Retinotopic organization of the visual cortex before and after decompression of the optic chiasm in a patient with pituitary macroadenoma

Case report

Philippe A. Chouinard Ph.D.1, Christopher L. Striemer Ph.D.1,2, Won Hyung A. Ryu M.Sc.3, Irene Sperandio Ph.D.1, Melvyn A. Goodale Ph.D.1, David A. Nicolle M.D.4, Brian Rotenberg M.D., M.P.H.5, and Neil Duggal M.D., M.Sc., F.R.C.S.C.3
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  • 1 Department of Psychology, Brain and Mind Institute, University of Western Ontario;
  • | 3 Departments of Clinical Neurological Sciences and
  • | 4 Ophthalmology, London Health Sciences Centre; and
  • | 5 Department of Otolaryngology, St. Joseph's Health Care London, London, Ontario; and
  • | 2 Department of Psychology, Grant MacEwan University, Edmonton, Alberta, Canada
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Compression induced by a pituitary tumor on the optic chiasm can generate visual field deficits, yet it is unknown how this compression affects the retinotopic organization of the visual cortex. It is also not known how the effect of the tumor on the retinotopic organization of the visual cortex changes after decompression. The authors used functional MRI (fMRI) to map the retinotopic organization of the visual cortex in a 68-year-old right-handed woman before and 3 months after surgery for a recurrent pituitary macroadenoma. The authors demonstrated that longitudinal changes in visual field perimetry, as assessed by the automated Humphrey visual field test, correlated with longitudinal changes in fMRI activation in a retinotopic manner. In other words, after decompression of the optic chiasm, fMRI charted the recruitment of the visual cortex in a way that matched gains in visual field perimetry. On the basis of this case, the authors propose that fMRI can chart neural plasticity of the visual cortex on an individual basis and that it can also serve as a complementary tool in decision making with respect to management of patients with chiasmal compression.

Abbreviations used in this paper:

fMRI = functional MRI; V1 = primary visual cortex.

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Contributor Notes

Address correspondence to: Neil Duggal, M.D., M.Sc., F.R.C.S.C., Division of Neurosurgery, Clinical Neurological Sciences, University Hospital, London Health Sciences Centre, 339 Windermere Road, London, Ontario N6A 5A5, Canada. email: neil.duggal@lhsc.on.ca.

Please include this information when citing this paper: published online June 8, 2012; DOI: 10.3171/2012.4.JNS112158.

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