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Mapping Connectivity Damage in the Case of Phineas Gage

1Laboratory of Neuro Imaging (LONI), Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
2Surgical Planning Laboratory, Department of Radiology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA.
Public Library of Science
Publication Date:
PLoS One
Volume Number:
Issue Number:
PLoS One 2012 May; 7(5): e37454.
PubMed ID:
Appears in Collections:
U54 EB005149/EB/NIBIB NIH HHS/United States
RC1 MH088194/MH/NIMH NIH HHS/United States
P41 RR013642/RR/NCRR NIH HHS/United States
Generated Citation:
van Horn J.D., Irimia A., Torgerson C.M., Chambers M.C., Kikinis R., Toga A.W. Mapping Connectivity Damage in the Case of Phineas Gage. PLoS One 2012 May; 7(5): e37454. PMID: 22616011. PMCID: PMC3353935.
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White matter (WM) mapping of the human brain using neuroimaging techniques has gained considerable interest in the neuroscience community. Using diffusion weighted (DWI) and magnetic resonance imaging (MRI), WM fiber pathways between brain regions may be systematically assessed to make inferences concerning their role in normal brain function, influence on behavior, as well as concerning the consequences of network-level brain damage. In this paper, we investigate the detailed connectomics in a noted example of severe traumatic brain injury (TBI) which has proved important to and controversial in the history of neuroscience. We model the WM damage in the notable case of Phineas P. Gage, in whom a ‘‘tamping iron’’ was accidentally shot through his skull and brain, resulting in profound behavioral changes. The specific effects of this injury on Mr. Gage’s WM connectivity have not previously been considered in detail. Using computed tomography (CT) image data of the Gage skull in conjunction with modern anatomical MRI and diffusion imaging data obtained in contemporary right handed male subjects (aged 25–36), we computationally simulate the passage of the iron through the skull on the basis of reported and observed skull fiducial landmarks and assess the extent of cortical gray matter (GM) and WM damage. Specifically, we find that while considerable damage was, indeed, localized to the left frontal cortex, the impact on measures of network connectedness between directly affected and other brain areas was profound, widespread, and a probable contributor to both the reported acute as well as long-term behavioral changes. Yet, while significantly affecting several likely network hubs, damage to Mr. Gage’s WM network may not have been more severe than expected from that of a similarly sized ‘‘average’’ brain lesion. These results provide new insight into the remarkable brain injury experienced by this noteworthy patient.

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