Analysis of pathways mediating preserved vision after striate cortex lesions.
This study investigated the neural substrates of preserved visual functioning in a patient with homonymous hemianopsia and Riddoch syndrome after a posterior cerebral artery stroke affecting the primary visual cortex (area V1). The limited visual abilities of this patient included above-chance verbal reports of movement and color change as well as discrimination of movement direction in the hemianopic field. Functional magnetic resonance imaging showed that motion and color-change stimuli presented to the hemianopic field produced activation in several extrastriate areas of the lesioned hemisphere that were defined using retinotopic mapping. Magnetoencephalographic recordings indicated that evoked activity occurred earlier in the higher-tier visual areas V4/V8 and V5 than in the lower-tier areas V2/V3 adjacent to the lesion. In addition, the functional magnetic resonance imaging analysis showed an increased functional connectivity between areas V4/V8 and V5 of the lesioned hemisphere in comparison with the same areas in the intact hemisphere during the presentation of color changes. These results suggest that visual perception after the V1 lesion in Riddoch syndrome is mediated by subcortical pathways that bypass V1 and project first to higher-tier visual areas V5 and V4/V8 and subsequently to lower-tier areas V2/V3.
Schoenfeld
Mircea Ariel
MA
Department of Neurology II, University of Magdeburg, 39120 Magdeburg, Germany. ariel@neuro2.med.uni-magdeburg.de
Noesselt
Toemme
T
Poggel
Dorothe
D
Tempelmann
Claus
C
Hopf
Jens-Max
JM
Woldorff
Martin G
MG
Heinze
Hans-Jochen
HJ
Hillyard
Steven A
SA
D000328:Adult; D001931:Brain Mapping / Q000379:methods*; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D015225:Magnetoencephalography / Q000379:methods; D008297:Male; D020521:Stroke / Q000473:pathology; D014785:Vision, Ocular / Q000502:physiology*; D014793:Visual Cortex / Q000473:pathology* / Q000502:physiology*; D014795:Visual Pathways / Q000473:pathology / Q000502:physiology*