Introduction

Mild TBI (mTBI) may cause alterations in cerebral perfusion leading to hypoperfusion, ischemia, and subsequent cellular damage. Disruption of the neurovascular unit may result in clinical sequalea reported in TBI. Studies have shown decreased perfusion following TBI at the acute stage (1,2). Previously, we demonstrated perfusion deficits in a group of mild TBI patients from a military population at the subacute stage using dynamic susceptibility contrast (DSC) imaging (3). This project attempted to characterize perfusion changes over time using DSC imaging in mTBI patients from a military population.

Methods

Study participants included 7 mTBI patients (29.7 ± 10.0 years) and 16 age matched controls (28.8 ± 8.6 years, p = 0.84). Patients were scanned at three intervals: Scan 1 was performed at 143 ± 56 days (range: 95 – 241 days) after injury; Scan 2 was performed at 277 ± 72 days after injury (range: 196 – 364 days); Scan 3 was performed at 918 ± 353 days after injury (range: 367 – 1214 days). Images were acquired on a 3T whole body scanner with a 32-channel phased array head coil. Structural T1 images were acquired with the 3D BRAVO sequence: TR/TE = 6.7/2.5 ms, FA = 12°, voxel size = 0.5 × 0.5 × 0.6 cm3. DSC images were acquired after 20 ml of Gd-DTPA administered at a rate of 5 ml/sec with the following parameters: TR/TE = 1590/22.3 ms, FA = 60°, voxel size = 2 × 2 × 4 cm³, 70 dynamics, 40 slices. The arterial input function (AIF) was manually selected from the right and left middle cerebral arteries. In the calculation of regional cerebral blood flow (rCBF), model independent deconvolution was performed with AFNI (http://afni.nimh.nih.gov/afni). Presented rCBF was normalized to the rCBF of the white matter. Freesurfer (http://freesurfer.net) segmentation was performed on the T1 images. 107 subcortical and cortical ROIs were extracted from the Freesurfer segmentation. Mean rCBF of each ROI was calculated accordingly.

Results

The mTBI patients demonstrated reduced rCBF in the right cerebellum, cuneus as well as posterior banks of the superior temporal sulcus (bankssts) and pericalcarine cortex compared to the controls as show in Table 1 (p values were compared to the controls). Nevertheless, the rCBF in all regions listed in Table 1 suggests a trend to increase over time compared to the rCBF at the initial scan. As a result, none of the regions listed in Table 1 demonstrated altered perfusion in the mTBI patients compared to controls at the last scan. Figure 1-3 demonstrated the rCBF in the left and right cerebellum, as well as cuneus in individual patient at all three scans (p values were computed with a paired t-test to Scan 1). The rCBF in the left cerebellum increased to 69.4 ± 12.5 ml/100g/min (p = 0.015) at Scan 2 and to 71.8 ± 13.0 ml/100g/mi (p = 0.015) at the Scan 3 from Scan 1 of 61.1 ± 10.1 ml/100g/min. Similarly the rCBF in the right cerebellum increased from Scan 1 at 60.7 ± 8.0 ml/100g/min to 67.2 ± 10.3 ml/100g/min (p = 0.019) at Scan 2 and 74.2 ± 2.3 ml/100g/min (p = 0.003) at Scan 3. The rCBF within the cuneus also increased from 54.1 ± 10.5 ml/100g/min to 64.9 ± 11.8 (p = 0.022) and 66.2 ± 11.6 (p = 0.035).

Conclusion and Discussion

Mild TBI patients scanned at around 5 months (143 days) after injury demonstrated reduced rCBF in various brain regions. In particular, the hypoperfusion in the cerebellum and cuneus is consistent with our pervious report in mTBI patients at the subacute stage (3). This longitudinal study, however, suggests that the rCBF in these brain regions with reduced perfusion may continue to recover over a 2-3 year period. This finding may provide important information regarding the evolution of mTBI and might contribute toward non-invasive assessment.

Disclaimer

The views expressed in this abstract are those of the authors and do not reflect the official policy of the Department of Army/Navy/Air Force, Department of Defense, or U.S. Government.

Acknowledgements

No acknowledgement found.