More than 2.5 million incidences of traumatic brain injury (TBI) occur in the United States every year, and approximately 2.2 million of those individuals are treated in emergency departments.1 These visits for TBI of varying severities (mild, moderate, and severe) result in more than 280,000 hospitalizations, 80–90,000 individuals with permanent disabilities, and more than 50,000 deaths, every year.2 In total, it is estimated that 5.3 million individuals in the United States continue to require long-term daily assistance due to a TBI. Worldwide, the reported incidence of TBI varies considerably by country—approximately 50 per 100,000 persons in China, to over 400 per 100,000 persons in Sweden, with Europe averaging 235 incidences per 100,000 persons.3 The variability in incidence and prevalence data across different nations may be attributed to such factors as injury awareness, sensitivity of diagnostic criteria, and reporting mechanisms, as well as cultural differences in vocational and avocational activities, which may expose their populations to greater risk. In total, the annual worldwide incidence of TBI is estimated at more than 10 million, and even this is believed to be a vast underestimation.
As with most traumas, the severity of anatomic damage associated with TBI can vary greatly. Furthermore, based on the location of damage within the brain, patients may manifest a wide variety of physical, cognitive, behavioral, or emotional symptoms. The resultant heterogeneity of TBI thus creates significant challenges in terms of classifying, characterizing, or selecting effective treatments for patients with brain injury. Although the initial or primary damage to the brain may be unavoidable in the trauma setting, all efforts should be made to help mitigate and prevent secondary injury (e.g., brain swelling, hypo/hypertension, hyperthermia, infection, hypo/hyperglycemia, repeated trauma, etc.). The goal must be to both treat the initial injury and also prevent, as much as possible, the development of secondary complications. As with the entire nervous system, early intervention is often regarded as the most valuable and effective, especially with more severe trauma; thus, early diagnosis of severity and detection of the type of injury is vital.
CASE 15-1
A 12-year-old girl presents to the emergency department (ED) having suffered a kick to the head during a soccer match approximately 3 hours earlier. According to her parents, she was walking and talking following injury, with no apparent loss of consciousness (LOC), although she described memory loss of a few moments following injury. The on-site athletic trainer also reported that she was confused and disoriented for several minutes before walking off the field and experienced low-level nausea and dizziness, which dissipated within 15–20 minutes. She currently has a mild headache.
TBI is a clinical diagnosis and defined as a trauma-induced structural injury and/or physiological disruption of brain function as a result of an external force followed by onset or worsening of any of the following symptoms shortly after the event:4
Any loss of memory for events immediately before or after injury
Any period of loss of consciousness
Any alteration in consciousness/mental state at the time of the injury (confusion, disorientation, slowed thinking, etc. —also known as alteration of consciousness [AOC])
Neurological deficits (weakness, loss of balance, visual changes, praxis, paresis/paraplegia, sensory loss, aphasia, etc.) that may or may not be transient
Intracranial lesion
The forces contributing to injury can include sudden deceleration or acceleration, penetrating objects, and the combined effects of multiple forces, as well as complex mechanisms such as those involved in blast trauma. TBI can also result without any contact to the head. Rapid deceleration or acceleration can cause the brain to come into contact with the interior of the skull. This is common in motor vehicle accidents.5 The term “concussion” is usually used interchangeably when referring to mild TBI (mTBI), and is the preferred term to use in clinical encounters with patients.
The results of TBI can be subtle and difficult to identify radiographically. Injuries may manifest as focal lesions such as skull fractures and contusions, or as more widespread injuries, such as subarachnoid hemorrhage (SAH), subdural hemorrhage (SDH), epidural hemorrhage (EDH), intraparenchymal hemorrhage (IPH), or diffuse axonal injury (DAI). The variable causes, manifestation, and effects necessitate individualized assessment of each individual who experiences a TBI.5
A number of other symptoms can be associated with TBI, but are not necessary to be prevalent for a diagnosis of TBI:
Coma is possible in the acute phase with moderate-to-severe TBI
Headache
Anisocoria—potential indication of more serious TBI
Blurred vision and/or changes in peripheral vision
Diplopia
Sensitivity to light and/or sound
Dizziness or vertigo
A feeling of sluggishness
Difficulty with concentration or attention (often develops in the weeks following injury)
Nausea/vomiting
Tinnitus (“ringing” in the ears)
Insomnia or hypersomnia
Fatigue
In cases of skull fracture, physicians should also be cognizant of the fact that while a skull fracture can accompany TBI, it does not necessarily indicate one has occurred.
CASE 15-1 (continued)
In Case 15-1, the history and mechanism of injury, memory loss, disorientation, and confusion indicate that the diagnosis of mTBI, otherwise known as concussion, is appropriate.
While attributable percentages vary by region, the most common causes of TBI in the civilian population are6–8:
Falls
Traffic accidents
Unintentional blunt trauma (including sports-related injuries and accidental head trauma caused by various objects)
Assaults
Figure 15-1 illustrates the different common causes of TBI and their distribution.
Figure 15-1
Causes of traumatic brain injury. The distribution of causes of TBI in nations and areas worldwide is disparate. This is most likely due to a lack of identification and reporting and different systems of classification as well as different mechanisms of injury. The most accurate and up-to-date estimates have been produced by the nations of North America and Europe, yet even these reports fluctuate region to region.
Previous concussion/mTBI or TBI
Being 0–4 years or >65 years of age
Being male (incidence 3 times higher than for females)
Airway, breathing, and circulation (ABC) must be checked (in accordance with advanced trauma lifesaving guidelines)
A comprehensive and systematic review of patient history and current condition. This includes:
Physical examination
Review of medical history
A review of mental health history and symptoms
Neurological examination including assessment of pupillary responses
Characterization of injury severity and assessment of damage to the brain
TBI comprises a heterogeneous group of conditions that can be the result of disparate injuries. Therefore, it is often best to characterize it by clinical severity as well as expected outcome and pathoanatomical features (the where and what for treatment purposes).9
Each TBI can be classified based on injury severity into one of three distinct levels:
Severe TBI10
Moderate TBI
Mild TBI (mTBI) often termed “concussion”
It should be noted that the term, “concussion,” can be used interchangeably with mTBI; however, many providers prefer to use the term “concussion” with their patients in order to help reinforce the predicted transient nature of their symptoms, rather than reinforcing misperceptions/concerns that may be associated with the terms “brain damage” or “brain injury.”
The classification of injury severity in the acute phase is typically made by using the Glasgow Coma Scale (GCS), which has a score range of 3–15, with a score of 8 or below indicating coma. Although numerous other scales and tests exist, the GCS is the standard of care tool. It must, however, be understood as a relative measure due to the subjective nature of the examination (scores are based on the interpretation of the evaluator). Relative GCS scores and corresponding diagnosis and symptoms can be found in Table 15-1. Several other scales are also available, including the Modified Glasgow Coma Scale for Infants and the Adelaide Pediatric Coma Scale (maximum score of 14). The Adelaide Pediatric Coma Scale has been rated for various age groups under the age of 5 and, therefore, provides a bit more clarity for clinicians in determining score relevance for young children (Table 15-1B).
According to the published Clinical Practice Guidelines published by the United States Department of Defense (DoD) and Department of Veterans Affairs (VA), mild, moderate, or severe TBI may be classified according to structural imaging changes, loss or alteration of consciousness, period of post-traumatic amnesia (PTA), or best GCS score (Table 15-1C).11
Diagnosing Traumatic Brain Injury Severity
A. | |||
---|---|---|---|
In Adults | In Children | In Infants | Score |
Eye Opening | Eye Opening | Eye Opening | |
Open spontaneously prior to stimulus | Spontaneous, prior to stimulus | Spontaneous, prior to stimulus | 4 |
Open after spoken or shouted request | After verbal stimuli | After verbal stimuli | 3 |
To pain only (fingertip pressure) | To pain (fingertip pressure) | To pain only (fingertip pressure) | 2 |
No opening at any time, no interfering factors | No response, no interfering factors | No response, no interfering factors | 1 |
Interference* | Interference | Interference | NT |
Verbal response | Verbal response | Verbal response | Score |
Can correctly give name, place, and date | Oriented | Coos and babbles | 5 |
Confused but communication coherent (forms sentences) | Confused but words possible | Irritable cries | 4 |
Intelligible single words | Vocal sounds | Cries to pain | 3 |
Only nonword sounds (moans and groans) possible | Cries | Moans to pain | 2 |
No audible response | No response | No response | 1 |
Interference* | Interference | Interference | NT |
Motor response | Motor response | Motor response | Score |
Obeys 2-part request | — | Moves spontaneously and purposefully | 6 |
Localizes cause of pain | Obeys commands | Withdraws to touch | 5 |
Withdraws in response to pain | Can localize pain | Withdraws in response to pain | 4 |
Flexion in response to pain | Flexion to pain | Abnormal flexion in response to pain | 3 |
Extension in response to pain | Extension to pain | Abnormal extension in response to pain | 2 |
The anatomic and pathologic classification is often most helpful for determination of a course of treatment for moderate-to-severe TBIs, although it can also be informative for mTBI/concussion. Anatomically, the causes of TBI tend to fall into one of the following groups:
Contusions
SAH and intraventricular hemorrhage (IVH)
Epidural hematoma, subdural hematoma, intraparenchymal hematoma
The determination of this categorization can typically be made by head computerized tomography (CT) or brain magnetic resonance imaging (MRI) scan (Fig. 15-2).
Based on imaging findings, it may be more appropriate to treat the injury using surgical intervention. Table 15-2 provides some examples of general clinical and radiological presentations for some of the most common classifications of injury, as well as treatments.
Figure 15-2
Heterogeneity of severe traumatic brain injury (TBI). Computed tomography (CT) scans of six different patients with severe TBI, defined as a Glasgow Coma Scale score of <8, highlighting the significant heterogeneity of pathological findings. CT scans represent patients with epidural hematomas (EDH), contusions and parenchymal hematomas (contusion/hematoma), diffuse axonal injury (DAI), subdural hematoma (SDH), subarach-noid hemorrhage and intraventricular hemorrhage (SAH/IVH), and diffuse brain swelling (diffuse swelling). Reproduced with permission from Saatman KE, Duhaime AC, Bullock R, et al. Classification of traumatic brain injury for targeted therapies, J Neurotrauma 2008 Jul;25(7):719–738.
Common Traumatic Brain Injury Clinical Presentations and General Treatment Measures
Specific Injury | Clinical Presentation | Specific Treatment Measures |
---|---|---|
Skull fracture |
| If the brain does not require decompressive measures due to injury, surgical intervention is recommended to repair the skull. Closed, nondisplaced fractures do not require immediate intervention. |
Cerebral contusion |
| Close monitoring of patient and frequent MRI or CT to monitor status is typically necessary. Contusion can enlarge within first 12 hours and worsen over first few days. |
IPH | Edema that can increase over time and may cause progressive neurological deterioration and mass effect. | If patients experience neurological decline or increased effect, neurosurgical consult is recommended for decompression surgery. |
EDH |
|
|
SDH |
|
|
SAH |
|
|
DAI |
|
|
What is the role of laboratory tests in TBI, especially mTBI/concussion, diagnosis and treatment in the acute phase?
Serum and other laboratory tests are regarded as a potential way to reduce unnecessary radiation exposure, hospital costs, and the duration of mTBI management and hospital stays; however, the practice and procedure are not firmly established.
The use of laboratory assays for predicting neurological changes in cases of mTBI is under investigation. Several studies have found that S100B, a protein found in astrocytes that is believed to be released by damaged neurons upon injury, can function as a sensitive negative predictor of radiological findings if assayed within 3–4 hours of brain injury. This finding was demonstrated to be consistent in both children and adults.12
Serum levels of S100B below 0.12 ng/mL successfully predicted a lack of radiological findings at a rate of 99.7%.
According to the Centers for Disease Control (CDC) and American College of Emergency Physicians (ACEP), in cases of mTBI/concussion without extensive external cranial injuries and S100B serum level of <0.1 ng/mL taken within 3 hours of injury, consideration can be given to not performing a CT or MRI scan.13 Such use, however, is not general practice at this time and reflects only a Level C recommendation in the eyes of the CDC and ACEP guidelines (the lowest level of recommendation given, implying that this recommendation is based on preliminary, inconclusive, or conflicting evidence or panel opinion).
Despite the potential value of this examination, it is not yet approved by the Food and Drug Administration (FDA) in the United States for clinical use and, thus, should be considered experimental at this time.
CT or MRI scans are indicated for those with moderate-to-severe TBI in order to assess the extent of injury and determine necessary treatment. Prompt imaging in the acute phase is critical to expedite diagnosis and care. Additionally, follow-up scans are suggested to monitor injury status and evolution of the condition.
While there is no indication that either a CT scan or MRI is better for assessing patients with TBI, MRI availability in the acute phase is limited and can be contraindicated in the presence of metal, which is especially relevant for military service members who may have other injuries from metal fragments or shrapnel. They also require more time and are expensive to perform. However, MRI provides greater sensitivity than CT, especially in cases of diffuse brain damage, and can also be used to evaluate infarction, ischemia, and edema. CT has the advantage in being able to quickly assess the entire brain and spinal column in a single set of scans and is easier to perform on patients who are agitated or have restricted mobility due to being on ventilator support or in spinal traction. For this reason, CT is commonly used for initial screening of patients with head trauma or neurological deficits. CT scans are able to identify SDH, EDH, SAH, IPH, IVH, contusions, cerebral edema, skull fractures, mass effect including midline shift, and ischemic infarction.5
Despite the reported benefit of CT, there is increasing concern that exposure to low levels of radiation during a scanning14 may be harmful, especially in children.
CT is, thus, recommended for initial assessment of acute trauma in order to image the entire CNS, while MRI is recommended for follow-up evaluations and in conjunction with neurological monitoring, if available.
In the unlikely event that both CT and MRI are unavailable, serial neurological examinations and evaluation of pupillary responses are of greater importance. Close monitoring of the patient for any change in their mental or neurological status is imperative in such a situation.
With a recent increase in research efforts focused on mTBI/concussion in sports and the military, there has been an increase in the number of CT and MRI scans used in the initial clinical assessment of those suspected to have sustained a TBI/concussion; although considerable debate continues to persist regarding this practice.
According to the recommendations of the United States CDC, imaging using a CT scan or MRI should be considered in patients with no LOC or PTA if there is “a focal neurologic deficit, vomiting, severe headache, age >65 years, physical signs of a basilar skull fracture, GCS score <15, coagulopathy, or a dangerous mechanism of injury” (including ejection from car, pedestrian struck by a vehicle, a fall from a height of more than 3 feet, substance intoxication).13 Imaging may also be warranted in the setting of ethanol or other substance use, as the etiology of the patient’s altered state of consciousness may not be discernable from the injury or substance use. Ultimately, clinical judgment will dictate whether the use of scanning is needed to determine the extent of injury.
If an MRI or CT scan is not available, discharge of someone with mTBI/concussion can be made based on clinical evaluation. In general, patients with a GCS score of 15 at a time of 4 or more hours after injury, along with an absence of PTA, nausea, skull fracture, severe headache, dizziness, confusion, blurred or altered vision, anisocoria, or other severe symptoms could be considered for discharge, provided that necessary rest and attention will be available and provided in the home environment. If laboratory assessments (such as S100B plasma concentrations) have been obtained, the results of these findings should be taken into account.
CASE 15-1 (continued)
Patient reported that she had suffered a head injury a year prior, but did not receive treatment. In that instance, there was no LOC and no PTA, just a headache that persisted for 2–3 days. No difficulty with memory or concentration was noted. There was no history of persistent headaches. Injury report and evaluation correspond to a negative evaluation for mild TBI/concussion.
Although CDC studies have estimated that 300,000 sports-related concussions/mTBI occur each year,15 terminology, reporting, and methods of diagnosis are not consistent across hospitals or individual physicians. Additionally, this report only included those who suffered an LOC. Since the majority of individuals who sustain an mTBI/concussion do not develop LOC, it has been estimated that up to 3.4 million sports-related incidents of mTBI may occur each year in the United States, or more than 600 per 100,000 population.16 Many of these go unreported, undiagnosed, and untreated. Similar numbers are seen in the European Union (∼300,000 concussions reported each year related to sports).17
Upwards of 85% of all instances of medically treated TBI are mTBI/concussion.18
By some estimates, concussions represented 15% of all sports-related injuries in high school athletes (up to age 18).19
A number of secondary health complications can arise following any TBI, although a particularly significant concern with mTBI/concussion is that the injury may go unnoticed or unrecognized, which may contribute to a more serious repeated injury or failure to receive appropriate treatment, leading to slower recovery or even persistent symptoms.
While often mild in its initial symptomatic expression, mTBI/concussion can lead to difficulty concentrating and memory problems that can have a negative impact on quality of life and academic performance, both of which should be taken into account, especially with younger patients in whom the brain is still developing.
Although rarer following mTBI than more severe head injuries, intracranial bleeding, diffuse axonal injury, and physical, cognitive, and psychosocial functional impairment can develop following a concussion. Patients should be monitored for the presence of such conditions. CT scans and MRIs may be helpful if available especially if neurological examination indicates that a more severe condition has evolved following the initial presentation.
A single mTBI/concussion increases the risk of repeated concussion.
Post-traumatic seizures (discussed further later in this section) are seen in 2.1% of those with mTBI/concussion.20
Full recovery can take days to months; however, most patients (95% based on published sports concussion literature) should see resolution of all symptoms within a week.
Repeated TBI is a serious concern. A single concussion can have significant and long-term consequences, and each incident increases the chance of repeat injury and requires progressively longer and possibly more difficult recovery periods.
Two concussions within a short period (within days of each other) can result in second-impact syndrome (SIS), an extremely rare, but potentially fatal, injury characterized by rapid diffuse brain swelling, brain herniation, and death, in a matter of hours.21 While the existence of SIS has been debated and noted almost exclusively in males under the age of 24, patients and physicians should be cognizant of the potential for this development and take precautions with return to play and/or return to rigorous or potentially harmful activities following initial and especially repeat mTBI. Such returns to play should be predicated on functional recovery and the end of all symptoms, with no recurrent symptoms even with exertion. A number of suggested timelines with functional standpoints exist. Perhaps the most widely utilized is the Consensus Statement on Concussion in Sport, which has been adopted by the CDC of the United States and provides strong guidelines for progressive re-integration (Table 15-3).22
A particular concern for those individuals who suffer multiple concussions is the potential development of more significant injuries. The cumulative effects of multiple mTBIs have been implicated in the development of neurodegenerative diseases such as chronic traumatic encephalopathy (CTE), amyotrophic lateral sclerosis (ALS), Parkinson disease (PD), and Alzheimer disease (AD), as well as neuroinflammation, changes in synaptic plasticity, cognitive deficits, increased rates of depression, and other psychosocial impairments.23,24
Graduated Return-to-Play Protocol for Sports-Related Concussion/TBI
Rehabilitation Stage | Functional Exercise at Each Stage of Rehabilitation | Objective of Each Stage |
---|---|---|
1. No activity | Symptom-limited physical and cognitive rest | Recovery |
2. Light aerobic exercise | Walking, swimming, or stationary cycling, keeping intensity <70% of maximum permitted heart rate; no resistance training | Increase heart rate |
3. Sport-specific exercise | Skating drills in ice hockey, running drills in soccer, etc. No head-impact activities | Add movement |
4. Noncontact training drills | Progression to more complex training drills (i.e., passing drills in football and ice hockey); may start progressive resistance training | Exercise, coordination, and cognitive load |
5. Full-contact practice | After medical clearance, participation in normal training activities | Restore confidence and assessment of functional skills by coaching staff |
Return to play | Normal game play |