Schizophrenia Flashcards
Biological explanation (AO1)
One aspect of the biological explanation for schizophrenia (SZ) is its genetic basis, which posits that SZ is heritable and influenced by inherited genetic factors. Family studies provide robust evidence supporting this view, demonstrating that the likelihood of developing SZ increases in proportion to genetic similarity with a relative who has the disorder. Gottesman (1991) conducted a meta-analysis that revealed an individual with an aunt who has SZ has a 2% risk of developing the disorder, compared to a 9% risk for those with an affected sibling, and a striking 48% concordance rate for monozygotic (identical) twins. This significant increase in risk underscores the role of shared genetic material in predisposing individuals to SZ.
Moreover, schizophrenia is considered polygenic, meaning it is influenced by multiple genes rather than a single gene. The genes most implicated are those involved in coding for neurotransmitter systems, particularly dopamine. However, research has identified a wide array of potential candidate genes across different studies, indicating that the genetic architecture of SZ is highly complex and aetiologically heterogeneous. This means that distinct combinations of genetic variations may contribute to the development of SZ in different individuals. SZ can also have a genetic origin in the absence of a family history of the disorder. One explanation for this is mutation in parental DNA triggered by enviromental factors such as radiation, poison or viral infection. This highlights a crucial interplay between genetic vulnerability and environmental influences in the aetiology of schizophrenia, exemplifing its complexity.
Neural correlates (AO1)
The genetic basis of schizophrenia is closely intertwined with neural correlates, as the implicated genes likely influence both neurotransmitter activity and brain structure. Neural explanations focus on the role of neurotransmitters like dopamine, which is critical for transmitting signals between neurons. In schizophrenia, individuals are thought to have an abnormally high number of D2 dopamine receptors on postsynaptic neurons, resulting in excessive dopamine binding and overactive neuronal firing. These receptors may also function atypically, contributing to dysregulation. Da neurons play a key role in guiding attention and so distburnces may explain problems with attention + thought experienced by suffers. This forms the foundation of the original dopamine hypothesis, which attributes positive symptoms like auditory hallucinations to hyperdopaminergia, particularly in Broca’s area. However, the revised dopamine hypothesis expands on this by including cortical hypodopaminergia, characterized by abnormally low dopamine levels in the brain’s cortex. Research by Goldman-Rakic et al. (2004) has associated hypodopaminergia in the prefrontal cortex with cognitive impairments and negative symptoms, such as disorganized thought and diminished motivation. Similarly, hypodopaminergia in the ventral striatum has been linked to avolition, highlighting how neurotransmitter imbalances can explain both positive and negative symptoms of schizophrenia.
In addition to neurotransmitter dysfunction, structural abnormalities in the brain are significant neural correlates of schizophrenia. One notable finding is the presence of enlarged ventricles—fluid-filled cavities in the brain responsible for nutrient delivery and waste removal. In individuals with schizophrenia, these ventricles are approximately 15% larger than in neurotypical brains, leading to reduced brain mass. Studies have found that up to 80% of patients exhibit these abnormalities, underscoring the physical changes associated with the disorder.
Together, genetic factors and neural correlates offer a comprehensive explanation for schizophrenia, with genes influencing both neurotransmitter systems and structural brain development, creating a biological foundation for the disorder’s complex symptoms.
Bio explanation (AO3)
One major criticism of the biological explanation of sz is its biologically reductionist nature, attempting to explain the disorder solely in terms of neurochemical imbalances—reducing the complex condition to the lowest level of explanation. This view overlooks the intricate interplay between biology, cognition, and environmental factors, focusing on neurotransmitters and genetic makeup in isolation. Research links schizophrenia to early trauma, prenatal complications, and drug use, all of which can play a crucial role in triggering the disorder. A more holistic approach, such as the diathesis-stress model, recognizes that while biological vulnerabilities may increase the risk of schizophrenia, these vulnerabilities are often activated by external stressors, making a purely neurochemical explanation insufficient. Therefore, while the biological perspective offers valuable insights, a more integrated approach is necessary to fully understand the complexity of schizophrenia.
However, despite its reductionist nature, the dopamine hypothesis has had high practical applications in leading to the development of antipsychotic drug treatments. The discovery that dopamine-blocking drugs, such as chlorpromazine, reduce positive symptoms has led to effective pharmacological interventions that have significantly improved the lives of many patients. This has provided strong empirical support for the role of dopamine in schizophrenia and has revolutionized psychiatric treatment, allowing many individuals to manage their symptoms and lead relatively stable lives. This demonstrates the real-world value of biological explanations in advancing medical treatments.
However, the success of antipsychotic drugs does not necessarily validate the dopamine hypothesis as a complete explanation for schizophrenia. The aetiological fallacy—assuming that because a treatment works, it must target the root cause—highlights the limitations of this view. Research has shown that other neurotransmitters, such as serotonin and glutamate, are also implicated in schizophrenia, suggesting that the disorder is far more neurochemically complex than originally thought. Additionally, antipsychotic drugs are not universally effective, with a significant proportion of patients experiencing little to no improvement in symptoms. This suggests that dopamine dysfunction alone cannot fully explain schizophrenia, and a more multifactorial approach is needed. The development of second-generation (atypical) antipsychotics, which target both dopamine and serotonin, further supports the idea that multiple neurotransmitter systems are involved. Therefore, while the dopamine hypothesis has contributed to valuable treatments, its narrow focus on a single neurotransmitter system means it remains an incomplete and overly simplistic explanation for schizophrenia.
