“resplendent peacock feathers and buildings.” Another saw sunsets almost too bright to bear and luminous landscapes of extraordinary beauty, “much prettier, I think, than anything I have ever seen. I really wish I could paint.”
Several mentioned spontaneous changes in their hallucinations; for one subject, a butterfly became a sunset, which changed to an otter and, finally, a flower. None of the subjects had any voluntary control over their hallucinations, which seemed to have “a mind” or “a will” of their own.
No hallucinations were experienced when subjects were engaged in challenging sensory activity of another mode, such as listening to television or music, talking, or even attempting to learn Braille. (The study was concerned not only with hallucinations but with the power of blindfolding to improve andheighten tactile skills and the ability to conceive of space and the world around one in nonvisual terms.)
Merabet et al. felt that the hallucinations reported by their subjects were entirely comparable with those experienced by patients with Charles Bonnet syndrome, and their results suggested to them that visual deprivation alone could be a sufficient cause for CBS. 2
B ut what exactly is going on in the brains of such experimental subjects—or in the brains of pilots who crash in cloudless blue skies, or truckers who see phantoms on an empty road, or prisoners watching their enforced “cinema” in darkness?
With the advent of functional brain imaging in the 1990s it became possible to visualize, at least in gross terms, how the brain might respond to sensory deprivation—and, if one was lucky (hallucinations are notoriously fickle, and the inside of an fMRI machine is not an ideal place for delicate sensory experiences), one might even catch the neural correlates of a fugitive hallucination. One such study, by Babak Boroojerdi and his colleagues, showed an increase in the excitability of the visual cortex when subjects were visually deprived, a change that occurred within minutes. Another group of researchers, in the neuroscience lab led by Wolf Singer, studied a single subject, a visual artist with excellent powers of visual imagery (an article on this by Sireteanu et al. was published in 2008).The subject was blindfolded for twenty-two days and spent several sessions in an fMRI machine, where she was able to indicate the exact times her hallucinations appeared and disappeared. The fMRI showed activations in her visual system, both in the occipital cortex and in the inferotemporal cortex, in precise coincidence with her hallucinations. (When, by contrast, she was asked to recall or imagine the hallucinations using her powers of visual imagery, there was, additionally, a good deal of activation in the executive areas of the brain, in the prefrontal cortex—areas that had been relatively inactive when she was merely hallucinating.) This made it clear that, at a physiological level, visual imagery differs radically from visual hallucination. Unlike the top-down process of voluntary visual imagery, hallucination is the result of a direct, bottom-up activation of regions in the ventral visual pathway, regions rendered hyperexcitable by a lack of normal sensory input.
T he deafferentation tanks used in the 1960s produced not only visual deprivation but every other sort of deprivation: of hearing, touch, proprioception, movement, and vestibular sensation, as well as, to varying degrees, deprivation of sleep and social contact—any of which may in themselves lead to hallucinations.
Hallucinations engendered by immobility, whether from motor system disease or external constraints, were frequently seen when polio was rampant. The worst afflicted, unable even to breathe by themselves, lay motionless in coffinlike “iron lungs” and would often hallucinate, as Herbert Leiderman and his colleagues described in a 1958 article. The immobility producedby other paralyzing diseases—or even splints and
Several mentioned spontaneous changes in their hallucinations; for one subject, a butterfly became a sunset, which changed to an otter and, finally, a flower. None of the subjects had any voluntary control over their hallucinations, which seemed to have “a mind” or “a will” of their own.
No hallucinations were experienced when subjects were engaged in challenging sensory activity of another mode, such as listening to television or music, talking, or even attempting to learn Braille. (The study was concerned not only with hallucinations but with the power of blindfolding to improve andheighten tactile skills and the ability to conceive of space and the world around one in nonvisual terms.)
Merabet et al. felt that the hallucinations reported by their subjects were entirely comparable with those experienced by patients with Charles Bonnet syndrome, and their results suggested to them that visual deprivation alone could be a sufficient cause for CBS. 2
B ut what exactly is going on in the brains of such experimental subjects—or in the brains of pilots who crash in cloudless blue skies, or truckers who see phantoms on an empty road, or prisoners watching their enforced “cinema” in darkness?
With the advent of functional brain imaging in the 1990s it became possible to visualize, at least in gross terms, how the brain might respond to sensory deprivation—and, if one was lucky (hallucinations are notoriously fickle, and the inside of an fMRI machine is not an ideal place for delicate sensory experiences), one might even catch the neural correlates of a fugitive hallucination. One such study, by Babak Boroojerdi and his colleagues, showed an increase in the excitability of the visual cortex when subjects were visually deprived, a change that occurred within minutes. Another group of researchers, in the neuroscience lab led by Wolf Singer, studied a single subject, a visual artist with excellent powers of visual imagery (an article on this by Sireteanu et al. was published in 2008).The subject was blindfolded for twenty-two days and spent several sessions in an fMRI machine, where she was able to indicate the exact times her hallucinations appeared and disappeared. The fMRI showed activations in her visual system, both in the occipital cortex and in the inferotemporal cortex, in precise coincidence with her hallucinations. (When, by contrast, she was asked to recall or imagine the hallucinations using her powers of visual imagery, there was, additionally, a good deal of activation in the executive areas of the brain, in the prefrontal cortex—areas that had been relatively inactive when she was merely hallucinating.) This made it clear that, at a physiological level, visual imagery differs radically from visual hallucination. Unlike the top-down process of voluntary visual imagery, hallucination is the result of a direct, bottom-up activation of regions in the ventral visual pathway, regions rendered hyperexcitable by a lack of normal sensory input.
T he deafferentation tanks used in the 1960s produced not only visual deprivation but every other sort of deprivation: of hearing, touch, proprioception, movement, and vestibular sensation, as well as, to varying degrees, deprivation of sleep and social contact—any of which may in themselves lead to hallucinations.
Hallucinations engendered by immobility, whether from motor system disease or external constraints, were frequently seen when polio was rampant. The worst afflicted, unable even to breathe by themselves, lay motionless in coffinlike “iron lungs” and would often hallucinate, as Herbert Leiderman and his colleagues described in a 1958 article. The immobility producedby other paralyzing diseases—or even splints and
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