The scientific literature on MTBI supports a functional rather than a structural etiology [45]. The model commonly used to understand the neurophysiological basis of MTBI, developed on the basis of animal models, is conceptualized as a multilayered neurometabolic cascade, involving a complex of interwoven cellular and vascular changes that occur following trauma to the brain [22]. According to this model, the pathophysiology of MTBI represents a temporary disruption of brain function secondary to ionic fluxes, abnormal energy transmission, diminished cerebral blood flow, and impaired neurotransmission rather than any readily identifiable form of structural brain damage. According to most accounts the neurophysiological changes associated with the acute stage of MTBI clear within a period of 7–10 days [41, 44].

Results from research on humans with MTBI have demonstrated a rather remarkable correspondence to the findings reported from animal studies. The evidence obtained through controlled investigations, using primarily athlete samples, have demonstrated a gradual resolution of symptoms, including headache, dizziness, and cognitive disturbance, within a period of 1–7 days (see Fig. 1). Findings from these and other studies led several panels, including the World Health Organization (WHO) Collaborating Centre Task Force on Mild Traumatic Brain Injury, to conclude that symptoms of MTBI are generally temporary and self-limiting in nature, with resolution observed within days to weeks post-injury in an overwhelming majority of cases [15].

From a structural standpoint, it appears that most of the injuries classified as MTBI are associated with, at most, low levels of axonal stretching, resulting in the temporary neurophysiological changes described above [22]. There is now accumulating evidence, obtained from studies using advanced neuroimaging (e.g., fMRI, nuclear magnetic resonance (NMR) spectroscopy, and diffusion tensor imaging (DTI)) and electrophysiological (e.g., quantitative EEG and evoked potentials) techniques indicating that signs of this non-permanent form of traumatic axonal injury can be detected in some subjects for up to 30–40 days following injury [19, 38, 73]. From a clinical standpoint, this might represent a period where the brain is more vulnerable to re-injury or effects of fatigue with suggestions that the brain might also require recruitment of additional neuronal resources to achieve its typical level of functioning [43]. From a clinical standpoint, this might represent the underlying cause for what many patients report as difficulties with resuming their pre-injury level of activity. However, it should be emphasized that this stage of recovery is temporary with no empirical evidence of any pathophysiological abnormalities persisting for more than a several week period. Contrary to what some believe, there is little evidence supporting the existence of any more serious form of diffuse axonal injury (DAI) resulting from a typical MTBI [3].

Patients reporting symptoms of MTBI extending for more than several weeks post-injury are often classified as having post-concussion syndrome (PCS). The exact number of patients reporting PCS remains controversial. While some argue for the existence of a “miserable minority” consisting of approximately 15 % of MTBI victims [3, 57], the results of most prospective studies and meta-analyses indicate that the number is more likely to be closer to 3 % [63]. There is no scientific evidence supporting claims that PCS symptoms are the results of direct physiologic effects of brain injury. The conclusion from the WHO task force was that symptoms extending beyond the typical recovery of several days to weeks are attributable to a number of “non-injury” factors such as depression, PTSD, chronic pain, life stress, or secondary gain [15]. There has been recent interest in identifying a number of psychological factors (e.g., misattribution, nocebo effect, “good-old-days” phenomena) underlying the tendency to report persisting symptoms following MTBI [27, 51].

Additional controversy surrounding MTBI has developed following reports of symptoms and neuropathological changes associated with dementia appearing in a small number of athletes exposed to repetitive head injury while participating in contact sports including football, boxing, and ice hockey [49]. While an association between more severe forms of TBI and the occurrence of Alzheimer’s disease has been established [67], investigators are claiming that the pattern of behavioral decline seen in this sample of athletes, in association with its unique underlying profile of pathology represents a distinctive form of dementia known as chronic traumatic encephalopathy (CTE) [49]. Based on existing evidence, the development of CTE does not appear to be related to the occurrence of discrete MTBI events, but rather the cumulative effects of repeated “sub-concussive” blows to the head. At this point, the validity of the CTE diagnosis and its relevance to the vast majority of MTBI victims remains unclear [48, 59].

In summary, the emerging evidence-based model of neurophysiological recovery from MTBI can be characterized as having three possible stages, which are depicted in Fig. 2. The first of these stages, characterized as an acute period of recovery, is based on temporary neurophysiological effects that recover within a period of 7–10 days, along with most clinical signs and symptoms. The second, “sub-acute” stage is characterized by continued brain recovery, which can be identified potentially through the use of advanced neurodiagnostic techniques obtained within a period of several weeks following the injury before full remission. Subsequently, there is a possibility of a third stage of recovery, explaining the potential for some individuals to experience a longer-term susceptibility to repeat injury and perhaps even the possibility of developing dementia later in life. While continued research is needed to confirm the presence and nature of these three stages of recovery, clinicians will find it useful to consider these stages of recovery when performing neuropsychological evaluations of individuals following a reported MTBI.

Patients with MTBI present with a complex combination of physical, cognitive, and emotional symptoms. When examining these individuals, neuropsychologists need to be aware of the evidence-based literature on recovery from MTBI and to be cognizant of which stage of recovery the individual falls in at the time of the assessment. With the exception of individuals working in an acute concussion clinic, sport setting, or the military, it is likely that most neuropsychologists will encounter MTBI patients long after the occurrence of the injury when patients are reporting symptoms of PCS. In that context, neuropsychologists are, by virtue of their training and use of empirically based assessment methods, uniquely qualified among health care professionals to assess the complex display of symptoms seen in individuals presenting with PCS.

When evaluating individuals with MTBI, it is important to be reminded of the distinction between neuropsychological testing and neuropsychological assessment [37]. There is perhaps no other clinical situation where it is more important to corroborate information obtained via self-report through other sources. The comprehensive assessment of an individual with MTBI should include a detailed record review, an interview with the patient, testing of neurocognitive functioning, and completion of self-report symptom inventories. Interviews with collateral sources, such as family members, employers, or witnesses to the injury are also helpful, if such individuals are available, cooperative, and knowledgeable about the patient and the reported injury.

Results of the neuropsychological evaluation will provide clinicians working with MTBI patients in a clinical setting with critical information on the presence of symptoms, their likely etiology, and the degree to which they are affected by the effects of comorbid physical and psychological conditions. After obtaining this information, the next step is to develop a plan for intervention. This plan will differ significantly depending on the clinical setting and the chronicity of the injury. Those working with patients in the early sub-acute stage of recovery will utilize strategies aimed at preventing the development of persistent PCS while interventions aimed at symptom reduction will be used in patients continuing to experience longer-term effects of the injury.

Psycho-education is the key to prevention of long-term symptoms in patients following MTBI. It was not too long ago that the public at large had very little information about MTBI, making the effects of the injury somewhat of a mystery, both to patients and clinicians. Now, with the explosion of information provided by the media and the internet, most injured patients have expectations of what might be expected following MTBI, with many of these expectations guided not so much by research findings but by misconceptions based on dramatic accounts of celebrities, athletes, and soldiers who have experienced difficult recoveries. The role of the clinician is therefore to relay information from the evidence-based literature while providing reassurance to their patients that, after a brief period of headache and other short-lived symptoms, the vast majority of individuals sustaining an MTBI achieve full recovery, enabling them to resume their lives with no long-term effects.

There are indications that psycho-educational interventions aimed at patients with MTBI are best initiated as early as possible following the injury [52]. Findings from research studies have indicated that providing information sheets or a single session intervention to patients at the time of the ER visit will reduce symptom expression and level of distress at longer-term follow-up. Communications to the patient that he or she will benefit from rest while they undergo a brief period of symptoms can prevent them from suffering setbacks as a result of a premature resumption of their regular activities. Most MTBI experts advocate a common sense approach for an initial return to activity, adapting concepts borrowed from return to play guidelines developed in the sports setting. This generally involves a graduated resumption of activities, as tolerated, until a full return to a pre-injury level of functioning can be achieved unaccompanied by symptoms [47].

The issue of complete cognitive and physical rest has become a controversial topic in the clinical management of MTBI. Recommendations for rest are based loosely on concepts obtained from animal studies where it is known that a premature activation of physiological activity during a period when the brain is undergoing a restorative process can have a negative effect on many of the neural factors important for recovery. Based on this information, it makes sense to recommend a few days rest following an injury. However, the clinician must be careful not to overextend recommendations of rest, which could have the potential of placing the recovering patient at risk for developing a maladaptive focus on their symptoms. At the current time, further information is needed on the long-term benefits of rest and the optimal amount and types of rest that are required for optimal recovery from MTBI [65].

Most health care professionals are well aware that patients with persistent PCS are difficult to treat. Interventions aimed at treating persistent PCS can be divided roughly into physiological and psychological approaches. It is not surprising that there is no consensus on what physiologic approaches to treatment should be used for treatment of PCS, given the fact that its underlying physiologic causes remain undetermined. Based on findings from the research literature, there is more empirical support for the use of psychological interventions for PCS, although there is clearly a need for more work in this area.

Pharmacological approaches to the treatment of patients with PCS focus primarily on treatment of comorbid depression and anxiety, as no medication has been shown to be effective in treating the primary symptoms of PCS [36, 39]. There is a growing interest in identifying oculomotor [21] and vestibular disturbances [5] in PCS patients, based on the possibility that these types of disturbances are often overlooked in this population. However, large-scale studies looking at the efficacy of vision and vestibular therapy are clearly needed. Based on findings that long-term cognitive effects of MTBI are minimal, the use of cognitive rehabilitation approaches with this group is unwarranted. There is no convincing published evidence that neurofeedback, hypnosis, or acupuncture are effective as “alternative” treatments for patients following MTBI [36].

There is now a growing trend to use cognitive behavioral therapy (CBT) for treatment of MTBI patients who have developed PCS. The theoretical basis for CBT interventions with this population is that (1) the symptoms that predominate in PCS are subjective in nature, (2) these symptoms overlap substantially with those seen in other psychological conditions, and (3) there are a number of cognitive-behavioral processes underlying the evolution and maintenance of symptoms in PCS [58]. While previous psychotherapeutic approaches to PCS emphasized a sequence of validation and identifying alternative interpretations for the attribution of symptoms, use of CBT enables the clinician to address maladaptive behavioral responses, cognitive appraisals, and the impact of symptoms on daily life [2].

A 12-session framework for CBT with PCS patients has been developed by Potter and Brown [58]. Beginning sessions utilize and extend the use of materials from psycho-educational interventions by providing information on the course of symptom recovery seen in the majority of patients. This is followed by a number of sessions identifying problem areas and developing appropriate responses. The goal is to help develop positive expectations while limiting the negative impact of perceived errors or mistakes. Later sessions focus on the techniques that worked and did not work in addition to developing longer-term behavioral plans for the future. In a recent systematic review of the research literature, it was determined that all ten randomized controlled trials demonstrated a therapeutic benefit, although small numbers and short durations of follow-up prevent the formation of robust conclusions about the ultimate efficacy of CBT with the MTBI population.

The presentation of MTBI differs significantly across settings. For the purposes of this chapter, we will focus on a discussion of similarities and differences as presented in patients with injuries resulting from sports, personal injury, or military service. These three diverse contexts provide markedly different means for documenting details regarding the injured person, the mechanisms of the injury, and its resulting effects. Further details regarding the differences among these three settings are listed in Table 4. For example, those in the sports and military settings are at an increased risk for sustaining an MTBI, which often provides a formal means for obtaining information on their pre-injury status through baseline testing. However, in the case of personal injury evaluations, the clinician is forced to estimate the individual’s premorbid state using information from available records and various psychometric methods. The level of available documentation of the injury itself and the course of acute and subsequent recovery varies widely across these three settings. There are also marked differences by which comorbid psychiatric factors and motivation can play a role in symptom presentation, depending on the nature and social context of the injury. Additional details on the differences among these settings are provided below.