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. 2016 May;37(5):774–781. doi: 10.3174/ajnr.A4636

Fig 3.

Fig 3.

Possible mechanisms of visual hallucinations. A, Deafferentation: lesions responsible for pathway complex visual hallucination in which deafferentation from ocular input results in “release” activity in the cortex. B, Disinhibition: lesions responsible for ascending complex visual hallucinations in which a loss of ascending inhibition to the geniculate results in a hyperexcited geniculate and excess glutamatergic activity in the optic radiation, with resultant poor-quality signal to the cortex. C, Central: lesions producing central complex visual hallucinations in which damage to the geniculate may again “deafferent” the striate cortex and lesions to the pulvinar of the thalamus may reduce the signal-to-noise ratio of cortical input due to a loss of the visual filter function of the pulvinar. Reproduced with permission from Dr. Ramon Mocellin.