Neuropsychiatry of complex visual hallucinations.
OBJECTIVE
To describe the phenomenology and pathophysiology of complex visual hallucinations (CVH) in various organic states, in particular Charles Bonnet syndrome and peduncular hallucinosis.


METHODS
Three cases of CVH in the setting of pontine infarction, thalamic infarction and temporoparietal epileptiform activity are presented and the available psychiatric, neurological and biological literature on the structures of the central nervous system involved in producing hallucinatory states is reviewed.


RESULTS
Complex visual hallucinations can arise from a variety of processes involving the retinogeniculocalcarine tract, or ascending brainstem modulatory structures. The cortical activity responsible for hallucinations results from altered or reduced input into these regions, or a loss of ascending inhibition of their afferent pathways.


CONCLUSIONS
A significant degree of overlaps exists between the concepts of Charles Bonnet syndrome and peduncular hallucinosis. The fluidity of these eponymous syndromes reduces their validity and meaning, and may result in an inappropriate attribution of the underlying pathology. An understanding of how differing pathologies may produce CVH allows for the appropriate tailoring of treatment, depending on the site and nature of the lesion and content of perceptual disturbance.
Mocellin
Ramon
R
Neuropsychiatry Unit, Royal Melbourne Hospital, and Melbourne Neuropsychiatry Centre, University of Melbourne, Victoria, Australia.
Walterfang
Mark
M
Velakoulis
Dennis
D
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D020520:Brain Infarction / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006212:Hallucinations / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008636:Mesencephalon / Q000473:pathology* / Q000503:physiopathology; D014795:Visual Pathways / Q000473:pathology* / Q000503:physiopathology