Schizophrenia: Classification, Dopamine, Family Dysfunction & Therapies

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Classification: Positive vs Negative Symptoms & Diagnosis Issues

1. Positive symptoms are excess/added distortions of normal functioning: Hallucinations (unreal sensory perceptions, most commonly auditory voices commenting on or criticising the individual) and Delusions (bizarre, fixed false beliefs not grounded in reality, such as delusions of persecution/paranoia, grandeur, or external control). 2. Negative symptoms are a loss or diminution of normal functioning: Speech Poverty (alogia, reduction in the amount and quality of speech) and Avolition (apathy, severe loss of motivation to initiate and persist with goal-directed activities like personal hygiene or work). In DSM-5, at least 1 positive symptom (delusions, hallucinations, or disorganised speech) is required alongside a second symptom for 1 month; in ICD-10, 2 or more negative symptoms suffice. Diagnostic validity and reliability are undermined by Low Inter-Rater Reliability (Cheniaux et al. 2009), Co-morbidity (Buckley et al. 2009: 50% also have depression, 47% substance abuse), Symptom Overlap with bipolar disorder (Ellason & Ross 1995), Gender Bias (Loring & Powell 1988), and Cultural Bias (Cochrane 1977: Afro-Caribbean men in the UK are 7-9x more likely to be diagnosed than white British men or people in the Caribbean).

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Biological Explanations: Genetics & Neural Correlates

1. Genetic basis: Gottesman (1991) conducted a landmark family study showing risk rises with genetic similarity: 1% in the general population, 2% in aunts/uncles, 9% in siblings, 17% in DZ twins, 46% in children of two schizophrenic parents, and 48% in identical MZ twins. Schizophrenia is polygenic and aetiologically heterogeneous: Ripke et al. (2014) compared 37,000 patients with 113,000 controls and identified 108 separate genetic loci (many coding for dopamine receptors and the immune system). 2. The dopamine hypothesis: The original hypothesis (Seeman 1987) focused purely on hyperdopaminergia in the subcortex (excess dopamine receptors in Broca's area / mesolimbic pathway causing positive symptoms like auditory hallucinations). Davis et al. (1991) added hypodopaminergia in the prefrontal cortex (too little dopamine in the mesocortical pathway causing negative symptoms and cognitive deficits), while Howes et al. (2017) linked both to excessive presynaptic dopamine synthesis. 3. Neural CORRELATES: Enlarged ventricles (Torrey 2002: 15% larger fluid-filled cavities, associated with negative symptoms) and reduced activity in the ventral striatum (Juckel et al. 2006: correlated with avolition).

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Psychological Explanations: Family Dysfunction & Cognitive Deficits

1. Family dysfunction: Fromm-Reichmann's (1948) 'Schizophrenogenic Mother': cold, rejecting, and controlling, creating a family climate of secrecy and distrust that breeds paranoid delusions. Bateson et al.'s (1972) Double-Bind Theory: the child repeatedly receives contradictory verbal and non-verbal messages from parents (e.g., mother asks for a hug then stiffens up coldly) and cannot comment on the contradiction, leaving them confused about what is real. Expressed Emotion (EE - Brown et al. 1972, Kuipers et al. 1983): high levels of verbal criticism, hostility, and emotional over-involvement from carers is primarily a maintenance/relapse factor (causing a 4x higher relapse rate in returning patients). 2. Cognitive explanations (Frith et al. 1992): Dysfunctional thought processing caused by: Metarepresentation dysfunction: inability to recognise one's own thoughts and inner speech as self-generated, attributing inner voice to an external source (explaining auditory hallucinations and delusions of thought insertion). Central Control dysfunction: inability to suppress automatic thoughts and associations triggered by each word, resulting in disorganised speech ('word salad' / derailment, tested using the Stroop task by Stirling et al. 2006).

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Biological Therapy: Typical vs Atypical Antipsychotics

1. Typical (First-Generation) antipsychotics (e.g., Chlorpromazine, discovered in the 1950s): Act as strong dopamine antagonists by binding to and blocking D2 dopamine receptors in the synapses of the mesolimbic pathway, reducing dopamine action to eliminate positive symptoms (and also acting as a histamine antagonist sedative). Evaluation: Thornley et al. (2003) meta-analysis of 1,121 patients showed Chlorpromazine significantly reduced symptom severity and relapse compared to placebo, but blocking dopamine in the basal ganglia causes severe extrapyramidal side effects - tardive dyskinesia (involuntary facial grimacing and tongue-twisting) and lethal Neuroleptic Malignant Syndrome. 2. Atypical (Second-Generation) antipsychotics (e.g., Clozapine and Risperidone): Temporarily occupy D2 receptors and then rapidly dissociate to allow normal dopamine transmission (reducing tardive dyskinesia), while also targeting serotonin and glutamate receptors to reduce depression, anxiety, and negative symptoms (Meltzer 2012 found Clozapine effective in 30-50% of treatment-resistant cases, though Clozapine requires regular blood tests due to the risk of fatal agranulocytosis).

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Psychological Therapies: CBTp, Family Therapy & Token Economies

1. Cognitive behavioural therapy for psychosis (CBTp - Tarrier 2005): Usually 5 to 20 sessions helping patients identify irrational delusions/hallucinations, challenge their reality through gentle reality-testing and Socratic questioning (e.g., 'If the CIA is watching you, why haven't they acted?'), and develop normalizing coping strategies to reduce distress (Jauhar et al. 2014 found a small-to-moderate significant therapeutic effect, especially when combined with antipsychotics). 2. Family therapy (Pharoah et al. 2010): Works with the patient and their family to reduce Expressed Emotion (EE), improve constructive communication, and form a therapeutic alliance (reducing hospital readmission and improving medication compliance). 3. Token economies (Ayllon & Azrin 1968): An operant conditioning behaviour modification system used in psychiatric wards to manage maladaptive institutionalised negative symptoms (e.g., avolition/poor hygiene): patients earn coloured plastic tokens (secondary reinforcers) immediately for carrying out desirable behaviours (making their bed, brushing teeth), which they exchange for tangible rewards/privileges (primary reinforcers like sweets, magazines, or yard walks).

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The Interactionist Approach to Schizophrenia (Diathesis-Stress)

Paul Meehl's (1962) original diathesis-stress model argued that diathesis was a single 'schizogene' producing a schizotypic personality, which developed into schizophrenia only if exposed to a schizophrenogenic mother. The modern Interactionist Model (Ripke 2014; Read et al. 2001) recognises that: 1. Diathesis is polygenic (108+ genes) and can also be caused by early neurodevelopmental trauma (such as severe childhood sexual/physical abuse or birth asphyxia altering the HPA axis and dopamine sensitivity); 2. Stress includes any later environmental trigger, not just high family Expressed Emotion, but also heavy cannabis use (Houston et al. 2008: childhood trauma + cannabis before age 16 multiplied psychosis risk) or urban upbringing (Vassos et al. 2012). Treatment combines antipsychotic medication with CBTp (Tarrier et al. 2004 showed combination groups had lower symptom levels than medication-only controls).

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1. Q1

   Outline and evaluate the biological explanation for schizophrenia, referring to both genetics and the dopamine hypothesis. (8 marks)

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   Click “Check Mark Scheme” to compare your answer, 1. [AO1 - 4 marks] Genetic explanations show schizophrenia runs in families: Gottesman (1991) found a 48% concordance rate in identical MZ twins vs 17% in DZ twins, and Ripke et al. (2014) demonstrated it is polygenic and aetiologically heterogeneous, identifying 108 distinct genetic loci coding for neurotransmitter and immune function. Neurochemically, the revised Dopamine Hypothesis proposes that hyperdopaminergia (excess dopamine D2 receptor activity) in the subcortex/Broca's area causes positive symptoms like auditory hallucinations, whereas hypodopaminergia (low dopamine) in the prefrontal cortex causes negative symptoms and cognitive deficits. 2. [AO3 Strength: Twin/adoption studies & drug efficacy - 2 marks] Adoption studies (Tienari et al. 2004) confirm that biological children of schizophrenic mothers retain higher genetic risk even when raised apart, and the dopamine hypothesis is strongly supported by pharmacological evidence, dopamine agonists like amphetamines/L-DOPA induce psychosis in healthy people, while dopamine antagonists (antipsychotics) alleviate positive symptoms. 3. [AO3 Limitation: Environmental triggers & glutamate/correlation-causation - 2 marks] Because MZ twin concordance is 48% rather than 100%, genetics alone cannot be a complete explanation (requiring an interactionist diathesis-stress model), and Moghaddam and Javitt (2012) argue that abnormal glutamate levels may be the primary neurochemical cause rather than dopamine.

2. Q2

   Compare family dysfunction and cognitive explanations as psychological explanations for schizophrenia. (6 marks)

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   Click “Check Mark Scheme” to compare your answer, 1. Outline of Family Dysfunction: Explains schizophrenia through abnormal interpersonal communication in childhood and the home, including Fromm-Reichmann's cold, controlling 'schizophrenogenic mother', Bateson et al.'s (1972) Double-Bind theory (contradictory verbal and non-verbal signals trapping the child), and High Expressed Emotion (criticism, hostility, and over-involvement triggering relapse) [2 marks]. 2. Outline of Cognitive Explanations: Frith et al. (1992) explain symptoms via internal information-processing deficits, failed Metarepresentation (attributing internal voices to external agents, causing hallucinations) and failed Central Control (inability to suppress automatic associations, causing disorganised speech) [2 marks]. 3. Evaluation and Comparison: Cognitive explanations have strong empirical laboratory support (Stirling et al. 2006 found patients took over twice as long as controls on the Stroop task) and avoid socially sensitive parent-blaming, whereas early family dysfunction theories (schizophrenogenic mother and double-bind) rely on retrospective clinical observations, lack empirical evidence, and cause immense guilt and stigma for parents caring for ill children [2 marks].

3. Q3

   Discuss the use of typical and atypical antipsychotic drugs in the treatment of schizophrenia. (8 marks)

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   Click “Check Mark Scheme” to compare your answer, 1. [AO1 - 4 marks] Typical antipsychotics (e.g., Chlorpromazine) are strong dopamine antagonists that block D2 receptors in the mesolimbic pathway to reduce positive symptoms and also act as histamine sedatives. Atypical antipsychotics (e.g., Clozapine and Risperidone) were developed to improve efficacy on negative symptoms and reduce motor side effects: they bind transiently to D2 receptors before rapidly dissociating, and additionally act on serotonin (5-HT2A) and glutamate receptors. 2. [AO3 Strength: Clinical effectiveness in trials - 2 marks] Thornley et al.'s (2003) review of 13 trials (1,121 participants) confirmed Chlorpromazine reduced symptom severity and relapse rates compared to placebo, while Meltzer (2012) showed Clozapine is more effective than typical antipsychotics and works in 30-50% of treatment-resistant cases (and reduces suicide risk). 3. [AO3 Limitation: Severe side effects, Healy's critique & 'chemical cosh' - 2 marks] Typical antipsychotics cause debilitating tardive dyskinesia in ~30% of long-term users and Clozapine can cause fatal agranulocytosis; Healy (2012) noted many drug trials exaggerate benefits by using short-term designs where control patients suffer withdrawal effects, and critics argue sedative antipsychotics are sometimes used as a 'chemical cosh' to pacify hospitalised patients rather than cure the underlying cause.

4. Q4

   Explain two issues affecting the validity and/or reliability of the classification and diagnosis of schizophrenia. (4 marks)

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   Click “Check Mark Scheme” to compare your answer, 1. Co-morbidity (Validity): Schizophrenia frequently co-occurs with other mental disorders: Buckley et al. (2009) found around 50% of patients with schizophrenia also have a diagnosis of depression and 47% have substance abuse (and 29% PTSD) - calling into question whether schizophrenia is a distinct, valid single condition [2 marks]. 2. Symptom Overlap (Validity and Reliability): Many positive and negative symptoms of schizophrenia (such as delusions and avolition) overlap with other disorders like Bipolar Disorder; Ellason and Ross (1995) noted that patients with Dissociative Identity Disorder (did) actually have more schizophrenic symptoms than people diagnosed with schizophrenia, leading to inconsistent diagnoses depending on whether ICD or DSM is used [2 marks].

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