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White matter changes in comatose survivors of anoxic ischemic encephalopathy and traumatic brain injury: comparative
Anke W van der Eerden1, Omid Khalilzadeh, Vincent Perlbarg
1From the Department of Neuroradiology (A.W.v.d.E., D.D., D.G.), the Neurosurgical ICU (P.S., L.P.), and the Medical ICU (C.E.L.), Hôpital Pitié-Salpêtrière, Assistance Publique-Hôpitaux de Paris, 47-83 boulevard de l'Hôpital, 75651 Paris Cedex 13, France; Departments of Radiology (A.W.v.d.E.) and Neurology (P.E.V.), Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands; INSERM, UMRS 678, Université Pierre et Marie Curie-Paris 6, Paris, France (V.P., H.B.); Department of Radiology, Massachusetts General Hospital, Boston, Mass (O.K., J.D., R.G.); Division of Neuroscience Critical Care, Department of Anesthesiology Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Md (R.D.S.); Department of Neuroradiology, Guy de Chauliac Hospital, Montpellier, France (N.M.d.C.); Department of Neuroradiology, Roger Salengro Hospital, Lille, France (C.D.); Department of Neuroradiology, Centre Hospitalier Universitaire, Rouen, France (E.T.); and Cyclotron Research Center, University of Liège, Liège, Belgium (S.L., A.V.).
Purpose:
To analyze white matter pathologic abnormalities by using diffusion-tensor (DT) imaging in a multicenter prospective cohort of comatose patients following cardiac arrest or traumatic brain injury (TBI).
Materials And Methods:
Institutional review board approval and informed consent from proxies and control subjects were obtained. DT imaging was performed 5-57 days after insult in 49 cardiac arrest and 40 TBI patients. To control for DT imaging-processing variability, patients' values were normalized to those of 111 control subjects. Automated segmentation software calculated normalized axial diffusivity (λ1) and radial diffusivity (λ⊥) in 19 predefined white matter regions of interest (ROIs). DT imaging variables were compared by using general linear modeling, and side-to-side Pearson correlation coefficients were calculated. P values were corrected for multiple testing (Bonferroni).
Results:
In central white matter, λ1 differed from that in control subjects in six of seven TBI ROIs and five of seven cardiac arrest ROIs (all P < .01). The λ⊥ differed from that in control subjects in all ROIs in both patient groups (P < .01). In hemispheres, λ1 was decreased compared with that in control subjects in three of 12 TBI ROIs (P < .05) and nine of 12 cardiac arrest ROIs (P < .01). The λ⊥ was increased in all TBI ROIs (P < .01) and in seven of 12 cardiac arrest ROIs (P < .05). Cerebral hemisphere λ1 was lower in cardiac arrest than in TBI in six of 12 ROIs (P < .01), while λ⊥ was higher in TBI than in cardiac arrest in eight of 12 ROIs (P < .01). Diffusivity values were symmetrically distributed in cardiac arrest (P < .001 for side-to-side correlation) but not in TBI patients.
Conclusion:
DT imaging findings are consistent with the known predominance of cerebral hemisphere axonal injury in cardiac arrest and chiefly central myelin injury in TBI. This consistency supports the validity of DT imaging for differentiating axon and myelin damage in vivo in humans.
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