Synonyms

Concussion; Mild brain injury; Sport-related concussion

Short Description or Definition

Mild traumatic brain injury (MTBI) is a trauma-induced alteration in neurological function caused by a direct blow to the head or from rapid acceleration, deceleration, rotational, or percussive forces on brain tissue. Common mechanisms associated with MTBI include a motor vehicle accident, fall, assault, or contact sports. The diagnosis of MTBI is made based on identifying an event with adequate force to cause a concussive injury and by examining acute injury indicators to grade the severity of injury. Standard neurological examination and neuroimaging studies should not be relied on to diagnose MTBI (have limited sensitivity). Common clinical signs of MTBI include an alteration of mental status or behavior and can be accompanied by other symptoms outlined below.

Diagnosis and Categorization

Mild Versus Moderate to Severe Brain Injury: Spectrum of Brain Injury Severity

MTBI is best understood when considered along a continuum of brain injury severity – from mild brain injury to severe brain injury. Brain injury severity is determined by acute injury characteristics such as length of unconsciousness (LOC), time to follow commands, duration of posttraumatic anterograde (PTA) or retrograde amnesia (RGA), and Glasgow Coma Scale rating (GCS: Teasdale and Jennett 1974). Many systems have been developed that use these injury characteristics to classify brain injury into mild, moderate, or severe. As an example, the American Congress of Rehabilitation Medicine (ACRM; Kay et al. 1993) indicates that a brain injury resulting in LOC less than or equal to 30 min, PTA less than 24 h, or a GCS of 13–15 is considered a MTBI. An individual with injury characteristics exceeding these criteria has a moderate to severe brain injury.

Definitions specific to MTBI have recently been articulated by the American Academy for Neurology (AAN 1997), the International Conferences on Concussion in Sports (McCrory et al. 2013), the Center for Disease Control (CDC) MTBI Work Group (National Center for Injury Prevention and Control 2003), and the WHO Collaborating Centre Task Force on MTBI (Holm et al. 2005). Some classification systems categorize MTBI into various grades of injury severity, such as MTBI grade 1, 2, or 3 (e.g., AAN 1997; Cantu 2001). A higher grade (grade 3) of MTBI is considered a more severe MTBI. Although there is considerable overlap in criteria among these systems, no universally accepted definition of MTBI exists.

Epidemiology

In their 2003 report to Congress, the CDC’s MTBI Work Group clearly outlines the public health burden associated with MTBI and discusses historical and current challenges in understanding and treating this elusive injury (National Center for Injury Prevention and Control 2003). The epidemiology of MTBI is arguably the most challenging to discover of all acquired brain injury. Incidence or prevalence estimates appear to grossly underestimate the frequency of MTBI because of imprecise surveillance systems, particularly given the high percentage of individuals who never present for evaluation or treatment following MTBI. Individuals may not even recognize that they sustained a MTBI due to the transient and nonspecific nature of symptoms following concussion. Variable MTBI definitions and methodological differences across studies further muddy current epidemiological estimates. In addition to the CDC’s report to Congress, McCrea (2008) provides a detailed overview of the challenges in uncovering the epidemiology of MTBI. This review of the literature suggests that roughly 85% of all brain injuries are mild in nature based on acute injury characteristics. Recent findings point to an incidence of at least 100/100,000 and possibly as high as 500/100,000 population, keeping in mind that incident rates vary across relevant demographics such as age and gender.

Natural History, Prognostic Factors, Outcomes

Neurobiology of MTBI

Several authors discuss the complex neurobiological abnormalities that occur within the brain following MTBI, which correspond to the onset and recovery of clinical symptoms (Giza and Hovda 2014; Hovda et al. 1999; Iverson 2005; McCrea 2008). For example, Hovda et al. (1999) discuss the “neurometabolic cascade” to characterize ionic fluxes, neurotransmission abnormalities, changes in brain metabolism, and cerebral blood flow abnormalities that result from MTBI, and highlight a challenging neurobiologic dilemma of MTBI – namely, the increased demand for glucose and oxygen at the same time that cerebral blood flow is diminished. Although affected brain cells appear more vulnerable to reinjury during the early recovery period given their tenuous state, it appears that most cells recover and do not die or degenerate. Animal studies suggest a resolution of aberrant neurological processes by 1–2 weeks post-injury (Giza and Hovda 2014).

Natural Recovery and Outcome Post-MTBI

The past few decades of sport concussion research have brought many scientific and methodological advances to the study of MTBI that earlier MTBI research paradigms could not offer. For example, the sport concussion research model allows access to a population “at risk” for concussion (allowing for prospective study of MTBI), access to concussed athletes for acute and follow-up investigation, and noninjured matched controls are readily available (McCrea 2008). These methodological advances have improved the understanding of the acute effects, natural recovery, and outcome associated with MTBI.

The clinical picture following a single MTBI consists of an acute onset of one or more of the following symptoms: alteration in consciousness, confusion, focal neurologic abnormalities (e.g., ataxia, language changes), cognitive deficits (e.g., amnesia, confusion, attention deficits), physical symptoms (e.g., headache), mood or behavior change. See Table 1 for a brief listing of possible acute MTBI symptoms. Most symptoms following a single MTBI resolve within 7–10 days, with few persons experiencing symptoms beyond 3 months (Belanger and Vanderploeg 2005; Iverson 2005; McCrea 2008). Animal models and functional imaging studies demonstrate a neurophysiologic recovery curve that follows a very similar timeframe as recovery of clinical symptoms post-injury (Giza and Hovda 2014), but the full timeframe for “brain recovery” remains a focus of ongoing study.

Mild Traumatic Brain Injury, Table 1 Common acute symptoms following mild traumatic brain injurya

Despite ample evidence of an overwhelmingly positive outcome from a single concussion, clinicians need to consider individual factors and medical history in modifying recovery and outcome expectations for patients. First, individuals appear more vulnerable to reinjury (repeat concussions) during the period of recovery from concussion. Animal research has revealed that the brain remains in a vulnerable state for a period of time following concussive injury, and clinical experience indicates that individuals with recent concussions appear more likely to sustain additional concussions, perhaps even from a lighter or less prominent force to the head. Second, although extremely rare, catastrophic injuries have been reported, such as, so-called second impact syndrome, when a person suffers additional trauma during this period of increased vulnerability. Third, individuals appear to have slower recovery, and may be at greater risk for incomplete recovery, after repetitive concussion when compared to their first concussion. Fourth, there is increasing concern that repetitive head trauma may present a risk for neurologic and cognitive deficits or later onset neurodegeneration (Mielke et al. 2014). Lastly, “complicated” MTBI (those with focal neurologic injuries such as intracranial bleeding or skull fractures) may be more commonly associated with a suboptimal recovery (Williams et al. 1990).

There is a minority of patients that appear to have a suboptimal outcome due to persisting symptoms or treatment-refractory symptoms following MTBI, a group that is sometimes diagnosed with postconcussion syndrome (PCS). Iverson (2005) does an excellent job discussing non-brain injury factors that can complicate recovery and outcome from MTBI by contributing to or magnifying symptoms of MTBI – such as comorbid injury factors, medication effects, and mood variables. Preinjury adverse life events, stress, post-traumatic stress disorder, psychiatric history, family psychiatric history, somatizing tendencies, preinjury health problems are all risk factors for a suboptimal outcome. Genetic risk factors for post-concussive syndrome are being explored, but no firm conclusions can yet be drawn about biological risk factors (Carroll et al. 2014; AAN 2013), though some underpinnings have been postulated (Giza and Hovda 2014). All non-MTBI variables need to be considered alongside the MTBI when conceptualizing and treating MTBI patients.

Evaluation

Acute Evaluation and Management of MTBI

Individuals sustaining a MTBI should seek medical consultation immediately after injury. At a minimum, a person should seek medical guidance from an appropriate emergency medicine specialist to determine if any workup is necessary to rule out a more catastrophic injury. Frequently, evaluations are conducted by emergency medicine physicians and include medical and neurological examination where there is also access to advances in technology that assists with ruling out intracranial abnormalities associated with MTBI. Computed tomography (CT) technology is most sensitive method for detecting acute intracranial abnormalities that can occur as complications to MTBI. Emergency medicine specialists also routinely screen for other comorbid injuries (e.g., spine or orthopedic injury). Acute evaluation ideally involves some intervention related to education about MTBI and expected recovery.

Post-Acute Evaluation and Management of MTBI

Evaluation and management may be indicated in the post-acute phase of recovery from MTBI to monitor and treat ongoing symptoms, track recovery over time, and help individuals make decisions about when it is appropriate to return to work, school, or other important activities.

Neuropsychological testing helps quantify acute and post-acute cognitive changes following MTBI, objectively tracks cognitive recovery for individuals over time, and provides valuable information to inform return to activity decision-making (i.e., work, school or sports). Neurocognitive testing may be particularly sensitive to subtle changes in cognition shortly after brain injury, making it an invaluable method for identifying symptoms in individuals who appear asymptomatic or who may be minimizing symptoms for personal gain (e.g., return to sports). See the sport-related concussion entry for a detailed discussion of acute and post-acute evaluation and management of MTBI in sports.

Treatment

In addition to traditional medical or pharmacologic management of symptoms following MTBI (medications for headache, physical therapy for comorbid injuries or pain problems), behavioral management techniques should be incorporated in any treatment of persons with MTBI. Models to treat MTBI are ideally interdisciplinary and should include biopsychosocial principles in any intervention administered. Treatment models should also encourage appropriate return to activity as soon as possible (i.e., an active rehabilitation approach to care). Education about MTBI, common symptoms of MTBI, and expected recovery and outcome from MTBI is an essential part of patient management following MTBI, perhaps because these ingredients help patients develop appropriate expectations about their injury, symptoms, and early recovery. Cognitive-behavioral therapeutic techniques, frequently employed by neuropsychologists or other brain injury specialists with behavioral management experience, are used to prevent or treat persistent symptoms associated with MTBI (McCrea and Powell 2012; Mittenberg et al. 2001, 1996). Interventions typically focus on reassurance, help people modify outcome expectations, challenge distorted self- or symptom-appraisals, promote the use of compensatory strategies, and encourage gradual increase in activity level and socialization.

Cross-References