Diffusion tensor imaging in hemorrhagic stroke

Abstract

Diffusion tensor imaging (DTI) has evolved considerably over the last decade to now be knocking on the doors of wider clinical applications. There have been several efforts over the last decade to seek valuable and reliable application of DTI in different neurological disorders. The role of DTI in predicting outcomes in patients with brain tumors has been extensively studied and has become a fairly established clinical tool in this scenario. More recently DTI has been applied in mild traumatic brain injury to predict clinical outcomes based on DTI of the white matter tracts. The resolution of white matter fiber tractography based on DTI has improved over the years with increased magnet strength and better tractography post-processing. The role of DTI in hemorrhagic stroke has been studied preliminarily in the scientific literature. There is some evidence that DTI may be efficacious in predicting outcomes of motor function in animal models of intracranial hemorrhage. Only a handful of studies of DTI have been performed in subarachnoid hemorrhage or intraventricular hemorrhage scenarios. In this manuscript we will review the evolution of DTI, the existing evidence for its role in hemorrhagic stroke and discuss possible application of this non-invasive evaluation technique of human cerebral white matter tracts in the future.

Keywords: Cerebral hemorrhage; Diffusion tensor imaging; Subarachnoid hemorrhage.

Figure 1

32 direction bilateral normal corticospinal tracts processed image from 3T MRI on a human subject performed at the authors’ institution. This demonstrates the current ability to perform diffusion tensor tractography on human subjects.

Figure 2

T2 and DTI MRI changes in the brain 6 days after intracerebral hemorrhage.

Figure 3

Deferoxamine reduces reddish zone around hematoma at day 3 and day 7 in a pig ICH model. Pigs received an injection of autologous blood into the right frontal lobe. Deferoxamine (50 mg/kg, IM) or vehicle was administered 2 hours after ICH and then every 12 hours up to 7 days. Animals were killed 3 or 7 days later to examine brain damage after ICH. Values are means±SD, n=4, # p<0.01 vs. vehicle. (Reproduced with permission from: Gu Y et al. Stroke, 2009;40:2241–2243)

Figure 4

Representative coronal T2 images (A) and NG2, β-amyloid precursor protein (β-APP) and degraded myelin basic protein (DMBP) immunohistochemistry in white matter of sham and WT and LCN2^−/− mice 24 hours after SAH (B). Quantification of each result (C). ^**P<0.01, ^*P<0.05 vs. WT, and ^##P<0.01, ^#P<0.05 vs. LCN2^−/− animals. Values are means±SD; n=4–6. Scale bar = 100μm. (Reproduced with permission from: Egashira Y et al. Stroke 2014;45:2141–2143)