Traumatic Brain Injury (TBI) continues to be one of the leading causes of death and disability in the pediatric population. Although the literature on neurocognitive outcomes is relatively rich, studies vary significantly in the methods used to group subjects on several moderating variables, including age at injury, injury severity, and time since injury, making it difficult to combine and summarize the data for comparison. Further complicating this effort is the wide range of measures used to document functional outcomes in key neurocognitive domains. In this meta-analytic review, 28 publications (1988 to 2007) that met inclusion criteria were summarized based on three distinct injury severity and time post injury groups for 14 key neurocognitive domains. Effect sizes were calculated to reflect the extent to which the above groups differed in case-control and case-case studies, as well as address recovery based on longitudinal studies. To the best of our knowledge, this is the first published quantitative summary of the literature on neurocognitive outcomes after pediatric TBI. Limitations of the current state of the literature as well as recommendations for future studies are discussed.

Traumatic Brain Injury (TBI) in children, while the brain is in a state of rapid change and development, can adversely impact their development, their extended environment, and their families. The extant literature has identified several physiological, genetic, and environmental variables that predict outcomes following pediatric TBI; nonetheless, the individual course of recovery and later development of a given child is uniquely shaped by injury-related factors (e.g., nature and extent of the injury itself, the developmental status of the child) as well as a number of personal and family variables (e.g., pre-injury cognitive, genetic, and psychological status of the child, family functioning and resources, coping style). Furthermore, the effects of a brain injury during development may or may not become evident immediately after injury depending on a number of factors. Instead, observing trajectories of development over time may allow for a better understanding of the long-term consequences in many functional domains that interest researchers, clinicians, and families. The current paper reviews the chronic aspects of medical/health, cognitive/academic, emotional/behavioral, and family/social outcomes following pediatric TBI, with the goal of providing monitoring and treatment strategies for affected children and their families, as well as serving as a resource for researchers designing studies to better understand this heterogeneous population.

Comprehensive reviews of neurocognitive outcomes following mild, uncomplicated traumatic brain injury (TBI) in children have shown minimal effects on neurocognition, especially in methodologically rigorous studies. In this study, we report longitudinal (1, 6, and 12 months post injury) results in four domains of neurocognitive functioning in a large sample of children with mild TBI (n = 124, ages 8–17 at injury) relative to two demographically matched control groups (other injury: n = 94 and non-injury: n = 106). After accounting for age and parental education, significant main effects of group were observed on 7 of the 10 neurocognitive tests. However, these differences were not unique to the TBI sample but were found between both the TBI and other injury groups relative to the non-injured group, suggesting a general injury effect. Effects were primarily within the domains measuring memory, psychomotor processing speed, and language. This is the largest longitudinal study to date of neurocognitive outcomes at discrete time points in pediatric mild TBI. When controlling for pre-injury factors, there is no evidence of long-term neurocognitive impairment in this group relative to another injury control group. The importance of longitudinal analyses and use of appropriate control groups are discussed in the context of evaluating the effects of mild TBI on cognition. (JINS, 2011, 17, 886–895)

Although more severe brain injuries have long been associated with persisting neurocognitive deficits, an increasing body of literature has shown that children/adolescents with single, uncomplicated mild traumatic brain injury (mTBI) do not exhibitlong-lastingneurocognitive impairments. Nonetheless, clinical experience and our previous report (Babikian, 2011) showed that a minority of children/adolescents exhibit persistent cognitive problems using performance based measures following what appear to be relatively mild injuries. Predictors of poor neurocognitive outcomes were evaluated in 76 mTBI and 79 Other Injury subjects to determine the relative contributions of indices of injury severity, clinical symptomatology, demographic factors, and premorbid functioning in predicting 1-month and 12-month neurocognitive impairment on computerized or paper and pencil measures. Injury severity indicators or type of injury (headvs.other body part) did not predict either 1-month or 12-month cognitive impairment status. Rather, premorbid variables that antedated the injury (parental education, premorbid behavior and/or learning problems, and school achievement) predicted cognitive impairments. When post-injury neurocognitive impairments are observed in survivors of mild injuries (head or other body part), a sound understanding of their etiology is critical in designing appropriate intervention plans. Clinical and research implications are discussed. (JINS, 2012,18, 1–10)

Diffuse axonal injury (DAI) secondary to traumatic brain injury (TBI) contributes to long-term functional morbidity. The corpus callosum (CC) is particularly vulnerable to this type of injury. Magnetic resonance spectroscopy (MRS) was used to characterize the metabolic status of two CC regions of interest (ROIs) (anterior and posterior), and their structural (diffusion tensor imaging; DTI) and neurobehavioral (neurocognitive functioning, bimanual coordination, and interhemispheric transfer time [IHTT]) correlates. Two groups of moderate/severe TBI patients (ages 12–18 years) were studied: post-acute (5 months post-injury; n = 10), and chronic (14.7 months post-injury; n = 8), in addition to 10 age-matched healthy controls. Creatine (energy metabolism) did not differ between groups across both ROIs and time points. In the TBI group, choline (membrane degeneration/inflammation) was elevated for both ROIs at the post-acute but not chronic period. N-acetyl aspartate (NAA) (neuronal/axonal integrity) was reduced initially for both ROIs, with partial normalization at the chronic time point. Posterior, not anterior, NAA was positively correlated with DTI fractional anisotropy (FA) (r = 0.88), and most domains of neurocognition (r range 0.22–0.65), and negatively correlated with IHTT (r = −0.89). Inverse corerlations were noted between creatine and posterior FA (r = −0.76), neurocognition (r range −0.22 to −0.71), and IHTT (r = 0.76). Multimodal studies at distinct time points in specific brain structures are necessary to delineate the course of the degenerative and reparative processes following TBI, which allows for preliminary hypotheses about the nature and course of the neural mechanisms of subsequent functional morbidity. This will help guide the future development of targeted therapeutic agents.