Visual activation of extra-striate cortex in the absence of V1 activation

Abstract

When the primary visual cortex (V1) is damaged, there are a number of alternative pathways that can carry visual information from the eyes to extrastriate visual areas. Damage to the visual cortex from trauma or infarct is often unilateral, extensive and includes gray matter and white matter tracts, which can disrupt other routes to residual visual function. We report an unusual young patient, SBR, who has bilateral damage to the gray matter of V1, sparing the adjacent white matter and surrounding visual areas. Using functional magnetic resonance imaging (fMRI), we show that area MT+/V5 is activated bilaterally to visual stimulation, while no significant activity could be measured in V1. Additionally, the white matter tracts between the lateral geniculate nucleus (LGN) and V1 appear to show some degeneration, while the tracts between LGN and MT+/V5 do not differ from controls. Furthermore, the bilateral nature of the damage suggests that residual visual capacity does not result from strengthened interhemispheric connections. The very specific lesion in SBR suggests that the ipsilateral connection between LGN and MT+/V5 may be important for residual visual function in the presence of damage to V1.

Fig. 1

(A) Visual fields measured with Goldman perimetry. The largest region of residual visual function is in the upper peripheral field. Note that the fields are drawn with high contrast stimuli of different sizes all at brightest intensity. (B) The locations of the Gabor patches used for behavioral testing and the detection rates at each point, superimposed on the sum of the monocular visual fields from the perimetry. The blue circle indicates the mean fixation position (radius = 95% confidence interval), red circles indicate stimulus detection rates at 100% and yellow squares are detection rates at 50% contrast. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)

Fig. 2

The gray matter of the posterior calcarine sulcus has a lower intensity than the surrounding gray matter (A). (B) The single voxel thickness masks used to compare the intensity of gray matter voxels in the calcarine and intra-parietal sulci. The very anterior region of spared CS is indicated with the yellow arrows (C). The extracted values from the T1-weighted image for each of these regions are shown in (D). The ratio of perfusion in the posterior CS (P-CS) compared to MT+/V5 and the anterior CS (A-CS) is shown in (E), indicating decreased perfusion to the posterior CS in SBR. Error bars show standard deviations and asterisk indicates SBR's data lying more than 2 standard deviations from the control mean.

Fig. 3

Activation in SBR to chequerboard stimuli placed (A) centrally, (B) in the lower and (C) in the upper visual field. In each case, there is bilateral activation of V5/MT (yellow arrows). There is V2/V3 activation when the stimulus is in the central and lower visual field, but not upper as would be predicted normally (black arrows). The calcarine sulcus itself (blue arrows) shows no significant activation on either bank in any condition. The ventral visual stream shows significant activation when the larger stimuli are used (Lower and Upper), but nothing for the smaller, central stimulus. The scale bar shows the significance of the activation, thresholded at z > 2.3, corrected.

Fig. 4

Left side shows tracts between the LGN and the Calcarine Sulcus, Dorsal V2/V3 and area MT+ in patient SBR. The orange/red regions are the areas activated by the central flashing chequerboard. The color bars in the centre of the figure indicate the probability of connectivity between the LGN and the three visual areas. The right side shows the FA and mean diffusivity for SBR and the controls in the white matter of each tract. Error bars show standard deviations and asterisk represents SBR's data lying more than 2 standard deviations from the control mean.