Pathophysiology of Schizophrenia

Schizophrenia is a mental disorder that affects multiple pathways within the human body. It impairs neurotransmitter systems, with experts now linking it to a drop in acetylcholine muscarinic concentrations. The pathophysiology of schizophrenia is best explained by investigating anatomical abnormalities, dysfunctional neurotransmission, and stress-related signaling cascades. Anatomical abnormalities in the structure of different regions in the brain have been linked to a susceptibility to schizophrenia.

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In particular, a change in the structure of the prefrontal cortex has revealed previously unknown effects on human brain circuits and now associated with neurological disorders such as schizophrenia (Abel, 2016, p. 65). Similarly, dysfunctional neurotransmission involving dopamine, glutamate, and gamma-aminobutyric acid (GABA) systems occasions dysfunctions in receptor function, which then elevates the risk of developing schizophrenia. Stress-related signaling cascades, such as a sudden rise in parvalbumin-positive interneurons, can disrupt standard mechanisms and eventually cause schizophrenia.

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The most common symptoms of schizophrenia are hallucinations, disorganized thinking, and abnormal motor behavior. Schizophrenia is usually diagnosed using the criteria provided by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (Kasper et al., 2018).

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However, a medical practitioner may also recommend a physical exam, magnetic resonance imaging (MRI) screenings, or a psychiatric evaluation based on an individual’s personal history. Hallucinations in people with schizophrenia are caused by a transformed neural circuitry, which impacts negatively on an individual’s ability to differentiate real and imagined stimuli.  Disorganized thinking in schizophrenia is caused by hebephrenia, which reduces the sufferer’s ability to project any coherent thoughts to their audience. Furthermore, schizophrenia typically results in abnormal body movements. These motor symptoms are a result of abnormal oligodendrocyte function, which is tasked with ensuring that it prevents any neurodevelopmental disturbances.

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