Traumatic brain injury: diffusion-weighted MR imaging findings.

TLDR

Diffuse axonal injury accounts for a significant portion of primary intra‑axial lesions in traumatic brain injury. The study aimed to use diffusion‑weighted MR imaging to characterize diffuse axonal injury in acute and subacute traumatic brain injury. Nine patients (ages 26–78) underwent conventional MR imaging and echo‑planar diffusion‑weighted imaging 1–18 days post‑injury, with lesions identified by location and conventional image appearance and trace ADC maps computed from diffusion data. Diffusion‑weighted imaging revealed hyperintense lesions with corresponding low ADC values, and decreased ADC persisted up to 18 days post‑injury, indicating that DAI can produce cytotoxic‑like diffusion restriction beyond the typical ischemic window.

Abstract

Diffuse axonal injury (DAI) accounts for a significant portion of primary intra-axial lesions in cases of traumatic brain injury. The goal of this study was to use diffusion-weighted MR imaging to characterize DAI in the setting of acute and subacute traumatic brain injury.Nine patients ranging in age from 26 to 78 years were examined with conventional MR imaging (including fast spin-echo T2-weighted, fluid-attenuated inversion-recovery, and gradient-echo sequences) as well as echo-planar diffusion-weighted MR imaging 1 to 18 days after traumatic injury. Lesions were characterized as DAI on the basis of their location and their appearance on conventional MR images. Trace apparent diffusion coefficient (ADC) maps were computed off-line with the diffusion-weighted and base-line images. Areas of increased signal were identified on the diffusion-weighted images, and regions of interests were used to obtain trace ADC values.In the nine patients studied, isotropic diffusion-weighted images showed areas of increased signal with correspondingly decreased ADC. In one case, decreased ADC was seen 18 days after the initial event.Decreased ADC can be demonstrated in patients with DAI in the acute setting and may persist into the subacute period, beyond that described for cytotoxic edema in ischemia.