Diffusion Tensor Imaging Detects Acute and Subacute Changes in Corpus Callosum in Blast-Induced Traumatic Brain Injury

Abstract

There is a critical need for understanding the progression of neuropathology in blast-induced traumatic brain injury using valid animal models to develop diagnostic approaches. In the present study, we used diffusion imaging and magnetic resonance (MR) morphometry to characterize axonal injury in white matter structures of the rat brain following a blast applied via blast tube to one side of the brain. Diffusion tensor imaging was performed on acute and subacute phases of pathology from which fractional anisotropy, mean diffusivity, axial diffusivity, and radial diffusivity were calculated for corpus callosum (CC), cingulum bundle, and fimbria. Ventricular volume and CC thickness were measured. Blast-injured rats showed temporally varying bilateral changes in diffusion metrics indicating persistent axonal pathology. Diffusion changes in the CC suggested vasogenic edema secondary to axonal injury in the acute phase. Axonal pathology persisted in the subacute phase marked by cytotoxic edema and demyelination which was confirmed by ultrastructural analysis. The evolution of pathology followed a different pattern in the cingulum bundle: axonal injury and demyelination in the acute phase followed by cytotoxic edema in the subacute phase. Spatially, structures close to midline were most affected. Changes in the genu were greater than in the body and splenium; the caudal cingulum bundle was more affected than the rostral cingulum. Thinning of CC and ventriculomegaly were greater only in the acute phase. Our results reveal the persistent nature of blast-induced axonal pathology and suggest that diffusion imaging may have potential for detecting the temporal evolution of blast injury.

Repeated blast mild traumatic brain injury and oxycodone self-administration produce interactive effects on neuroimaging outcomes

“…DTI measurements also tend to be exacerbate with time post-injury: we have reported an increase in the volume of microstructural damage between post-injury day 4 and 30 13 , and Badea et al have reported greater changes in DTI at 90 days relative to 7 days post-injury 61 . Another study found region-specific changes in DTI between 1 and 14 days after injury, reflecting regional differences in time to vasogenic or cytotoxic edema and demyelination 62 . In the present study, we did not observe a significant effect of rbTBI on FA in the prefrontal cortex or nucleus accumbens, but we did observe a significant interaction between rbTBI and oxycodone self-administration in the nucleus accumbens.…”

Emerging Utility of Applied Magnetic Resonance Imaging in the Management of Traumatic Brain Injury

“…This pattern is thought to be the MR representation of a trauma-induced disturbance in the microstructure of the axonal tissue [ 36 ]. Furthermore, certain local brain regions, including the frontal lobes, the corpus callosum, the centrum semiovale, and the internal capsule, may be more susceptible to these changes after TBI than others [ 42 , 44 , 45 , 46 , 47 , 48 ]. Although detecting these changes may be helpful in the diagnosis of CT-negative mild TBI, it is less clinically relevant for those in whom TBI has already been confirmed.…”

18F-FDG PET Combined With MR Spectroscopy Elucidates the Progressive Metabolic Cerebral Alterations After Blast-Induced Mild Traumatic Brain Injury in Rats

“…Even though the acute symptoms of mTBI may be mild and transient, experimental and clinical studies have found metabolic, biochemical, and structural changes caused by mTBI. Mild TBI causes a complex pathophysiological cascade, including dramatic alterations in ionic homeostasis ( Katayama et al, 1991 ), disruption of the blood–brain barrier (BBB) ( Walls et al, 2016 ; Kuriakose et al, 2018 ), injury-induced neuroinflammation ( Kokiko-Cochran and Godbout, 2018 ; Missault et al, 2019 ), and diffuse axonal injury ( Ling et al, 2012 ; Venkatasubramanian et al, 2020 ). However, majority of mTBI patients experience neurological dysfunction with no findings on conventional clinical imaging methods, such as structural magnetic resonance imaging (MRI) or computed tomography (CT) ( Le and Gean, 2009 ).…”

“…Several advanced in vivo imaging techniques have been used to investigate TBI to better understand the temporal microstructural and functional changes following TBI, such as diffusion tensor imaging (DTI), functional MRI (fMRI), MR spectroscopy (MRS), positron emission tomography (PET), etc. ( Croall et al, 2014 ; Zhuo et al, 2015 ; Harris et al, 2016 ; Jaiswal et al, 2019 ; Kulkarni et al, 2019 ; Venkatasubramanian et al, 2020 ). DTI has been widely used to investigate the microstructural responses after mTBI.…”

“…DTI has been widely used to investigate the microstructural responses after mTBI. Many different regions have been found to be affected, since DTI is highly sensitive to axonal damage related to mTBI ( Mayer et al, 2010 ; Tang et al, 2017 ; Badea et al, 2018 ; Venkatasubramanian et al, 2020 ). In contrast to the structural information offered by DTI regarding brain integrity, some studies have explored functional and biochemical changes following brain injury using other imaging modalities.…”