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Correspondence |

Atrophy After Traumatic Axonal Injury

Satoru Takeuchi, MD; Hiroshi Nawashiro, MD
Arch Neurol. 2011;68(8):1090. doi:10.1001/archneurol.2011.205.
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We read with great interest the recent article by Warner et al1 in which the authors analyzed the spatial distribution of cortical and subcortical volume loss in patients with diffuse traumatic axonal injury and assessed the relationship between regional atrophy and functional outcome. The authors reported that decreases in volume were seen in several brain regions including the amygdala, hippocampus, thalamus, corpus callosum, putamen, precuneus, postcentral gyrus, paracentral lobule, and parietal and frontal cortices, and described that posttraumatic volume loss may occur primarily as a consequence of axonal injury. We wish to provide further comment on this issue. The cingulum bundle (CB) is a white matter tract that underlies the cingulate cortex, and all connections entering and exiting the cingulate gyrus pass through this bundle. These pathways include projections between prefrontal and parahippocampal cortices and projections to the median raphe nucleus that terminate in the dorsal hippocampus, and the CB is involved in attention, emotions, spatial orientation, and memory. Recently several authors reported that the CB is susceptible to traumatic axonal injury because of its long, coursing nature, and this injury is detectable by diffusion tensor imaging in studies involving mild to severe traumatic brain injury at both an acute and chronic phase.24 However, the authors unexpectedly reported that atrophies were not seen in any cingulates. This fact may conflict the authors' hypothesis that posttraumatic volume loss may occur primarily as a consequence of axonal injury. We suggest that a study of the relationship between diffusion tensor imaging findings at an acute stage and the following atrophy (especially in the cingulate cortex or the CB) should be performed with the authors' great method in the future.



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