Figure 2.

Left hemisphere structural lesions. Axial T₁-weighted MRI showing a small infarction in the patient with transcortical motor aphasia (A) involving the left sensorimotor cortex and medial insula (white arrows). The lesion is superficial sparing the deep white matter. The MRI in the patient with conduction aphasia shows a small infarction involving the left posterior temporal gyrus and supramarginal gyrus extending deeply into the lateral ventricle wall (B) (white arrows). The left hemisphere is represented on the left side of the images. DTI, MRI, and PET of the corpus callosum. Brain imaging of the corpus callosum. Midsaggital DTI (C) and ¹⁸FDG-PET images (D) and coronal T₁-weighted MRI (E) of the corpus callosum in patients RTP (top panel) and JGG (bottom panel). In RPT the corpus callosum was structurally (C) and functionally intact (D). Although RTP had an infarction in the left sensorimotor cortex, this did not result in noticeable changes in the anterior segments of the corpus callosum. The rostral body of corpus callosum in JGG shows diminished streamlines (C), bottom panel (yellow arrowheads) and decrement of metabolic activity (D), bottom panel (yellow arrow). The fact that structural and functional involvement of the anterior corpus callosum in JGG does not interrupt fibers interconnecting the damaged left temporoparietal cortex with its homologous in the right hemisphere suggests that corpus callosum involvement was unrelated to the stroke lesion. Anatomical MRIs show normal septum pellucidum (grade 0, normal) (yellow arrow) in RTP (E), top panel and an enlarged cavum septum pellucidum (grade 4, severe) (Degreef et al., 1992; DeLisi et al., 1993; Kim and Peterson, 2003) in JGG (yellow arrows) (E, bottom panel).