When the brain experiences hallucinations, brain imaging reveals complex and dynamic changes in activity across multiple regions, reflecting how perception can be altered without external stimuli. These changes involve disruptions in normal sensory processing pathways, imbalances between excitatory and inhibitory signals, and alterations in neurotransmitter systems such as dopamine.
During visual hallucinations, for example, brain scans show abnormal activation patterns in the visual cortex—the area responsible for processing what we see. This activation can occur even when no actual visual input is present. One way this happens is through a disruption of the brain’s predictive coding system. Normally, the brain constantly predicts incoming sensory information and updates these predictions based on real input; during hallucinations, this balance is disturbed so that internally generated signals override or distort external reality. Rhythmic or excessive inputs from deeper structures like the thalamus to the cortex may interfere with how prediction errors are computed, leading to vivid but false percepts such as geometric shapes or colors that appear real despite no corresponding stimulus.
In conditions like Charles Bonnet syndrome—where people with vision loss experience complex visual hallucinations—brain imaging suggests an imbalance between excitatory (glutamate) and inhibitory (GABA) neurotransmitters within visual areas might contribute to these experiences. However, some studies have not found consistent chemical differences at rest between those who do and do not experience hallucinations; this implies that transient neural dynamics during episodes might be more critical than static neurochemical levels.
Auditory verbal hallucinations commonly seen in schizophrenia also show distinct patterns on functional MRI scans: weakened connectivity between certain cortical regions involved in language processing correlates with hallucinatory experiences of hearing voices. Structural changes such as altered sulcal depth—a measure of cortical folding—in relevant auditory areas have been observed alongside these functional disruptions.
A key player implicated across many types of psychotic symptoms including hallucinations is dopamine—a neurotransmitter involved in reward signaling and salience detection. Positron emission tomography (PET) studies measuring dopamine synthesis capacity reveal increased dopamine activity linked directly to positive psychotic symptoms regardless of diagnostic category (schizophrenia, bipolar disorder with psychosis, major depression with psychosis). This suggests that heightened dopaminergic signaling may amplify internally generated perceptions or beliefs into hallucinatory phenomena by assigning inappropriate significance to them.
Overall then:
– Hallucination episodes correspond to abnormal spontaneous activity within sensory cortices even without external stimuli.
– Disrupted predictive coding mechanisms cause internal expectations or errors to dominate perception.
– Imbalances between excitation and inhibition alter neural circuit stability.
– Altered connectivity among language-related areas underlies auditory verbal hallucinations.
– Increased dopamine synthesis amplifies aberrant salience attribution contributing to hallucinatory content.
Brain imaging techniques like fMRI capture blood flow changes reflecting regional neural activity; PET scans measure specific neurochemical processes such as dopamine production; magnetic resonance spectroscopy can assess local concentrations of neurotransmitters though results vary depending on timing relative to episodes.
These findings illustrate how a combination of structural abnormalities (like cortical folding), functional disconnections among networks responsible for integrating sensory information and cognition, plus neurochemical dysregulation converge during hallucinatory states — turning subjective internal events into vivid perceptual realities experienced by individuals despite absence of corresponding external inputs. The complexity revealed by modern imaging underscores why treating hallucinations often requires targeting multiple aspects—from restoring network balance through medication affecting neurotransmitters like dopamine—to cognitive therapies aimed at recalibrating perception versus expectation mismatches within the brain’s predictive framework.
