Schizophrenia: Causes and Symptoms — Comprehensive Notes

Disturbances in schizophrenia: overview

• Schizophrenia involves disturbances in nearly every dimension of human psychology: thought, perception, behaviour, language/communication, and emotion. It is one of the most debilitating disorders because of its broad impact across multiple domains.

• The most distinctive features are disturbances of thought, perception, and language.

• Core experiences often include delusions (false beliefs despite evidence) and hallucinations (perceptual experiences without external stimuli).

• Visual hallucinations can occur, but auditory hallucinations are the most common in schizophrenia.

• Thought processes are frequently characterized by loose associations,

• Example of loose associations: a person might say, "I like to dance. Everyone has hands while the river is flowing." (illustrates tangential or illogical connections)

• Distinction between positive and negative symptoms: positive symptoms are the addition of experiences or behaviours not present before; negative symptoms are the removal or subtraction of normal behaviours or thoughts.

• Understanding positive vs negative symptoms is clinically important because they involve different neural circuits and respond to different medications.

Symptoms

• Positive symptoms: reflect the presence of something that is not normally there; subdivided into disorganized and psychotic categories.

  • Disorganized symptoms: inappropriate emotions, disordered thoughts, bizarre behaviour.

  • Psychotic symptoms: delusions and hallucinations.

• Delusions (types):

  • Persecution: belief that others are spying on or harming them.

  • Reference: objects, events, or people have a special significance for them.

  • Grandeur: belief of possessing great knowledge, power, or talent.

  • Identity: belief that they are someone else, often a significant figure.

  • Guilt: belief that they have committed a terrible sin.

  • Control: belief that thoughts and behaviours are controlled by external forces.

• Hallucinations: perceptual experiences without external stimuli; most commonly auditory, but can be visual.

• Disorganized thinking and speech: e.g., loose associations, derailment, and tangential speech.

• Negative symptoms: relatively chronic and include flattening of affect, lack of motivation (avolition), withdrawal from social interactions, inappropriate social behaviour, and impoverished thought.

• In contrast to positive symptoms, negative symptoms involve the subtraction or reduction of usual behaviours/thought processes.

• The presence of both positive and negative symptoms contributes to the overall functional impairment.

Delusions in depth

• Diagram of delusion types (overview): the spectrum includes persecution, reference, grandeur, identity, guilt, and control.

• Delusions contribute to distress and impairment through misinterpretation of reality and potential interference with daily functioning.

Positive vs negative symptoms: neural and treatment implications

• Positive symptoms tend to be associated with specific neural circuits involved in salience attribution, reward, and perception.

• Negative symptoms may involve deficits in motivation, social cognition, and affective processing circuits.

• Because these symptoms involve different neural substrates, they often respond differently to pharmacological and psychosocial interventions.

Diathesis-stress model and etiology

• The diathesis-stress model posits that schizophrenia arises from an underlying biological vulnerability (diathesis) that remains latent until activated by severe stress.

• Genetic predisposition is a key component, but early brain damage can also contribute to the risk.

• Some individuals are genetically above threshold for the illness and may develop it even without an environmental trigger; others are near threshold and require only a small stressor to precipitate an episode; some at risk may never develop the disorder without substantial negative environmental triggers.

• Key idea: biological vulnerability + environmental stressor = onset/recurrence of episodes.

Genetic contribution and heritability

• Research involving more than 30,000 monozygotic and dizygotic twins indicates heritability of schizophrenia is about h^2
  oughly 0.79 (≈ 79%).

• More conservative estimates place heritability around h^2
  oughly 0.50 (≈ 50%).

• These figures reflect the proportion of variance in liability to schizophrenia that can be attributed to genetic factors across twin studies.

• Genetics play a notable role, but environmental factors also contribute to risk and expression of the disorder.

Dopamine hypothesis and neurochemistry

• The dopamine hypothesis posits that people with schizophrenia produce too much dopamine, contributing to positive symptoms (delusions and hallucinations).

• Evidence supporting dopamine hypothesis:

  • Amphetamines increase dopamine activity and, at high doses, can induce psychotic-like symptoms in both typical and predisposed individuals.

  • Antipsychotic medications that block dopamine receptors reduce dopamine activity and yield reductions or eliminations of positive symptoms.

• Limitations and nuances:

  • Not all patients respond to medications that block dopamine receptors.

  • Other neurotransmitters may be involved (serotonin and glutamate), and the exact mechanism remains unclear.

  • It could be that dopamine inhibition leads to reduced glutamate activity, or that dopamine dysfunction exists independently of glutamate; the precise interaction is still being studied.

• In summary, while the dopamine system is central to many cases, schizophrenia likely involves multiple neurochemical pathways and circuits.

Environmental and cultural factors

• Environment still plays a part alongside biological vulnerability.

• Adoption studies:

  • Biological children of people with schizophrenia show increased susceptibility if raised in adoptive families with hostile or confusing communication patterns; this risk is attenuated if the adoptive family is well-functioning.

• Expressed emotion (EE): a key environmental variable.

  • EE refers to criticism or emotional overinvolvement/intrusiveness expressed by family members.

  • Relapse risk associated with EE: about 65 ext%-75 ext% of patients with high EE relapse relatively quickly after returning home, compared to about 25 ext% relapse with low EE.

• Childhood abuse and trauma:

  • A 2003 New Zealand study by Reader and Tau found that patients abused as children were four times more likely to experience hallucinations and 15 times more likely to hear voices compared to those not abused.

• Cross-cultural considerations:

  • Expressed emotion and relapse rates are culturally variable; relapse rates tend to be lower in some non-Western, more collectivist societies (e.g., India) where EE tends to be lower and there is greater social support.

  • Collectivist societies emphasize group responsibility and less blame toward individuals with schizophrenia, which may influence relapse dynamics and social outcomes.

• Cultural context and stigma can influence help-seeking, treatment adherence, and social integration.

Birth and early developmental factors

• Other possible environmental and biological contributors include birth complications, viral exposure, and malnutrition.

• In utero factors:

  • Exposure to famine and rubella (German measles) during the first trimester doubles the risk of developing schizophrenia later in life.

  • Exposure during the second and third trimesters is more strongly associated with mood disorders rather than schizophrenia.

• Perinatal and delivery factors:

  • Differences between monozygotic twins with discordant outcomes may be partly explained by complications during delivery (e.g., prolonged labour) affecting brain development.

Brain structure associated with schizophrenia

• Comparisons of monozygotic twins discordant for schizophrenia show structural brain differences in the affected twin: larger ventricles and smaller hippocampus.

• Such findings suggest that neurodevelopmental factors and perinatal events can contribute to brain changes linked with the disorder.

Summary and takeaway

• Schizophrenia involves disturbances across thought, perception, language, emotion, and behavior.

• Positive symptoms (presence) include delusions, hallucinations, disorganized thinking, and bizarre behaviours; negative symptoms (absence) include flat affect, avolition, social withdrawal, and impoverished thought.

• Delusions are diverse (persecution, reference, grandeur, identity, guilt, control); hallucinations are most often auditory.

• The diathesis-stress model provides a framework for understanding how biological vulnerability interacts with environmental stress to trigger episodes.

• The genetic contribution to schizophrenia is substantial but imperfect (heritability estimates around h^2
  oughly 0.79 to h^2
  oughly 0.50); environmental and developmental factors also play important roles.

• The dopamine hypothesis remains influential, supported by amphetamine effects and antipsychotic dopamine blockade, but other neurotransmitters (serotonin, glutamate) and neural circuits are also involved.

• Environmental factors such as expressed emotion and childhood abuse influence relapse risk and symptom expression, with cross-cultural differences in EE and relapse rates.

• Early life factors (birth complications, in utero exposure to famine or rubella) and brain structure differences (ventricular enlargement, reduced hippocampal volume) contribute to risk and manifestation.

• Overall, schizophrenia emerges from a complex interplay of genetic, neurochemical, developmental, and environmental factors that shape its onset, course, and response to treatment.