Schizophrenia Notes

Schizophrenia Part 1: Definition and Symptoms

• Schizophrenia is a psychotic disorder characterised by severely impaired thinking, emotions, and behaviours.

• Patients often struggle to filter sensory stimuli, leading to enhanced perceptions.

• Sufferers experience positive and/or negative symptoms.

• Positive Symptoms: Enhance the typical experience, occurring in addition to normal experiences. Examples include hallucinations and delusions.

• Negative Symptoms: Represent a 'loss' of typical experiences. Examples include speech poverty and avolition.

• Hallucinations: Distorted perceptions of real stimuli or perceptions with no basis in reality.

  • Auditory hallucinations may involve voices of loved ones or the deceased, caused by excess dopamine receptors in Broca’s area (a neural correlate).

• Delusions: Beliefs with no basis in reality.

  • Types: persecutory, delusions of grandeur, delusional jealousy, erotomania, and somatic delusional disorders.

• Speech Poverty: Abnormally low frequency and quality of speech.

  • A common type is 'derailment,' potentially caused by dysfunctions in central control (Frith et al, 1992), hindering the suppression of automatic associations.

• Avolition: Reduction in interests, desires, and goals; behavioural reduction of self-initiated and purposeful acts.

  • Inability to cope with normal pressures and motivations.

• Classification Systems for Mental Disorders:

  • Diagnostic and Statistical Manual (DSM-V)

  • International Classification of Diseases (ICD-10)

• DSM-V vs. ICD-10:

  • DSM-V: Requires at least two of the following: delusions, hallucinations, disorganised speech, and catatonic behaviour; persistence of symptoms for at least 1 month, more specific diagnostic criteria.

  • ICD-10: Broader approach, stating the clinical picture is dominated by stable, often paranoid delusions, accompanied by hallucinations; persistence of symptoms for at least 1 month.

• Differences between DSM and ICD:

  • Originating organisations: WHO vs. American Psychiatric Association.

  • Number and specificity of symptoms required for diagnosis.

  • Recognition of different subtypes of schizophrenia.

• Subtypes of Schizophrenia:

  • Positive schizophrenia: Prominent delusions, hallucinations, and positive formal thought disorders.

  • Mixed schizophrenia: Prominent symptoms are either both negative and positive, or neither is prominent.

  • Subtypes are currently recognised in the ICD-10 only.

• Co-morbidity:

  • Significant co-morbidity exists between schizophrenia and other mental health disorders like OCD and PTSD (Buckley et al, 2009).

    • Buckley et al (2009) found that 29% of SZ patients suffered from post-traumatic stress disorder, whilst 50% suffered depression

  • High co-morbidity with depression raises questions about the validity of differentiating SZ from other disorders.

Validity and Bias in Schizophrenia Diagnosis

• Gender Bias:

  • Longenecker et al (2010) noted a post-1980s increase in male SZ diagnoses without explanation.

  • Cotton et al (2009) suggest that there are no differences in genetic susceptibility for men and women in terms of SZ, then gender bias must be to blame.

  • Dispositional traits in women may mask symptoms or distort their severity.

  • Current diagnostic systems may not account for functional differences between men and women.

• Cultural Bias:

  • Escobar et al (2012) suggest that African Americans are more likely to be diagnosed with SZ compared to Western cultures.

  • Increased openness about admitting certain symptoms may appear normal in their cultures.

  • Hearing voices may be seen as a sign of increased spirituality and connectedness with ancestors.

  • Classification systems may misinterpret cultural phenomena as SZ characteristics.

Biological Explanations for Schizophrenia

• Genetic Basis:

  • Schizophrenia appears to run in families, suggesting a genetic basis.

  • Gottesman (1991) demonstrated a positive correlation between genetic similarity and risk of developing schizophrenia. Concordance rates are:

    • Monozygotic twins (48%)

    • Dizygotic twins (17%)

    • Siblings (9%)

    • Parents (6%)

  • However, no 100% concordance rates indicate environmental influences.

• Candidate Genes:

  • Ripke et al (2013) genome-wide study identified 22 loci at genome-wide significance, Researchers found “22 loci associated at genome-wide significance; 13 of these are new, and 1 was previously implicated in bipolar disorder”, alongside 8300 separate candidate genes.

    • Each gene marginally increases the risk of developing SZ.

  • Therefore, SZ is a polygenic disorder.

• Dopamine Hypothesis:

  • Original hypothesis: Hyperdopaminergia (abnormally high dopamine levels) in the subcortex is responsible for SZ.

  • Revised hypothesis: Hypodopaminergia (abnormally low dopamine levels) in the cortex is responsible for SZ.

  • Modern understanding: Both hyper- and hypodopaminergia in different brain areas contribute to SZ.

    • Hyperdopaminergia in the frontal lobe (Broca’s area) may cause auditory hallucinations.

    • Goldman, Rakic et al (2004) suggested that hypodopaminergia in the prefrontal cortex causes negative symptoms like speech poverty and avolition.

      • Prefrontal cortex: logical thinking; abnormally low dopamine levels; impaired ability to construct grammatical sentences or make decisions about day-to-day functioning.

  • Implications for drug treatments: antipsychotics/dopamine antagonists.

• Neural Correlates:

  • Specific patterns of cortical activity or neural structures that coincide with specific psychological symptoms.

  • Juckel et al (2006) suggested that abnormally low levels of activation in the ventral striatum may be associated with avolition.

    • Ventral striatum = evaluating reward values, predictability and risks.

  • Allen et al (2007) found that misidentification of self-generated speech is associated with functional abnormalities in the anterior cingulate and left temporal cortex.

    • SZ patients made more mistakes compared to the control group.

• Evidence Supporting Biological and Genetic Basis:

  • Brown et al (2002) found that the risk of having offspring with SZ increased by over 1.3% if the father was over 50 years old, compared to if the father was under the age of 25.

  • Mutations in DNA containing candidate genes (serotonin and dopamine production) suggest a strong heritability and biological basis.

• Mixed Evidence for the Dopamine Hypothesis:

  • Support: Tauscher et al (2014) found that antipsychotics alleviate symptoms.

  • Criticism: Moghaddam and Javitt (2012) argue that glutamate and serotonin may also play a key role.

    • Meltzer (2012) suggested that Clozapine acts upon both of these substances and is more effective than other atypical antipsychotics in reducing SZ symptoms

• Issues with Neural Correlates:

  • Correlational evidence does not demonstrate causation.

  • Third variable problem: An unstudied factor could be affecting both outcomes (lower activation levels and hallucinations). Could be the lowered activation levels causing the hallucinations, or the hallucinations themselves causing the lowered activation levels.

Psychological Explanations for Schizophrenia

• Abnormal family communication styles, including:

  • Schizophrenogenic mother

  • Double-bind theory

  • Expressed emotion

• These factors are contributory, not explicit causes, in the development and maintenance of schizophrenia.

• Schizophrenogenic Mother:

  • Fromm-Reichmann characterised the mother as cold and rejecting.

    • Creates a tense family climate lacking honesty, leading to paranoia and anxiety that manifests as paranoid delusions.

• Double-Bind Theory (Bateson):

  • The child receives mixed messages from parents about what is right or wrong.

    • Tense atmosphere prevents clarification, and mistakes are punished with withdrawal of love, leading to confusion and disorganised thinking.

• Expressed Emotion:

  • The level and type of emotion shown towards the patient by their carer.

    • High levels lead to stress, reduced medication adherence, and increased relapse due to verbal criticism, needless sacrifices, and violence with hostility.

• Dysfunctional Thought Processes (Frith et al, 1992):

  • Metarepresentation and central control.

    • Metarepresentation: cognitive ability to differentiate between our own actions and the actions of others, allowing us insight into the intentions and emotions as others, as well as maintaining a realistic/functional view of our own goals and intentions.

      • Dysfunctions associated with auditory hallucinations and thought insertion because to the inability to differentiate between our own thoughts and those of others. This may lead to paranoid delusions due to the contents of inserting others’ thoughts into the mind of the patient.

    • Central Control: Carrying out a deliberate action whilst suppressing an automatic response, often measured using the Stroop Test.

      • People with SZ often have dysfunctional central control abilities, and so often suffer from derailment because they cannot suppress the automatic associations that each new word in a sentence brings, and so begin to talk off-topic.

• Evidence Supporting Dysfunctional Thought Processes:

  • Stirling et al (2006) found that SZ sufferers made more mistakes and took longer to complete tasks, compared to a healthy neurotypical control group.

  • Dysfunctional thought processing explains the indirect proximal causes but not the distal causes, which limits its utility.

• Comparison Between Biological and Psychological Explanations:

  • Psychological explanations do not accommodate biological factors.

    • Weakness as a biological factors can explain distal origins.

  • Psychological explanations focus on proximal causes, which are more likely to be affected by psychological factors.

• Lack of Support for Family-Based Explanations:

  • The idea of the schizophrenogenic mother was based upon historical observations of families with SZ members, where observers would be searching for ‘crazy-making characteristics’, which is hardly an objective and reliable indicator of the likelihood of developing SZ.

  • Places blame on families and caregivers, without genetic or biological predisposition.

    • Further hurt when they are forced to accept responsibility for their patient’s schizophrenia, which is likely to have already upset family life and relationships through the development of severe and intrusive negative and positive symptoms.

Biological Therapies for Schizophrenia - Drug Therapy

• Two types of antipsychotics: typical and atypical.

• Antipsychotics are dopamine antagonists that bind to complementary dopamine receptors on the postsynaptic membrane, preventing dopamine molecules from binding.

  • The result is an inhibitory effect, where there is a lower rate of action potential generation in the postsynaptic membranes, and so returns neurotransmission (e.g. in the prefrontal cortex and subcortices) to a normal level.

• Typical Antipsychotics:

  • First-generation drugs, such as Chlorpromazine.

    • Favoured for calming and sedative effects, acting upon histamine receptors in addition to dopamine receptors (particularly favoured in psychiatric institutions).

• Atypical Antipsychotics:

  • Second-generation drugs, developed to add to the effectiveness of first-generation medications, and also alleviate the serious side effects

  • Target other neurotransmitter receptors on postsynaptic membranes.

    • Clozapine: targets serotonin and glutamate receptors.

    • Risperidone: acts on dopamine and serotonin receptors.

• Key Advantages:

  • Clozapine: improvements in cognitive functioning and mood.

  • Risperidone: Smaller doses are required because it acts more strongly on dopamine receptors compared to Clozapine

• Development Based on the Dopamine Hypothesis:

  • Paradox: appears to alleviate symptoms by reducing the action of dopamine. This action is not in line with the revised version of the dopamine hypothesis, which suggests that abnormally low levels of dopamine in the cortex are responsible for symptoms. Therefore, a further reduction in dopamine levels should make symptoms worse, and not better. This paradox has caused some to question the validity of the use of antipsychotics, as well as the accuracy of the dopamine hypothesis as an explanation for schizophrenia.

• Side Effects:

  • Short-term effects of typical antipsychotics: agitation and weight gain

  • Long-term risks include tardive dyskinesia (characterised by involuntary contraction and relaxation of the facial muscles) and neuroleptic malignant syndrome (NMS; characterised by fever, altered mental states, muscle rigidity and autonomic dysfunction and is thought to be caused by dopamine receptor blockage or central nervous system infections).

  • Atypical: agranulocytosis (severe leukopenia) with Clozapine, requiring continuous monitoring.

Psychological Therapies for Schizophrenia

• Main Therapies:

  • Cognitive Behaviour Therapy (CBT)

  • Family Therapy

  • Token Economy Systems

• Cognitive Behaviour Therapy (CBT):

  • Initial assessment to clarify symptoms and problems.

    • Emphasises understanding the causes of symptoms, which reduces the intrusive effects of their symptoms and increases their self-awareness, reassures patients that they are not ‘crazy’.

  • Effective behaviours are put into place by questioning the reality of the patient’s beliefs and considering other, more reasonable alternatives.

• Family Therapy:

  • Aims to reduce stress by improving families’ beliefs and attitudes towards schizophrenia.

  • Reduces stress, increases self-efficacy, and trains families to look for signs preceding an episode.

• Token Economy Systems:

  • Based upon behaviourist principles

  • Target, desirable behaviours are identified.

    • Patients are rewarded with a token (secondary reinforcer) exchanged for a reward or privilege (primary reinforcer). Therefore, patients are motivated by the primary reinforcer to carry out the desirable behaviours, and their frequency of doing so increases as they are positively reinforced.

  • Rewards may include extra TV time, exercise taken outside of the grounds of the hospitals and favourite magazines.

• Limitations:

  • Simply improve their quality of life by making the symptoms more manageable. For example, token economies increase the likelihood that the patients act in accordance with hospital rules and break disruptive patterns of behaviour, whilst family therapies reduce stress within a schizophrenic family and so increase the likelihood of the patient complying with their medical advice, whereas CBT improves the patient’s understanding of their symptoms.

• Ethical Issues:

  • Ethical issues associated with the use of psychological therapies, and specifically concerning token economies.

The Interactionist Approach to Schizophrenia

• Integrates biological and psychological explanations and therapies.

  • Central to the idea of an interactionist approach is the use of the diathesis-stress model

• Diathesis-Stress Model:

  • Meehl (1962) - Outdated:

    • Diathesis: biological in origin (i.e. a single ‘schizogene’) which causes a schizotypic personality which in turn eventually manifests itself as schizophrenia. However,

    • Stressor: purely psychological stressor (excessive exposure to stress, particularly through the schizophrenogenic mother)

  • Modern Understanding:

    • Stress: need not be biological in origin but could also be psychological, such as in the form of childhood trauma, as suggested by Ingram and Luxton (2005).

    • Diathesis: not limited to psychological factors but could also be biological in nature, as long as it increases the risk of developing SZ, as according to Houston et al (2008).

• Evidence:

  • Tienari et al's 2004 adoption study: Found family ratings were a significant predictor of schizophrenia spectrum disorders.

• Therapeutic Advantage:

  • Tarrier et al (2004): Tarrier et al (2004). The researchers studied 315 patients who were randomly allocated to one of three conditions, where the last control group received no treatment and the first two groups received a combination of psychological and biological treatments. The researchers found that, after an 18-month follow-up, “there were significant advantages for CBT and supportive counselling over TAU (treatment as usual) alone on symptom measures at 18 months, but no group difference was seen for relapse or re-hospitalisation.