Common short-term cognitive symptoms of pediatric brain injury, such as impaired attention, processing speed, visual perception, working memory, motor functioning, emotional lability, and hyperactivity, have been observed and documented by numerous studies over the years [7–9]. It appears that these symptoms may affect virtually all areas of functioning in children. For instance, in addition to having trouble sustaining focus, quickly and accurately processing new information, and retaining new facts, concussed children tend to have fewer friends and experience poor social skills and increased emotional lability [10–12]. Their family relationships may be compromised as well [13] and their academic performance is likely to decline [14, 15].

Moreover, Wozniak et al. [16] showed that traumatic injury to the white matter in the supracallosal region is specifically related to overt behavioral deficits, such as hyperactivity, aggression, and attention deficit. In this study, while children with mild and moderate brain injury did not differ from controls in general intelligence scores, their sustained focus and behavioral and emotional regulation were impaired when assessed 6–12 months after the brain injury. This finding is very important in the understanding of post-TBI functioning and performance, as it illustrates that, unlike the core intellectual abilities, which remain largely resilient to a mild white matter trauma, regulatory functions and efficiency skills are much more susceptible to impairment. This is a critical aspect of post-TBI life, as regulatory functions and efficiency skills are essential functions that allow one to utilize core intellectual abilities while completing academic tasks, listening to and following daily directions, and navigating social conflicts and relationships.

As our understanding of a mild TBI expands, we see that many children may quickly recover from the external head trauma and return to school, but some of them remain irritable, easily angered, hyperactive, and fidgety and have difficulty sustaining focus, effectively planning and organizing their activities and study material, adequately capturing and processing new concepts and rules, retaining new facts and retrieving information they have recently learned. They may also omit and misread social cues and display inappropriate reactions to daily stressors and changes in their environment. As we know, cognitive skills, academic abilities, and emotional stability are closely intertwined in many educational and social activities that children engage on a daily basis. Thus, it is difficult to separate where poor focus and retention problems end and irritability and frustration begin, when a child fails to listen to and follow directions, inhibit impulses, and sustain his focus to solve a math problem and, instead, fidgets and talks in class and disrupts his classmates. As a result, while these children have seemingly recovered from their mild head injury that they might have sustained on a playground or while playing sports, their entire life, including behaviors, relationships, and academic performance, come under assault of residual cognitive deficits and mood changes that cause ongoing disruption and anguish.

Over the past decades, we have learned a lot about the immediate head injury symptoms that children may experience during the first days and weeks post TBI. While immediate symptoms of a mild brain injury in children have been extensively documented, more recent research studies focus on identifying long-term cognitive symptoms, such as memory impairment that persists in some children 2 years post TBI [17]. Barlow and her colleagues [6] investigated mild brain injury in children and showed that 11 % of children displayed post-concussion symptoms 3 months after their injury and 1 year later these symptoms were still seen in 2.3 % of injured children. These studies helped us develop a better understanding of how and why some children’s recovery patterns differ from the majority of their peers, who have also sustained a mild TBI, and how persistent post-injury symptoms alter their normal developmental trajectory.

We can glean answers to these questions from the unique developmental processes that take place in a growing child’s brain. Children’s brains differ significantly from the adult brain and it is not just by virtue of being less mature or less capable. There are multiple developmental processes that are constantly changing the matrix of a child’s brain, making it more or less sensitive to various brain insults, treatment efforts, and environmental changes and stressors. Some of those developmental factors include ongoing myelination, sensitivity to oxidative stress, higher water content, open sutures, and brain plasticity [18, 19]. In fact, it is believed that maturation of white matter continues until approximately 30 years of age, as summarized by Maxwell [19]. Since the brain development is such a fluid process, any insult to the growing brain at any specific time would technically produce a different outcome because the brain was at a different state of development, with certain developmental goals already accomplished and certain developmental goals still at various stages of completion.

Over the past two decades, several authors have suggested that the damage caused by a traumatic injury to a developing brain can interfere with such processes as neuronal myelination and frontal lobe maturation [20, 21]. Indeed, during childhood and adolescence, a child’s brain is constantly undergoing a major construction of complex cortical networks, making it possible for the child to utilize self-regulation of emotions and behavior, sustain focus on lengthy assignments, organize his belongings and activities, and reflect on, compare, and associate various concepts. It is a complex, multidimensional scaffolding process that would be suspended and/or interrupted if some aspects of it are damaged and cannot, at least for some period of time, play their role in advancing the higher-order skills and supporting the associated cerebral functions. Levin [22] specifically questioned whether diffuse injury, which often occurs in mild brain injury cases, disrupts the development of networks that support higher-order cognitive functions in childhood.

Thus, if a mild cerebral insult produces diffuse injury, it may not be always detected by the traditional neuroimaging studies [4]. Yet, it still sets off a disruption of the ongoing myelination and maturation of white matter in a child’s brain. How long can this disruption last for before it generates long lasting effects on the cognitive, academic, and emotional maturity of a child? If some skill development is suspended for some time after the mild TBI, how does it affect the development of associated skills and how long does it take for the specific skill expansion, or evolution, to catch up with its original developmental goal?

In the past decades, numerous research findings have provided tremendous advances in understanding the short-term and long-term effects of focal brain damage on cognitive functioning. For example, studies that used neuropsychological measures of cognitive abilities and MRI results have determined that extrafrontal and temporal lesion volume predicted memory deficits as late as 1 year after the brain injury [23]. Also, Power and colleagues [24] have concluded that combined frontal and extrafrontal lesions predicted attention deficit 5 years after TBI, while the severity of individual frontal lesions were not predictive of attentional function.

However, if a mild TBI produces mainly diffuse white matter injury, which is not always detected by the traditional MRI scans, how can we illuminate the disruption of a complex web of constantly evolving cortical networks and its protracted effect over time on a child’s functioning at home and in school? Such interruption in the maturation of white matter of a child’s brain may not only delay the advancement of the existing skills but also delay the acquisition of more complex abilities. Indeed, in a growing child’s brain which undergoes rapid restructuring and layering of cognitive and emotional skills, a delay in maturation of lower-level abilities may significantly disrupt the scaffolding of higher-level abilities. While this hypothesis is not entirely new, recent studies investigating mild TBI have offered more support as they have found persistent cognitive impairments, as measured by neuropsychological tests, that correlate with metabolic disruptions and structural impairments in the brain.

It has been noted that conventional MRI can measure small lesions or hemorrhages and MRI findings correlate with neuropsychological and psychiatric outcome, but MRI may also underestimate diffuse axonal injury that is frequently seen in mild TBI [16]. While traditional MRI studies are not always able to detect structural impairment in mild brain injury cases [4], a newer neuroimaging technique, diffusion tensor imaging (DTI), offers a much more precise method of measuring post-concussion changes that occur in the white matter and contribute to persistent post-concussion symptoms and functional impairment months after the mild TBI.

DTI study measures the integrity of the white matter fibers via diffusion of water molecules [25]. If some axons are damaged and myelin sheath has diminished, the inter-axonal water volume increases. Therefore, DTI can detect injured axons and destroyed myelin even in mild TBI by measuring the integrity of white matter fibers; such axonal injury was observed months after the brain injury [16]. This is a new advancement in the detection of neuronal injury over the traditional MRI scan, which is not able to “see” such minor brain damage. In addition to being able to detect minor, yet important changes in white matter shortly after the brain injury, DTI allows the detection of long-term axonal injuries. For example, Bendlin and colleagues [26] described long-term impairments of white matter, as seen in DTI studies, 1 year after the injury. Her group detected specific axonal injury via fractional anisotropy and mean diffusivity reduction that was much greater than normal white matter changes expected in age-matched peers.

Thus, DTI technique allows us to detect some structural abnormalities in concussed individuals that were not visible on traditional neuroimaging studies, but those abnormalities remained for months or more post TBI. While these structural abnormalities might be minor, they are not inconsequential and do contribute to significant functional impairment that disturbs a brain injured person’s ability to complete daily chores, learn new information, and effectively interact with and adapt to his environment. In the recent years, such functional dysfunction, which is traditionally measured by neuropsychological tests, was found to correlate with structural abnormalities, as detected by DTI, further supporting the idea that even a mild brain injury may produce long-term cognitive functional impairments in some individuals.