Author(s): Steven Flanagan, MD, Jessie Chan, MD
Originally published: November 16, 2011 Last updated: February 12, 2026
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Disease/Disorder

Definition

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

Etiology

Unintentional falls (49.1%) and motor vehicle accidents (24.5%) are the most common causes of TBI-related hospitalizations for adults.2 Similarly, the most common mechanisms of injury in children aged 0-17 are falls (7.7 per 100,000) and motor vehicle accidents (6.8 per 100,000). Other causes include colliding with a moving or stationary object and assaults, with the caveat that many cases are often classified as either other or unknown.2 Among deployed service members, 22.6% reported sustaining a TBI, with blast/bullet (53.8%), fall (10.8%), and motor vehicle crash (6.6%) as the most common causes of service-related TBI.3 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 military-related TBI.4

Epidemiology including risk factors and primary prevention

There are approximately 225,000 non-fatal TBI-related hospitalizations annually in the United States, 7.8% of whom were children and adolescents.5  Recent evidence suggests that approximately 11.4 million individuals age ≥40 with a history of TBI with loss of consciousness in the United States have a disability in at least one domain of function.6 Hospitalization rates are highest among those age 75 or older, followed by 65-74, then 55-64.2 Among children hospitalized for TBI, falls and motor vehicle accidents are the most common mechanisms of injury.2

Slightly more than 60,000 TBI related deaths are reported annually in the U.S. Rates of TBI-related deaths are highest among adults over age 55, with the highest rates in that group among those 75 and older. The most common mechanisms are suicide (35.5%), unintentional falls (29.9%), and motor vehicle accidents (17%). Adults aged 75 and older account for the majority of those who had TBI-related deaths due to suicide and falls, whereas people aged 15-34 have the highest rates of deaths due to motor vehicle accidents. 4.1% of all TBI deaths are among children under age 18, and the most common mechanisms are motor vehicle accidents and homicide.7 By age, TBI-related deaths decrease over time in people aged 25 and younger but increase in those aged 50 and older, with the most significant increase seen in those 75 years or older.8

Men are twice as likely as women to be hospitalized due to TBI and thrice as likely to experience a TBI-related death.9 Men have significantly higher age-adjusted rates of unintentional and intentional injury secondary to falls, motor vehicles accidents (twofold higher), being struck by or against an object (more than twofold higher), intentional self-harm (more than twofold higher), and assault (more than fourfold higher).2

Compared to the general population, people who experience homelessness are 2-4 times more likely to have a history of TBI and 10 times more likely to have a history of moderate to severe TBI.9

American Indian and Alaska Native children and adults are at higher risk of TBI-related hospitalization and death compared to other ethnic groups.7 Between 1999 and 2018, TBI-related mortality rates declined among Asian and Pacific Islander and Hispanic individuals, remained stable among Black individuals, and increased among White individuals.8 Racial and ethnic minority groups are less likely to receive post-TBI medical care and rehabilitation than non-Hispanic white patients.9 The 2007-2010 National Trauma Data Bank findings reveal that Hispanic and black patients are less likely to be discharged to high level rehabilitation than are non-Hispanic white patients despite comparable TBI severities, even after adjusting for insurance status.4

A United States study of patients with severe TBI in 2016 found that mortality was similar across geographical regions, teaching vs nonteaching hospital, and hospital size. 51% were discharged home, 16% to inpatient rehabilitation facilities (IRF), 14% to skilled nursing facilities (SNF), and 11% were deceased. There was geographical variation in discharge destination, with southern patients more likely to be discharged to home whereas northeastern patients were more likely to be discharged to IRF.10

Patho-anatomy/physiology

TBI-related pathophysiology can be conceptualized into primary injury at the moment of impact and secondary injuries that occur after the initial insult. Primary injury includes cerebral contusions, intracranial hemorrhages, traumatic axonal injury, and lacerations. Traumatic axonal injury (also referred to as diffuse axonal injury), results from shearing forces impacting white matter tracks, which is inconsistently seen on standard neuroimaging studies. 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 traumatic axonal injury in the brain and spinal cord.11 Secondary injury includes the evolution of primary intracerebral damage in addition to edema, excitatory neurotransmitter release, free-radical damage, hypotension, metabolic and ionic 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, traumatic axonal injury, and cerebral edema.12

Chronic traumatic encephalopathy (CTE) has become the focus of public interest in recent years. It is a neurodegenerative tauopathy associated with chronic repeated head trauma, most commonly experienced by athletes and military veterans with blast injuries.13 Diagnostic criteria for CTE, determined by a consensus panel convened by the National Institutes of Health includes the presence of phosphorylated-tau aggregates in neurons, astrocytes, and cell processes around small blood vessels in the depths of cortical sulci, which is considered pathognomonic. The presence and quantity of locations of neurofibrillary tangles in other cerebral regions, in combination with the pathognomonic lesion determines disease burden or whether the specimen is non-diagnostic.14 In 2021, consensus guidelines were established to diagnose the clinical manifestations of CTE, called traumatic encephalopathy syndrome (TES). A diagnosis of TES requires substantial exposure to repetitive head impacts (RHI), cognitive impairment, and/or neurobehavioral dysregulation that are progressive over a period of at least one year without RHI, which  cannot be fully accounted for by other conditions.15

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 provide some information for prognostication. Severe TBI can result in a disorder of consciousness (DOC), which often starts its progression in an unresponsive wakefulness syndrome (formerly referred to as a vegetative state) with no discernable awareness of, or interaction with the external environment. This can progress to a minimally conscious state with observable, repeated 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.16

Specific secondary or associated conditions and complications

Medical complications after TBI can include infections, hydrocephalus, posttraumatic seizures, spasticity, heterotopic ossification, and neuroendocrine and autonomic disturbances. Cognitive/behavioral problems include impulsivity, agitation, mood impairments, apathy, decreased processing speed, impaired judgment, and decreased insight into deficits.17 TBI has also been described as a chronic condition, manifested by decreased life expectancy, increased risk of multiple conditions such as neurodegenerative diseases, psychiatric conditions, sleep disorders, and changes in function over time.18

Essentials of Assessment

History

  • The following should be assessed when evaluating a person with TBI
    • Mechanism of injury
    • Loss of consciousness and duration
    • Associated injuries
    • Residual impairments (including cognitive)
    • Initial assessment at the time of injury (e.g. Glasgow Coma Scale)
    • Early predictors of prognosis including duration of posttraumatic amnesia
    • Prior functional status, previous psychiatric history, drug and alcohol history, medical history, prior TBIs, learning disabilities, and social support.

Physical examination

The rehabilitation exam continually evaluates cognitive, behavioral, neurologic, and musculoskeletal status, neurologic and functional progress, prognosis for recovery, and rehabilitation potential, which guides treatment planning. Serial neurologic examinations are fundamental to rehabilitation as a worsening in neurologic status may indicate new intracranial pathology or medical problems.  Assessments of the following are essential to comprehensive management:

  • Mental status examination
    • Alertness/arousal
    • Attention
    • Short-term memory
    • Encoding/recall
    • Judgment/reasoning
    • Problem solving
  • Cranial nerves, including vestibular/ocular-motor examination
  • 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

TBI variably affects physical, cognitive, and emotional functions, which further impacts a person’s societal roles, including those at home, school/work, and vocational activities and can be measured by a readily available assessment tools.19 Neuropsychologist-administered screening/testing can further evaluate a patient’s cognitive/behavior, and affective states.20

Laboratory studies

Need for laboratory studies will vary with the patient in the acute phase with electrolyte imbalance and endocrine abnormalities commonly found. Although no widely accepted guidelines exist, endocrine testing has been recommended in the acute hospitalization if clinically indicated, then again at 3 months and 12 months post-injury.21

Imaging

Structural imaging for TBI includes computed tomography (CT) and magnetic resonance imaging (MRI). Initial evaluation should include a non-contrast CT of the brain to rule out epidural, subdural, subarachnoid, and intraparenchymal hemorrhages. Head CTs are also utilized to identify and follow the evolution of lesions, diagnose hydrocephalus, and locate radio-opaque foreign bodies. MRI has higher resolution than CT, providing greater sensitivity in identifying small focal traumatic lesions, hemorrhagic axonal damage, and contusions that may be missed on CT. Additional MR technologies, such as functional MRI, diffusion tensor imaging, diffusion kurtosis imaging, and magnetic resonance spectroscopy, as well as single-photon emission computed tomography (SPECT) and positron emission tomography (PET) are currently available primarily for research.16

Supplemental assessment tools

Early assessment of TBI includes the GCS which assesses initial injury severity by evaluating visual, motor, and verbal responses.  Each category is assigned a value, which are summed to determine a final score and stratify TBI into 3 categories: severe (GCS 3-8), moderate (GCS 9-12), and mild (GCS 13-15). It is a useful tool to assess for changes in neurological status acutely after injury. After the acute phase, multiple factors are typically used to grade TBI severity, including neuroimaging results, duration of altered or loss of consciousness and length of posttraumatic amnesia, in addition to the highest GCS score during the first 24 hours after injury. A new model is being proposed to more precisely and personalize assess injury severity.  It incorporates clinical, biomarker and imaging data as well as various modifiers such as preexisting medical conditions, environmental factors, age, living situation and how the injury occurred that is intended to better describe injury impact and trajectory over time.22

The Ranchos Los Amigos Levels of Cognitive Functioning categorizes the patient’s cognitive and behavioral function and recovery over time. The Galveston Orientation and Amnesia Test (GOAT) is used to determine if someone remains in or has emerged from posttraumatic amnesia (PTA) noting the length of PTA is a strong prognostic indicator for functional recovery. This can also be measured by the O-log.23 The Coma Recovery Scale-Revised assesses auditory, visual, motor, oromotor/verbal, and communication skills as well as arousal arranged in a hierarchical format to assess patients with disorders of consciousness.16,24 Several tools are used to determine the degree of community integration, including the Community Integration Questionnaire, Participation Assessment with Recombined Tools-Objective, and the Participation Objective and Participation Subjective tool.12 Agitation can be assessed and monitored with the Agitated Behavior Scale.25 Impairment-based outcome measurements for TBI include the Extended Glasgow Outcome Scale (GOS-E) 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.26

Early predictions of outcomes

There can be significant heterogeneity in outcome; some factors can be helpful for prognostication, with the caveat that individual patients’ outcomes can vary.

  • Good recovery is unlikely if
    • 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
    • Time to follow commands is less than 2 weeks
    • Duration of PTA is less than 2 months.12,27

Environmental

Balance, coordination, mobility, and cognitive/behavioral deficits from TBI often require increased supervision and structured environment to maintain the patient in their community. Structural accommodations may also be required for home discharge of the patient. Environmental modification to decrease sensory stimulation during the acute stage of recovery is a core component of early management to mitigate agitation.12

Social role and social support system

The importance of the person with TBI’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.12

Professional issues

Ethical/legal issues that healthcare providers often address in the management of TBI include decision-making capacity, worker’s compensation, medical malpractice, and in very severe injury, withdrawal of care. The rehabilitation team must advocate for the patient’s interests and coordinate with multiple professionals and stake holders, including but not limited to other medical consultants, ethics committee members, insurance providers, family members, and attorneys.28

Rehabilitation Management and Treatments

At different disease stages

Initial management starts at the scene of injury by assessing and addressing alterations in vital signs, breathing, and vascular issues along with concomitant injuries. Acute hospital interventions often include diligent monitoring and management of intracranial and mean arterial pressure to ensure adequate cerebral perfusion. Surgical intervention may be necessary in patients with significant intracranial hematoma or midline shift.

Routine seizure prophylaxis is recommended for the first week post injury following severe TBI, noting management is generally guided by various clinical indications thereafter.   Agitation, autonomic dysregulation, bowel/bladder dysfunction, wounds, vertigo, headaches, spasticity, and cognitive impairment should be monitored and addressed as needed. Prevention of venous thrombosis is important at this phase. Cognitive and motor recovery as well as emergence of challenging behaviors often commences during the acute hospitalization, requiring the initiation of early rehabilitation interventions.  This needs to be continued into the subacute and long-term phases to adequately identify and address unique challenges and to optimize outcomes.29

Long-term management includes assisting patients with reintegration into their communities and return to pre-injury life roles and vocation. This may involve support/counseling, driving evaluations, vocational rehabilitation, medication, ongoing rehabilitation therapies, and referrals to other healthcare professionals. Continued medical support for TBI-related comorbidities, such as depression, anxiety, cognitive impairments, weakness, heterotopic ossification, headaches, and spasticity among others is often necessary.30

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

Patient & family education

Educating the patient and family includes careful discussion of expected short- and long-term recovery and impact on the family. Changing life roles within the family tend to require various levels of intervention and may include education, support groups, formal therapy, or other intervention.12,31

Emerging/unique interventions

Serum and CSF biomarkers are being investigated as potential tools to aid in assessing, diagnosing and managing TBI.  Most of the scientific literature on biomarkers include those released by stressed, injured, and dying neurons and astroglia such as intracellular soluble molecules UCH-L1, NSE, and S100B as well as structural proteins GFAP, NF-L, and tau. There has also been increased focus on TBI-related vascular injury which has led to studies on markers of endothelial stress (CEGF, vWF, ADAMTS13), damage to endothelial tight junctions (claudin-5, occludin), cell-cell adhesion disruption (VCAM-1, CNX43, MMP9), and inflammatory processes (S100A8/9, hsp70, HMGB1, CXCL12).32  Acute serum levels of UCH-L1 and GFAP are correlated with intracranial hemorrhages detectable by CT as well as the need for neurosurgical intervention, and are available for clinical use.

Neuromodulation, brain-computer interfaces, and innovative means to address spasticity are being explored as potential means to facilitate recovery and improve function.33

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

The 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 additions to augment function. Many people with TBI are unaware of their cognitive and behavioral challenges, complicating the management for healthcare providers and family members.12,31,34

Gaps in the Evidence-Based Knowledge

Accurate estimates of the incidence and frequency of TBI is hampered by several factors, including not seeking care following concussion, insufficient epidemiological data from many states, and discrepancies in arising from different sources.35 Although the evidence base for assessment and treatment of TBI continues to grow, significant gaps of knowledge persist. These include pharmacologic and biologic roles in recovery and treatment, the clinical role of advanced neuroimaging technologies, mechanisms of cognitive and physical decline over time, accurate prognostication, and more meaningful assessments of severity over time.

References

  1. Department of Veterans Affairs, Department of Defense. VA/DoD Clinical Practice Guideline for the Management and Rehabilitation of Post-Acute Mild Traumatic Brain Injury. Clin Pract Guidel. Published online June 2021. https://www.healthquality.va.gov/HEALTHQUALITY/guidelines/Rehab/mtbi/VADODmTBICPGFinal508.pdf
  2. Peterson AB, Zhou H, Thomas KE, Daugherty J. Traumatic brain injury-related hospitalizations and deaths by age group, sex, and mechanism of injury : United States 2016/2017. Published online 2021. https://stacks.cdc.gov/view/cdc/111900
  3. Jannace KC, Pompeii L, Gimeno Ruiz De Porras D, et al. Risk of Traumatic Brain Injury in Deployment and Nondeployment Settings Among Members of the Millennium Cohort Study. J Head Trauma Rehabil. 2025;40(2):E102-E110. doi:10.1097/HTR.0000000000000970
  4. Whiteneck G, Williams W, Almeida E, Bidelspach D, Culpepper W, Picon LM, Eagye CB, Dr Mellick D. Two Decades of Department of Veterans Affairs Traumatic Brain Injury Care and Benefits for Veterans of Post-9/11 Conflicts. J Head Trauma Rehabil. 2024 Sep-Oct 01;39(5):E462-E469. doi: 10.1097/HTR.0000000000000952. Epub 2024 Sep 10. PMID: 38652670; PMCID: PMC11387123.
  5. Peterson AB, Thomas KE. Incidence of Nonfatal Traumatic Brain Injury-Related Hospitalizations – United States, 2018. MMWR Morb Mortal Wkly Rep. 2021;70(48):1664-1668. doi:10.15585/mmwr.mm7048a3
  6. Schneider ALC, Wang D, Gottesman RF, Selvin E. Prevalence of Disability Associated With Head Injury With Loss of Consciousness in Adults in the United States: A Population-Based Study. Neurology. 2021;97(2):e124-e135. doi:10.1212/WNL.0000000000012148
  7. Peterson AB, Thomas KE, Zhou H. Surveillance Report of Traumatic Brain Injury-related Deaths by Age Group, Sex, and Mechanism of Injury – United States, 2018 and 2019. Published online 2022. https://www.cdc.gov/traumatic-brain-injury/media/pdfs/TBI-surveillance-report-2018-2019-508.pdf
  8. Shaik NF, Law CA, Elser H, Schneider ALC. Trends in Traumatic Brain Injury Mortality in the US. JAMA Neurol. 2024;81(2):194. doi:10.1001/jamaneurol.2023.4618
  9. Understanding Health Disparities in Traumatic Brain Injury & Concussion. Accessed September 28, 2025. https://www.cdc.gov/traumatic-brain-injury/media/pdfs/CDC_TBI_Health_Disparities-508.pdf
  10. Stanley SP, Truong EI, DeMario BS, et al. Variations in Discharge Destination Following Severe Traumatic Brain Injury across the United States. J Surg Res. 2022;271:98-105. doi:10.1016/j.jss.2021.10.023
  11. Rosenfeld JV, McFarlane AC, Bragge P, Armonda RA, Grimes JB, Ling GS. Blast-related traumatic brain injury. Lancet Neurol. 2013;12(9):882-893. doi:10.1016/S1474-4422(13)70161-3
  12. Silver JM, McAllister TW, Arciniegas DB, eds. Textbook of Traumatic Brain Injury. Third edition. American Psychiatric Association Publishing.; 2019.
  13. 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
  14. Bieniek KF, Cairns NJ, Crary JF, et al. The Second NINDS/NIBIB Consensus Meeting to Define Neuropathological Criteria for the Diagnosis of Chronic Traumatic Encephalopathy. J Neuropathol Exp Neurol. 2021;80(3):210-219. doi:10.1093/jnen/nlab001
  15. Katz DI, Bernick C, Dodick DW, et al. National Institute of Neurological Disorders and Stroke Consensus Diagnostic Criteria for Traumatic Encephalopathy Syndrome. Neurology. 2021;96(18):848-863. doi:10.1212/WNL.0000000000011850
  16. Weitzel L, Bavishi S. Disorders of Consciousness. Phys Med Rehabil Clin N Am. 2024;35(3):493-506. doi:10.1016/j.pmr.2024.02.003
  17. Allred D. Management of Medical Complications during the Rehabilitation of Moderate–Severe Traumatic Brain Injury. Phys Med Rehabil Clin N Am. 2024;35(3):507-521. doi:10.1016/j.pmr.2024.02.004
  18. Brett BL, Gardner RC, Godbout J, Dams-O’Connor K, Keene CD. Traumatic Brain Injury and Risk of Neurodegenerative Disorder. Biol Psychiatry. 2022;91(5):498-507. doi:10.1016/j.biopsych.2021.05.025
  19. Corrigan JD, Smith-Knapp K, Granger CV. Validity of the functional independence measure for persons with traumatic brain injury. Arch Phys Med Rehabil. 1997;78(8):828-834. doi:10.1016/S0003-9993(97)90195-7
  20. Torregrossa W, Torrisi M, De Luca R, et al. Neuropsychological Assessment in Patients with Traumatic Brain Injury: A Comprehensive Review with Clinical Recommendations. Biomedicines. 2023;11(7):1991. doi:10.3390/biomedicines11071991
  21. Mahajan C, Prabhakar H, Bilotta F. Endocrine Dysfunction After Traumatic Brain Injury: An Ignored Clinical Syndrome? Neurocrit Care. 2023;39(3):714-723. doi:10.1007/s12028-022-01672-3
  22. Manley GT, Dams-O’Connor K, Alosco ML, et al. A new characterisation of acute traumatic brain injury: the NIH-NINDS TBI Classification and Nomenclature Initiative. Lancet Neurol. 2025;24(6):512-523. doi:10.1016/S1474-4422(25)00154-1
  23. Cognitive Impairments. In: Brain Injury Medicine, Third Edition: Principles and Practice. 3rd ed. Springer Publishing Company; 2021.
  24. Assessment and Rehabilitative Management of Individuals With Disorders of Consciousness. In: Brain Injury Medicine, Third Edition: Principles and Practice. 3rd ed. Springer Publishing Company; 2021.
  25. Neuropsychiatric Symptoms and Syndromes. In: Brain Injury Medicine, Third Edition: Principles and Practice. 3rd ed. Springer Publishing Company; 2021.
  26. Functional Assessment in Traumatic Brain Injury. In: Brain Injury Medicine, Third Edition: Principles and Practice. 3rd ed. Springer Publishing Company; 2021.
  27. Prognosis After Moderate to Severe Traumatic Brain Injury: A Practical, Evidence-Based Approach. In: Brain Injury Medicine, Third Edition: Principles and Practice. 3rd ed. Springer Publishing Company; 2021.
  28. Clinicolegal Issues. In: Brain Injury Medicine, Third Edition: Principles and Practice. 3rd ed. Springer Publishing Company; 2021.
  29. Acute Care. In: Brain Injury Medicine, Third Edition: Principles and Practice. 3rd ed. Springer Publishing Company; 2021.
  30. Psychosocial Functioning, Community Re-Entry, and Productivity. In: Brain Injury Medicine, Third Edition: Principles and Practice. 3rd ed. Springer Publishing Company; 2021.
  31. Practical Approaches to Family Assessment and Intervention. In: Brain Injury Medicine, Third Edition: Principles and Practice. 3rd ed. Springer Publishing Company; 2021.
  32. Hicks AJ, Carrington H, Bura L, et al. Blood-Based Protein Biomarkers in the Chronic Phase of Traumatic Brain Injury: A Systematic Review. J Neurotrauma. 2025;42(9-10):759-797. doi:10.1089/neu.2024.0294
  33. Calderone A, Cardile D, Gangemi A, De Luca R, Quartarone A, Corallo F, Calabrò RS. Traumatic Brain Injury and Neuromodulation Techniques in Rehabilitation: A Scoping Review. Biomedicines. 2024 Feb 16;12(2):438. doi: 10.3390/biomedicines12020438. PMID: 38398040; PMCID: PMC10886871.
  34. Education, Training, and Certification for Health Care Providers. In: Brain Injury Medicine, Third Edition: Principles and Practice. 3rd ed. Springer Publishing Company; 2021.
  35. Stopa BM, Harary M, Jhun R, et al. Divergence in the epidemiological estimates of traumatic brain injury in the United States: comparison of two national databases. J Neurosurg. 2021;135(2):584-593. doi:10.3171/2020.7.JNS201896

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.

Lindsay A. Smith, MD, Blessen C. Eapen, MD. Traumatic Brain Injury. 1/12/2023.

Author Disclosure

Steven Flanagan, MD
Nothing to Disclose

Jessie Chan, MD
Nothing to Disclose