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Brain 2007 130(5):1244-1253; doi:10.1093/brain/awm045
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© The Author (2007). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Recovery from optic neuritis: an ROI-based analysis of LGN and visual cortical areas

Kirsten Korsholm1, Kristoffer H. Madsen1,2, Jette L. Frederiksen3, Arnold Skimminge1,2 and Torben E. Lund1

1Danish Research Centre for Magnetic Resonance, Copenhagen University Hospital, Hvidovre, 2Informatics and Mathematical Modelling, Technical University of Denmark, Lyngby and 3Department of Neurology, Copenhagen University Hospital, Glostrup, Denmark

Correspondence to: Kirsten Korsholm, Danish Research Centre for Magnetic Resonance, Copenhagen University Hospital, Hvidovre, 2650 Hvidovre, Denmark E-mail: kirstenk{at}drcmr.dk

Optic neuritis (ON) is the first clinical manifestation in ~20% of patients with multiple sclerosis (MS). The inflammation and demyelination of the optic nerve are characterized by symptomatic visual impairment and retrobulbar pain, and associated with decreased visual acuity, decreased colour and contrast sensitivity, delayed visual evoked potentials and visual field defects. Spontaneous recovery of vision typically occurs within weeks or months after onset, depending on the resolution of inflammation, remyelination, restoration of conduction in axons which persist demyelinated and neuronal plasticity in the cortical and subcortical visual pathways. To assess where recovery takes place along the visual pathway, visual activation was studied in the lateral geniculate nucleus (LGN), the main thalamic relay nucleus in the visual pathway and in three areas of the visual cortex: the lateral occipital complexes (LOC), V1 and V2. We conducted a longitudinal functional magnetic resonance imaging (fMRI) study of regions of interest (ROI) of activation in LGN and visual cortex in 19 patients with acute ON at onset, 3 and 6 months from presentation. With fMRI we measured the activation in the ROIs and compared activation during monocular stimulation of the affected and unaffected eye. In the acute phase the activation of LGN during visual stimulation of the affected eye was significantly reduced (P < 0.01) compared to the unaffected eye. This difference in LGN activation between the affected and unaffected eye diminished during recovery, and after 180 days the difference was no longer significant (P = 0.59). The decreased difference during recovery was mainly due to an increase in the fMRI signal when stimulating the affected eye, but included a component of a decreasing fMRI signal from LGN when stimulating the unaffected eye. In LOC, V1 and V2 activation during visual stimulation of the affected eye in the acute phase was significantly reduced (P < 0.01) compared to the unaffected eye, and during recovery the difference diminished with no significant differences left after 180 days. As the pattern of activation in LOC, V1 and V2 resembled the development in LGN we found no evidence of additional cortical adaptive changes. The reduced activation of the LGN to stimulation of the unaffected eye is interpreted as a shift away from early compensatory changes established in the acute phase in LGN and may indicate very early plasticity of the visual pathways.

Key Words: optic neuritis; lateral geniculate nucleus; lateral occipital complex (LOC); functional magnetic resonance imaging; regeneration

Abbreviations: LGN, lateral geniculate nucleus; LOC, lateral occipital complexes; MRI, magnetic resonance imaging; ON, optic neuritis; ROI, region of interest

Received October 24, 2006. Revised February 5, 2007. Accepted February 13, 2007.


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