies into the dopamine hypothesis have shown that schizophrenics who take amphetamines show increased symptom severity, but non-schizophrenics given the same dose showed no symptoms of schizophrenia, suggesting that schizophrenics have a higher sensitivity towards dopamine, rather than objectively higher levels.

The relative levels of success in the use of dopamine antagonists (reducing activity) as treatment supports the dopamine hypothesis, however, 1 in 3 schizophrenics do not respond to antagonists, suggesting that there must be other factors.

This suggests that the dopamine hypothesis is overly reductionist - factors other than neurotransmitter levels must play a role in the development of such a complex condition, as the hypothesis cannot explain all of the symptoms. 

Amphetamine psychosis only explains the positive symptoms of schizophrenia - excess dopamine levels in addicts can lead to the positive symptoms, but not the negative symptoms. Dopamine antagonists are also only useful for the treatment of these positive symptoms, suggesting that the dopamine hypothesis can only really explain the symptoms such as hallucinations, delusions and thought disturbances.

Genes

There is evidence to suggest that genes can play a causal role in the development of schizophrenia, as concordance rates are higher between more genetically similar individuals. Several concordance studies support this.

Gottesman carried out a meta-analysis of 40 European studies into schizophrenia which looked at the condition's incidence rates.

• General public: 1%
• Sibling of schizophrenic: 10%
• Son or daughter of schizophrenic: 10%
• Dizygotic (non-identical) twin of schizophrenic: 17%
• Monozygotic (identical) twin of schizophrenic: 48%

These results would seem to support the concept of a genetic basis for schizophrenia, but not a purely causal relationship.

More genetically similar individuals have more environmental similarities - upbringing, how they are treated. These environmental similarities could help explain the greater incidence rates.

A methodological flaw emerges in the use of a meta-analysis. Different studies analysed used different research methods and diagnosis classifications, lowering the validity of the research. Additionally, there were large variations in concordance rates between studies.

The results suggest schizophrenia is not completely genetic, or else monozygotic twins would have an 100% concordance rate due to being genetically identical. Therefore, these results support the diathesis-stress hypothesis, the idea that schizophrenia is a result of genetic predisposition requiring an environmental trigger to cause development of the disorder.

Heston (1966) studied adoptees, seeking to eliminate the interference between genetics and upbringing in establishing a concordance rate. He studied 47 adopted children that were born to a schizophrenic mother and then adopted by non-schizophrenics. A control group was used to counter the stress of adoption potentially contributing to the development of schizophrenia. 

• 5/47 of the children developed schizophrenia, just over 10%, the same as the rate of incidence in children of schizophrenics found in Gottesman's study. 

This supports the concept of a definite role of genetics in the development of schizophrenia.

Even though they were adopted at birth, the children still spent 9 months in their mothers' womb during gestation - they could have been exposed to schizophrenogenic drugs, so a shared environment cannot be completely ruled out.

Heston didn't investigate the children until adulthood, so all sorts of environmental factors in childhood and adolescence could have played a role in schizophrenia development.

Sorri studied Swedish adoptees with schizophrenic biological mothers. He found that the chance of schizophrenia development depended on the quality of adoptive parenting - these children still had a greater risk of schizophrenia development, but it was upbringing-dependent. This further supports the diathesis-stress hypothesis, that schizophrenia has a genetic basis that requires environmental activation. 

Gottesman and Shields compared concordance in a meta-analysis of 5 studies on severe schizophrenics, and found a concordance rate of between 75% and 91% - strongly supporting a genetic basis to at least the most severe cases of schizophrenia.

Overall, the studies into the genetic hypothesis suggests that genes can provide a biological basis, making an individual more predisposed to schizophrenia, which will then require certain environmental triggers to cause the condition's full development.

Brain anatomy

There is evidence to suggest a smaller brain size in schizophrenics - enlarged ventricles in the brain lead to an overall reduction in the volume of brain matter. The first evidence came from early autopsies of schizophrenics - meaning cause and effect could not be established, as it could be that schizophrenia caused the anatomical differences, not vice versa. Also, these patients had had a long history of antipsychotic medication, which could have affected anatomy, along with potential physical trauma or substance abuse.

Brain scans are a more contemporary method of studying neuroanatomy. Early CAT scans showed that 25% of schizophrenics had enlarged ventricles, compared to a miniscule proportion of healthy controls. However, 25% is very inconclusive - it meant that 75% had no anatomical differences to healthy individuals.

Crowe et al (1989) used Magnetic Resonance Imaging (MRI) to study schizophrenics, and found a reduction in brain matter in the hippocampus in the temporal lobe, especially on the left hand side of the brain. 

Goldstein et al' (1999) used MRI to find a reduction in brain matter volume in the paralimbic cortex, a group of brain structures involved in emotion processing, goal setting, motivation and self control - all functions that the symptoms of schizophrenia impair in some way.

MRI technology is not specific enough to reliably pinpoint specific parts of the brain as being dysfunctional. It shows blood flow to regions, which, while roughly correlational, is not a direct measure of brain activity.

Enlarged ventricles are found to be a predisposing factor for many disorders, and are more likely to be an indicator of general susceptibility to psychiatric disorders than schizophrenia specifically.

The viral explanation

Research suggests that if the mother contracts the flu virus (influenza A) during the 2nd trimester of pregnancy, the child is significantly more likely to develop schizophrenia. 

O'Callaghan et al (1991) looked at the 1957 influenza outbreak, and found that children in the 4th-6th month of gestation during the outbreak had a particularly incidence of schizophrenia.

Sham et al (1992) examined the relationship between flu outbreaks and reported schizophrenia incidence across several decades. They concluded that schizophrenia was more common amongst those who had been in the womb during the outbreaks. However, the majority of schizophrenics had not been exposed to influenza A in utero, alone, this hypothesis is not a complete explanation of schizophrenia. 

Correlations cannot show cause and effect - a third, intervening variable that explains the correlation between antenatal influenza A exposure and schizophrenia development.

Overall evaluation of the biological explanation of schizophrenia

While biological factors such as dopamine levels, genes, neuroanatomy and viral exposure cannot fully explain the development of schizophrenia, and are reductionist in their simplification of schizophrenia to merely the result of certain biological processes, there is evidence to suggest that biology can provide a predisposition to schizophrenia, which then requires environmental circumstances to trigger the disorder's development. The diathesis-stress hypothesis is the model of schizophrenia most likely to be correct, stating that nature provides a basis to schizophrenia, which then requires environmental activation to lead to the full development of the illness.