Variables associated with subjective cognitive change among Iraq and Afghanistan war Veterans with blast-related mild traumatic brain injury

Introduction: This study investigated variables associated with subjective decline in executive function among Veterans of Operations Enduring Freedom, Iraqi Freedom, and New Dawn (OEF/OIF/OND) following a history of blast-related mild traumatic brain injury (mTBI).

Method: Fifty-six male U.S. Veterans (M_Age = 35.3 ± 8.8 years) with a history of blast-related mTBI (6.6 ± 3.2 years post injury) completed a battery of self-report questionnaires and neuropsychological measures. Participants rated current and retrospectively estimated pre-mTBI executive function difficulties on the Frontal Systems Behavior Scale (FrSBe). A difference score (post- minus pre-mTBI ratings) was the dependent variable (?FrSBe). Linear regression models examined variables predicting ?FrSBe, including: pre-injury characteristics (education, premorbid intelligence), injury-related characteristics (number of blast exposures, losses of consciousness), post-injury clinical symptoms (PTSD Checklist–Military version; Pittsburgh Sleep Quality Index), and post-injury neuropsychological performances on executive function measures (Trail Making Test Part B; Controlled Oral Word Association Test; Auditory Consonant Trigrams; Wisconsin Card Sorting Test).

Results: While 11% of participants had a clinically elevated pre-injury FrSBe total score, 82% had a clinically elevated post-injury FrSBe total score. Only self-reported PTSD symptom severity independently predicted perceived change in executive function.

Conclusions: Many OEF/OIF/OND Veterans with a history of blast-related mTBI experience subjective decline in executive function following injury. Perceived executive function decline was associated with higher PTSD symptom severity, aligning with previous research associating PTSD with cognitive complaints. Results did not support a correspondence between perceived cognitive change and neuropsychological performances.     

Longitudinal white matter microstructural changes in pediatric mild traumatic brain injury: An A‐CAP study

In the largest sample studied to date, white matter microstructural trajectories and their relation to persistent symptoms were examined after pediatric mild traumatic brain injury (mTBI). This prospective, longitudinal cohort study recruited children aged 8–16.99 years with mTBI or mild orthopedic injury (OI) from five pediatric emergency departments. Children''s pre‐injury and 1‐month post‐injury symptom ratings were used to classify mTBI with or without persistent symptoms. Children completed diffusion‐weighted imaging at post‐acute (2–33 days post‐injury) and chronic (3 or 6 months via random assignment) post‐injury assessments. Mean diffusivity (MD) and fractional anisotropy (FA) were derived for 18 white matter tracts in 560 children (362 mTBI/198 OI), 407 with longitudinal data. Superior longitudinal fasciculus FA was higher in mTBI without persistent symptoms relative to OI, d (95% confidence interval) = 0.31 to 0.37 (0.02, 0.68), across time. In younger children, MD of the anterior thalamic radiations was higher in mTBI with persistent symptoms relative to both mTBI without persistent symptoms, 1.43 (0.59, 2.27), and OI, 1.94 (1.07, 2.81). MD of the arcuate fasciculus, −0.58 (−1.04, −0.11), and superior longitudinal fasciculus, −0.49 (−0.90, −0.09) was lower in mTBI without persistent symptoms relative to OI at 6 months post‐injury. White matter microstructural changes suggesting neuroinflammation and axonal swelling occurred chronically and continued 6 months post injury in children with mTBI, especially in younger children with persistent symptoms, relative to OI. White matter microstructure appears more organized in children without persistent symptoms, consistent with their better clinical outcomes.     

Ethyl pyruvate improves white matter remodeling in rats after traumatic brain injury

BackgroundSevere traumatic brain injury (TBI) results in long‐term neurological deficits associated with white matter injury (WMI). Ethyl pyruvate (EP) is a simple derivative of the endogenous energy substrate pyruvate with neuroprotective properties, but its role in recovery from WMI has not been explored.AimsThis study examines the effect of EP treatment on rats following TBI using behavioral tests and white matter histological analysis up to 28 days post‐injury.Materials and MethodsAnaesthetised adult rats were subjected to TBI by controlled cortical impact. After surgery, EP or Ringers solution (RS) was administrated intraperitoneally at 15 min after TBI and again at 12, 24, 36, 48, and 60 h after TBI. Sensorimotor deficits were evaluated up to day 21 after TBI by four independent tests. Immunofluorescence and transmission electron microscopy (TEM) were performed to assess white matter injury. Microglia activation and related inflammatory molecules were examined up to day 14 after TBI by immunohistochemistry or real‐time PCR.ResultsHere, we demonstrate that EP improves sensorimotor function following TBI as well as improves white matter outcomes up to 28 d after TBI, as shown by reduced myelin loss. Furthermore, EP administration during the acute phase of TBI recovery shifted microglia polarization toward the anti‐inflammatoryM2 phenotype, modulating the release of inflammatory‐related factors.ConclusionEP treatment may protect TBI‐induced WMI via modulating microglia polarization toward M2.     

Examining the relationship between blast‐induced mild traumatic brain injury and posttraumatic stress‐related traits

Emerging evidence suggests that mild traumatic brain injury (mTBI) resulting from blast exposure may contribute to the occurrence of posttraumatic stress disorder (PTSD) and related affective sequelae, such as anxiety and depression. Many studies have used survey techniques to describe blast exposure leading to comorbid mTBI and related persistent postconcussive symptoms (PPCS) with PTSD in military populations. Despite this, there is a lack of literature that examines possible biological mechanisms by which blast exposure contributes to the development of PTSD sequelae. This Mini‐Review addresses the current literature on potential neurophysiological changes that may contribute to PTSD‐like traits as a result of a single or multiple exposures to blast events. Evidence from clinical blast‐induced mTBI populations and animal models of blast‐induced mTBI was evaluated with an emphasis on behavioral and physiological symptoms similar to those seen in PTSD populations and models. From the analysis, we propose potential mechanisms that merit further investigation for better understanding of how blast exposures may produce a higher rate of comorbid PPCS, PTSD, and affective phenomena. An improved understanding of PTSD‐like outcomes resulting from blast exposure will ultimately help facilitate the development of future treatments and contribute to a better understanding of PTSD sequelae that develop from physical trauma. © 2015 Wiley Periodicals, Inc.     

Gliovascular changes precede white matter damage and long‐term disorders in juvenile mild closed head injury

Traumatic brain injury (TBI) is a leading cause of hospital visits in pediatric patients and often leads to long‐term disorders even in cases of mild severity. White matter (WM) alterations are commonly observed in patients months or years after the injury assessed by magnetic resonance imaging (MRI), but little is known about WM pathophysiology early after mild pediatric TBI. To evaluate the status of the gliovascular unit in this context, mild TBI was induced in postnatal‐day 17 mice using a closed head injury model with two grades of severity (G1, G2). G2 resulted in significant WM edema (increased T2‐signal) and BBB damage (IgG‐extravasation immunostaining) whereas decreased T2 and the increased levels of astrocytic water‐channel AQP4 were observed in G1 mice 1 day post‐injury. Both severities induced astrogliosis (GFAP immunolabeling). No changes in myelin and neurofilament were detected at this acute time point. One month after injury G2 mice exhibited diffusion tensor imaging MRI alterations (decreased fractional anisotropy) accompanied by decreased neurofilament staining in the WM. Both severities induced behavioral impairments at this time point. In conclusion, long‐term deficits and WM changes similar to those found after clinical TBI are preceded by distinct early gliovascular phenotype alterations after juvenile mild TBI, revealing AQP4 as a potential candidate for severity‐based treatments.     

Diffusion tensor imaging and white matter lesions at the subacute stage in mild traumatic brain injury with persistent neurobehavioral impairment

Mild traumatic brain injury (mTBI) can induce long‐term behavioral and cognitive disorders. Although the exact origin of these mTBI‐related disorders is not known, they may be the consequence of diffuse axonal injury (DAI). Here, we investigated whether MRI at the subacute stage can detect lesions that are associated with poor functional outcome in mTBI by using anatomical images (T₁) and diffusion tensor imaging (DTI). Twenty‐three patients with mTBI were investigated and compared with 23 healthy volunteers. All patients underwent an MRI investigation and clinical tests between 7 and 28 days (D15) and between 3 and 4 months (M3) after injury. Patients were divided in two groups of poor outcome (PO) and good outcome (GO), based on their complaints at M3. Groupwise differences in gray matter partial volume between PO patients, GO patients and controls were analyzed using Voxel‐Based Morphometry (VBM) from T₁ data at D15. Differences in microstructural architecture were investigated using Tract‐Based Spatial Statistics (TBSS) and the diffusion images obtained from DTI data at D15. Permutation‐based non‐parametric testing was used to assess cluster significance at p < 0.05, corrected for multiple comparisons. Twelve GO patients and 11 PO patients were identified on the basis of their complaints. In PO patients, gray matter partial volume was significantly lower in several cortical and subcortical regions compared with controls, but did not differ from that of GO patients. No difference in diffusion variables was found between GO and controls. PO patients showed significantly higher mean diffusivity values than both controls and GO patients in the corpus callosum, the right anterior thalamic radiations and the superior longitudinal fasciculus, the inferior longitudinal fasciculus and the fronto‐occipital fasciculus bilaterally. In conclusion, PO patients differed from GO patients by the presence of diffusion changes in long association white matter fiber tracts but not by gray matter partial volume. These results suggest that DTI at the subacute stage may be a predictive marker of poor outcome in mTBI. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.     

Structural connectome differences in pediatric mild traumatic brain and orthopedic injury

Sophisticated network‐based approaches such as structural connectomics may help to detect a biomarker of mild traumatic brain injury (mTBI) in children. This study compared the structural connectome of children with mTBI or mild orthopedic injury (OI) to that of typically developing (TD) children. Children aged 8–16.99 years with mTBI (n = 83) or OI (n = 37) were recruited from the emergency department and completed 3T diffusion MRI 2–20 days postinjury. TD children (n = 39) were recruited from the community and completed diffusion MRI. Graph theory metrics were calculated for the binarized average fractional anisotropy among 90 regions. Multivariable linear regression and linear mixed effects models were used to compare groups, with covariates age, hemisphere, and sex, correcting for multiple comparisons. The two injury groups did not differ on graph theory metrics, but both differed from TD children in global metrics (local network efficiency: TD > OI, mTBI, d = 0.49; clustering coefficient: TD < OI, mTBI, d = 0.49) and regional metrics for the fusiform gyrus (lower degree centrality and nodal efficiency: TD > OI, mTBI, d = 0.80 to 0.96; characteristic path length: TD < OI, mTBI, d = −0.75 to −0.90) and in the superior and middle orbital frontal gyrus, paracentral lobule, insula, and thalamus (clustering coefficient: TD > OI, mTBI, d = 0.66 to 0.68). Both mTBI and OI demonstrated reduced global and regional network efficiency and segregation as compared to TD children. Findings suggest a general effect of childhood injury that could reflect pre‐ and postinjury factors that can alter brain structure. An OI group provides a more conservative comparison group than TD children for structural neuroimaging research in pediatric mTBI.     

Strategic white matter injury associated with long‐term information processing speed deficits in mild traumatic brain injury

Deficits in information processing speed (IPS) are among the earliest and most prominent cognitive manifestations in mild traumatic brain injury (mTBI). We investigated the impact of white matter fiber location on IPS outcome in an individual basis assessment. A total of 112 acute mild TBI with all CT negative underwent brain DTI and blood sampling for inflammation cytokines within 7 days postinjury and 72 age‐ and sex matched healthy controls with same assessments were enrolled. IPS outcome was assessed by the trail making test at 6–12 month postinjury in mild TBI. Fractional anisotropy (FA) features were extracted using a novel lesion‐load analytical strategy to capture spatially heterogeneous white matter injuries and minimize implicit assumptions of uniform injury across diverse clinical presentations. Acute mild TBI exhibited a general pattern of increased and decreased FA in specific white matter tracts. The power of acute FA measures to identify patients developing IPS deficits with 92% accuracy and further improved to 96% accuracy by adding inflammation cytokines. The classifiers predicted individual's IPS and working memory ratings (r = .74 and .80, respectively, p < .001). The thalamo‐cortical circuits and commissural tracts projecting or connecting frontal regions became important predictors. This prognostic model was also verified by an independent replicate sample. Our findings highlighted damage to frontal interhemispheric and thalamic projection fiber tracts harboring frontal‐subcortical neuronal circuits as a predictor for processing speed performance in mild TBI.     

Memory retrieval brain–behavior disconnection in mild traumatic brain injury: A magnetoencephalography and diffusion tensor imaging study

Mild traumatic brain (mTBI) injury is often associated with long‐term cognitive and behavioral complications, including an increased risk of memory impairment. Current research challenges include a lack of cross‐modal convergence regarding the underlying neural–behavioral mechanisms of mTBI, which hinders therapeutics and outcome management for this frequently under‐treated and vulnerable population. We used multi‐modality imaging methods including magnetoencephalography (MEG) and diffusion tensor imaging (DTI) to investigate brain–behavior impairment in mTBI related to working memory. A total of 41 participants were recruited, including 23 patients with a first‐time mTBI imaged within 3 months of injury (all male, age = 29.9, SD = 6.9), and 18 control participants (all male, age = 27.3, SD = 5.3). Whole‐brain statistics revealed spatially concomitant functional–structural disruptions in brain–behavior interactions in working memory in the mTBI group compared with the control group. These disruptions are located in the hippocampal–prefrontal region and, additionally, in the amygdala (measured by MEG neural activation and DTI measures of fractional anisotropy in relation to working memory performance; p < .05, two‐way ANCOVA, nonparametric permutations, corrected). Impaired brain–behavior connections found in the hippocampal–prefrontal and amygdala circuits indicate brain dysregulation of memory, which may leave mTBI patients vulnerable to increased environmental demands exerting memory resources, leading to related cognitive and emotional psychopathologies. The findings yield clinical implications and highlight a need for early rehabilitation after mTBI, including attention‐ and sensory‐based behavioral exercises.     

Abnormalities of cortical thickness,subcortical shapes,and white matter integrity in subcortical vascular cognitive impairment

Subcortical vascular cognitive impairment (sVCI) is caused by lacunar infarcts or extensive and/or diffuse lesions in the white matter that may disrupt the white matter circuitry connecting cortical and subcortical regions and result in the degeneration of neurons in these regions. This study used structural magnetic resonance imaging (MRI) and high angular resolution diffusion imaging (HARDI) techniques to examine cortical thickness, subcortical shapes, and white matter integrity in mild vascular cognitive impairment no dementia (VCIND Mild) and moderate‐to‐severe VCI (MSVCI). Our study found that compared to controls (n = 25), VCIND Mild (n = 25), and MSVCI (n = 30) showed thinner cortex predominantly in the frontal cortex. The cortex in MSVCI was thinner in the parietal and lateral temporal cortices than that in VCIND Mild. Moreover, compared to controls, VCIND Mild and MSVCI showed smaller shapes (i.e., volume reduction) in the thalamus, putamen, and globus pallidus and ventricular enlargement. Finally, compared to controls, VCIND Mild, and MSVCI showed an increased mean diffusivity in the white matter, while decreased generalized fractional anisotropy was only found in the MSVCI subjects. The major axonal bundles involved in the white matter abnormalities were mainly toward the frontal regions, including the internal capsule/corona radiata, uncinate fasciculus, and anterior section of the inferior fronto‐occipital fasciculus, and were anatomically connected to the affected cortical and subcortical structures. Our findings suggest that abnormalities in cortical, subcortical, and white matter morphology in sVCI occur in anatomically connected structures, and that abnormalities progress along a similar trajectory from the mild to moderate and severe conditions. Hum Brain Mapp 35:2320–2332, 2014. © 2013 Wiley Periodicals, Inc .     

亚低温在治疗急性颅脑创伤中的疗效和争议

二十世纪90年代初,国内外对亚低温脑保护的作用有了新认识。动物实验研究发现亚低温对实验性颅脑外伤具有显著的治疗保护作用。大多数前瞻性临床应用研究发现30～33℃亚低温能显著降低重型颅脑伤患者的死残率。但美国Clifton教授牵头的9个医学中心合作研究发现亚低温治疗组与对照组无统计学差异.仅能显著提高GCS 6～8分、年龄<45岁、伤后6h内达到亚低温水平的病人的治疗效果。最近一项欧州5家医院多中心前瞻性随机临床研究结果令人兴奋,他们研究证明亚低温对心跳骤停脑缺血缺氧病人有显著治疗保护作用。目前国内外有关亚低温治疗的争议焦点是亚低温治疗的指征、时间窗和时程。     

Task switching in traumatic brain injury relates to cortico‐subcortical integrity

Suppressing and flexibly adapting actions are a critical part of our daily behavioral repertoire. Traumatic brain injury (TBI) patients show clear impairments in this type of action control; however, the underlying mechanisms are poorly understood. Here, we tested whether white matter integrity of cortico‐subcortical pathways could account for impairments in task switching, an important component of executive functioning. Twenty young adults with TBI and eighteen controls performed a switching task requiring attention to global versus local stimulus features. Diffusion weighted images were acquired and whole brain tract‐based spatial statistics (TBSS) were used to explore where white matter damage was associated with switching impairment. A crossing fiber model and probabilistic tractography further identified the specific fiber populations. Relative to controls, patients with a history of TBI had a higher switch cost and were less accurate. The TBI group showed a widespread decline in fractional anisotropy (FA) throughout the TBSS skeleton. FA in the superior corona radiata showed a negative relationship with switch cost. More specifically, this involved cortico‐subcortical loops with the (pre‐)supplementary motor area and superior frontal gyrus. These findings provide evidence for damage to frontal‐subcortical projections in TBI, which is associated with task switching impairments. Hum Brain Mapp 35:2459–2469, 2014. © 2013 Wiley Periodicals, Inc.     

Investigating the prevalence of complex fiber configurations in white matter tissue with diffusion magnetic resonance imaging

It has long been recognized that the diffusion tensor model is inappropriate to characterize complex fiber architecture, causing tensor‐derived measures such as the primary eigenvector and fractional anisotropy to be unreliable or misleading in these regions. There is however still debate about the impact of this problem in practice. A recent study using a Bayesian automatic relevance detection (ARD) multicompartment model suggested that a third of white matter (WM) voxels contain crossing fibers, a value that, whilst already significant, is likely to be an underestimate. The aim of this study is to provide more robust estimates of the proportion of affected voxels, the number of fiber orientations within each WM voxel, and the impact on tensor‐derived analyses, using large, high‐quality diffusion‐weighted data sets, with reconstruction parameters optimized specifically for this task. Two reconstruction algorithms were used: constrained spherical deconvolution (CSD), and the ARD method used in the previous study. We estimate the proportion of WM voxels containing crossing fibers to be ～90% (using CSD) and 63% (using ARD). Both these values are much higher than previously reported, strongly suggesting that the diffusion tensor model is inadequate in the vast majority of WM regions. This has serious implications for downstream processing applications that depend on this model, particularly tractography, and the interpretation of anisotropy and radial/axial diffusivity measures. Hum Brain Mapp 34:2747–2766, 2013. © 2012 Wiley Periodicals, Inc.     

亚低温对重型脑损伤后血清IL-18含量的影响

目的 观察重型创伤性脑损伤(TBI)患者血清白细胞介素18(IL-18)的含量变化.方法 60例患者随机分成常温治疗组和亚低温治疗组,两组均于伤后第1 d、3 d、7 d 和10d 采用酶联免疫吸附(ELISA)法测定血清中IL-18 含量.结果 两组IL-18 含量均高于对照组(P ＜ 0.01).亚低温治疗组IL-18 含量在3d、7 d、10d 低于常温治疗组(P ＜0.01),而在伤后第1 d 差异无统计学意义(P ＞0.05).结论 亚低温治疗能够降低sTBI 患者血清IL-18 含量.     

Postconcussional disorder and PTSD symptoms of military‐related traumatic brain injury associated with compromised neurocircuitry

Traumatic brain injury (TBI) is a common combat injury, often through explosive blast, and produces heterogeneous brain changes due to various mechanisms of injury. It is unclear whether the vulnerability of white matter differs between blast and impact injury, and the consequences of microstructural changes on neuropsychological function are poorly understood in military TBI patients. Diffusion tensor imaging (DTI) techniques were used to assess the neurocircuitry in 37 US service members (29 mild, 7 moderate, 1 severe; 17 blast and 20 nonblast), who sustained a TBI while deployed, compared to 14 nondeployed, military controls. High‐dimensional deformable registration of MRI diffusion tensor data was followed by fiber tracking and tract‐specific analysis along with region‐of‐interest analysis. DTI results were examined in relation to post‐concussion and post‐traumatic stress disorder (PTSD) symptoms. The most prominent white matter microstructural injury for both blast and nonblast patients was in the frontal fibers within the fronto‐striatal (corona radiata, internal capsule) and fronto‐limbic circuits (fornix, cingulum), the fronto‐parieto‐occipital association fibers, in brainstem fibers, and in callosal fibers. Subcortical superior‐inferiorly oriented tracts were more vulnerable to blast injury than nonblast injury, while direct impact force had more detrimental effects on anterior‐posteriorly oriented tracts, which tended to cause heterogeneous left and right hemispheric asymmetries of white matter connectivity. The tractography using diffusion anisotropy deficits revealed the cortico‐striatal‐thalamic‐cerebellar‐cortical (CSTCC) networks, where increased post‐concussion and PTSD symptoms were associated with low fractional anisotropy in the major nodes of compromised CSTCC neurocircuitry, and the consequences on cognitive function were explored as well. Hum Brain Mapp 35:2652–2673, 2014. © 2013 Wiley Periodicals, Inc .     

轻度认知功能障碍与脑白质弥散张量成像的相关性研究

目的通过磁共振弥散张量成像研究不同区域脑白质损害与轻度认知功能(MCI)的关系。方法纳入2015年7月至2016年2月我院的住院患者56例为研究对象,其中MCI组34例,认知功能正常组22例。所有研究对象进行一般情况检查,完成神经心理学量表检测。通过头颅磁共振弥散张量成像(DTI)检查对不同脑区白质纤维进行部分各向异性(FA)值测量。结果 MCI组患者与认知功能正常组相比,右侧额叶FA值(0.335±0.068)、左侧颞叶白质FA值(0.391±0.032)及胼胝体膝部FA值(0.658±0.053)降低,差异具有统计学意义(P0.05)。将上述FA值和MMSE、Mo CA量表中各认知域进行典型相关分析,结果显示右侧额叶白质FA值与注意与计算力呈正相关,左侧颞叶白质和胼胝体膝部FA值与记忆力呈正相关(P0.05)。结论 MCI患者注意与计算力的障碍可能与右侧额叶白质损害有关,而左侧颞叶白质及胼胝体膝部白质的损害可能导致早期的记忆障碍。DTI可能成为超早期识别与诊断MCI的新方法。     

MRI-based brain volumetry in chronic whiplash patients: no evidence for traumatic brain injury

Introduction –  Cognitive complaints, such as poor concentration and memory deficits, are frequent after whiplash injury and play an important role in disability. The origin of these complaints is discussed controversially. Some authors postulate brain lesions as a consequence of whiplash injuries. Potential diffuse axonal injury (DAI) with subsequent atrophy of the brain and ventricular expansion is of particular interest as focal brain lesions have not been documented so far in whiplash injury.
Objective –  To investigate whether traumatic brain injury can be identified using a magnetic resonance (MR)-based quantitative analysis of normalized ventricle–brain ratios (VBR) in chronic whiplash patients with subjective cognitive impairment that cannot be objectively confirmed by neuropsychological testing.
Materials and methods –  MR examination was performed in 21 patients with whiplash injury and symptom persistence for 9 months on average and in 18 matched healthy controls. Conventional MR imaging (MRI) was used to assess the volumes of grey and white matter and of ventricles. The normalized VBR was calculated.
Results –  The values of normalized VBR did not differ in whiplash patients when compared with that in healthy controls ( F  = 0.216, P  = 0.645).
Conclusions –  This study does not support loss of brain tissue following whiplash injury as measured by VBR. On this basis, traumatic brain injury with subsequent DAI does not seem to be the underlying mechanism for persistent concentration and memory deficits that are subjectively reported but not objectively verifiable as neuropsychological deficits.     

Postconcussion symptom reporting is not associated with diffusion tensor imaging findings in the subacute to chronic phase of recovery in military service members following mild traumatic brain injury

Introduction: The purpose of this study was to examine the relation between white matter integrity of the brain and postconcussion symptom reporting following mild traumatic brain injury (MTBI).

Method: Participants were 109 U.S. military service members (91.7% male) who had sustained a MTBI (n = 88) or orthopedic injury without TBI (trauma controls, TC, n = 21), enrolled from the Walter Reed National Military Medical Center, Bethesda, Maryland. Participants completed a battery of neurobehavioral symptom measures and underwent diffusion tensor imaging (DTI; General Electric 3T) of the whole brain, on average 44.9 months post injury (SD = 42.3). Measures of fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD) were generated for 18 regions of interest (ROIs). Participants in the MTBI group were divided into two subgroups based on International Classification of Diseases–10th Revision (ICD–10) Category C criteria for postconcussion syndrome (PCS): PCS-present (n = 41) and PCS-absent (n = 47).

Results: The PCS-present group had significantly worse scores on all 13 neurobehavioral measures than the PCS-absent group (p < .001, d = 0.87–2.50) and TC group (p < .003, d = 0.84–2.06). For all ROIs, there were no significant main effects across the three groups for FA, MD, AD, and RD (all ps >.03). Pairwise comparisons revealed no significant differences for all ROIs when using FA and RD, and only two significant pairwise differences were found between PCS-present and PCS-absent groups when using MD and AD [i.e., anterior thalamic radiation and cingulate gyrus (supracallosal) bundle].

Conclusions: Consistent with past research, but not all studies, postconcussion symptom reporting was not associated with white matter integrity in the subacute to chronic phase of recovery following MTBI.