Vivid visual hallucinations from occipital lobe infarction
Philip LClatworthy, Neurosciences, University of Cambridge, Box 83, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQplc12@cam.ac.uk
Elizabeth A Warburton, Jean-Claude Baron
Submitted January 04, 2006
We read the article by Flint et al with interest. [1] While hallucinations in cases of visual cortical damage are well-documented, their exacerbation by light in this case is intriguing; the patient modified her spectacles to exclude light as far as possible from the affected hemifield. Disinhibition of higher visual areas is not a complete explanation for this phenomenon. It also requires visually-induced neural activity to reach those areas no longer receiving input from affected areas of visual cortex.
Two explanations are possible. First, that visual information reaches intact extrastriate visual areas via pathways that bypass the main geniculostriate route, whether from the lateral geniculate nucleus or other subcortical areas such as pulvinar. These pathways have been documented in primates. [2,3]
The second possibility is that neural plasticity causes surviving areas of primary visual cortex to stimulate regions of higher visual areas that are not usually excited by this activity. Plasticity has been postulated as a possible mechanism for changes in response properties in extrastriate visual cortex following long-term damage to primary visual cortex in humans [4] and has been found to occur locally following lesions to primary visual cortex in cats. [5]
These possibilities should be testable using appropriately designed experiments involving visually provoked hallucinations combined with fMRI in patients with cerebral damage due to stroke.
2. Cowey A, Stoerig P. Projection patterns of surviving neurons in the dorsal lateral geniculate nucleus following discrete lesions of striate
cortex: implications for residual vision. Exp Brain Res 1989;75:631-638.
3. Weller RE, Steele GE, Kaas JH. Pulvinar and other subcortical connections of dorsolateral visual cortex in monkeys. J Comp Neurol 2002;450:215-240.
4. Baseler HA, Morland AB, Wandell BA. Topographic organization of human visual areas in the absence of input from primary cortex. J Neurosci 1999;19:2619-2627.
5. Zepeda A, Vaca L, Arias C, Sengpiel F. Reorganization of visual cortical maps after focal ischemic lesions. J Cereb Blood Flow Metab 2003;23:811-820.
We read the article by Flint et al with interest. [1] While hallucinations in cases of visual cortical damage are well-documented, their exacerbation by light in this case is intriguing; the patient modified her spectacles to exclude light as far as possible from the affected hemifield. Disinhibition of higher visual areas is not a complete explanation for this phenomenon. It also requires visually-induced neural activity to reach those areas no longer receiving input from affected areas of visual cortex.
Two explanations are possible. First, that visual information reaches intact extrastriate visual areas via pathways that bypass the main geniculostriate route, whether from the lateral geniculate nucleus or other subcortical areas such as pulvinar. These pathways have been documented in primates. [2,3]
The second possibility is that neural plasticity causes surviving areas of primary visual cortex to stimulate regions of higher visual areas that are not usually excited by this activity. Plasticity has been postulated as a possible mechanism for changes in response properties in extrastriate visual cortex following long-term damage to primary visual cortex in humans [4] and has been found to occur locally following lesions to primary visual cortex in cats. [5]
These possibilities should be testable using appropriately designed experiments involving visually provoked hallucinations combined with fMRI in patients with cerebral damage due to stroke.
References
1. Flint AC, Loh JP, Brust JC. Vivid visual hallucinations from occipital lobe infarction. Neurology 2005; 65: 756.
2. Cowey A, Stoerig P. Projection patterns of surviving neurons in the dorsal lateral geniculate nucleus following discrete lesions of striate cortex: implications for residual vision. Exp Brain Res 1989;75:631-638.
3. Weller RE, Steele GE, Kaas JH. Pulvinar and other subcortical connections of dorsolateral visual cortex in monkeys. J Comp Neurol 2002;450:215-240.
4. Baseler HA, Morland AB, Wandell BA. Topographic organization of human visual areas in the absence of input from primary cortex. J Neurosci 1999;19:2619-2627.
5. Zepeda A, Vaca L, Arias C, Sengpiel F. Reorganization of visual cortical maps after focal ischemic lesions. J Cereb Blood Flow Metab 2003;23:811-820.