PMC4412053_01
Stroke sites and corresponding visual field deficits on perimetry. Top Row: day 8 T2-weighted MRI scan, axial slices (radiological convention, so images are flipped) through occipital cortex showing left acute occipital lesion and demonstrating midbrain lesion (traced or circled in white). Despite the fact that his midbrain lesion was right-sided, the patient had persistent left ptosis, with left lid artifact present on perimetry (white arrow). T2 images are shown as subacute ischemic lesions are difficult to see on T1 images. His right partial homonymous visual deficit can be seen on his perimetric visual field maps (black arrows). Note that perimetric tests were 90  visual field tests. Bottom row: repeat MRI at 6 months, axial T1-weighted slices through occipital lobes, revealed interval infarction in the right occipital pole (traced in white). Lid artifact still present from ptosis (white arrow), but perimetry revealed almost complete resolution of right homonymous deficit despite interval development of partial left inferior quadrantanopia (gray speckled arrow). LE, left eye; RE, right eye.
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Admission MRI scanning confirmed the presence of a left inferior occipital infarct and right-midline midbrain infarct (see Figure 1). On day 5, automated perimetry was performed, and revealed incomplete resolution of the right homonymous visual deficit, restricted to the superior quadrant for the left eye and peripheral loss crossing the horizontal meridian in the right eye (Figure 1). Repeat MR scanning at 6 months as part of our fMRI research study confirmed the presence of a further right-sided stroke, affecting the superior occipital gyrus and cuneus (Figure 1). There was evidence of diaschisis on initial perimetry, associated with a symmetrical constriction in the unaffected hemifield:see Figure 1.
(A) Control subject t-test SCRF maps (individual exemplar) overlaid onto corresponding T1-weighted images, 3 coronal slices through occipital pole and calcarine cortices, demonstrating symmetrical activation in striate (calcarine) and extrastriate regions. Normal visual field in seen on perimetry, right of figure. (B) Patient t-test SCRF maps overlaid onto corresponding T1-weighted images, 3 coronal slices through occipital pole and calcarine cortices (radiological convention), demonstrating reduced extrastriate activation and bilaterally absent calcarine activation, common acutely secondary to diaschisis. Stroke site traced in pink. Corresponding visual deficit again shown, highlighted with pink arrow. Note the white arrows highlighting sites of activation in the middle occipital lobe. (C) Patient t-test SCRF maps overlaid onto corresponding T1-weighted images, 3 coronal slices through occipital pole and calcarine cortices (radiological convention), demonstrating bilateral return of striate (calcarine) activation, despite the presence of a further stroke, stroke site traced in green. Corresponding visual deficit shown, green arrow. Note that the new stroke site has affected an area of activation demonstrated in the initial fMRI, but visual cortical reorganization has continued despite the recurrent lesion. Blue arrows point out regions of activation not present on initial fMRI.
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Diaschisis may also have contributed to the overall reduction in bihemispheric activation seen on early scanning (Bosley et al.,; Brodtmann et al.,):see Figure 2.