Advances in neuroimaging of traumatic brain injury and posttraumatic stress disorder

Abstract

Improved diagnosis and treatment of traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD) are needed for our military and veterans, their families, and society at large. Advances in brain imaging offer important biomarkers of structural, functional, and metabolic information concerning the brain. This article reviews the application of various imaging techniques to the clinical problems of TBI and PTSD. For TBI, we focus on findings and advances in neuroimaging that hold promise for better detection, characterization, and monitoring of objective brain changes in symptomatic patients with combat-related, closed-head brain injuries not readily apparent by standard computed tomography or conventional magnetic resonance imaging techniques.

Figure 1

Diffusion-weighting. In practice, different degrees of diffusion-weighted images can be obtained by varying the weighting factor, which is carried out by varying time and strength of gradient pulses (represented by orange triangle). (a) The larger the weighting factor, the more the signal intensity (SI) becomes attenuated in image. This attenuation, though, is modulated by the diffusion coefficient: signal in structures with fast diffusion (e.g., water-filled ventricular cavities) decays very fast with the weighting factor, while signal in tissues with low diffusion (e.g., gray and white matter) decreases more slowly. By fitting signal decay as a function of weighting factor, one obtains the Apparent Diffusion Coefficient (ADC) for each elementary volume (voxel) of image. (b) Calculated diffusion images (ADC maps), depending solely on diffusion coefficient, can then be generated and displayed using gray (or color) scale: high diffusion, as in ventricular cavities, appears bright, while low diffusion appears dark.

Figure 2

Imaging the hippocampal subfields. (a) High-resolution magnetic resolution imaging. (b) Histological section. (c) Manual marking. CA = cornu ammonis, Sub = subiculum.

Figure 3

Arterial spin labeling perfusion. Magnetic resonance imaging perfusion-based group activation maps obtained during letter 2-back working-memory task from control subjects (left) and patients with traumatic brain injury studied following either placebo (middle) or methylphenidate (MPH) (right). Frontal activation in patients is reduced on placebo when compared with activation in controls, but normal-appearing activation is restored after MPH administration. Source: Unpublished data courtesy of Junghoon Kim and John Whyte, Moss Rehabilitation Institute.

Figure 4

Susceptibility-weighted image (SWI) example. Comparison of (a) T2-weighted, (b) SWI filtered phase, (c) processed magnitude, and (d) maximum intensity projection images on patient with traumatic brain injury, acquired on 3 T TRIO Siemens system. SWI has the following acquisition parameters: echo time/repetition time (TR/TE): 29/20 ms, flip angle: 15°, bandwidth: 120 Hz/pixel, 8-channel phased array coil with a parallel imaging factor of two, field of view (FOV): 256 × 256 mm², slice thickness: 2 mm, acquisition matrix: 512 × 416 × 64, spatial resolution: 0.5 × 0.5 × 2 mm³. T2-weighted image acquired with T2 fast spin echo with TR/TE: 5000/113 ms, FOV: 256 × 256 mm², slice thickness: 2 mm, acquisition matrix: 320 × 320. Red arrows label multiple possible microhemorrhages invisible on both T1- and T2-weighted images (some not labeled). In this case, SWI data clearly demonstrate multiple possible microhemorrhages in brain.

Figure 5

Positron emission tomography (PET) example. PET images obtained with the amyloid-imaging agent Pittsburgh Compound B ([¹¹C] PIB) in normal control (far left), three different patients with mild cognitive impairment (MCI) (three center images), and patient with mild Alzheimer disease (AD) (far right). Some MCI patients have control-like levels of amyloid, some have AD-like levels, and some have intermediate levels. DVR = distribution volume ratio.

Figure 6

Positron emission tomography (PET) amyloid-β (Aβ) plaque example. Increased retention of tracer in right frontal cortical area is seen over 2 years during which 74-year-old subject remained cognitively normal. Similar longitudinal PET imaging studies in traumatic brain injury subjects may help assess role and dynamics of Aβ deposition. Source: Unpublished data courtesy of University of Pittsburgh.