Cortical activation in hemianopia after stroke
ABSTRACT Changes in neuronal activity of the visual cortex have been described in patients with hemianopia. The anatomical areas that are involved in neuroplastic changes have not been studied in a larger group of stroke patients with a homogenous structural pathology of the visual cortex. Brain activation was measured in 13 patients with a single ischemic lesion of the striate cortex and partially recovered hemianopia and in 13 age-matched control subjects using blood oxygen level dependent (BOLD) functional magnetic resonance imaging (fMRI). Differences in activation between rest and visual hemifield stimulation were assessed with statistical parametric mapping using group and multi-group studies. In normal subjects, the most significant activation was found in the contralateral primary visual cortex (area 17) and bilaterally in the extrastriate cortex (areas 18 and 19). In patients, these areas were also activated when the intact hemifield was stimulated. During stimulation of the hemianopic side, bilateral activation was seen within the extrastriate cortex, stronger in the ipsilateral (contralesional) hemisphere. Stimulation of the hemianopic visual field is associated with ipsilateral activation of the extrastriate visual cortex. This pattern of activation suggests extensive neuronal plasticity within the visual cortex after postgeniculate ischemic lesions and may have implications for therapeutic interventions.
- SourceAvailable from: Michał Bola
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- "It has been shown that the visual cortex lesion affects activity and connectivity of down-stream visual structures (Goebel et al., 2001; Schoenfeld et al., 2002; Nelles et al., 2007). Crucially, unilateral cortical lesions alter activity of visual cortical areas not only in the damaged, but also in the seemingly unaffected (uninjured) hemisphere, which has been shown in animal model (Rushmore and Payne, 2003) and in patients (Henriksson et al., 2007; Nelles et al., 2007). Changes in activity are related to modification of anatomical (Bridge et al., 2008) and functional connectivity (Silvanto et al., 2009) between both hemispheres . "
ABSTRACT: Unilateral visual cortex lesions caused by stroke or trauma lead to blindness in contralateral visual field - a condition called homonymous hemianopia. Although the visual field area processed by the uninjured hemisphere is thought to be "intact," it also exhibits marked perceptual deficits in contrast sensitivity, processing speed, and contour integration. Such patients are "sightblind" - their blindness reaches far beyond the primary scotoma. Studies showing perceptual deficits in patients' intact fields are reviewed and implications of these findings are discussed. It is concluded that consequences of partial blindness are greater than previously thought, since perceptual deficits in the "intact" field likely contribute to subjective vision loss in patients with visual field defect. This has important implications for vision diagnosis and rehabilitation.Frontiers in Neurology 06/2013; 4:80. DOI:10.3389/fneur.2013.00080
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- "These different authors reported functional and anatomical modifications in the intact and/or the damaged hemisphere, including within the occipital lobe. For example, it has been shown that the intact occipital lobe (the extrastriate areas) was engaged in the processing of visual information from the ipsilateral visual field (i.e. the contralesional blind visual field) in addition to its normal implication in the processing of visual information from the contralateral visual field (Henriksson et al. 2007; Nelles et al. 2007 "
ABSTRACT: The current study aims to investigate visual scene perception and its neuro-anatomical correlates for stimuli presented in the central visual field of patients with homonymous hemianopia, and thereby to assess the effect of a right or a left occipital lesion on brain reorganization. Fourteen healthy participants, three left brain damaged (LBD) patients with right homonymous hemianopia and five right brain damaged (RBD) patients with left homonymous hemianopia performed a visual detection task (i.e. "Is there an image on the screen?") and a categorization task (i.e. "Is it an image of a highway or a city?") during a block-designed functional magnetic resonance imaging recording session. Cerebral activity analyses of the posterior areas-the occipital lobe in particular-highlighted bi-hemispheric activation during the detection task but more lateralized, left occipital lobe activation during the categorization task in healthy participants. Conversely, in patients, the same network of activity was observed in both tasks. However, LBD patients showed a predominant activation in their right hemisphere (occipital lobe and posterior temporal areas) whereas RBD patients showed a more bilateral activation (in the occipital lobes). Overall, our preliminary findings suggest a specific pattern of cerebral activation depending on the task instruction in healthy participants and cerebral reorganization of the posterior areas following brain injury in hemianopic patients which could depend upon the side of the occipital lesion.Brain Topography 01/2013; 26(2):264-277. DOI:10.1007/s10548-012-0244-z · 2.52 Impact Factor
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- "There are only very rare cases of spontaneous vision recovery beyond this time point (Poggel et al., 2001). Nelles et al. (2002, 2007) studied patients with ischemic lesions of the visual cortex using functional imaging. While in a control group, they observed the maximum activity in hemifield stimulation in the contralateral visual cortex and bilaterally in the extrastriate cortex, the patients showed increased ipsilateral activation in the extrastriate cortex when stimulating the hemianopic hemifield. "
ABSTRACT: Vision loss after retinal or cerebral visual injury (CVI) was long considered to be irreversible. However, there is considerable potential for vision restoration and recovery even in adulthood. Here, we propose the "residual vision activation theory" of how visual functions can be reactivated and restored. CVI is usually not complete, but some structures are typically spared by the damage. They include (i) areas of partial damage at the visual field border, (ii) "islands" of surviving tissue inside the blind field, (iii) extrastriate pathways unaffected by the damage, and (iv) downstream, higher-level neuronal networks. However, residual structures have a triple handicap to be fully functional: (i) fewer neurons, (ii) lack of sufficient attentional resources because of the dominant intact hemisphere caused by excitation/inhibition dysbalance, and (iii) disturbance in their temporal processing. Because of this resulting activation loss, residual structures are unable to contribute much to everyday vision, and their "non-use" further impairs synaptic strength. However, residual structures can be reactivated by engaging them in repetitive stimulation by different means: (i) visual experience, (ii) visual training, or (iii) noninvasive electrical brain current stimulation. These methods lead to strengthening of synaptic transmission and synchronization of partially damaged structures (within-systems plasticity) and downstream neuronal networks (network plasticity). Just as in normal perceptual learning, synaptic plasticity can improve vision and lead to vision restoration. This can be induced at any time after the lesion, at all ages and in all types of visual field impairments after retinal or brain damage (stroke, neurotrauma, glaucoma, amblyopia, age-related macular degeneration). If and to what extent vision restoration can be achieved is a function of the amount of residual tissue and its activation state. However, sustained improvements require repetitive stimulation which, depending on the method, may take days (noninvasive brain stimulation) or months (behavioral training). By becoming again engaged in everyday vision, (re)activation of areas of residual vision outlasts the stimulation period, thus contributing to lasting vision restoration and improvements in quality of life.Progress in brain research 01/2011; 192:199-262. DOI:10.1016/B978-0-444-53355-5.00013-0 · 5.10 Impact Factor