Traumatic Brain Injury (TBI) is a major global public health problem. Neurological damage from TBI may be mild, moderate, or severe and occurs both immediately at the time of impact (primary injury) and continues to evolve afterwards (secondary injury). In mild (m)TBI, common symptoms are headaches, dizziness and fatigue. Visual impairment is especially prevalent. Insomnia, attentional deficits and memory problems often occur. Neuroimaging methods for the management of TBI include computed tomography and magnetic resonance imaging. The location and the extent of injuries determine the motor and/or sensory deficits that result. Parietal lobe damage can lead to deficits in sensorimotor function, memory, and attention span. The processing of visual information may be disrupted, with consequences such as poor hand-eye coordination and balance. TBI may cause lesions in the occipital or parietal lobe that leave the TBI patient with incomplete homonymous hemianopia. Overall, TBI can interfere with everyday life by compromising the ability to work, sleep, drive, read, communicate and perform numerous activities previously taken for granted. Treatment and rehabilitation options available to TBI sufferers are inadequate and there is a pressing need for new ways to help these patients to optimize their functioning and maintain productivity and participation in life activities, family and community.

Mild traumatic brain injury (mTBI) accounts for more than 80% of the total number of TBI cases. The mechanism of injury for patients with mTBI has a variety of neuropathological processes. However, the underlying neurophysiological mechanism of the mTBI is unclear, which affects the early diagnosis, treatment decision-making, and prognosis evaluation. More and more multimodal magnetic resonance imaging (MRI) techniques have been applied for the diagnosis of mTBI, such as functional magnetic resonance imaging (fMRI), arterial spin labeling (ASL) perfusion imaging, susceptibility-weighted imaging (SWI), and diffusion MRI (dMRI). Various imaging techniques require to be used in combination with neuroimaging examinations for patients with mTBI. The understanding of the neuropathological mechanism of mTBI has been improved based on different angles. In this review, we have summarized the application of these aforementioned multimodal MRI techniques in mTBI and evaluated its benefits and drawbacks.

Mild traumatic brain injury (mTBI) can be accompanied by structural damage to the brain. Here, we investigated how the presence of intracranial traumatic computed tomography (CT) pathologies relates to the global functional outcome in young patients one year after mTBI. All patients with mTBI (Glasgow Coma Scale: 13–15) ≤24 years in the multi-center, prospective, observational Collaborative European NeuroTrauma Effectiveness Research in TBI (CENTER-TBI) study were included. Patient demographics and CT findings were assessed at admission, and the Glasgow Outcome Scale Extended (GOSE) was evaluated at 12 months follow-up. The association between a “positive CT” (at least one of the following: epidural hematoma, subdural hematoma, traumatic subarachnoid hemorrhage (tSAH), intraventricular hemorrhage, subdural collection mixed density, contusion, traumatic axonal injury) and functional outcome (GOSE) was assessed using multi-variable mixed ordinal and logistic regression models. A total of 462 patients with mTBI and initial brain CT from 46 study centers were included. The median age was 19 (17–22) years, and 322 (70%) were males. CT imaging showed a traumatic intracranial pathology in 171 patients (37%), most commonly tSAH (48%), contusions (40%), and epidural hematomas (37%). Patients with a positive CT scan were less likely to achieve a complete recovery 12 months post-injury. The presence of any CT abnormality was associated with both lower GOSE scores (odds ratio [OR]: 0.39 [0.24–0.63]) and incomplete recovery (GOSE <8; OR: 0.41 [0.25–0.68]), also when adjusted for demographical and clinical baseline factors. The presence of intracranial traumatic CT pathologies was predictive of outcome 12 months after mTBI in young patients, which might help to identify candidates for early follow-up and additional care.

To determine the clinical relevance, if any, of traumatic intracranial findings on early head computed tomography (CT) and brain magnetic resonance imaging (MRI) to 3-month outcome in mild traumatic brain injury (MTBI).One hundred thirty-five MTBI patients evaluated for acute head injury in emergency departments of 3 LEVEL I trauma centers were enrolled prospectively. In addition to admission head CT, early brain MRI was performed 12 ± 3.9 days after injury. Univariate and multivariate logistic regression were used to assess for demographic, clinical, socioeconomic, CT, and MRI features that were predictive of Extended Glasgow Outcome Scale (GOS-E) at 3 months postinjury.Twenty-seven percent of MTBI patients with normal admission head CT had abnormal early brain MRI. CT evidence of subarachnoid hemorrhage was associated with a multivariate odds ratio of 3.5 (p = 0.01) for poorer 3-month outcome, after adjusting for demographic, clinical, and socioeconomic factors. One or more brain contusions on MRI, and ≥4 foci of hemorrhagic axonal injury on MRI, were each independently associated with poorer 3-month outcome, with multivariate odds ratios of 4.5 (p = 0.01) and 3.2 (p = 0.03), respectively, after adjusting for head CT findings and demographic, clinical, and socioeconomic factors.In this prospective multicenter observational study, the clinical relevance of abnormal findings on early brain imaging after MTBI is demonstrated. The addition of early CT and MRI markers to a prognostic model based on previously known demographic, clinical, and socioeconomic predictors resulted in a >2-fold increase in the explained variance in 3-month GOS-E.Copyright © 2012 American Neurological Association.

Background: Only in 7–15% of patients with mild traumatic brain injury (mTBI), traumatic CT-abnormalities are found. Nevertheless, 40% of mTBI patients suffer from posttraumatic complaints not resolving after 6 months. We discuss the ability of susceptibility-weighted imaging (SWI), sensitive for microbleeds, to detect more subtle brain abnormalities. Summary: After a search on PubMed, we selected 15 studies on SWI in adult mTBI patients; 11 studies on 3T MRI, and 4 studies on 1.5T MRI. All 1.5T studies showed that, compared to T2, gradient echo, diffusion-weighted imaging, or fluid-attenuated inversion recovery sequences, SWI is more sensitive for microbleeds. Only two 1.5T studies described the association between SWI findings and outcome. In 3 of the 4 studies, no control group was present. The mean number of microbleeds varied from 3.2 to 6.4 per patient. In the 3T studies, the percentage of patients with traumatic microbleeds varied from 5.7 to 28.8%, compared to 0–13.3% in normal controls. Microbleeds were particularly located subcortical or juxtacortical. The number of microbleeds in mTBI varied from 1 to 10 per patient. mTBI patients with microbleeds appeared to have higher symptom severity at 12 months and perform worse on tests of psychomotor speed and speed of information processing after 3 and 12 months, compared to mTBI patients without microbleeds. Key Messages: There is some evidence that traumatic microbleeds predict cognitive outcome and persistent posttraumatic complaints in patients with mTBI.

Mild traumatic brain injury (mTBI), frequently referred to as concussion, is one of the most common neurological disorders. The underlying neural mechanisms of functional disturbances in the brains of concussed individuals remain elusive. Novel forms of brain imaging have been developed to assess patients postconcussion, including functional magnetic resonance imaging (fMRI), susceptibility-weighted imaging (SWI), diffusion MRI (dMRI), and perfusion MRI [arterial spin labeling (ASL)], but results have been mixed with a more common utilization in the research environment and a slower integration into the clinical setting. In this review, the benefits and drawbacks of the methods are described: fMRI is an effective method in the diagnosis of concussion but it is expensive and time-consuming making it difficult for regular use in everyday practice; SWI allows detection of microhemorrhages in acute and chronic phases of concussion; dMRI is primarily used for the detection of white matter abnormalities, especially axonal injury, specific for mTBI; and ASL is an alternative to the BOLD method with its ability to track cerebral blood flow alterations. Thus, the absence of a universal diagnostic neuroimaging method suggests a need for the adoption of a multimodal approach to the neuroimaging of mTBI. Taken together, these methods, with their underlying functional and structural features, can contribute from different angles to a deeper understanding of mTBI mechanisms such that a comprehensive diagnosis of mTBI becomes feasible for the clinician.© 2021 The Authors. Human Brain Mapping published by Wiley Periodicals LLC.

Mild traumatic brain injury (mTBI) is neurological impairment induced by biomechanical forces without structural brain damage, currently without an objective diagnostic tool. Downstream injury stems from oxidative damage leading to the production of neurotoxic aldehydes. A collagen-based 3D corticomimetic in vitro model of concussion was developed, confirming aldehyde production following impact. Total aldehyde levels were mapped in vivo following mTBI using a novel CEST-MRI contrast agent, ProxyNA, in a new model of closed-head, awake, single-impact concussion in aged and young mice with aldehyde dehydrogenase 2 (ALDH2) deficiency. ProxyNA-MRI was performed before impact, and on days two- and seven- post-impact. MRI signal enhancement significantly increased at two days post-injury prior to astrocyte activation at seven days post-injury. The data suggest that advanced age and ALDH2 deficiency contribute to increased aldehydic load following mTBI. Overall, ProxyNA was capable of mapping concussion-associated aldehydes, supporting its application as an objective diagnostic tool for concussion.© 2025. The Author(s).

According to the US Defense and Veterans Brain Injury Center (DVBIC) and Centers for Disease Control and Prevention (CDC), mild traumatic brain injury (mTBI) is a common form of head injury. Medical imaging data provides clinical insight into tissue damage/injury and injury severity, and helps medical diagnosis. Computational modeling and simulation can predict the biomechanical characteristics of such injury, and are useful for development of protective equipment. Integration of techniques from computational biomechanics with medical data assessment modalities (e.g., magnetic resonance imaging or MRI) has not yet been used to predict injury, support early medical diagnosis, or assess effectiveness of personal protective equipment. This paper presents a methodology to map computational simulations with clinical data for interpreting blunt impact TBI utilizing two clinically different head injury case studies. MRI modalities, such as T1, T2, diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC), were used for simulation comparisons. The two clinical cases have been reconstructed using finite element analysis to predict head biomechanics based on medical reports documented by a clinician. The findings are mapped to simulation results using image-based clinical analyses of head impact injuries, and modalities that could capture simulation results have been identified. In case 1, the MRI results showed lesions in the brain with skull indentation, while case 2 had lesions in both coup and contrecoup sides with no skull deformation. Simulation data analyses show that different biomechanical measures and thresholds are needed to explain different blunt impact injury modalities; specifically, strain rate threshold corresponds well with brain injury with skull indentation, while minimum pressure threshold corresponds well with coup–contrecoup injury; and DWI has been found to be the most appropriate modality for MRI data interpretation. As the findings from these two cases are substantiated with additional clinical studies, this methodology can be broadly applied as a tool to support injury assessment in head trauma events and to improve countermeasures (e.g., diagnostics and protective equipment design) to mitigate these injuries.

背景：既往尚无新生儿化脓性脑膜炎在不同颅脑并发症下ADC值的纵向变化研究。目的：回顾性总结新生儿化脓性脑膜炎在发病后不同病程阶段的头颅MR表现，在髓鞘化过程中分析不同颅脑并发症下脑组织ADC值随病程的变化规律。设计：病例对照研究。方法：以足月新生儿化脓性脑膜炎并行头颅MR检查者为病例组，基于颅脑并发症中有无脑实质损伤灶和脑积水分为病例1组（无脑实质损伤灶和脑积水）、病例2组（有脑实质损伤灶，无脑积水）、病例3组（有脑积水无脑实质损伤灶）和病例4组（有脑实质损伤灶和脑积水）。以发病至头颅MR检查间隔时间0~7 d、~28 d、~60 d和~120 d分为病程A~D组；根据MR检查时患儿日龄，病程A组分为A1组（0~14 d）和A2组（~28 d），病程B组分为B1组（~28 d）和B2组（~60 d）。与病例组同期因其他疾病在同院行常规头颅MR且未观察到异常病变的儿童为对照组。主要结局指标：相同日龄或相同病程下MR评估新生儿化脓性脑膜炎脑实质ADC值变化趋势。结果：173例新生儿化脓性脑膜炎进入本文分析，病例组MR检查302例次，病程A~D组有241例次MR检查的ADC值进入本文分析；对照组20例。随着日龄的增加，对照组和病例组ADC值均呈降低趋势。不同病程(相同日龄)比较结果中，大脑皮层、深部白质在各个病程中，病例1~3组和对照组ADC值差异均无统计学意义（胼胝体压部的部分病程除外）；皮层下白质在病程0~60 d中，病例2和3组ADC值明显低于对照组，病例3组及部分病程中病例2组ADC值明显低于病例1组，皮层下白质在病程61~120 d中，病例2、3组和对照组ADC值差异无统计学意义，病例1组(除外顶叶白质)ADC值明显高于对照组；深部灰质核团在病程0~30 d中，病例1~3组ADC值明显低于对照组，在病程31~120 d中，病例1~3组和对照组ADC值差异均无统计学意义。结论：在新生儿化脓性脑膜炎患儿，皮层下白质在病程1~2个月ADC值降低，病程3~4个月时ADC值正常或升高，提示髓鞘化进程受阻；深部灰质核团ADC值在病程1个月内降低，而病程2~4个月时恢复正常。MR DWI定量ADC值有助于对无脑结构损伤的新生儿脑膜炎微观损伤的评估。

\n Diffusion tensor imaging (DTI) literature on single-center studies contains conflicting results regarding acute effects of mild traumatic brain injury (mTBI) on white matter (WM) microstructure and the prognostic significance. This larger-scale multi-center DTI study aimed to determine how acute mTBI affects WM microstructure over time and how early WM changes affect long-term outcome. From Transforming Research and Clinical Knowledge in Traumatic Brain Injury (TRACK-TBI), a cohort study at 11 United States level 1 trauma centers, a total of 391 patients with acute mTBI ages 17 to 60 years were included and studied at two weeks and six months post-injury. Demographically matched friends or family of the participants were the control group (\n n\n  = 148). Axial diffusivity (AD), fractional anisotropy (FA), mean diffusivity (MD), and radial diffusivity (RD) were the measures of WM microstructure. The primary outcome was the Glasgow Outcome Scale Extended (GOSE) score of injury-related functional limitations across broad life domains at six months post-injury. The AD, MD, and RD were higher and FA was lower in mTBI versus friend control (FC) at both two weeks and six months post-injury throughout most major WM tracts of the cerebral hemispheres. In the mTBI group, AD and, to a lesser extent, MD decreased in WM from two weeks to six months post-injury. At two weeks post-injury, global WM AD and MD were both independently associated with six-month incomplete recovery (GOSE <8 vs = 8) even after accounting for demographic, clinical, and other imaging factors. DTI provides reliable imaging biomarkers of dynamic WM microstructural changes after mTBI that have utility for patient selection and treatment response in clinical trials. Continued technological advances in the sensitivity, specificity, and precision of diffusion magnetic resonance imaging hold promise for routine clinical application in mTBI.\n

A magnetic resonance imaging method is presented for quantifying the degree to which water diffusion in biologic tissues is non-Gaussian. Since tissue structure is responsible for the deviation of water diffusion from the Gaussian behavior typically observed in homogeneous solutions, this method provides a specific measure of tissue structure, such as cellular compartments and membranes. The method is an extension of conventional diffusion-weighted imaging that requires the use of somewhat higher b values and a modified image postprocessing procedure. In addition to the diffusion coefficient, the method provides an estimate for the excess kurtosis of the diffusion displacement probability distribution, which is a dimensionless metric of the departure from a Gaussian form. From the study of six healthy adult subjects, the excess diffusional kurtosis is found to be significantly higher in white matter than in gray matter, reflecting the structural differences between these two types of cerebral tissues. Diffusional kurtosis imaging is related to q-space imaging methods, but is less demanding in terms of imaging time, hardware requirements, and postprocessing effort. It may be useful for assessing tissue structure abnormalities associated with a variety of neuropathologies.

Conventional imaging is unable to detect damage that accounts for permanent cognitive impairment in patients with mild traumatic brain injury (mTBI). While diffusion tensor imaging (DTI) can help to detect diffuse axonal injury (DAI), it is a limited indicator of tissue complexity. It has also been suggested that the thalamus may play an important role in the development of clinical sequelae in mTBI. The purpose of this study was to determine if diffusional kurtosis imaging (DKI), a novel quantitative magnetic resonance imaging (MRI) technique, can provide early detection of damage in the thalamus and white matter (WM) of mTBI patients, and can help ascertain if thalamic injury is associated with cognitive impairment. Twenty-two mTBI patients and 14 controls underwent MRI and neuropsychological testing. Mean kurtosis (MK), fractional anisotropy (FA), and mean diffusivity (MD) were measured in the thalamus and several WM regions classically identified with DAI. Compared to controls, patients examined within 1 year after injury exhibited variously altered DTI- and DKI-derived measures in the thalamus and the internal capsule, while in addition to these regions, patients examined more than 1 year after injury also showed similar differences in the splenium of the corpus callosum and the centrum semiovale. Cognitive impairment was correlated with MK in the thalamus and the internal capsule. These findings suggest that combined use of DTI and DKI provides a more sensitive tool for identifying brain injury. In addition, MK in the thalamus might be useful for early prediction of permanent brain damage and cognitive outcome.

Traumatic brain injury (TBI) is one of the highest public health priorities, especially among military personnel where comorbidity with post-traumatic stress symptoms and resulting consequences is high. Brain injury and post-traumatic stress symptoms are both characterized by dysfunctional brain networks, with the amygdala specifically implicated as a region with both structural and functional abnormalities.

Mild traumatic brain injuries (mTBIs) are the most common form of acquired brain injury. Symptoms of mTBI are thought to be associated with a neuropathological cascade, potentially involving the dysregulation of neurometabolites, lipids, and mitochondrial bioenergetics. Such alterations may play a role in the period of enhanced vulnerability that occurs after mTBI, such that a second mTBI will exacerbate neuropathology. However, it is unclear whether mTBI-induced alterations in neurometabolites and lipids that are involved in energy metabolism and other important cellular functions are exacerbated by repeat mTBI, and if such alterations are associated with mitochondrial dysfunction.

Various cognitive disorders have been reported for mild traumatic brain injury (mTBI) patients during the acute stage. This acute stage provides an opportunity for clinicians to optimize treatment protocols, which are based on the evaluation of brain structural connectivity. So far, most brain functional magnetic resonance imaging studies are focused on moderate to severe traumatic brain injuries (TBIs). In this study, we prospectively collected resting state data on 50 mTBI within 3 days of injury and 50 healthy volunteers and analyzed them using Amplitude of low-frequency fluctuation (ALFF), Regional Homogeneity (ReHo), graph theory methods and behavior measure, to explore the dysfunctional brain regions in acute mTBI. In our study, a total of 50 patients suffering <3 days mTBI and 50 healthy subjects were tested in rs-fMRI, as well as under neuropsychological examinations including the Wechsler Intelligence Scale and Stroop Color and Word Test. The correlation analysis was conducted between graph theoretic parameters and neuropsychological results. For the mTBI group, the ReHo of the inferior temporal gyrus and the cerebellum superior are significantly lower than in the control group, and the ALFF of the left insula, the cerebellum inferior, and the middle occipital gyrus were significantly higher than in the control group, which implies the dysfunctionality usually observed in Parkinson's disease. Executive function disorder was significantly correlated with the global efficiencies of the dorsolateral superior frontal gyrus and the anterior cingulate cortex, which is consistent with the literature: the acute mTBI patients demonstrate abnormality in terms of motor speed, association, information processing speed, attention, and short-term memory function. Correlation analysis between the neuropsychological outcomes and the network efficiency for the mTBI group indicates that executive dysfunction might be caused by local brain changes. Our data support the idea that the cerebral internal network has compensatory reactions in response to sudden pathological and neurophysiological changes. In the future, multimode rs-fMRI analysis could be a valuable tool for evaluating dysfunctional brain regions after mTBI.

Neuroimaging is being increasingly applied to the study of paediatric mild traumatic brain injury (mTBI) to uncover the neurobiological correlates of delayed recovery post-injury. The aims of this systematic review were to: (i) evaluate the neuroimaging research investigating neuropathology post-mTBI in children and adolescents from 0-18 years, (ii) assess the relationship between advanced neuroimaging abnormalities and PCS in children, (iii) assess the quality of the evidence by evaluating study methodology and reporting against best practice guidelines, and (iv) provide directions for future research. A literature search of MEDLINE, PsycINFO, EMBASE, and PubMed was conducted. Abstracts and titles were screened, followed by full review of remaining articles where specific eligibility criteria were applied. This systematic review identified 58 imaging studies which met criteria. Based on several factors including methodological heterogeneity and relatively small sample sizes, the literature currently provides insufficient evidence to draw meaningful conclusions about the relationship between MRI findings and clinical outcomes. Future research is needed which incorporates prospective, longitudinal designs, minimises potential confounds and utilises multimodal imaging techniques.Copyright © 2020 Elsevier Ltd. All rights reserved.

The insula is an important part of the posttraumatic headache (PTH) attributed to mild traumatic brain injury (mTBI) neuropathological activity pattern. It is composed of functionally different subdivisions and each of which plays different role in PTH neuropathology.Ninety-four mTBI patients were included in this study. Based on perfusion imaging data obtained from arterial spin labelling (ASL) perfusion magnetic resonance imaging (MRI), this study evaluated the insular subregion perfusion-based functional connectivity (FC) and its correlation with clinical characteristic parameters in patients with PTH after mTBI and non-headache mTBI patients.The insular subregions of mTBI + PTH (mTBI patients with PTH) and mTBI-PTH (mTBI patients without PTH) group had positive perfusion-based functional connections with other insular nuclei and adjacent discrete cortical regions. Compared with mTBI-PTH group, significantly increased resting-state perfusion-based FC between the anterior insula (AI) and middle cingulate cortex (MCC)/Rolandic operculum (ROL), between posterior insula (PI) and supplementary motor area (SMA), and decreased perfusion-based FC between PI and thalamus were found in mTBI + PTH group. Changes in the perfusion-based FC of the left posterior insula/dorsal anterior insula with the thalamus/MCC were significant correlated with headache characteristics.Our findings provide new ASL-based evidence for changes in the perfusion-based FC of the insular subregion in PTH patients attributed to mTBI and the association with headache features, revealing the possibility of potential neuroplasticity after PTH. These findings may contribute to early diagnosis of the disease and follow-up of disease progression.© 2024. The Author(s).

Traumatic brain injury (TBI) causes neuroinflammation and can lead to long-term neurological dysfunction, even in cases of mild TBI (mTBI). Despite the substantial burden of this disease, the management of TBI is precluded by an incomplete understanding of its cellular mechanisms. Sphingolipids (SPL) and their metabolites have emerged as key orchestrators of biological processes related to tissue injury, neuroinflammation, and inflammation resolution. No study so far has investigated comprehensive sphingolipid profile changes immediately following TBI in animal models or human cases. In this study, sphingolipid metabolite composition was examined during the acute phases in brain tissue and plasma of mice following mTBI.Wildtype mice were exposed to air-blast-mediated mTBI, with blast exposure set at 50-psi on the left cranium and 0-psi designated as Sham. Sphingolipid profile was analyzed in brain tissue and plasma during the acute phases of 1, 3, and 7 days post-TBI via liquid-chromatography-mass spectrometry. Simultaneously, gene expression of sphingolipid metabolic markers within brain tissue was analyzed using quantitative reverse transcription-polymerase chain reaction. Significance (P-values) was determined by non-parametric t-test (Mann-Whitney test) and by Tukey's correction for multiple comparisons.In post-TBI brain tissue, there was a significant elevation of 1) acid sphingomyelinase (aSMase) at 1- and 3-days, 2) neutral sphingomyelinase (nSMase) at 7-days, 3) ceramide-1-phosphate levels at 1 day, and 4) monohexosylceramide (MHC) and sphingosine at 7-days. Among individual species, the study found an increase in C18:0 and a decrease in C24:1 ceramides (Cer) at 1 day; an increase in C20:0 MHC at 3 days; decrease in MHC C18:0 and increase in MHC C24:1, sphingomyelins (SM) C18:0, and C24:0 at 7 days. Moreover, many sphingolipid metabolic genes were elevated at 1 day, followed by a reduction at 3 days and an absence at 7-days post-TBI. In post-TBI plasma, there was 1) a significant reduction in Cer and MHC C22:0, and an increase in MHC C16:0 at 1 day; 2) a very significant increase in long-chain Cer C24:1 accompanied by significant decreases in Cer C24:0 and C22:0 in MHC and SM at 3 days; and 3) a significant increase of C22:0 in all classes of SPL (Cer, MHC and SM) as well as a decrease in Cer C24:1, MHC C24:1 and MHC C24:0 at 7 days.Alterations in sphingolipid metabolite composition, particularly sphingomyelinases and short-chain ceramides, may contribute to the induction and regulation of neuroinflammatory events in the early stages of TBI, suggesting potential targets for novel diagnostic, prognostic, and therapeutic strategies in the future.© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.

Traumatic brain injury (TBI) is associated with persistent functional and cognitive deficits, which may be susceptible to secondary insults. The implications of exposure to surgery and anesthesia after TBI warrant investigation, given that surgery has been associated with neurocognitive disorders.