Dataset Information

Diagnostic Problems in Diffuse Axonal Injury.

ABSTRACT: In this study, three problems associated with diagnosing diffuse axonal injury (DAI) in patients with traumatic brain injury are reviewed: the shortage of scientific evidence supporting the 6-hour loss of consciousness (LOC) diagnostic criterion to discriminate concussion and DAI, the low sensitivity of conventional brain MRI in the detection of DAI lesions, and the inappropriateness of the term diffuse in DAI. Pathological study by brain biopsy is required to confirm DAI; however, performing a brain biopsy for the diagnosis of DAI in a living patient is impossible. Therefore, the diagnosis of DAI in a living patient is clinically determined based on the duration of LOC, clinical manifestations, and the results of conventional brain MRI. There is a shortage of scientific evidence supporting the use of the 6-hour LOC criterion to distinguish DAI from concussion, and axonal injuries have been detected in many concussion cases with a less than 6-hour LOC. Moreover, due to the low sensitivity of conventional brain MRI, which can only detect DAI lesions in approximately half of DAI patients, diagnostic MRI criteria for DAI are not well established. In contrast, diffusion tensor imaging (DTI) has been shown to have high sensitivity for the detection of DAI lesions. As DTI is a relatively new method, further studies aimed at the establishment of diagnostic criteria for DAI detection using DTI are needed. On the other hand, because DAI distribution is not diffuse but multifocal, and because axonal injury lesions have been detected in concussion patients, steps to standardize the use of terms related to axonal injury in both concussion and DAI are necessary.

SUBMITTER: Jang SH

PROVIDER: S-EPMC7168326 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Diagnostic Problems in Diffuse Axonal Injury.

Jang Sung Ho SH

Diagnostics (Basel, Switzerland) 20200221 2

In this study, three problems associated with diagnosing diffuse axonal injury (DAI) in patients with traumatic brain injury are reviewed: the shortage of scientific evidence supporting the 6-hour loss of consciousness (LOC) diagnostic criterion to discriminate concussion and DAI, the low sensitivity of conventional brain MRI in the detection of DAI lesions, and the inappropriateness of the term diffuse in DAI. Pathological study by brain biopsy is required to confirm DAI; however, performing a ...[more]

PMID: 32098060

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Project description:Regarding the determination of the biomechanical parameters in a reliable in vitro cell model for diffuse axonal injury (DAI), our study aimed to demonstrate connections between those parameters and secondary axotomy through examination of morphological alterations under a variety of traumatic conditions. An in vitro cell model for DAI was established in primary cultured mouse neurons by uniaxial mechanical stretching of non-myelinated axons under various traumatic conditions: strain (?) = 5, 10, 20, and 50%; strain time (t) = 500, 100, and 20 ms; strain rate ranging between 0.1 and 25 s-1. Axonal real strains (strainaxon) were measured as 4.53 ± 0.27, 9.02 ± 0.91, 17.75 ± 1.65, and 41.8 ± 4.4%. Axonal real strain rates (SRaxon) ranged between 0.096 ± 0.0054 and 20.9 ± 2.2 s-1. Results showed there was no obvious abnormality of axons with a lower strain condition (strainaxon < 17.75 ± 1.65%) during the acute phase within 30 min after injury. In contrast, acute axonal degeneration (AAD) was observed in the axons following injury with a higher strain condition (SRaxon > 17.75 ± 1.65%). In addition, the incidence and degree of AAD were closely correlated with strain rate. Specifically, AAD occurred to all axons that were examined, when ? = 50% (strainaxon = 41.8 ± 4.4%) for 20 ms, while no spontaneous rupture was observed in those axons. Besides, the concentration of Ca2+ within the axonal process was significantly increased under such traumatic conditions. Moreover, the continuity of axon cytoskeleton was interrupted, eventually resulting in neuronal death during subacute stage following injury. In this study, we found that there is a minimum strain threshold for the occurrence of AAD in non-myelinated axons of primary cultured mouse neurons, which ranges between 9.02 ± 0.91 and 17.75 ± 1.65%. Basically, the severity of axonal secondary axotomy post DAI is strain rate dependent under a higher strain above the threshold. Hence, a reliable and reproducible in vitro cell model for DAI was established, when ? = 50% (strainaxon = 41.8 ± 4.4%) for 20 ms.

Project description:Axonal injury is a major contributor to the clinical symptomatology in patients with traumatic brain injury. Conventional neuroradiological tools, such as CT and MRI, are insensitive to diffuse axonal injury (DAI) caused by trauma. Diffusion tensor MRI parameters may change in DAI lesions; however, the nature of these changes is inconsistent. Multidimensional MRI is an emerging approach that combines T1, T2, and diffusion, and replaces voxel-averaged values with distributions, which allows selective isolation of specific potential abnormal components. By performing a combined post-mortem multidimensional MRI and histopathology study, we aimed to investigate T1-T2-diffusion changes linked to DAI and to define their histopathological correlates. Corpora callosa derived from eight subjects who had sustained traumatic brain injury, and three control brain donors underwent post-mortem ex vivo MRI at 7 T. Multidimensional, diffusion tensor, and quantitative T1 and T2 MRI data were acquired and processed. Following MRI acquisition, slices from the same tissue were tested for amyloid precursor protein (APP) immunoreactivity to define DAI severity. A robust image co-registration method was applied to accurately match MRI-derived parameters and histopathology, after which 12 regions of interest per tissue block were selected based on APP density, but blind to MRI. We identified abnormal multidimensional T1-T2, diffusion-T2, and diffusion-T1 components that are strongly associated with DAI and used them to generate axonal injury images. We found that compared to control white matter, mild and severe DAI lesions contained significantly larger abnormal T1-T2 component (P = 0.005 and P < 0.001, respectively), and significantly larger abnormal diffusion-T2 component (P = 0.005 and P < 0.001, respectively). Furthermore, within patients with traumatic brain injury the multidimensional MRI biomarkers differentiated normal-appearing white matter from mild and severe DAI lesions, with significantly larger abnormal T1-T2 and diffusion-T2 components (P = 0.003 and P < 0.001, respectively, for T1-T2; P = 0.022 and P < 0.001, respectively, for diffusion-T2). Conversely, none of the conventional quantitative MRI parameters were able to differentiate lesions and normal-appearing white matter. Lastly, we found that the abnormal T1-T2, diffusion-T1, and diffusion-T2 components and their axonal damage images were strongly correlated with quantitative APP staining (r = 0.876, P < 0.001; r = 0.727, P < 0.001; and r = 0.743, P < 0.001, respectively), while producing negligible intensities in grey matter and in normal-appearing white matter. These results suggest that multidimensional MRI may provide non-invasive biomarkers for detection of DAI, which is the pathological substrate for neurological disorders ranging from concussion to severe traumatic brain injury.

Dataset Information

Diagnostic Problems in Diffuse Axonal Injury.

Publications

Diagnostic Problems in Diffuse Axonal Injury.

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