Letter to the Editor: The Concept of Mild Traumatic Brain Injury: Response to Palacios and Colleagues

To the Editor:

“Whatever we observe is not nature itself, but nature exposed to our method.” Werner Heisenberg

I read with interest the thought-provoking article by Palacios and colleagues, ¹ a clinical study augmented by diffusion tensor imaging (DTI)-magnetic resonance imaging. This asserts, inter alia, that mild traumatic brain injury (mTBI) may be a misnomer because there may be a substantial degree of incomplete recovery. A similar conclusion was reached by another recent study. ² Neither study, however, addressed the prominent attrition of mTBI patients. In contrast, an extensive older literature ^{3 –6} suggests that complete recovery is the rule, and incomplete recovery may be associated with pre-existing psychological problems or secondary gain. ⁴ Since attrition is plausibly explained by complete recovery, ⁶ failure to address it could help explain the newer findings.

Palacios and colleagues interpreted measures of fractional anisotropy (FA) and diffusivity in mTBI patients versus controls ¹ as evidence of axonal injury. Decreased FA was seen in the thalamus, internal and external capsules, and centrum semiovale, all regions prone to watershed ischemia. Yet there was a striking lack of involvement of the corpus callosum, a structure extremely vulnerable to TBI, but not to ischemia.

Other interpretations might therefore be considered. For example, mild diffuse hypoperfusion, ⁷ in regions prone to ischemia, may be associated with increased deoxyhemoglobin. Blood oxygenation level–dependent dephasing is largely isotropic and independent of motion, and this effect would be amplified by deoxyhemoglobin, consistent with decreased FA. Unlike axonal injury, it would also be reversible.

Clinically, recovery at 6 months was assessed using the subjective Glasgow Coma Outcome Scale (GCOS), which may be biased by secondary gain. ^8,9 Complete recovery was GCOS = 8; incomplete recovery was GCOS <8. The large majority of patients (68%) were quickly lost to follow-up. This attrition is most plausibly due to complete recovery, ⁶ yet was not addressed. Of the remainder, at 6 months, 15% had GCOS = 8, 17% had GCOS <8. Therefore, the incomplete recovery group was 17% of the total, in line with the 16% estimate from a recent meta-analysis of the older literature. ⁶ Finally, initial radiological deficits correlated with complete, but not with incomplete, recovery. ¹ This is consistent with symptom amplification by those with secondary gain.

Putting these findings together, another explanation of Palacios and colleagues might now be offered:

DTI is sensitive to mTBI, but the changes may be more physiological than structural.