User Tools

Site Tools


mild_traumatic_brain_injury

Mild traumatic brain injury mTBI

The most frequently used definition of Mild traumatic brain injury (TBI) 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).

Epidemiology

Mild traumatic brain injury (TBI) or concussion is estimated to occur in 3.8 million each year in the US.

The peak ages for these injuries are in adolescence and young adulthood, and sport-related concussions are particularly common among young persons 2).

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).

Classification

A definition of mild TBI has been developed by the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine. Within the spectrum of injury severity in mild TBI there are several classification systems, primarily used in management of acute mild TBI, that breakdown mild TBI into grades of injury severity. These are based upon the presence or absence of mental status changes, amnesia, loss of consciousness, anatomical lesion or neurological deficit 5).

see also Pediatric mild traumatic brain injury.

see Sports related concussion.

see Explosive blast mild traumatic brain injury.

Neurometabolic cascade

Recommendation: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3211100/

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 6).

Glutamate release and ionic disequilibrium

As a result of mechanical trauma, neuronal cell membranes and axons undergo disruptive stretching, leading to temporary ionic disequilibrium 7).

As a result, levels of extracellular potassium increase drastically, and indiscriminate glutamate release occurs 8).

Glutamate release activates N-methyl-D-aspartate receptors, which leads to accumulation of intracellular calcium 9) 10) 11) , causing mitochondrial respiration dysfunction, protease activation, and often initiating apoptosis 12) 13). 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 14). Additionally, sodium channel upregulation, fueled by ATPase proteins depending on glucose for energy, is observed following axonal stretch injuries 15).

Energy crisis and mitochondrial dysfunction

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 16).

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 17). This acidosis, caused by hyperglycolysis, has been shown to worsen membrane permeability, ionic disequilibrium, and cerebral edema 18).

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 19). 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.

Alterations in cerebral blood flow

Some studies have shown that cerebral blood flow decreases immediately following the insult, and the amount of time it remains lowered seems to depend on the severity of the injury 20) 21).

Other studies, however, show no significant differences in CBF following mild TBI in subjects over 30 years of age 22). In pediatric studies, CBF has been seen to increase during the first day following mild TBI, followed by decreased CBF for many days after 23) 24). Data comparing cerebral blood flow in pediatric TBI patients has shown impaired autoregulation in 42% of moderate and severe and 17% of mild injuries 25).

Histopathologic changes

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 26).

Clinical Features

Posttraumatic headache is one of the most common symptoms following mild traumatic brain injury in children.

From the available evidence, slowed reaction time, impaired verbal learning and memory, impaired balance, and disorientation or confusion were found to be significantly prevalent in early samples of exposed individuals. There is insufficient evidence to assess the relationships among these measures.At a minimum, future studies should include comparison groups; take measures at fixed and relevant time points; report distinct signs, symptoms, and deficits in terms of frequencies and correlations; and follow standards for minimizing bias and confound 27).

Symptoms are typically short-lived, and may correlate to physiologic changes in the acute period after injury. There are many available tools that can be utilized on the sideline as well as in the clinical setting for assessment and diagnosis of concussion. It is important to use validated tests in conjunction with a thorough history and physical examination. Neurocognitive testing may be helpful in the subacute period.

Possible findings

vacant stare or befuddled expression

delayed verbal & motor responses: slow to answer questions or follow instructions

easy distractibility, difficult focusing attention, inability to perform normal activities

disorientation: walking in the wrong direction, unaware of date, time or place.

speech alterations: slurred or incoherent, disjoined or incomprehensible statements

incoordination: stumbling, inability to tandam walk

exaggerated emotionality: inappropriate crying, distraught appearance

memory deficits: repeatedly asking same question that has been answered cannot name 3 out of 3 objects after 5 minutes

any period of LOC: paralytic coma, unresponsiveness to stimuli.

Confusion

May be evident immediately following the blow, or may take several minutes to develop.

Loss of consciousness (LOC)

Loss of consciousness is not a requirement.

Patients themselves may be unaware whether or not they experienced LOC.

When there is LOC, the fact that it is often virtually instantaneous (there may be a latency of a few seconds), and the usually rapid return of function with no evidence of microscopic changes suggests that the LOC is due to a transient disturbance in neuronal function. Levels of glutamate (an excitatory neurotransmitter) rise after concussion and the brain enters a hyperglycolytic and hypermetabolic state which may persist up to 7-10 days after the injury.

During this period the brain may be more susceptible to a second impact syndrome.

Diagnosis

Concussion grading

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.

Management

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).

Guideline

Outcome

Case series

2017

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).

1)
Teasdale G, Maas A, Lecky F, Manley G, Stocchetti N, Murray G. The Glasgow Coma Scale at 40 years: standing the test of time. Lancet Neurol. 2014 Aug;13(8):844-54. doi: 10.1016/S1474-4422(14)70120-6. Review. Erratum in: Lancet Neurol. 2014 Sep;13(9):863. PubMed PMID: 25030516.
2)
Langlois JA, Rutland-Brown W, Thomas KE. The incidence of traumatic brain injury among children in the United States: differences by race. J Head Trauma Rehabil. 2005;20(3):229–238.
4)
Cassidy, J. D., Carroll, L. J., Peloso, P. M. et al.: Incidence, risk factors and prevention of mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. J. Rehabil. Med., 2004, 43 (Suppl.), p. 28-60.
5)
Esselman PC, Uomoto JM. Classification of the spectrum of mild traumatic brain injury. Brain Inj. 1995 May-Jun;9(4):417-24. Review. PubMed PMID: 7640688.
6)
Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. 2014 Oct;75 Suppl 4:S24-33. doi: 10.1227/NEU.0000000000000505. PubMed PMID: 25232881.
7)
Farkas O, Lifshitz J, Povlishock JT. Mechanoporation induced by diffuse traumatic brain injury: an irreversible or reversible response to injury? J Neurosci. 2006 Mar 22;26(12):3130–3140.
8)
Katayama Y, Becker DP, Tamura T, Hovda DA. Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury. J Neurosurg. 1990 Dec;73(6):889–900.
9)
Osteen CL, Giza CC, Hovda DA. Injury-induced alterations in N-methyl-D-aspartate receptor subunit composition contribute to prolonged 45 calcium accumulation following lateral fluid percussion. Neuroscience. 2004;128(2):305–322.
10)
Osteen CL, Moore AH, Prins ML, Hovda DA. Age-dependency of 45calcium accumulation following lateral fluid percussion: acute and delayed patterns. J Neurotrauma. 2001 Feb;18(2):141–162.
11)
Fineman I, Hovda DA, Smith M, Yoshino A, Becker DP. Concussive brain injury is associated with a prolonged accumulation of calcium: a 45Ca autoradiographic study. Brain Research. 1993;624(1–2):94–102.
12)
Raghupathi R. Cell death mechanisms following traumatic brain injury. Brain Pathol. 2004 Apr;14(2):215–222.
13)
Sullivan PG, Rabchevsky AG, Waldmeier PC, Springer JE. Mitochondrial permeability transition in CNS trauma: cause or effect of neuronal cell death? J Neurosci Res. 2005 Jan 1–15;79(1–2):231–239.
14)
Reinert M, Hoelper B, Doppenberg E, Zauner A, Bullock R. Substrate delivery and ionic balance disturbance after severe human head injury. Acta Neurochir Suppl. 2000;76:439–444.
15)
Yuen TJ, Browne KD, Iwata A, Smith DH. Sodium channelopathy induced by mild axonal trauma worsens outcome after a repeat injury. J Neurosci Res. 2009 Dec;87(16):3620–3625.
16)
Yoshino A, Hovda DA, Kawamata T, Katayama Y, Becker DP. Dynamic changes in local cerebral glucose utilization following cerebral concussion in rats: evidence of a hyper- and subsequent hypometabolic state. Brain Research. 1991;561(1):106–119.
17)
Kawamata T, Katayama Y, Hovda DA, Yoshino A, Becker DP. Lactate accumulation following concussive brain injury: the role of ionic fluxes induced by excitatory amino acids. Brain Research. 1995;674(2):196–204.
18)
Kalimo H, Rehncrona S, Soderfeldt B. The role of lactic acidosis in the ischemic nerve cell injury. Acta Neuropathol Suppl (Berl) 1981;7:20–22.
19)
Glenn TC, Kelly DF, Boscardin WJ, et al. Energy dysfunction as a predictor of outcome after moderate or severe head injury: indices of oxygen, glucose, and lactate metabolism. J Cereb Blood Flow Metab. 2003 Oct;23(10):1239–1250.
20)
Golding EM, Steenberg ML, Contant CF, Jr, Krishnappa I, Robertson CS, Bryan RM., Jr Cerebrovascular reactivity to CO(2) and hypotension after mild cortical impact injury. Am J Physiol. 1999 Oct;277(4 Pt 2):H1457–1466.
21)
Grindel SH. Epidemiology and pathophysiology of minor traumatic brain injury. Curr Sports Med Rep. 2003 Feb;2(1):18–23.
22)
Chan KH, Miller JD, Dearden NM. Intracranial blood flow velocity after head injury: relationship to severity of injury, time, neurological status and outcome. J Neurol Neurosurg Psychiatry. 1992 Sep;55(9):787–791.
23)
Mandera M, Larysz D, Wojtacha M. Changes in cerebral hemodynamics assessed by transcranial Doppler ultrasonography in children after head injury. Childs Nerv Syst. 2002 Apr;18(3–4):124–128.
24)
Becelewski J, Pierzchala K. Cerebrovascular reactivity in patients with mild head injury. Neurol Neurochir Pol. 2003 Mar-Apr;37(2):339–350.
25)
Vavilala MS, Lee LA, Boddu K, et al. Cerebral autoregulation in pediatric traumatic brain injury. Pediatr Crit Care Med. 2004;5(3):257–263.
26)
Lucke-Wold BP, Phillips M, Turner RC, Logsdon AF, Smith KE, Huber JD, Rosen CL, Regele JD. Elucidating the role of compression waves and impact duration for generating mild traumatic brain injury in rats. Brain Inj. 2016 Nov 23:1-8. [Epub ahead of print] PubMed PMID: 27880054.
27)
Carney N, Ghajar J, Jagoda A, Bedrick S, Davis-OʼReilly C, du Coudray H, Hack D, Helfand N, Huddleston A, Nettleton T, Riggio S. Concussion guidelines step 1: systematic review of prevalent indicators. Neurosurgery. 2014 Sep;75 Suppl 1:S3-S15. doi: 10.1227/NEU.0000000000000433. PubMed PMID: 25006974.
28)
Stiell IG, Wells GA, Vandemheen K, Clement C, Lesiuk H, Laupacis A, McKnight RD, Verbeek R, Brison R, Cass D, Eisenhauer ME, Greenberg G, Worthington J. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001 May 5;357(9266):1391-6. PubMed PMID: 11356436.
29)
Smits M, Dippel DW, Steyerberg EW, de Haan GG, Dekker HM, Vos PE, Kool DR, Nederkoorn PJ, Hofman PA, Twijnstra A, Tanghe HL, Hunink MG. Predicting intracranial traumatic findings on computed tomography in patients with minor head injury: the CHIP prediction rule. Ann Intern Med. 2007 Mar 20;146(6):397-405. PubMed PMID: 17371884.
30)
Borg J, Holm L, Cassidy JD, Peloso PM, Carroll LJ, von Holst H, Ericson K; WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. Diagnostic procedures in mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. J Rehabil Med. 2004 Feb;(43 Suppl):61-75. Review. PubMed PMID: 15083871.
31)
Foks KA, Cnossen MC, Dippel DW, Maas A, Menon D, van der Naalt J, Steyerberg EW, Lingsma H, Polinder S. Management of mild traumatic brain injury at the emergency department and hospital admission in Europe: A survey of 71 neurotrauma centers participating in the CENTER-TBI study. J Neurotrauma. 2017 Apr 11. doi: 10.1089/neu.2016.4919. [Epub ahead of print] PubMed PMID: 28398105.
32)
Choe MC, Giza CC. Diagnosis and Management of Acute Concussion. Semin Neurol. 2015 Feb;35(1):29-41. Epub 2015 Feb 25. PubMed PMID: 25714865.
33)
Overton TL, Shafi S, Cravens GF, Gandhi RR. Can trauma surgeons manage mild traumatic brain injuries? Am J Surg. 2014 Apr 28. pii: S0002-9610(14)00179-2. doi: 10.1016/j.amjsurg.2014.02.012. [Epub ahead of print] PubMed PMID: 24933668.
34)
Joseph B, Aziz H, Sadoun M, Kulvatunyou N, Tang A, O'Keeffe T, Wynne J, Gries L, Green DJ, Friese RS, Rhee P. The acute care surgery model: managing traumatic brain injury without an inpatient neurosurgical consultation. J Trauma Acute Care Surg. 2013 Jul;75(1):102-5; discussion 105. doi: 10.1097/TA.0b013e3182946667. PubMed PMID: 23778447.
35)
Ditty BJ, Omar NB, Foreman PM, Patel DM, Pritchard PR, Okor MO. The nonsurgical nature of patients with subarachnoid or intraparenchymal hemorrhage associated with mild traumatic brain injury. J Neurosurg. 2014 Dec 19:1-5. [Epub ahead of print] PubMed PMID: 25526270.
36)
Kreitzer N, Lyons MS, Hart K, Lindsell CJ, Chung S, Yick A, Bonomo J. Repeat neuroimaging of mild traumatic brain-injured patients with acute traumatic intracranial hemorrhage: clinical outcomes and radiographic features. Acad Emerg Med. 2014 Oct;21(10):1083-91. doi: 10.1111/acem.12479. PubMed PMID: 25308130.
37)
Huang X, Wan D, Lin Y, Xue N, Hao J, Ma N, Pei X, Li R, Zhang W. Endothelial Progenitor Cells Correlated with Oxidative Stress after Mild Traumatic Brain Injury. Yonsei Med J. 2017 Sep;58(5):1012-1017. doi: 10.3349/ymj.2017.58.5.1012. PubMed PMID: 28792147.
mild_traumatic_brain_injury.txt · Last modified: 2017/08/17 13:18 by administrador