Acceleration/deceleration injuries, rather than direct blows to the head, are the most frequently cause of concussions [64]. When a force is applied to the body or to the head itself, the brain experiences these forces as angular rotation rather than translational (Figs. 29.2 and 29.3). The spinal cord and the brain stem are generally fixed in space by the confines of the spinal column and attachments at the base of the skull (e.g., vessels, cranial nerves). The upper midbrain, thalamus, and cerebral hemispheres are suspended on the brain stem within the skull, surrounded by fluid and connective tissue. These structures are not fixed within this space and are free to move within the skull to varying degrees. The cerebrospinal fluid around the brain acts as somewhat of an inertial damper, redirecting forces that are transmitted to the skull around the brain rather than through it. But it can only dampen so much force, and what force is applied causes the brain to rotate around its more fixed and deep structures. The brief loss or alteration of consciousness associated with concussion is likely an effect of these forces acting on the junction of the upper midbrain and thalamus, leading to a transient disruption in the functioning of the reticular neurons that maintain alertness [76].

Forces applied to the brain become angular rotational forces due to the structures that constrain the base of the brain [5, 6]. White matter, likely due to the myelin sheaths around axons , is stiffer than gray matter, so the strain generally concentrates at the intersections of these two areas. In concussion, these strains are not associated with visible structural abnormalities on conventional neuroimaging. In a more severe traumatic brain injury, however, large magnitudes of force applied in the same fashion will frequently cause disruptions at the gray-white junction (i.e., diffuse axonal injury) (Fig. 29.4) [58].

While human pathophysiology studies have tried to describe the motion of the brain in concussive injuries, the chemical and neuronal response to concussion has mostly been described in animal models [4, 14]. After the initial mechanical trauma to the brain, there is a complex neurochemical and neurometabolic response. Neuronal axons are stretched, leading to membrane deformation and a release of neurotransmitters and ions. This shift leads to an alteration in glucose metabolism and mitochondrial functioning. Cells respond by downregulating excitatory neurotransmitter receptors and eventually reset themselves to their normal state over several days. Depending on the severity of the injury, the mechanical stretching on axonal cell membranes can cause disruption of the cytoskeleton and likely reversible axonal injury.

With the initial trauma, axonal stretching leads to membrane deformation and an indiscriminate flux of ions through previously regulated ion channels [22]. There is a large efflux of potassium and a release of excitatory amino acids, especially glutamate [37]. This release of glutamate leads to indiscriminate activation of neuronal cells through binding to NMDA and AMPA ionic channels [21]. At the same time, cells work to restore the normal ionic balance through the ATP-dependent Na+/K+ pumps. Due to the shift in ions beyond a normal physiologic level, cellular metabolism is strained and lactate production increases, leading to local acidosis, increased membrane permeability, and cerebral edema [36, 38, 104].

After an initial period of hyperglycolysis, lasting approximately 6 h, a prolonged period of glucose hypometabolism can occur [105]. Activation of NMDA channels leads to an influx of calcium ions, which accumulate in mitochondria and lead to dysfunction in glucose oxidation [43, 75, 100, 104]. In studies of humans with moderate to severe TBI , PET imaging has shown glucose hypometabolism to last for months [7]. While no short-duration, longitudinal, within-subject studies have confirmed it, it is believed that a similar disruption in mild TBI and concussion recovers much more rapidly.

Likely in response to over-activation by glutamate, NMDA receptors are downregulated by post-injury day 2–4 and appear to return to normal by day 7 [25]. NMDA channels are associated with learning and long-term potentiation (LTP ), and post-injury animal models have shown a decrease in LTP induction after post-injury day 2 [73, 84]. While this generally recovers after 1–2 weeks, it has been seen to take up to 8 weeks to fully return to normal [79]. Human fMRI studies have shown abnormal activation of neural circuits in patients with cognitive deficits at 1 week after injury [32]. When these changes have been observed, the affected individuals seem to have a prolonged clinical recovery [45, 50].

In addition to the neurometabolic effects that occur after axonal stretching, disruptions of the cytoskeleton can occur as well. Acutely, neurofilament compaction can occur due to phosphorylation or sidearm proteolysis [34, 92]. As calcium accumulates, microtubules can become destabilized [49]. Axonal transport can be interrupted, and eventually blebbing and disconnection can occur [68, 78].

This process has been observed in animal dissection studies and more recently in human studies using advanced MRI and DTI techniques (Fig. 29.6) [61, 88]. Using DTI , it has been observed that fractional anisotropy, a measure of linear water diffusion, is decreased in several white matter regions after mild TBI . These decreases have been correlated to decreased attention control and memory in adults, as well as to changes in motor speed, executive function, and behavior in children (Fig. 29.7) [62, 101].

The most dreaded consequence of concussion is the reported “second impact syndrome.” When a second concussion occurs in close temporal proximity to an initial concussion, a catastrophic syndrome of cerebral edema can result in coma, severe neurologic deficit, and death [10, 11, 80]. It is unclear how long concussion patients are at risk for second impact syndrome, leading to the extensive debate over return to play timelines [41, 71]. Several animal studies have demonstrated a period of transient metabolic and physiologic vulnerability that may exacerbate the cellular injury caused by repeated mild injury [44, 95, 97].

After the initial injury, the previously described alterations in metabolism and brain activity occur. In a rat model, repeated mild injuries occurring 3 days after an initial mild injury cause damage similar to that which occurs after a single severe TBI [97, 99]. When the second injury occurred after 5 days, the resulting perturbations were similar to the initial injury itself. Given that translating such a time window to humans is difficult, it is reasonable that individuals who have suffered from a concussion do not put themselves in harms way while they are still symptomatic from the initial injury.

While the majority of the biomechanical experiments on mild TBI have occurred in adult populations, there are a few special items to consider in the pediatric population. Given the relative size of the head to the rest of the body in children, angular motion of the head is likely intensified. In helmeted sports in particular, the added weight of the helmet itself compared to the weight of the head and body leads to an increase in angular motion and likely a proportional increase in the forces transferred to the brain [17]. While the overall smaller size of the brain in children may be somewhat protective (i.e., more force is required to cause injury), the increases in force described in helmeted sports likely negate this protection [65].

When a patient is brought to you for an evaluation after concussion, it is important to perform a detailed history and physical. A history of headaches (especially migraines), prior concussion, depression, anxiety, post-traumatic stress disorder, and attention deficit hyperactivity disorder all increase the risk that a patient will endure prolonged symptoms. Female sex and a higher intelligence quotient are also associated with prolonged symptoms [55]. The patient’s pre-injury functioning should be assessed: How have they done in school? Do they have difficulties in any particular subject area? When did they meet important developmental milestones?

Regarding the concussion itself, it is important to note the patient’s initial response: Was there loss of consciousness? Does the patient remember the events leading up to the injury? Does the patient remember the events after the injury? Was there a convulsive event before or after? If the answer is “yes” to any of these questions, documenting the length of time (e.g., length of loss of consciousness, how many minutes were forgotten before or after) should also be done.

The next step generally involves a concussion symptom scale, such as the Pittsburgh Post-Concussion Scale (Fig. 29.8) [107]. In adults and older adolescents, you can ask the patient to fill out the scale before hand, rating each of 21 symptoms on a scale of 0–6, where 0 is no symptom and 6 is severe. In younger children, you may need to go through the symptoms individually to get a response. While younger children may have difficulty differentiating between a 3 and a 6 in terms of symptom severity, they generally understand if something is better or worse than previously (e.g., “is your headache worse today or was it worse yesterday?”). In our practice, we ask that patients fill out the scale for the evening of the injury, the day after the injury, and the day of the evaluation, which allows us to track symptom progress over time.

Finally, a detailed neurological exam should be performed. In concussion, there should be no focal neurological deficits. However, it is not uncommon to see a decrease in short-term memory (e.g., recalling two of three objects 5 min after registration), coarse eye movements on visual pursuit, mild dysmetria, or gait/balance disturbances. Focal neurological deficits should be evaluated as neurological emergencies and triaged to the ER accordingly. If symptoms persist beyond 2–3 days, patients should be evaluated by a neurologist or another medical professional that specializes in concussions. Cognitive complaints (e.g., decreased attention, decreased memory) may require detailed testing by a neuropsychologist .

Several sideline assessment tools have been designed to aid in the evaluation of a concussion patient [51, 52]. While these tools have been widely studied, it is not recommended that these tools be used to decide if a patient can return to play after sustaining a head injury. If a concussion may have occurred and these tests are to be performed, then it is the current recommendation of multiple medical associations that the individual be withheld from same-day return to play and receive a complete evaluation from a fully licensed and trained medical professional. Several of the sideline assessment tools may be used as part of a clinical decision to allow someone to return to play, but their use as a stand-alone tool should be limited. When these tools are used, serial documentation of a subject’s performance should be documented, including baseline testing prior to participation in a sport. These tools allow for initial documentation of symptoms (e.g., headache), physical signs (e.g., LOC, amnesia), behavioral changes (e.g., irritability), and cognitive impairment (e.g., memory deficits) (Fig. 29.9) [53].

Several neurocognitive testing paradigms have been developed for the evaluation of patients with concussion. The most widely used, the Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT), scores patients with six modules and a symptom scale. It derives composite scores on verbal memory, visual memory, reaction time, visual motor processing speed, and impulse control to identify specific cognitive domains that a concussed patient may have difficulty with. In a recent study on high school athletes, researchers were able to correctly classify patients as control or post-concussion utilizing composite scores from the ImPACT test battery in approximately 85 % of cases [81].

Given the competitive nature of many athletes, relying on self-reported symptoms can lead to the underdiagnosis of concussion and premature return to play decisions. In one recent study, the sensitivity of concussion diagnosis increased by 19 % when self-reported symptom scores were combined with computerized neurocognitive testing , compared to symptom scores alone [98]. Further, neurocognitive testing can help determine if patients have fully returned to baseline after a concussion, even after previously reported symptoms have resolved [19, 24]. However, the limitations of neurocognitive testing alone have been demonstrated in a large study on professional football players, where evaluations by clinical staff kept athletes out of participation despite resolution of neurocognitive test scores due to other clinical variables [66].

As with sideline assessments, neurocognitive testing should not be interpreted in a vacuum. Testing can provide a window into specific areas that a subject may be deficient in and can help guide further diagnostic testing by neuropsychologists. It is most useful when patients have pre-participation testing performed to act as a baseline. However, in children, these tools are generally more limited given the varied pace at which individuals progress. Even baseline testing can be unreliable in children, as their scores on neurocognitive tests can improve dramatically over time, and peer-to-peer comparisons are frequently just as fraught with variation.

More formalized neuropsychological testing, performed by a psychologist specially trained in cognitive testing, may be indicated if patients exhibit chronic deficits in any cognitive domains, even if their overall functioning has appeared to return to baseline. It is important that children especially get these evaluations to insure their return to school occurs in an organized and productive manner.

As described at the beginning of this section, the vast majority of patients who suffer concussions do not require neuroimaging. Standard CT and MRI imaging will be negative in a concussion, but can be used to evaluate for more serious brain injuries. CT is useful for the evaluation of bone fractures, intracranial bleeding, cerebral contusions, and general mass effects; it should only be used in the acute setting if clinically indicated and is generally not useful in patients with persistent symptoms. MRI , on the other hand, is more sensitive for evaluating symptoms that worsen or persist beyond a reasonable period of time. For example, if a patient has headaches that start to worsen or become positional, if they develop seizures after the injury, or if they have persistent balance or neurocognitive deficits, MRI can be used to evaluate brain architecture very finely.