Evaluation of Delayed Neuronal and Axonal Damage Secondary to Moderate and Severe Traumatic Brain Injury Using Quantitative MR Imaging Techniques

Department of Radiology, Cancer Hospital of Barretos-Fundacao Pio XII, Barretos, Sao Paulo, Brazil.
American Journal of Neuroradiology (Impact Factor: 3.59). 02/2009; 30(5):947-52. DOI: 10.3174/ajnr.A1477
Source: PubMed


Traumatic brain injury (TBI) is a classic model of monophasic neuronal and axonal injury, in which tissue damage mainly occurs at the moment of trauma. There is some evidence of delayed progression of the neuronal and axonal loss. Our purpose was to test the hypothesis that quantitative MR imaging techniques can estimate the biologic changes secondary to delayed neuronal and axonal loss after TBI.
Nine patients (age, 11-28 years; 5 male) who sustained a moderate or severe TBI were evaluated at a mean of 3.1 years after trauma. We applied the following techniques: bicaudate (BCR) and bifrontal (BFR) ventricle-to-brain ratios; T2 relaxometry; magnetization transfer ratio (MTR); apparent diffusion coefficient (ADC); and proton spectroscopy, by using an N-acetylaspartate/creatine (NAA/Cr) ratio measured in normal-appearing white matter (NAWM) and the corpus callosum (CC). The results were compared with those of a control group.
BCR and BFR mean values were significantly increased (P < or = .05) in patients due to secondary subcortical atrophy; increased T2 relaxation time was observed in the NAWM and CC, reflecting an increase in water concentration secondary to axonal loss. Increased ADC mean values and reduced MTR mean values were found in the NAWM and CC, showing damage in the myelinated axonal fibers; and decreased NAA/Cr ratio mean values were found in the CC, indicating axonal loss.
These quantitative MR imaging techniques could noninvasively demonstrate the neuronal and axonal damage in the NAWM and CC of human brains, secondary to moderate or severe TBI.

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    • "Axial diffusivity is believed to be sensitive to axonal integrity and radial diffusivity reflects myelin integrity (Song et al., 2002, 2003). Previous TBI studies on both humans and animals have shown altered MD (Alsop et al., 1996; Huisman et al., 2003; Liu et al., 1999; Mamere et al., 2009), and FA in white matter regions (Arfanakis et al., 2002; Bazarian et al., 2007; Huisman et al., 2004; Mac Donald et al., 2007a,b; Mayer et al., 2010; Wilde et al., 2006; Wozniak et al., 2007) anywhere from 24 h to several days after injury. "
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