The most frequently used definition of Mild traumatic brain injury (mTBI) is a GCS score between 13-15 and loss of consciousness of less than 30 minutes or amnesia not extending beyond 24 hours after blunt head injury 1).
Mild traumatic brain injury (TBI) or concussion is estimated to occur in 3.8 million each year in the US.
It accounts for 80% of all craniocerebral injuries 3).
The incidence worldwide is approximately 600/100,000 pop. per year, with the incidence requiring hospitalization in the range of 100 to 300/100,000 pop. per year.
It occurs in men twice as often as in the female population, with the age group at highest risk being those aged 15-24 years.
The main causes of MBI are traffic accidents and falls 4).
The initial ionic flux and glutamate release result in significant energy demands and a period of metabolic crisis for the injured brain. These physiological perturbations can now be linked to clinical characteristics of concussion, including migrainous symptoms, vulnerability to repeat injury, and cognitive impairment. Furthermore, advanced neuroimaging now allows a research window to monitor postconcussion pathophysiology in humans noninvasively. There is also increasing concern about the risk for chronic or even progressive neurobehavioral impairment after concussion/mild traumatic brain injury. Critical studies are underway to better link the acute pathobiology of concussion with potential mechanisms of chronic cell death, dysfunction, and neurodegeneration 5).
As a result of mechanical trauma, neuronal cell membranes and axons undergo disruptive stretching, leading to temporary ionic disequilibrium 6).
Glutamate release activates N-methyl-D-aspartate receptors, which leads to accumulation of intracellular calcium 8) 9) 10) , causing mitochondrial respiration dysfunction, protease activation, and often initiating apoptosis 11) 12). Elevated glutamate levels were also found to be significantly correlated with derangements in lactate, potassium, brain tissue pH, and brain tissue CO2 levels in human studies 13). Additionally, sodium channel upregulation, fueled by ATPase proteins depending on glucose for energy, is observed following axonal stretch injuries 14).
In combination, the cellular response to the above-mentioned ionic shifts and the downstream effects of the neurotransmitter release lead to an acute energy crisis. This occurs when, to restore ionic equilibrium, adenosine-triphosphate (ATP) -dependent sodium-potassium ion transporter pump activity increases, which augments local cerebral glucose demand 15).
Further metabolic demand is incurred by ATP-dependent sodium channel upregulation. This occurs in the face of mitochondrial dysfunction, leading cells to primarily utilize glycolytic pathways instead of aerobic metabolism for energy, and causing extracellular lactate accumulation as a byproduct 16). This acidosis, caused by hyperglycolysis, has been shown to worsen membrane permeability, ionic disequilibrium, and cerebral edema 17).
Some evidence shows that the lactate produced by this process may eventually be utilized as a source of energy by the neurons once mitochondrial oxidative respiration normalizes; in fact, one study showed that in moderate to severe TBI the incidence of abnormally high levels of lactate uptake were seen in 28% of subjects 18). The same study showed that patients exhibiting a higher rate of brain lactate uptake relative to arterial lactate levels tended to have more favorable outcomes compared to others with lower relative lactate uptake.
Other studies, however, show no significant differences in CBF following mild TBI in subjects over 30 years of age 21). In pediatric studies, CBF has been seen to increase during the first day following mild TBI, followed by decreased CBF for many days after 22) 23). Data comparing cerebral blood flow in pediatric TBI patients has shown impaired autoregulation in 42% of moderate and severe and 17% of mild injuries 24).
The underlying histopathologic changes that occur are relatively unknown. In order to improve understanding of acute injury mechanisms, appropriately designed pre-clinical models must be utilized.
The clinical relevance of compression wave injury models revolves around the ability to produce consistent histopathologic deficits. Mild traumatic brain injuries activate similar neuroinflammatory cascades, cell death markers and increases in amyloid precursor protein in both humans and rodents. Humans, however, infrequently succumb to mild traumatic brain injuries and, therefore, the intensity and magnitude of impacts must be inferred. Understanding compression wave properties and mechanical loading could help link the histopathologic deficits seen in rodents to what might be happening in human brains following concussions 25).
The Glasgow coma scale is too insensitive for use.
Many concussion grading systems have been proposed, the two most widely used are those of Cantu, and that of the American Academy of Neurology (AAN)
LOC by itself may not be a significant discriminant (e.g. confusion > 30 minutes may be worse than LOC for a few seconds). Most systems consider a concussion to be mild if there is a change in sen- sorium without loss of consciousness, however they differ mostly in the deﬁnotion of “change in sensorium”.
There is no scientiﬁc basis to recommend one system over another.
Recommendation: select one system and use it consistently. Do not place undue emphasis on grading.
Even though admitting a patient with a mild traumatic brain injury (TBI) to the ICU might be the appropriate decision to ensure proper interventions in the case of secondary neurological worsening, existing data do not support this 26) 27).
Because of the low risk of intracranial damage, a head computed tomography or hospital admission is not always necessary in these patients. To estimate the risk of intracranial abnormalities in mild TBI, various prediction rules and guidelines have been developed, for example the Canadian CT head rule, National Institute for Health and Care Excellence (NICE) guidelines for head injury and CHIP prediction rule 28) 29) 30).
Previous studies have indicated that there is no consensus about management of mild traumatic brain injury (mTBI) at the emergency department (ED) and during hospital admission 31).
Management should begin with removal from risk if a concussion is suspected, and once diagnosis is made, education and reassurance should be provided. Once symptoms have resolved, a graded return-to-play protocol can be implemented with close supervision and observation for return of symptoms. Management should be tailored to the individual, and if symptoms are prolonged, further diagnostic evaluation may be necessary 32).
Implementation of a selective neurosurgical consultation policy reduced neurosurgical consultations without any impact on patient outcomes, suggesting that trauma surgeons can effectively manage these patients 33) 34).
Patients with the constellation of traumatic subarachnoid hemorrhage and/or intraparenchymal hemorrhage IPH and mTBI do not require neurosurgical consultation, and these findings should not be used as the sole criteria to justify transfer to tertiary centers 35).
Since 2000, center's standard practice has been to obtain a repeat head computed tomography (CT) at least 6 hours after initial imaging. Patients are eligible for discharge if clinical and CT findings are stable. Whether this practice is safe is unknown.
Discharge after a repeat head CT and brief period of observation in the ED allowed early discharge of a cohort of mild TBI patients with traumatic ICH without delayed adverse outcomes. Whether this justifies the cost and radiation exposure involved with this pattern of practice requires further study 36).
Peripheral blood samples were collected from 20 patients with mild TBI at day-1, day-2, day-3, day-4, and day-7 post TBI. The number of circulating Endothelial progenitor cells EPCs and the plasma levels of superoxide dismutase (SOD) and Malondialdehyde (MDA) were measured.
The average of circulating EPCs in TBI patients decreased initially, but increased thereafter, compared with healthy controls. Plasma levels of SOD in TBI patients were significantly lower than those in healthy controls at day-4 post-TBI. MDA levels showed no difference between the two groups. Furthermore, when assessed on day-7 post-TBI, the circulating EPC number were correlated with the plasma levels of SOD and MDA.
These results suggest that the number of circulating EPCs is weakly to moderately correlated with plasma levels of SOD and MDA at day-7 post-TBI, which may offer a novel antioxidant strategy for EPCs transplantation after TBI 37).