A review of neuroimaging findings in repetitive brain trauma

Abstract

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease confirmed at postmortem. Those at highest risk are professional athletes who participate in contact sports and military personnel who are exposed to repetitive blast events. All neuropathologically confirmed CTE cases, to date, have had a history of repetitive head impacts. This suggests that repetitive head impacts may be necessary for the initiation of the pathogenetic cascade that, in some cases, leads to CTE. Importantly, while all CTE appears to result from repetitive brain trauma, not all repetitive brain trauma results in CTE. Magnetic resonance imaging has great potential for understanding better the underlying mechanisms of repetitive brain trauma. In this review, we provide an overview of advanced imaging techniques currently used to investigate brain anomalies. We also provide an overview of neuroimaging findings in those exposed to repetitive head impacts in the acute/subacute and chronic phase of injury and in more neurodegenerative phases of injury, as well as in military personnel exposed to repetitive head impacts. Finally, we discuss future directions for research that will likely lead to a better understanding of the underlying mechanisms separating those who recover from repetitive brain trauma vs. those who go on to develop CTE.

Keywords: neuroimaging; repetitive head injury.

Figure 1

Soccer players experience repetitive subconcussive head impacts while heading the ball. A recent study investigated the white matter microstructure using diffusion tensor imaging in a group of professional soccer players compared with swimmers. Tract‐based spatial statistics revealed increased radial diffusivity in widespread white matter regions in soccer players. Journal of the American Medical Association [see 78].

Figure 2

We present a multistage disease model of short‐ and long‐term consequence following repetitive brain trauma. Quality of life is indicated by symptom load, which is expressed as a function of time, thereby allowing for the differentiation between at least three main trajectories of the disease including an acute/subacute phase, a chronic/static phase and a phase of possible neurodegeneration.

Figure 3

Three‐dimensional reconstruction of the hippocampus. The hippocampus has been associated with memory impairment in traumatic brain injury and repetitive brain trauma.

Figure 4

Surface lines of pial (yellow) and white matter (red) superimposed on a T1‐weighted image. Surface segmentation was performed using FreeSurfer 5.1 in a retired national football league player, the surfaces can then be used to calculate cortical thickness and perform group comparisons as well as associations with, for example, neuropsychological test evaluations.

Figure 5

Susceptibility‐weighted image (SWI) with superimposed lesion mask. SWI is sensitive to detect microhemorrhages following brain trauma. Typically, the hemorrhages appear dark in SWI making them difficult to separate from blood vessels. A threshold mask is used such that lesions are hyperintense and can be used to calculate the hypointensity burden [see 66].

Figure 6

Spectrum obtained using magnetic resonance spectroscopy. Cho = choline; Cr = creatine; Glx = glutamate; mI = myoinositol; NAA = N‐acetyl aspartate. [see 86]

Figure 7

Comparison between single‐tensor streamline tractography (A) and two‐tensor tractography (B) of the corpus callosum. The same region of interest was used to seed fibers (A) and to select fibers from a two‐tensor whole‐brain tractography (B). Note that two‐tensor fiber reconstruction includes numerous fibers in the periphery while the single‐tensor approach only detects more central fibers.