Positive and negative symptoms

Schizophrenia is a severe mental disorder affecting roughly 1% of the population, in which thought and contact with reality are impaired. It is diagnosed using the DSM-5 or the ICD.

• Positive symptoms — additional experiences beyond ordinary existence.
  • Hallucinations — unusual sensory experiences, which may be auditory (hearing voices, often criticising) or visual, olfactory or tactile.
  • Delusions — irrational beliefs held with total conviction: delusions of grandeur (being an important historical figure), of persecution (being spied on), or of control (the body is under external control).
• Negative symptoms — the loss of usual abilities and experiences.
  • Avolition — a severe loss of motivation and an inability to initiate or persist in goal-directed activity. Andreasen identified three signs: poor hygiene and grooming, lack of persistence in work or education, and lack of energy.
  • Speech poverty (alogia) — reduced fluency and quantity of speech. The DSM now places more emphasis on speech disorganisation, in which speech becomes incoherent or the speaker changes topic mid-sentence.

Diagnosis requires (DSM-5) two or more symptoms present for a significant portion of a one-month period, with at least one being a positive symptom — and continuous signs of disturbance for at least six months.

Problems with the diagnosis of schizophrenia

• Reliability — diagnosis must be consistent. Inter-rater reliability has historically been poor: Cheniaux et al. (2009) had two psychiatrists independently diagnose 100 patients using both DSM and ICD criteria. One diagnosed schizophrenia in 26 patients using DSM and 44 using ICD; the other diagnosed 13 using DSM and 24 using ICD. The agreement between the two clinicians was poor, and both diagnosed more cases with ICD than DSM.
• Validity — co-morbidity. Schizophrenia is commonly diagnosed alongside other conditions. Buckley et al. (2009) concluded that co-morbid depression occurs in about 50% of patients with schizophrenia, substance abuse in about 47%, PTSD in about 29% and OCD in about 23%. If half of the people with schizophrenia also have depression, schizophrenia may not be a distinct condition at all.
• Validity — symptom overlap. Schizophrenia and bipolar disorder share both delusions and avolition. Under the ICD a patient might be diagnosed with schizophrenia, and under the DSM with bipolar disorder — so the two may not be separate conditions.
• Gender bias. Men are diagnosed more often than women (a ratio of about 1.4:1). Cotton et al. (2009) suggest women typically function better than men — they are more likely to work and to have good family relationships — which may mask the symptoms and mean some women who would benefit from treatment are not diagnosed. Clinicians may also be more likely to attribute symptoms in women to a mood disorder.
• Culture bias. People of African-Caribbean origin in Britain are several times more likely to be diagnosed than white British people, although rates in Africa and the Caribbean are not elevated. This suggests the difference is not genetic but a product of culture bias in diagnosis: hearing voices is more acceptable in some cultures (e.g. as communication with ancestors), and reporting such experiences to a white psychiatrist may be misread as bizarre.

Positive or negative?

Reliability or validity?

Genetics and the dopamine hypothesis

Genetic explanation. Schizophrenia runs in families, and risk increases with genetic similarity to a relative with the diagnosis. Gottesman's large-scale family study found a concordance rate of about 48% for identical (MZ) twins, about 17% for non-identical (DZ) twins, and about 9% for siblings — against a general population risk of about 1%.

• Schizophrenia is polygenic and aetiologically heterogeneous — different combinations of genes can lead to the condition. Ripke et al. (2014) combined the genome-wide studies of 37,000 patients and 113,000 controls and identified 108 separate genetic variations associated with increased risk.
• Mutation is also possible: schizophrenia can occur in people with no family history, and it has been correlated with paternal age, which is associated with increased sperm mutation.

The dopamine hypothesis. Dopamine (DA) is important in the functioning of brain systems related to the symptoms.

• The original hypothesis: hyperdopaminergia in the subcortex. An excess of dopamine, or too many D2 receptors, in subcortical areas — for example, an excess in Broca's area — could explain speech poverty and auditory hallucinations.
• The updated hypothesis: hypodopaminergia in the cortex. Goldman-Rakic et al. identified abnormally low dopamine in the prefrontal cortex, which is responsible for thinking and decision-making. Low cortical dopamine could explain the negative symptoms. Modern versions of the hypothesis therefore propose both high subcortical and low cortical dopamine.

Evaluation: the dopamine hypothesis has strong support from drug studies: amphetamines increase dopamine and can produce schizophrenia-like symptoms in people without the disorder, while antipsychotics, which block dopamine, reduce the symptoms. But it is at best incomplete — glutamate has also been consistently implicated in post-mortem and imaging studies, and clozapine, the most effective antipsychotic, acts on serotonin and glutamate as well as dopamine. On genetics, the MZ concordance of 48% is decisive evidence that environment matters too: identical twins share 100% of their genes, so if genes were the whole story concordance would be 100%.

Read the concordance

Family dysfunction and cognitive explanations

Family dysfunction

• The schizophrenogenic mother (Fromm-Reichmann, 1948) — a psychodynamic account based on patients' accounts of their childhoods. The 'schizophrenia-causing' mother is cold, rejecting and controlling, and creates a family climate of tension and secrecy. This leads to distrust that develops into paranoid delusions.
• Double-bind theory (Bateson et al., 1972) — the child is trapped in a situation where they receive contradictory messages and are punished whatever they do, but cannot comment on the unfairness or leave. They come to see the world as confusing and dangerous, which is reflected in disorganised thinking and paranoid delusions. Bateson was clear this is a risk factor, not the sole cause.
• Expressed emotion (EE) — the level of negative emotion expressed by carers towards a patient: verbal criticism (sometimes with violence), hostility (including rejection) and emotional over-involvement. High EE is a serious source of stress and is a well-evidenced predictor of relapse. Note that EE is primarily an explanation of relapse, not of the original onset.

Cognitive explanations. Frith et al. (1992) identified two kinds of dysfunctional thought processing:

• Metarepresentation dysfunction — metarepresentation is the ability to reflect on our own thoughts and behaviour, and to recognise our thoughts and actions as our own. Disruption to it would explain why patients experience their own thoughts as voices (auditory hallucinations) and their own actions as controlled by others (delusions of control).
• Central control dysfunction — the ability to suppress automatic responses while performing deliberate ones. Disruption would explain disorganised speech and thought: patients cannot suppress the automatic associations triggered by each word, so they derail into a chain of associations.

Evaluation: the family-based explanations rest on very weak evidence — support for the schizophrenogenic mother is based on informal assessments of patients' mothers, and it has led to parent-blaming, causing enormous distress to families already coping with a severely ill relative. The cognitive explanations have far better support: Stirling et al. (2006) compared 30 patients with schizophrenia and 18 controls on the Stroop task and found the patients took over twice as long to name the ink colours — direct evidence of central control dysfunction. But cognitive explanations are proximal, not distal: they explain what is happening now in the patient's mind, not how it came to be that way.

Typical and atypical antipsychotics

• Typical antipsychotics — chlorpromazine. In use since the 1950s. It is a dopamine antagonist: it blocks dopamine receptors in the synapse, reducing the action of dopamine. Initially this increases dopamine production, but after a time production is reduced, and symptoms — especially the hallucinations — subside. Chlorpromazine is also an effective sedative, and is often used to calm patients on admission. Typical dose has declined over time and now runs up to a maximum of about 1,000 mg a day, with treatment usually starting at a much smaller dose.
• Atypical antipsychotics — clozapine. Developed in the 1970s. It binds to dopamine receptors but also acts on serotonin and glutamate receptors. It is believed to improve mood and cognitive functioning as well as the positive symptoms, and is therefore prescribed when a patient is at high risk of suicide — an important consideration, since a substantial proportion of people with schizophrenia attempt suicide. Clozapine was withdrawn for a period after some patients died from agranulocytosis (a fatal blood condition), so patients on it must have regular blood tests and it is not available as an injection.
• Risperidone — a more recent atypical antipsychotic, developed to be as effective as clozapine without the serious side effects. It binds more strongly to dopamine receptors than clozapine, so is effective in much smaller doses, and appears to lead to fewer side effects.

Evaluation: antipsychotics are effective: Thornley et al. (2003) reviewed studies comparing chlorpromazine with a placebo and found, in data from 13 trials with a total of 1,121 participants, that chlorpromazine was associated with better overall functioning and reduced symptom severity. But there are serious side effects: dizziness, agitation, sleepiness, weight gain and — most seriously — tardive dyskinesia (involuntary facial movements caused by dopamine supersensitivity) and the potentially fatal neuroleptic malignant syndrome. There is also an important ethical criticism: antipsychotics have been used in hospitals as a chemical cosh to sedate and control patients for the convenience of staff rather than for the patients' benefit, which is a serious abuse of human rights.

Typical or atypical?

CBT and family therapy

• CBT for psychosis (CBTp). Typically 5 to 20 sessions, individually or in groups. It does not aim to eliminate the symptoms but to help the patient make sense of them and reduce the distress they cause. Delusions are gently challenged — a patient who believes he is being pursued by government agents can be helped to see how unlikely it is that agents would take that trouble. Normalisation — explaining that many people hear voices — reduces anxiety and the sense of isolation. NICE reviews of the evidence show CBT is effective in reducing symptom severity and improving functioning.
• Family therapy. Takes place with the family as a whole, and aims to reduce stress within the family — in particular, to reduce the level of expressed emotion. Burbach's model works through phases: sharing information and identifying resources, encouraging mutual understanding, identifying unhelpful patterns of interaction, and skills training (stress management, communication). Pharoah et al. (2010) reviewed 53 studies conducted across Europe, Asia and North America and concluded that family therapy leads to moderate improvements in mental state and a reduced likelihood of relapse and readmission. It also has an important benefit for the whole family, who provide the bulk of the care.

Evaluation: neither therapy is a cure — both manage symptoms and improve quality of life. A serious methodological problem is that CBTp studies vary enormously in the techniques used and in the symptoms of the patients studied, so combining them into an overall verdict is misleading. The evidence for family therapy is stronger on relapse than on symptom reduction. There is also an ethical objection to CBTp: gently challenging a patient's delusions can be experienced as disrespectful of their reality, and some argue it is used to make patients easier to manage. In practice, both therapies are used alongside antipsychotics — you generally have to be stable on medication to engage with the psychological work — which is exactly the interactionist argument.

Spec check: token economies have been removed from 7182 v1.4. The named psychological treatments for schizophrenia are now CBT and family therapy only.

The diathesis-stress model

The interactionist approach acknowledges that biological, psychological and societal factors all matter. In schizophrenia it takes the form of the diathesis-stress model: a person develops schizophrenia only if they have a vulnerability (diathesis) and experience a stressor that triggers it.

• Meehl's original model (1962) — the diathesis was entirely genetic: a single 'schizogene' produced a 'schizotypic' personality. On this model, someone without the gene could never develop schizophrenia, however great the stress.
• The modern model — there is no single schizogene (Ripke found 108 variants), and the diathesis need not be genetic at all. Read et al. (2001) proposed a neurodevelopmental model in which early trauma alters the developing brain — for example by making the HPA system over-active — creating a biological vulnerability. The stressor has likewise been broadened beyond parenting to anything that increases risk, including cannabis use, which increases risk up to about seven times at the highest doses because it interferes with the dopamine system.
• Evidence: Tienari et al. (2004) studied 19,000 Finnish children adopted away from mothers with schizophrenia. Adoptive parents were assessed for child-rearing style. A high level of criticism, conflict and low empathy in the adoptive family was strongly associated with the development of schizophrenia — but only in the children who had a high genetic risk. In children with low genetic risk, family style made no significant difference. Genetic vulnerability and family stress together predicted the disorder; neither alone did.

Treatment implications. The interactionist model requires combined treatment — antipsychotics plus CBT. This is standard in Britain but, as Turkington et al. point out, it is possible to believe in biological causes and still practise CBT, so the model is not always applied coherently. Note also the 'treatment-causation fallacy': the fact that a drug reduces symptoms does not prove that the biology it acts on caused them — just as paracetamol relieving a headache does not mean the headache was caused by a lack of paracetamol.

Interpret Tienari

Which therapy?

Which dopamine hypothesis?

Which cognitive dysfunction?

Culture bias in diagnosis

Which explanation?

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Term and meaning

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The big ideas to know

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