Psychosis is a condition that impacts how the brain processes information, leading to a disconnect from reality. When a person experiences psychosis, their thoughts and perceptions can be disrupted, making it difficult to distinguish between what is real and what is not. This state is a collection of symptoms rather than a specific illness. To understand these symptoms, scientists compare the brains of those experiencing psychosis with “typical” brains, identifying differences in structure, function, and chemistry.
Altered Brain Structures
Researchers use tools like Magnetic Resonance Imaging (MRI) to examine the brain’s physical architecture, revealing anatomical differences in some individuals with psychosis. One consistent finding involves changes in gray matter, the tissue containing most of the brain’s neuronal cell bodies. Reductions in gray matter volume are observed in areas such as the prefrontal cortex, involved in decision-making, and the temporal lobes, important for processing sounds and language.
The hippocampus, a structure in the temporal lobe associated with memory formation, may also show reduced volume. These changes are localized to specific regions. Scientists also examine the brain’s white matter, which consists of myelinated nerve fibers that connect different brain regions. The integrity of these tracts can be compromised, affecting how efficiently different parts of the brain communicate.
Another observed structural difference is the enlargement of the ventricles, the fluid-filled spaces within the brain. The exact reasons for this enlargement are still under investigation, but it is a frequently noted characteristic in brain scans of individuals with a history of psychosis.
Differences in Brain Function and Communication
Beyond physical structures, the way a brain operates and communicates is also different during psychosis. Functional imaging techniques, such as fMRI and PET, allow scientists to observe brain activity. These studies reveal altered levels of activity in specific regions. For example, a state known as “hypofrontality,” or reduced activity in the prefrontal cortex, is sometimes observed, impacting planning and executive functions.
Conversely, other areas might show hyperactivity. The amygdala, a region associated with processing fear, and the striatum, involved in motivation and reward, can exhibit heightened activity. This may relate to the intense emotional and perceptual experiences during a psychotic episode. These are not constant states but can fluctuate depending on the person’s mental state.
These functional differences also extend to the large-scale networks that coordinate brain activity. Neural circuits, such as the default mode network (active when the mind is at rest) and the salience network (helps determine what stimuli deserve attention), can show disrupted connectivity. This less coherent communication between network hubs can affect the seamless integration of information.
Neurotransmitter Systems and Psychosis
The brain’s chemical messaging systems, managed by neurotransmitters, are also implicated in psychosis. The “dopamine hypothesis” suggests that an excess of dopamine activity in certain pathways contributes to psychotic experiences. Conversely, a deficit of dopamine in other areas, such as the mesocortical pathway leading to the prefrontal cortex, might be linked to other symptoms.
While dopamine has been a primary focus, research has expanded to include other neurotransmitters. Glutamate, the main excitatory neurotransmitter, is now a significant area of investigation. Theories suggest that underactivity of the NMDA receptor, a specific type of glutamate receptor, could disrupt the delicate balance between excitation and inhibition in brain circuits.
Serotonin, a neurotransmitter known for its role in mood regulation, sleep, and appetite, also appears to be involved. There is significant interplay between the serotonin and dopamine systems, and alterations in serotonin levels can influence dopamine activity.
Consequences for Cognition and Behavior
The structural, functional, and chemical brain differences culminate in the cognitive and behavioral changes characteristic of psychosis. These manifestations are categorized into distinct symptom groups. “Positive symptoms” refer to experiences added to a person’s reality, such as hallucinations (seeing or hearing things that are not there) and delusions (firmly held false beliefs). These may be linked to hyperactivity in sensory processing areas and dysregulated dopamine activity.
Another category is “negative symptoms,” which involve a reduction or absence of typical functions. This includes avolition, a severe lack of motivation to complete purposeful tasks, and anhedonia, a reduced ability to experience pleasure. Social withdrawal is also common. These symptoms may be associated with structural changes like reduced gray matter in the prefrontal cortex and functional issues like hypofrontality.
Cognitive impairments are also a frequent consequence. Individuals may experience disorganized thought and speech, making it difficult to follow a conversation or express coherent ideas. Problems with attention, working memory, and executive functions are also prevalent, arising from the widespread disruptions in neural communication and chemical imbalances.