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      Effects of dexamethasone in traumatic brain injury patients with pericontusional vasogenic edema : A prospective-observational DTI-MRI study

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          Abstract

          Cerebral edema is a frequent and serious complication in traumatic brain injury (TBI) patients. The objective is to study the effect of dexamethasone in patients with brain contusions, and to assess its effect on the vasogenic component of the pericontusional edema.

          Prospective-observational study to quantify, using magnetic resonance imaging, the volume of the edema before and after 10 days of dexamethasone in patients with brain contusions. Using diffusion tensor imaging, we have examined the effect of dexamethasone on fractional anisotropy (FA) and apparent diffusion coefficient (ADC). To assess changes, the pre- and post-treatment values for each patient were compared using a paired-samples Student t test.

          We included 30 TBI patients, 15 in each group. The volume of the vasogenic edema in the group of patients treated with dexamethasone decreased from 22 to 19 mL and this decrease was statistically significant ( P < .05). Nevertheless, in the non-steroids group the volume of the vasogenic edema increased from 11 to 15 mL. There was a significant decrease in the ADC value (from 1.78–1.59; P < .05); and a significant increase in the FA value (0.09–0.11; P < .05) in the patients treated with dexamethasone.

          Using diffusion tensor imaging we have shown in a selected group of TBI patients with vasogenic pericontusional edema, a reduction of edema volume, a decrease in the ADC and an increase in the FA after treatment with dexamethasone. However, we have no data if such results are beneficial in terms of improving functional outcome.

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          Most cited references23

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          Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months.

          MRC CRASH is a randomised controlled trial (ISRCTN74459797) of the effect of corticosteroids on death and disability after head injury. We randomly allocated 10,008 adults with head injury and a Glasgow Coma Scale score of 14 or less, within 8 h of injury, to a 48-h infusion of corticosteroid (methylprednisolone) or placebo. Data at 6 months were obtained for 9673 (96.7%) patients. The risk of death was higher in the corticosteroid group than in the placebo group (1248 [25.7%] vs 1075 [22.3%] deaths; relative risk 1.15, 95% CI 1.07-1.24; p=0.0001), as was the risk of death or severe disability (1828 [38.1%] vs 1728 [36.3%] dead or severely disabled; 1.05, 0.99-1.10; p=0.079). There was no evidence that the effect of corticosteroids differed by injury severity or time since injury. These results lend support to our earlier conclusion that corticosteroids should not be used routinely in the treatment of head injury.
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            Blood-brain barrier breakdown as a therapeutic target in traumatic brain injury.

            Traumatic brain injury (TBI) is the leading cause of death in young adults and children. The treatment of TBI in the acute phase has improved substantially; however, the prevention and management of long-term complications remain a challenge. Blood-brain barrier (BBB) breakdown has often been documented in patients with TBI, but the role of such vascular pathology in neurological dysfunction has only recently been explored. Animal studies have demonstrated that BBB breakdown is involved in the initiation of transcriptional changes in the neurovascular network that ultimately lead to delayed neuronal dysfunction and degeneration. Brain imaging data have confirmed the high incidence of BBB breakdown in patients with TBI and suggest that such pathology could be used as a biomarker in the clinic and in drug trials. Here, we review the neurological consequences of TBI, focusing on the long-term complications of such injuries. We present the clinical evidence for involvement of BBB breakdown in TBI and examine the primary and secondary mechanisms that underlie such pathology. We go on to consider the consequences of BBB injury, before analyzing potential mechanisms linking vascular pathology to neuronal dysfunction and degeneration, and exploring possible targets for treatment. Finally, we highlight areas for future basic research and clinical studies into TBI.
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              Diffusion tensor imaging of mild traumatic brain injury.

              Mild traumatic brain injury (mTBI) remains a challenge to accurately assess with conventional neuroimaging. Recent research holds out the promise that diffusion tensor imaging (DTI) can be used to predict recovery in mTBI patients. Unlike computed tomography or conventional magnetic resonance imaging, DTI is sensitive to microstructural axonal injury, the neuropathology that is thought to be most responsible for the persistent cognitive and behavioral impairments that often occur after mTBI. Through the use of newer DTI analysis techniques such as automated region of interest analysis, tract-based voxel-wise analysis, and quantitative tractography, researchers have shown that frontal and temporal association white matter pathways are most frequently damaged in mTBI and that the microstructural integrity of these tracts correlates with behavioral and cognitive measures. Future longitudinal DTI studies are needed to elucidate how symptoms and the microstructural pathology evolve over time. Moving forward, large-scale investigations will ascertain whether DTI can serve as a predictive imaging biomarker for long-term neurocognitive deficits after mTBI that would be of value for triaging patients to clinical trials of experimental cognitive enhancement therapies and rehabilitation methods, as well as for monitoring their response to these interventions.

                Author and article information

                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MEDI
                Medicine
                Lippincott Williams & Wilkins (Hagerstown, MD )
                0025-7974
                1536-5964
                23 October 2020
                23 October 2020
                : 99
                : 43
                : e22879
                Affiliations
                [a ]Radiology Department
                [b ]Neurosurgical Department, Son Espases Hospital
                [c ]Neuropsychology and Cognition Research Group, Research Institute on Health IDISBA & IUNICS-UIB
                [d ]Research Institute on Health IDISBA, Son Espases Hospital
                [e ]Intensive Care Department, Son Espases Hospital, Palma de Mallorca, Spain.
                Author notes
                []Correspondence: Jon Pérez-Bárcena, Intensive Care Department. Son Espases Hospital, Carretera de Valldemossa, 79, Palma de Mallorca (Islas Baleares) 07120, Spain (e-mail: juan.perez@ 123456ssib.es ).
                Author information
                http://orcid.org/0000-0003-4147-8636
                Article
                MD-D-20-03505 22879
                10.1097/MD.0000000000022879
                7581187
                33120830
                e6b70dc2-a699-45dc-bfcf-e72eb0e3b681
                Copyright © 2020 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC), where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc/4.0

                History
                : 20 April 2020
                : 18 September 2020
                : 24 September 2020
                Categories
                3900
                Research Article
                Observational Study
                Custom metadata
                TRUE

                brain contusions,dexamethasone,diffusion tensor imaging,pericontusional edema,traumatic brain injury

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