CAUSES
Disorders cannot be explained by one factor alone. Many times, it is the interaction of development, culture, genetics, neurobiology, psychology and society that brings about the onset of a disorder. The model used to explain these multi-faceted disorders is called the integrative model.
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Development:
- Early in development, children may show early clinical features that tend to indicate a later onset of schizophrenia (physical abnormalities, poor motor coordination, cognitive problems, and social problems). The problem with this, however, is that these features do not necessarily mean that the child will develop Schizophrenia. Some of these children might develop another type of disorder.
- Before clinically significant symptoms arise, around 85% of people who develop Schizophrenia go through a prodromal stage. This stage is characterized by less severe symptoms (ideas of reference, magical thinking, illusions, isolation, impairment in functioning, lack of initiative, interest, and/or energy) that precede more serious symptoms by 1-2 years.
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Culture:
- Different stressors that are more recurrent in one culture when compared to another contribute to worse prognoses (might also be due to predominant biological differences).
- Imbalances in diagnoses may may also be due to the stress brought about by the societal discrimination of a culture.
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Genetics:
- There is no single gene that can be identified as influential to the onset of the disorder
- Genes are most definitely responsible for making a person more vulnerable to schizophrenia or predisposing them.
- Genetics and environment work together in an integrative model called the diathesis-stress model which proposes that genetics predispose a person to develop a disorder, but acute, stressful stimulus triggers the onset of the disorder
- It seems that children inherit a predisposition towards all forms of the Schizophrenia Spectrum (e.g., schizophrenia, schizophreniform disorder, schizoaffective disorder, etc.) when a parent has one form of Schizophrenia.
- Studies indicate that the risk of developing Schizophrenia increases the more genes are shared with the person diagnosed with the disorder.
- Most reliable genetic influences: Chromosome 8 (Neuregulin 1), 6 (dystrobrevin-binding protein 1), and 22 (catecholamine O-methyl transferase). The latter is of the biggest interest because it influences the dopaminergic system - system that is predominantly disrupted in people with Schizophrenia.
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Neurobiology:
- The dopamine hypothesis of schizophrenia proposes that the dopamine system might be overly active in people with schizophrenia.
- Evidence:
1. Most effective drugs for treating schizophrenia are dopamine antagonists (inhibit dopamine system)
2. L-dopa, a dopamine agonist (promotes production and/or release of dopamine) that is used to treat dopamine deficiency, produces psychotic symptoms in some people.
3. Amphetamines (dopamine agonists) worsen the symptoms of people with Schizophrenia
- Counter-Evidence:
1. A number of people with the disorder do not exhibit a better prognosis when given the dopamine antagonists
2. Dopamine antagonists act quickly, but symptoms only begin to fade after days or weeks of drug use
3. Drugs only help in reducing some negative symptoms
- Current theory: at least three neurochemical imbalances have an influence on the brains of people with the disorder
- Brain structure indicators: the brains of people with schizophrenia (or a predisposition to it) tend to have larger ventricles
- Hypofrontality (a less active frontal lobe) and hyperfrontality (an excessively active frontal lobe) are present in different schizophrenia patients, indicating that a dysfunction in the lobe could be an influential factor.
- Dysfunctional brain areas in Schizophrenia patients: prefrontal cortex, related cortical regions, and subcortical circuits such as the thalamus and the striatum (related to dopamine)
- Other possible influential factors:
1. Prenatal exposure to influenza
2. Seeming correlation between marijuana use and schizophrenia (chronic use of marijuana may contribute to an onset of the disorder)
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Psychology:
- Stress: This relates back to what was mentioned under the category of genetics: a genetic predisposition might be triggered by environmental stressors, thus causing the onset of this disorder.
- The previously mentioned model is not unilateral, however, since people that already have the disorder might react different to stress
- Families also seem to have a high influence on the relapse rate of patients with the disorder. In fact, emotional overinvolvement or overexpression (expressed emotion or EE) on the family's part actually increased the likelihood that a patient diagnosed with Schizophrenia would relapse.
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Terminology
- Ideas of Reference: Belief that events relate directly to a person
- Magical Thinking: Belief that the person has supernatural abilities
- Illusions: Misrepresentations of real stimulus (e.g., a child that sees the outline of a coat and believes it to be a monster)
- Expressed Emotion (EE): Levels of criticism, hostility, and emotional involvement displayed by behaviors
- Saran, Manish, et al. (2007). Biological Markers and the Future of Early Diagnosis and Treatment in Schizophenia. PsychiatricTimes. Retrieved from: http://www.psychiatrictimes.com/articles/biological-markers-and-future-early-diagnosis-and-treatment-schizophrenia
- Oliver D. Howes, Shitij Kapur; The Dopamine Hypothesis of Schizophrenia: Version III—The Final Common Pathway, Schizophrenia Bulletin, Volume 35, Issue 3, 1 May 2009, Pages 549–562, https://doi.org/10.1093/schbul/sbp006
- Brown GW, Monck EM, Carstairs GM, et al. Influence of Family Life on the Course of Schizophrenic Illness
Journal of Epidemiology & Community Health 1962;16:55-68.