Source: Abnormal Psychology textbook (University of Florida)
Tags: schizophrenia, genetics, dopamine hypothesis, neurotransmitters, brain abnormalities, neurodevelopmental, psychosocial, expressed emotion, schizoaffective, schizophreniform, brief psychotic disorder, delusional disorder, schizotypal personality disorder
Difficulty: Intermediate | Prerequisites: Part 1 of these notes (Symptoms and Diagnosis). Familiarity with basic neuroscience concepts (neurotransmitters, brain structures) is helpful.
This section covers why schizophrenia develops and the other psychotic disorders that sit alongside it on the spectrum. The biological theories span genetics, brain structure, prenatal damage, and neurotransmitter systems. The psychosocial theories examine stress, family dynamics, and cognitive explanations. The other psychotic disorders, from schizoaffective disorder to schizotypal personality disorder, share features with schizophrenia but differ in severity, duration, or symptom profile. Understanding causes is essential for understanding treatment (covered in Part 3).
Schizophrenia has strong genetic roots (MZ twin concordance around 46%) but is not purely genetic; prenatal insults, brain structural abnormalities, and neurotransmitter dysregulation (especially dopamine) all contribute. Psychosocial factors such as chronic stress, expressed emotion in families, and urban upbringing increase risk or trigger relapse. Several related psychotic disorders sit on the same spectrum, distinguished primarily by duration, severity, and the presence or absence of mood symptoms.
Concordance rate
The probability that both members of a twin pair will have a disorder if one twin has it. For schizophrenia, the MZ concordance rate is approximately 46% and the DZ rate approximately 14%. In simple terms, if one identical twin has schizophrenia, there is roughly a coin-flip chance the other will too, but it is not guaranteed, which tells us genetics are not the whole story.
Mesolimbic pathway
A subcortical dopamine pathway involved in processing salience and reward. Excessive dopamine activity here is linked to positive symptoms of schizophrenia (hallucinations, delusions). Think of it as the brain's "this matters" signal firing too often, causing the person to attach importance to things that do not warrant it.
Prefrontal cortex
The brain region responsible for language, emotional expression, planning, and carrying out plans. It connects to all other cortical regions, the limbic system, and the basal ganglia. Low dopamine activity here is associated with negative symptoms.
Perinatal hypoxia
Oxygen deprivation at birth or in the few weeks before or after birth. It interacts with genetic vulnerability to increase the risk of developing schizophrenia.
Expressed emotion
A pattern in families characterised by overinvolvement, overprotectiveness, self-sacrificing attitudes, low warmth, and high criticism directed at the family member with schizophrenia. High expressed emotion is linked to higher rates of relapse. In simple terms, families that are simultaneously too involved and too critical create an environment that makes symptoms worse.
Social drift
The process by which schizophrenia symptoms interfere with education and employment, causing the person to drift downward in social class relative to their family of origin.
Schizoaffective disorder
A condition involving a mix of schizophrenia symptoms and prominent mood symptoms (meeting criteria for major depressive or manic episode). Requires at least two weeks of hallucinations or delusions without mood symptoms.
Schizophreniform disorder
Meets the core criteria (A, D, E) for schizophrenia but symptoms last only one to six months. An intermediate condition between brief psychotic disorder and schizophrenia.
Brief psychotic disorder
Sudden onset of delusions, hallucinations, disorganised speech, and/or disorganised behaviour lasting between one day and one month, after which symptoms completely resolve.
Delusional disorder
Delusions lasting at least a month that concern plausible real-life situations. No other psychotic symptoms are present, and the person generally functions well apart from the delusion. More common in females; typical onset around age 40 to 49.
Schizotypal personality disorder
A lifelong pattern of significant oddities in self-concept, relationships, thinking, and behaviour. The person has odd perceptions and beliefs but retains a basic grasp on reality. Classified under both the schizophrenia spectrum and personality disorders.
Double bind theory
Gregory Bateson's (now largely discredited) theory that parents of people with schizophrenia placed their children in contradictory communication situations (e.g. physically comforting but verbally abusing), leading to distorted perceptions of reality.
Family, twin, and adoption studies consistently show a genetic component.
No single genetic abnormality accounts for schizophrenia; it is polygenic.
Irving Gottesman's research showed that children of parents with schizophrenia and MZ twins share the greatest number of risk genes and the greatest risk of developing the disorder.
Lower genetic similarity corresponds to lower risk, though higher genetic similarity does not guarantee development, only higher risk.
Key adoption studies:
Pekka Tienari tracked children of mothers with schizophrenia who were adopted away. These children still developed the disorder at higher rates.
Seymour Kety studied biological relatives of people with schizophrenia and found they were more likely to develop it.
Key statistics:
MZ twin concordance: approximately 46%
DZ twin concordance: approximately 14%
A Finnish study attributed approximately 83% of variation in schizophrenia to genetic factors.
Environmental and other biological factors still play a role, even in genetically at-risk individuals.
Twins concordant for schizophrenia show more gene differences than twins who are both unaffected.
Major structural and functional deficits are present in people with schizophrenia.
The disorder is increasingly viewed as a neurodevelopmental condition, where various factors lead to abnormal brain development in the uterus and early life.
Grey matter:
Gross reduction in grey matter in the cortex, particularly in the medial temporal, superior temporal, and prefrontal areas.
People at risk show abnormal activity in the prefrontal cortex, which connects to the limbic system (emotion and cognition) and basal ganglia (motor movement).
Abnormalities in brain development during adolescence (a critical period) are linked to schizophrenia.
Hippocampus:
Abnormalities in volume and shape are associated with schizophrenia.
Similar abnormalities appear in first-degree relatives.
White matter:
Reductions and abnormalities in white matter (the material connecting brain regions), particularly in areas related to working memory.
These abnormalities can be present before overt symptoms appear, making them potential early markers.
White matter problems disrupt coordination between brain areas, contributing to the severe deficits seen in the disorder.
Ventricles:
Enlargement of the ventricles (fluid-filled spaces in the brain) suggests atrophy or deterioration in surrounding brain tissue.
People with enlarged ventricles show social, emotional, and behavioural deficits long before core symptoms emerge.
They tend to have more severe symptoms and respond less well to medication.
Birth complications:
Serious prenatal and birth difficulties are more frequent in people who develop schizophrenia.
Obstetric difficulties increase the likelihood of developing the full syndrome.
Perinatal hypoxia may be particularly important. The effects of oxygen deprivation interact with genetic vulnerability, though most people who experience perinatal hypoxia do not develop schizophrenia.
Prenatal viral exposure:
Higher rates of schizophrenia when the mother was exposed to viral infections during pregnancy, especially during the second trimester (a critical period for brain development).
People with schizophrenia are more likely to have been born in spring months (consistent with maternal flu exposure during autumn/winter).
Viral infection may activate the mother's immune system in ways that negatively affect the development of brain cells and dopamine systems in the foetus.
The dopamine hypothesis (original):
Symptoms of schizophrenia were thought to be caused by excess dopamine in the prefrontal cortex and limbic system.
Drugs that reduce dopamine (phenothiazines/neuroleptics) reduce symptoms.
Drugs that increase dopamine (e.g. amphetamines) increase positive symptoms.
Neuroimaging shows more dopamine receptors and higher dopamine levels in some brain areas of people with schizophrenia.
Problems with the original theory:
Many people did not respond to neuroleptics.
Those who did respond saw reduction in positive symptoms only, and the effect was not immediate.
Dopamine is therefore not the sole determinant.
The revised dopamine theory:
Different types of dopamine receptors and different dopamine levels in various brain areas contribute to different symptoms.
Excessive dopamine in the mesolimbic pathway leads to attributing salience to innocuous stimuli, producing hallucinations, delusions, and motivational deficits.
Low dopamine in the prefrontal cortex leads to negative symptoms (consistent with structural abnormalities in that region and explaining why phenothiazines do not alleviate negative symptoms).
Atypical antipsychotics may work by binding to specific dopamine receptor types and blocking their action.
Other neurotransmitters:
Serotonin: Serotonin neurons regulate dopamine neurons in the mesolimbic system. The interaction between serotonin and dopamine may be crucial. Newer drugs bind to serotonin receptors.
GABA: Abnormal levels are linked to schizophrenia. Deficiencies may contribute to cognitive and emotional symptoms.
Glutamate: Excitatory pathways linking the cortex, limbic system, and thalamus. Drugs that block glutamate receptors (PCP, ketamine) produce hallucinations and delusions.
Dysregulation of the dopamine system appears involved in multiple forms of psychosis, not just schizophrenia.
People with schizophrenia are more likely to experience chronically stressful circumstances.
Social drift: symptoms interfere with education and employment, pushing the person downward in social class.
People with schizophrenia were more likely to be born in large cities. Torry and Yolken argue this is because pregnant women in cities face greater exposure to infectious agents.
Immigration, as a stressful life event, is associated with increased risk.
Stressful circumstances may trigger new episodes.
Some apparently negative life events preceding relapse may themselves be prodromal symptoms rather than independent triggers.
Early (now discredited) theories:
Overprotective and rejecting mothers were blamed for causing schizophrenia.
Bateson's double bind theory proposed that contradictory messages from parents (e.g. physical comfort paired with verbal abuse) led to distorted perceptions. This theory did not hold up to scientific scrutiny and caused considerable guilt in families.
Expressed emotion (supported by research):
Families high in expressed emotion are overinvolved, overprotective, critical, hostile, and resentful, while voicing self-sacrificing attitudes.
They often speak as though the person with schizophrenia can control their symptoms.
High expressed emotion is linked to increased risk of relapse and full syndrome.
However, more negative symptoms may provoke more expressed emotion, so the relationship is not necessarily one-directional.
Family members high in expressed emotion often have psychological disorders themselves, meaning the person with schizophrenia may be genetically prone to relapse independently of the emotional environment.
Interventions that reduce expressed emotion do reduce relapse rates.
Fundamental difficulties in attention, inhibition, and communication rules lead people with schizophrenia to conserve limited cognitive resources by adopting certain biases and thinking styles.
Delusions arise as attempts to explain strange perceptual experiences.
Hallucinations result from hypersensitivity to perceptual input combined with a tendency to attribute internal experiences to external sources.
Negative symptoms arise from expectations that social interactions will be aversive and from the need to withdraw and conserve cognitive resources.
Cognitive therapies help patients identify and cope with stressful circumstances, dispute delusional beliefs, and develop more positive expectations about social engagement.
These therapies show greater success in reducing symptoms than supportive therapy alone.
Cultures vary in how they explain schizophrenia.
Most societies have a biological explanation for the disorder.
Other cultural theories attribute it to stress, lack of spiritual piety, or family dynamics.
All of the following share features with schizophrenia and fall along a continuum of severity. Schizophrenia has the worst long-term outcome.
A mix of schizophrenia and a mood disorder.
Psychotic symptoms present alongside prominent mood symptoms meeting criteria for major depressive or manic episode.
Mood symptoms must be present for the majority of the illness period.
Requires at least two weeks of hallucinations or delusions in the absence of mood symptoms (to distinguish it from a mood disorder with psychotic features).
Meets criteria A, D, and E for schizophrenia but symptoms last only one to six months.
Functional impairment may be present but is not required for diagnosis.
Good prognostic features include quick onset, prior good functioning, and confusion without blunted or flat affect.
The majority of people with this diagnosis will eventually be rediagnosed with schizophrenia or schizoaffective disorder.
Sudden onset of delusions, hallucinations, disorganised speech, and/or behaviour.
Lasts between one day and one month; symptoms then resolve completely.
Sometimes follows a major stressor, sometimes appears without one.
More common in women, particularly postpartum.
High relapse risk, but overall outcomes are excellent.
Delusions lasting at least one month about plausible real-life situations.
No other psychotic symptoms.
Functioning is generally preserved apart from the delusion itself.
More common in females; onset typically around age 40 to 49.
Lifelong pattern of oddities in self-concept, relating to others, thinking, and behaviour.
Weak or unstable sense of self; difficulty setting realistic goals.
Restricted or inappropriate emotional expression.
Few close relationships; perceives others as deceitful and hostile.
Odd thinking and behaviour, but retains a basic grasp on reality.
May believe random events are related to them; has odd perceptions.
Easily distracted or prone to fixating; lost in thought or fantasy.
Shows deficits in working memory, learning, and recall (similar to but less severe than schizophrenia).
Shares genetic and neurological abnormalities with schizophrenia.
Some people with schizotypal personality disorder experience brief psychotic episodes and eventually develop schizophrenia.
Classified under both the schizophrenia spectrum and personality disorders.
Students often think the dopamine hypothesis is a single, settled theory. It has been significantly revised: the current view involves different dopamine levels in different brain pathways (excess in mesolimbic, deficit in prefrontal), not a simple "too much dopamine" explanation.
The double bind theory and "schizophrenogenic mother" concept are frequently confused with the expressed emotion research. The former are discredited; expressed emotion is supported by evidence but the causal direction is not straightforward.
Students sometimes assume that if MZ twin concordance is 46%, genes account for 46% of the cause. Concordance rates and heritability estimates are different metrics. The Finnish study estimated heritability at 83%.
Brief psychotic disorder is often mistaken for schizophrenia on exams. The key distinction is duration: brief psychotic disorder resolves within one month.
⚠️ Know the concordance rates for MZ (46%) and DZ (14%) twins, and what they imply about the gene-environment interaction.
⚠️ Be able to explain the revised dopamine theory: mesolimbic excess (positive symptoms) vs. prefrontal deficit (negative symptoms).
⚠️ Understand expressed emotion, how it relates to relapse, and the caveats about causal direction.
⚠️ Be able to distinguish between schizoaffective, schizophreniform, brief psychotic, and delusional disorders by duration and symptom profile.
⚠️ Schizotypal personality disorder sits on the schizophrenia spectrum; know its relationship to schizophrenia.
⚠️ Prenatal viral exposure and perinatal hypoxia as environmental risk factors are commonly tested.
True or False: If one identical twin has schizophrenia, the other will definitely develop it too. False. The MZ concordance rate is approximately 46%, not 100%.
Fill in the blank: Excessive dopamine in the ______ pathway is linked to positive symptoms, while low dopamine in the ______ is linked to negative symptoms. Mesolimbic pathway; prefrontal cortex.
True or False: The double bind theory of schizophrenia is well supported by research. False. It did not hold up to scientific scrutiny.
Fill in the blank: Brief psychotic disorder resolves within ______, while schizophreniform disorder lasts between ______. One month; one to six months.
True or False: Expressed emotion in families is a proven direct cause of schizophrenia. False. It is associated with relapse, but the causal relationship is not clear-cut, and the person's symptoms may provoke the expressed emotion.
Q: Explain the revised dopamine theory of schizophrenia.
A: The revised theory proposes that different symptoms arise from different dopamine levels in different brain pathways. Excessive dopamine activity in the mesolimbic pathway causes the person to attribute salience to innocuous stimuli, leading to hallucinations, delusions, and motivational deficits (positive symptoms). Low dopamine activity in the prefrontal cortex leads to deficits in attention, motivation, and organisation of behaviour (negative symptoms). This dual-pathway model explains why traditional antipsychotics, which broadly reduce dopamine, alleviate positive symptoms but not negative ones.
Q: What evidence supports a genetic contribution to schizophrenia?
A: Family studies show that closer genetic relatives of people with schizophrenia have higher risk. Twin studies show MZ concordance of approximately 46% vs. DZ concordance of approximately 14%. Adoption studies by Tienari and Kety found that biological relatedness predicts risk regardless of rearing environment. A Finnish study attributed 83% of variation to genetic factors. However, the fact that MZ concordance is well below 100% confirms that environment also matters.
Q: How does schizoaffective disorder differ from schizophrenia?
A: Schizoaffective disorder involves prominent mood symptoms (meeting criteria for major depressive or manic episode) present for the majority of the illness, alongside psychotic symptoms. It also requires at least two weeks of hallucinations or delusions in the absence of mood symptoms. In schizophrenia, mood symptoms are not a required or prominent feature.
Q: Describe the role of expressed emotion in schizophrenia relapse.
A: Expressed emotion refers to a family environment marked by overinvolvement, criticism, hostility, and low warmth. People with schizophrenia living in high-expressed-emotion families show higher rates of relapse. However, the relationship may be bidirectional: severe negative symptoms can provoke more criticism and overinvolvement. Family members high in expressed emotion may also have their own psychological disorders, contributing genetic risk. Interventions that reduce expressed emotion do reduce relapse rates.
Q: What distinguishes schizotypal personality disorder from schizophrenia?
A: People with schizotypal personality disorder have oddities in thinking, behaviour, self-concept, and relationships, but they retain a basic grasp on reality. They may have odd perceptions and beliefs but do not experience full-blown hallucinations or delusions (unless they develop brief psychotic episodes). Their cognitive deficits are similar to but less severe than those in schizophrenia. It is classified as both a personality disorder and part of the schizophrenia spectrum.
The neurotransmitter theories link to biological psychology and pharmacology. The dopamine hypothesis connects to the study of Parkinson's disease (dopamine deficit) and substance abuse (amphetamines increasing dopamine). Expressed emotion research ties into health psychology and the broader study of how family systems affect mental health outcomes. The other psychotic disorders connect to mood disorders (schizoaffective disorder) and personality disorders (schizotypal).
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