Eight distinct models of complex visual hallucinations have been proposed since 2000, each based on different views of brain organization. Researchers from each model group have now agreed on an integrated Visual Hallucination Framework that aligns with current theories of both real and hallucinatory vision. The Framework identifies cognitive systems involved in hallucinations and enables systematic investigation of how hallucination experiences relate to changes in underlying cognitive structures. The episodic nature of hallucinations points to separate factors for their onset, persistence, and end, suggesting a complex relationship between temporary states and long-term traits of hallucination risk. The Framework also suggests new research directions and potential treatments for distressing hallucinations.
Visual hallucinations in Lewy body diseases (Parkinson's disease and dementia with Lewy bodies) and those induced by serotonergic psychedelics (psilocybin, mescaline) share overlapping phenomenology and neural mechanisms, despite different underlying causes. Both conditions produce visual aberrations from minor distortions to complex hallucinations, including illusory motion and entity encounters. Neuroimaging shows a common pattern of overactive associative cortex and underactive sensory cortex. Serotonin 2A receptor modulation is involved in both: psychedelics act through 5-HT2A and 5-HT1A receptors, while in Lewy body diseases, 5-HT2A receptor upregulation correlates with increased hallucinations, and blocking it with pimavanserin reduces them. Shared cortical signatures include reduced visual evoked responses and shifts toward visual excitation.