Definition and epidemiology
Traumatic brain injury is an alteration in brain function, or other evidence of brain pathology, caused by an external force. It is classified by severity (mild, moderate, severe using GCS), mechanism (blunt, penetrating, blast), and morphology (focal lesions such as contusion or hematoma versus diffuse injury such as diffuse axonal injury).
TBI is a major global health burden. It is one of the leading causes of death and disability in people under 45 years old. Falls are the most common cause overall, especially in children and older adults, while motor vehicle collisions and assaults are major contributors in adolescents and young adults. Males are affected roughly twice as often as females across most age groups.
- GCS 13-15 mild, 9-12 moderate, 8 or less severe TBI
- Non-contrast CT head is the first-line imaging study
- Cushing's triad (hypertension, bradycardia, irregular breathing) signals raised ICP/herniation
- Hypoxia and hypotension are the two most important secondary insults to avoid
- Epidural hematoma classically shows a lucid interval then rapid decline
- Battle sign and raccoon eyes suggest basilar skull fracture
- Diffuse axonal injury is best seen on MRI, not CT, and reflects shear injury
- Decompressive craniectomy is reserved for refractory intracranial hypertension
Etiology and risk factors
- Falls (most common cause overall, especially at the extremes of age)
- Motor vehicle, motorcycle, and pedestrian collisions
- Assault and interpersonal violence (blunt or penetrating)
- Sports-related impacts (common cause of mild TBI/concussion)
- Blast injury and combat-related trauma
Risk factors
- Young adult male
- Alcohol or substance intoxication
- Advanced age (increased fall risk, anticoagulant use)
- Anticoagulant or antiplatelet therapy (increases hemorrhage risk and lowers threshold for imaging)
- Prior TBI (cumulative risk, especially in repetitive concussion)
Pathophysiology
Injury occurs in two phases.
Primary injury
Direct mechanical damage occurs at the moment of impact: contusion, laceration, diffuse axonal injury from shear/rotational forces, and vascular tearing causing epidural, subdural, subarachnoid, or intraparenchymal hemorrhage.
Secondary injury
Evolves over hours to days and is the main target of clinical management:
- Cerebral edema and raised intracranial pressure (ICP)
- Ischemia from reduced cerebral perfusion pressure (CPP = MAP − ICP)
- Excitotoxicity (glutamate release), calcium influx, and free radical damage
- Inflammation and blood-brain barrier breakdown
- Herniation syndromes if mass effect and raised ICP go uncontrolled
The Monro-Kellie doctrine underlies ICP physiology: the skull is a fixed volume containing brain, blood, and CSF; an increase in one component (e.g., hematoma) must be compensated by a decrease in another, or ICP rises sharply once compensation is exhausted.
Clinical features
- Altered level of consciousness, ranging from brief confusion to coma
- Headache, nausea, vomiting
- Amnesia (retrograde and/or anterograde) around the event
- Focal neurologic deficits (hemiparesis, aphasia) depending on lesion location
- Pupillary asymmetry or a blown pupil (concerning for herniation)
- Cushing's triad (hypertension, bradycardia, irregular respirations) suggests raised ICP and impending herniation
- Battle sign, raccoon eyes, hemotympanum, or CSF rhinorrhea/otorrhea suggest basilar skull fracture
- Seizures (early, within 7 days, or late, after 7 days)
Severity grading (GCS)
| Severity | GCS |
|---|---|
| Mild | 13-15 |
| Moderate | 9-12 |
| Severe | 3-8 |
Diagnosis
Diagnosis is clinical, supported by imaging.
Initial assessment
- Primary survey (ABCDE) with cervical spine precautions
- Serial GCS and pupillary exam
- Screen for intoxication, coagulopathy, and other injuries (TBI is often part of polytrauma)
Imaging
- Non-contrast CT head is the first-line and most important investigation; it rapidly identifies hemorrhage, fracture, midline shift, and mass effect
- Clinical decision rules (e.g., Canadian CT Head Rule, New Orleans Criteria) help decide who needs CT after mild TBI
- MRI is more sensitive for diffuse axonal injury and subacute lesions but is not first-line in the acute setting
- CT angiography if vascular injury (dissection) is suspected
Monitoring
- Invasive ICP monitoring is considered in severe TBI (GCS 8 or less) with an abnormal CT or risk factors for raised ICP
- Continuous neurologic observation (e.g., hourly GCS) in admitted patients
Differential diagnosis
- Toxic-metabolic encephalopathy (hypoglycemia, intoxication, hepatic/uremic encephalopathy)
- Non-traumatic intracranial hemorrhage (e.g., spontaneous subarachnoid or intracerebral hemorrhage)
- Stroke (ischemic or hemorrhagic) presenting after an incidental fall
- Seizure (postictal state) causing the fall and confusion
- Spinal cord injury (can coexist and mimic or mask neurologic findings)
- Meningitis/encephalitis if fever and altered mental status are present
Management
Management is guided by severity and follows ATLS and major neurotrauma guideline principles (Brain Trauma Foundation, WHO).
Mild TBI (GCS 13-15)
- Observation, symptomatic treatment (analgesia, antiemetics)
- Clear return-to-activity/return-to-play guidance for concussion
- Discharge with head injury advice if CT is normal and no high-risk features
Moderate to severe TBI
- Secure airway early (intubation if GCS 8 or less) and maintain oxygenation and normotension
- Avoid hypoxia and hypotension, both strongly linked to worse outcomes
- Elevate head of bed, maintain normocapnia
- ICP/CPP-directed therapy: hyperosmolar therapy (mannitol or hypertonic saline) for raised ICP, sedation, and temperature control
- Avoid prophylactic hyperventilation except as a temporizing measure for acute herniation
- Seizure prophylaxis may be used short-term in severe TBI per some protocols; evidence and duration vary by guideline
- Correct coagulopathy, including reversal of anticoagulants when indicated
Surgical management
- Emergent evacuation of significant epidural, subdural, or intraparenchymal hematomas with mass effect
- Decompressive craniectomy considered in refractory intracranial hypertension
Rehabilitation
- Multidisciplinary rehabilitation (physical, occupational, speech therapy, neuropsychology) for moderate-severe TBI survivors
Complications and prognosis
- Raised ICP and herniation (uncinate, central, tonsillar) — can be rapidly fatal
- Post-traumatic seizures/epilepsy
- Diffuse axonal injury carries a poor prognosis if severe
- Post-concussion syndrome (headache, dizziness, cognitive and mood symptoms persisting weeks to months)
- Chronic traumatic encephalopathy with repetitive head injury (seen in some contact-sport athletes)
- Cognitive, behavioral, and psychiatric sequelae (memory impairment, depression, personality change)
- Hormonal dysfunction (post-traumatic hypopituitarism)
- Prognosis correlates strongly with initial GCS, pupillary findings, age, and CT findings; mild TBI generally has a good prognosis, while severe TBI carries substantial mortality and disability risk.
"TRAUMA" for severe TBI priorities: Tube (airway/intubate if GCS ≤8), Resuscitate BP (avoid hypotension), Avoid hypoxia, Up the head of bed, Mannitol/hypertonic saline for ICP, Antiepileptics if indicated, CT head urgently.
Practice questions
1. A 22-year-old man is brought to the emergency department after a motorcycle collision. He was briefly unconscious, then became alert and talked normally with paramedics. On arrival 40 minutes later he is drowsy and his left pupil is now larger than the right. Which of the following is the most likely diagnosis?
2. A 68-year-old woman on warfarin falls at home and strikes her head. She is alert with GCS 15 and has no focal deficits. Her INR is supratherapeutic. What is the most appropriate next step?
3. A 35-year-old man with severe TBI (GCS 7) is intubated and sedated in the ICU. His intracranial pressure monitor shows sustained ICP of 28 mmHg despite head elevation and sedation. Which of the following is the most appropriate next step in management?
Frequently asked questions
What causes traumatic brain injury?
TBI is caused by an external mechanical force to the head, most often from falls, motor vehicle collisions, assaults, or sports impacts. The force can cause direct tissue damage (contusion, hemorrhage) and trigger secondary injury from swelling and reduced blood flow over the following hours to days. Alcohol use, old age, and anticoagulant therapy increase both the risk and severity.
What are the first symptoms of TBI?
Early symptoms include headache, confusion, dizziness, nausea or vomiting, and brief loss of consciousness or amnesia around the event. More severe injuries present with persistent altered consciousness, focal weakness, unequal pupils, or seizures. Any worsening headache, repeated vomiting, or increasing drowsiness after a head injury warrants urgent medical evaluation.
How is TBI diagnosed?
TBI is diagnosed clinically using the history of head trauma plus neurologic examination, with the Glasgow Coma Scale used to grade severity. A non-contrast CT scan of the head is the key first-line test to detect hemorrhage, fracture, or swelling. Clinical decision rules help determine which patients with mild injury actually need a CT scan.
Is TBI curable?
Mild TBI (concussion) usually resolves fully within days to weeks with rest and gradual return to activity. Moderate to severe TBI often leaves some degree of permanent cognitive, physical, or behavioral impairment, though significant recovery can occur with rehabilitation over months to years. Outcome depends heavily on injury severity, age, and how quickly secondary injury is controlled.
Epidural vs subdural hematoma — what is the difference?
Epidural hematoma is bleeding between the skull and dura, classically from a torn middle meningeal artery, and often shows a lucid interval before rapid deterioration; on CT it appears as a lens-shaped (biconvex) collection that does not cross suture lines. Subdural hematoma is bleeding between the dura and arachnoid, usually from torn bridging veins, appears crescent-shaped on CT, and can cross suture lines.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: S06
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.