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Traumatic brain injury (TBI) is a disruption of brain function due to an external force or blow to the head resulting in any of the following: decreased level of consciousness, memory loss before or after injury, alteration of mental status, neurologic deficits, or intracranial lesion.1


In 2014 the U.S. reported 2.5 million TBI-related ED visits, of which 812,000 were pediatric.13 Falls (47.9%), unintentional strike by or against an object (17.1%), and motor vehicle/traffic (13.2%), were the main causes of TBI-related emergency department visits.13 Falls were the most frequent cause in young children and older adults, while motor vehicle collisions were most common in patients 15-24 years old.2,13 In 2016 and 2017, unintentional falls were the primary etiology of TBI-related hospitalizations among both men and women.14 Among post-9/11 military veterans, 17.3% sustained a TBI during military service, with blast (33.1%), object hitting head (31.7%), and fall (13.5%) as the most common causes of war-related TBI.17

Epidemiology including risk factors and primary prevention

At least 5.3 million people in the U.S. have a TBI-related disability.18 In 2017 224,000 people were hospitalized in the U.S. for TBI-related reasons.14 Hospitalization rates were highest among those age 75 or older, followed by 65-74, then 55-64.14 Among children hospitalized for TBI, falls and motor vehicle crashes were the most common mechanisms of injury.14

In 2017 61,000 people died of TBI-related causes in the U.S, representing an increase from 56,000 in 2013.14,15 In 2013, TBI-related death rates were highest among adults over age 55, with the highest rates among those 75 and older. 4.5% of all TBI deaths were among children under age 18.14 Suicide (34.7%) and unintentional falls (28%) caused most TBI-related deaths, which reflects an overall increase in suicide rates in the U.S.14

Males are four times more likely to experience a TBI18 and are at higher risk of TBI-related hospitalization than females across all mechanisms of injury. Men were more than four times as likely as women to be hospitalized for TBI due to assault, and twice as likely to be hospitalized for TBI due to motor vehicle crash, unintentionally being struck by/with an object, or intentional self-harm.14

American Indian/Alaska Native children and adults are at higher risk of TBI-related hospitalization and death compared to other ethnic groups.16 Racial and ethnic minority groups are less likely to receive post-TBI medical care and rehabilitation than non-Hispanic white patients.16 The 2007-2010 National Trauma Data Bank findings reveal that Hispanic and black patients were less likely to be discharged to high level rehabilitation than were non-Hispanic white patients despite comparable TBI severities, even after adjusting for insurance status.17

In 2004, 22% of hospitalized patients with TBI were transferred to a rehabilitation or nursing facility. From 2006 to 2010, TBI patients (not including multitrauma) made up 3.9% of patients in acute rehabilitation and had an average length of stay of 17.5 days.5 In a longitudinal study examining brain-injured patients five years after acute rehabilitation, 12% required long-term care.18 Approximately a third of all injury-related deaths involve a TBI.6


TBI can be divided into primary injury at the moment of impact and secondary injuries that occur after the initial insult. The primary injury, including cerebral contusions of gray matter, vascular injuries, contusions, and lacerations, occur at the moment of impact. Another primary injury, traumatic axonal injury (also referred to as diffuse axonal injury), occurs with shearing forces in white matter and is not consistently seen on imaging. Bladed weapons and projectiles may cause penetrating injuries, destroy brain tissue in their path, and create waves of injury that stretch and tear distant brain tissue. Blast injury involves negative pressure waves following an explosion and is hypothesized to result in diffuse axonal injury in the brain and spinal cord.3 Secondary injury involves evolution of primary intracerebral damage and extra-cerebral insults such as edema, excitatory neurotransmitter release, free-radical damage, hypotension, metabolic derangements, and ischemia. Additionally, TBI can be divided into focal and diffuse injuries. Focal injuries include lacerations, skull fractures, contusions, and intracranial hemorrhage. Diffuse injuries examples include ischemic injury, diffuse axonal injury, and cerebral edema.7

Though first described in 1928 in boxers, chronic traumatic encephalopathy (CTE) has become the focus of public interest in recent years. CTE is a neurodegenerative tauopathy associated with chronic repeated head trauma, such as that experienced by athletes and military veterans with blast injuries.19 Currently there is no consensus on diagnostic criteria for CTE, and research is ongoing.20 Definitive diagnosis is confirmed by pathognomonic p-tau aggregates on brain autopsy.19

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

The natural history of TBI varies with regard to amount and speed of recovery. Outcome metrics from the early phase can give some information for prognostication. Severe TBI can start its progression in an unresponsive wakefulness syndrome (formerly referred to as a vegetative state) with no purposeful behavior. This can progress to a minimally conscious state with intermittent purposeful behaviors. As a patient continues to improve, recovery will be observed to varying degrees in motor control, memory, and behavior. However, during the early phase of this transition, there can be significant memory impairment, behavioral disturbances, and lack of insight into one’s impairment.

Specific secondary or associated conditions and complications

Medical complications after TBI can include infections, normal pressure hydrocephalus, posttraumatic seizures, spasticity, and neuroendocrine disturbances. Cognitive/behavioral problems include impulsivity, agitation, mood impairments, apathy, decreased processing speed, impaired judgment, and decreased insight into deficits.

Essentials of Assessment


  • The following should be assessed when evaluating a patient:
    • Mechanism of injury
    • Loss of consciousness and duration
    • Associated injuries
    • Residual impairments (including cognitive)
    • Information about the available scores on Glasgow Coma Scale (GCS) to assess severity of injury
    • Early predictors of prognosis including duration of posttraumatic amnesia
    • Prior functional status, previous psychiatric history, drug and alcohol history, previous history of TBI, social support.
    • Physical examination

The rehabilitation exam evaluates all cognitive, behavioral, neurologic, and musculoskeletal impairments; the assessment of neurologic progress, prognosis for recovery, rehabilitation potential, and general planning is generally derived herein. Emphasis is placed on the cognitive evaluation, while a detailed neuro-musculoskeletal evaluation may identify focal abnormality or asymmetry. Serial neurologic examinations are fundamental to rehabilitation as a worsening in neurologic status may indicate new intracranial pathology, and improvements are important for functional gains. The following examinations should be completed:

  • Mental status examination
    • Alertness/arousal
    • Attention
    • Short-term memory
    • Encoding/recall
    • Judgment/reasoning
    • Problem solving
  • Cranial nerves, including vestibular/ocular-motor examination15
  • Strength
  • Reflexes
  • Sensation
  • Cerebellar, fine motor testing
  • Range of motion: assessment of tone, contracture, unidentified injury
  • Special tests: Babinski and Hoffman reflexes, frontal release signs, others

Functional assessment

The Functional Independence Measure (FIM) contains 18 items with 13 covering activities of daily living, mobility, bowel/bladder, and 5 covering communication and cognition. These tests are scored from total assistance (1) to complete independence (7). The Functional Assessment Measure is an adjunct to the FIM that adds 12 items to more adequately assess domains affected in TBI including behavioral, cognitive, communication, and community function measures.8 Neuropsychologist-administered screening/testing can further evaluate a patient’s cognitive/behavior, and affective states.

Laboratory studies

Need for laboratory studies will vary with the patient in the acute phase with electrolyte imbalance and endocrine abnormalities commonly found. Endocrine testing is recommended in the acute hospitalization only if clinically indicated, then again at 3 months and 12 months post-injury.9


Structural imaging for TBI includes computed tomography (CT) and magnetic resonance imaging (MRI). Initial evaluation should include a noncontrasted CT of the brain to rule out intracranial hemorrhage as well as serve limited prognostic utility. A head CT can also be utilized to follow progression, evaluate hydrocephalus, and locate radio-opaque foreign bodies. CT findings after TBI may include subdural hematoma, epidural hematoma, intraparenchymal hemorrhage, contusion, or subarachnoid hemorrhage.15 MRI has higher resolution than CT, can give additional information regarding specific injuries, and can follow changes over time. MRI has higher sensitivity for identifying small, focal traumatic lesions, hemorrhagic axonal damage, and contusions that may be missed on CT.15

Functional imaging for TBI is possible and available looking at blood flow (single-photon emission computed tomography scan) and metabolism (positron emission tomography scan). Additional techniques including functional MRI and magnetic resonance spectroscopy are currently available primarily for research.

Supplemental assessment tools

Early assessment of TBI includes the GCS which serves as assessment of severity of initial injury. The GCS uses visual, motor, and verbal responses to describe cognitive status and stratify TBI into 3 categories: severe (GCS 3-8), moderate (GCS 9-12), and mild (GCS 13-15). After the acute phase, additional scales can aid in assessment. The Department of Defense (DoD) uses multiple factors to grade TBI severity, including neuroimaging results, duration of altered or loss of consciousness, length of posttraumatic amnesia, and highest GCS score during the first 24 hours after injury.15

The Ranchos Los Amigos Scale of cognitive functioning categorizes the patient’s current cognitive function.10 The Galveston Orientation and Amnesia Test provides assessment of posttraumatic amnesia (PTA).12 This can also be measured by the O-log.10 The Coma Recovery Scale-Revised is predictive of outcome in patients with disorders of consciousness.12 The Community Integration Scale can be completed by the patient, significant other or provider.7 Agitation can be assessed with the Agitated Behavior Scale.12

Protein biomarkers are an emerging area of TBI research but are not currently used outside of academic settings to diagnose or guide treatment. Biomarkers currently under investigation may one day be used to evaluate neuronal cell body injury (UCH-L1, NSE), astrogliosis or cell injury (GFAP, S100B), axonal injury (SBDPs, Tau, NFs), demyelination (MBP), postsynaptic injury (Neurogranin), and autoimmunity (AutoAbGFAP, AutoS100b).21  

Early predictions of outcomes

  • Good recovery is unlikely if:11
    • Time to follow commands is longer than one month
    • Duration of PTA is greater than 3 months
    • Age 65 or older
  • Severe disability is unlikely if:11
    • Time to follow commands is less than 2 weeks
    • Duration of PTA is less than 2 months.


Balance, coordination, mobility, and cognitive/behavioral deficits from TBI often require increased supervision and structured environment to maintain the patient in the home. Structural accommodations may also be required for home discharge of the patient.

Social role and social support system

Importance of the TBI patient’s social support system cannot be overstated. Disposition from the hospital setting is often dependent on the ability, availability, and willingness of family members to support mobility and assist with care. Social support may promote safety and prevent medical and psychological complications.

Professional issues

Ethical/legal focuses are decision-making capacity, worker’s compensation, medical malpractice, and in very severe TBI, withdrawal of care. The rehabilitation team must advocate for the patient’s interests and coordinate with other professionals including psychiatry, ethics committee members, insurance providers, and attorneys.

Rehabilitation Management and Treatments

At different disease stages

Initial management starts at the scene of injury with monitoring of respiratory, cardiac, and vascular issues. Concomitant injuries will need to be addressed. Intracranial pressure should be monitored acutely and maintained below 20 millimeters of mercury (mmHg). Surgical intervention may be necessary in patients with significant intracranial hematoma or midline shift.

Sub-acute management includes initiation of rehabilitation efforts. Seizure prophylaxis/management is necessary. Agitation, autonomic problems, bowel/bladder, wounds, vertigo, headaches, and cognitive impairment also need management. Prevention of venous thrombosis and treatment of spasticity are important at this phase. Cognitive and motor recovery occurs during this phase. Rehabilitation is ongoing and the patient’s unique challenges need to be recognized to optimize rehabilitation.

Chronic management includes gradual return to life roles and vocation for those patients able. This may involve support/counseling, driving evaluations, vocational rehabilitation, medication, and referrals. Continued medical support for issues that may include depression, anxiety, ongoing cognitive impairment, weakness, heterotopic ossification, headaches, and spasticity among others is necessary.

Management of several individual complications and consequences of TBI is covered under separate topics

Patient & family education

Educating the patient and family should include careful discussion of expected short- and long-term recovery and impact on the family. The changing life roles within the family tend to require various levels of intervention and may include education, support groups, formal therapy, or other intervention.

Emerging/unique interventions

Impairment-based outcome measurements for TBI include the Extended Glasgow Outcome Scale (GOS-E), the FIM with the addition of the TBI-focused Functional Assessment Measure (FAM) to derive a FIM and FAM score, and the Disability Rating Scale (DRS). The Craig Handicap Assessment and Reporting Technique (CHART) assesses participation by TBI patients, and the Craig Hospital Inventory of Environmental Factors (CHIEF) assesses environmental issues. The Center for Outcome Measurement in Brain Injury (COMBI) website provides a description and list of many scales used to assess outcome after TBI.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

TBI population is diverse in severity and symptomatology of patients. Caring for this population requires patience and flexibility. Pharmacologic management includes removal of medications detrimental to recovery and function as well as evaluating potential medication to augment function. Many of these patients have cognitive impairment that may include frontal lobe injury with executive dysfunction and a lack of insight into their own deficits. This situation can be difficult for the treating physician as well as the patient.

Gaps in the Evidence-Based Knowledge

Although the evidence base for treatment of brain injury patients continues to grow, significant gaps of knowledge persist. These include pharmacologic and biologic roles in recovery and treatment, the role of functional imaging, and evidence for cognitive rehabilitation. Controversy continues in mild TBI/concussion, particularly in sports-related concussion, and the chronic effects of these injuries.


  1. Management of Concussion/mTBI Working Group: Department of Veterans Affairs/Department of Defense, U.S.A. VA/DoD Clinical Practice Guideline for Management of Concussion/mTBI. J Rehabil Res Dev. 2009;46:CP1-68.
  2. Faul M, Xu L, Wald MM, Coronado VG. Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations and Deaths 2002–2006. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2010.
  3. Champion HR, Holcomb JB, Young LA. Injuries from explosions. J Trauma. 2009;66:1468–1476.
  4. Coronado VG, Xu L, Basavaraju SV, et al. Suveillance for brain injury related deaths–United States 1997-2007. CDC Morbidity & Mortality Weekly Report. May 6, 2011. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/ss6005a1.htm. Accessed November 4, 2011.
  5. Uniform Data System for Medical Rehabilitation. 2011. Amherst, NY. www.udsmr.org. Accessed June, 2011.
  6. Centers for Disease Control and Prevention. Quickstats: injury and traumatic brain injury (TBI)-related death rates, by age group—United States, 2006. MMWR Morb Mortal Wkly Rep. 2010;59(10):303.
  7. Smith C. Neuropathology. In: Silver JM, McAllister TW, Yudofsky SC, eds. Textbook of Traumatic Brain Injury. 2nd ed. Washington, DC: American Psychiatric Publishing, Inc; 2011:23-35.
  8. Wright, J. (2000). The Functional Assessment Measure. The Center for Outcome Measurement in Brain Injury.http://www.tbims.org/combi/FAM ( accessedMarch 19, 2015
  9. Ghigo E, Masel B, Aimaretti G, et al. Consensus guidelines on screening for hypopituitarism following traumatic brain injury. Brain Inj. 2005;19(9):711-724
  10. Mysiw WJ, Fugate LP, Clinchot DM. Assessment, early rehabilitation intervention, and tertiary prevention. In: Zasler ND, Katz DI, Zafonte RD, eds. Brain Injury Medicine. New York, NY: Demos; 2007:283-304.
  11. Santa Clara Valley Medical Center. The Center for Outcome Measurement in Brain Injury. 2006. Available at: http://www.tbims.org/combi. Accessed August 4, 2011.
  12. Kothari S. Prognosis after severe TBI: a practical, evidence-based approach. In: Zasler ND, Katz DI, Zafonte RD, eds. Brain Injury Medicine. New York, NY: Demos; 2007:169-199.
  13. Centers for Disease Control and Prevention. 2014 Surveillance Report: Traumatic Brain Injury-related Emergency Department Visits, Hospitalizations, and Deaths. https://www.cdc.gov/traumaticbraininjury/pdf/TBI-Surveillance-Report-FINAL_508.pdf
  14. Centers for Disease Control and Prevention. 2016-2017 Surveillance Report: Traumatic Brain Injury-related Hospitalizations and Deaths by Age Group, Sex, and Mechanism of Injury. https://www.cdc.gov/traumaticbraininjury/pdf/TBI-surveillance-report-2016-2017-508.pdf
  15. National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Board on Health Care Services; Committee on the Review of the Department of Veterans Affairs Examinations for Traumatic Brain Injury. Evaluation of the Disability Determination Process for Traumatic Brain Injury in Veterans. Washington (DC): National Academies Press (US); 2019 Apr 10. 1, Introduction. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542605/
  16. https://www.cdc.gov/traumaticbraininjury/health-disparities-tbi.html
  17. Lindquist LK, Love HC, Elbogen EB. Traumatic Brain Injury in Iraq and Afghanistan Veterans: New Results From a National Random Sample Study. J Neuropsychiatry Clin Neurosci. 2017 Summer;29(3):254-259. doi: 10.1176/appi.neuropsych.16050100. Epub 2017 Jan 25. PMID: 28121256; PMCID: PMC5501743.
  18. Mary Alexis Iaccarino, Saurabha Bhatnagar, Ross Zafonte. Chapter 26 – Rehabilitation after traumatic brain injury. Editor(s): Jordan Grafman, Andres M. Salazar. Handbook of Clinical Neurology. Elsevier, Volume 127, 2015, Pages 411-422. ISSN 0072-9752, ISBN 9780444528926. https://doi.org/10.1016/B978-0-444-52892-6.00026-X.
  19. Mckee AC, Abdolmohammadi B, Stein TD. The neuropathology of chronic traumatic encephalopathy. Handb Clin Neurol. 2018;158:297-307. doi: 10.1016/B978-0-444-63954-7.00028-8. PMID: 30482357.
  20. Smith DH, Johnson VE, Trojanowski JQ, Stewart W. Chronic traumatic encephalopathy – confusion and controversies. Nat Rev Neurol. 2019 Mar;15(3):179-183. doi: 10.1038/s41582-018-0114-8. PMID: 30664683; PMCID: PMC6532781.
  21. Wang KK, Yang Z, Zhu T, Shi Y, Rubenstein R, Tyndall JA, Manley GT. An update on diagnostic and prognostic biomarkers for traumatic brain injury. Expert Rev Mol Diagn. 2018 Feb;18(2):165-180. doi: 10.1080/14737159.2018.1428089. Epub 2018 Jan 23. PMID: 29338452; PMCID: PMC6359936.


McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport–the 3rd International Conference on concussion in sport, held in Zurich, November 2008. J Clin Neurosci. 2009;16:755-63.

Original Version of the Topic

Christopher Wolf, DO, Matthew McLaughlin, MD, Michael Khadavi, MD, Fred Murdock, PhD, Elizabeth A Barton, MD. Traumatic Brain Injury. 11/16/2011.

Previous Revision(s) of the Topic

Christopher Wolf, DO, Matthew McLaughlin, MD, Michael Khadavi, MD, Fred Murdock, PhD, Elizabeth A Barton, MD. Traumatic Brain Injury. 10/8/2015.

Author Disclosure

Lindsay A. Smith, MD
Nothing to Disclose

Blessen C. Eapen, MD
Nothing to Disclose