Data from recent scientific studies conclusively show that schizophrenia, like Alzheimer’s disease and bipolar disorder, is a biological disease of the brain. For starters, it is now understood that schizophrenia is inherited and somewhat influenced by genetics. Another is that schizophrenia and normal brains differ structurally as shown by current non-invasive brain imaging techniques like Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI). Up to 25% less gray matter, particularly in the temporal and frontal lobes (thought to be crucial for thinking and judgment coordination), is present in the brains of those with schizophrenia. Patients with the worst loss of brain tissue also frequently have the worst symptoms.
Real-time maps of regional cerebral blood flow and metabolism can now be created utilizing functional brain-scanning techniques like Positron Emission Tomography (PET) and functional MRI, opening another window into the differences between schizophrenic and healthy brains. When compared to healthy individuals used as control subjects, such investigations typically reveal low levels of activation in the middle frontal cortex and inferior parietal cortex of schizophrenia patients. Findings of low activity are also connected to increased negative symptoms. In other words, those with more negative symptoms are more likely to have lower levels of brain activity in critical parts of the brain.
Thus, the total amount of tissue and the level of activity is (on average) different in schizophrenia-affected brains. However, the majority of the time there isn’t a clear-cut instance of structural damage (a “lesion”) to identify as the precise region of the brain where schizophrenia is taking place.
Schizophrenic brains have neurochemical variations in addition to morphological variations when compared to healthy brains. The brain’s millions of individual neurons communicate with one another using a variety of chemical messengers called neurotransmitters. Fundamentally, it seems that schizophrenic brains are more susceptible to the neurotransmitter dopamine than normal brains are. The “dopamine hypothesis” of schizophrenia asserts that too much dopamine (or excessive sensitivity to dopamine) is the root cause of the disorder. This theory is supported by a number of important sources.
First, medications that block dopamine’s actions in the brain are known to be effective antipsychotics (they, for example, lessen the severity and frequency of hallucinations). Second, it’s known that stimulant drugs like cocaine and methamphetamine, which either mimic dopamine’s effects or make dopamine more active in the brain, can cause hallucinations and delusions in non-schizophrenic people if enough of those drugs are consumed. It is also well-recognized that Parkinson’s disease is caused by a lack of dopamine and that prolonged use of antipsychotic drugs, which block dopamine, can cause tardive dyskinesia, a Parkinson’s-like disorder.
The long-standing dopamine theory has been challenged by new research, and it is no longer as certain that dopamine is the only factor contributing to schizophrenia. Today, it seems more likely that other neurotransmitters, such as glutamate (which is known to be involved in the hallucinogenic effects of the drug PCP (“angel dust”)) and serotonin (implicated in depression and anxiety), are responsible for the development of conditions for schizophrenia and psychosis. However, the fundamental neurochemical foundation of schizophrenia has been pretty clearly established and would now appear to be beyond doubt, even though the specifics of neurochemical participation in schizophrenia alter as new information becomes available.
Individuals suffering from schizophrenia exhibit evident functional deficiencies when compared to the general population as a whole. Functional deficits are issues that people have with basic mental and physical abilities, including the ability to recall information, use executive functioning (the ability to quickly switch between tasks, make decisions, etc.), infer rules from consequences, and have strong grips. In general, schizophrenic individuals have slower memory, attention spans, executive functioning, and reaction times than average individuals. For instance, they are similarly capable of recalling long-term memories but have comparatively more trouble than normal persons recalling what they acquired five minutes prior. They find it more difficult to plan and solve problems than other individuals do, and they tend to be more easily distracted.
Schizophrenic patients exhibit sensory processing abnormalities as well. Schizophrenic individuals frequently display ‘soft’ neurological indications, which include things like being unable to discriminate between two simultaneous touches or being unable to recognize numerals written on their hand’s palm. Additionally, they frequently mistake the right and left sides of the body for one other. Such well-reported sensory processing issues point to brain-wiring deficiencies or anomalies in schizophrenia sufferers.
Electroencephalogram (EEG) data, which measures the electrical activity of the brain, provide still more proof that schizophrenia affects the brain neurologically. A third of those with schizophrenia exhibit aberrant electrical brain impulses, which further suggests that the brains of those with schizophrenia are not wired normally.
Together, these numerous and methodologically diverse findings provide persuasive evidence that schizophrenia is primarily a brain disorder with a biological basis.
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