The first mechanism involves irritation (e.g., seizure activity) of cortical centers responsible for visual processing. Irritation of the primary visual cortex causes simple elementary visual hallucinations, while irritation of the visual association cortices causes more complex visual hallucinations. These data are supported by both electroencephalographic (EEG) recordings and direct stimulation experiments.
Lesions that cause differentiation of the visual system may lead to cortical release phenomenon, including visual hallucinations. Normal inputs are thought to be under the control of inhibitory processes that are effectively removed by differentiation. It has been further suggested that differenced neurons undergo specific biochemical and molecular changes that lead to an overall increase in excitability.
A multitude of lesions can cause this loss of input and inhibit other cognitive functions. Of note, visual hallucinations may be induced by prolonged visual deprivation. One study reported visual hallucinations in 10 of 13 healthy subjects blindfolded for a period of 5 days; this finding lends strong support to the idea that the simple loss of normal visual input is sufficient to cause visual hallucinations.
Finally, due to its role in the maintenance of arousal, the reticular activating system has been implicated in the genesis of visual hallucinations. Lesions of the brainstem have led to visual hallucinations (as in peduncular hallucinosis). Further, visual hallucinations are common in those with certain sleep disorders, and occur more frequently in those who are drowsy. The observation that visual hallucinations occur more frequently in those who are drowsy (even in the absence of frank sleep pathology) suggests that the reticular activating system plays a role in visual hallucinations, although the precise mechanism has not yet been established.
First published in SUNDAY FREAK - 3rd Edition - VISIONARY ART
HALLUCINATIONS