Concussion & Traumatic Brain Injury

Overview & Definition

TBI is a disruption of brain function — or other evidence of brain pathology — caused by an external mechanical force. The force is contact (a blow, a fall, a projectile) or acceleration–deceleration (whiplash, blast). The spectrum runs from confusion that clears in minutes to coma, mass lesions, and death.[1]

It is one of the commonest killers of young adults worldwide — roughly 30 to 50 percent of all trauma deaths — and the whole discipline rests on one sentence. Learn it, then say it on every ward round: primary injury is fixed; secondary injury is preventable — and is the target of all treatment. The brain cannot be un-hit. The hours after impact are where you earn your salary.[1][4]

Concussion — mild TBI — is the Concussion in Sport Group's defined entity: a brain injury from direct or indirect biomechanical force, producing symptoms that may or may not include loss of consciousness, with no abnormality on standard structural imaging. Two facts examiners love to prise out: LOC is not required for the diagnosis, and the scan is usually normal — concussion is a functional disturbance, not a structural one. That is what separates it from moderate and severe TBI, where contusion, haematoma, and axonal shearing are visible on CT.[9][10]

Your job at the bedside is three moves. Triage correctly — who needs CT, who goes home, who needs ICU. Prevent secondary injury — the avoidable deaths from hypoxia, hypotension, and rising ICP. Manage the complications — expanding haematomas, seizures, herniation, and the long tail of post-concussion syndrome, post-traumatic epilepsy, and chronic traumatic encephalopathy. The serial GCS is the one observation that stitches all three together: the trend matters more than any single value.[1][2]

Classification — three axes, one scale that decides everything

TBI is sorted along three independent axes — severity (the GCS), mechanism and morphology (focal vs diffuse, primary vs secondary), and pathology (fracture, contusion, the named haematomas). Record all three at first contact; each predicts a different piece of management and prognosis.[1][4]

Severity by the Glasgow Coma Scale

The GCS (Teasdale and Jennett, 1974) grades the depth of impaired consciousness from 15 down to 3. Three components — Eye opening (E1 to E4), Verbal (V1 to V5), Motor (M1 to M6) — recorded separately, then summed. The motor response carries the most prognostic weight; test it to a central painful stimulus. Severe is 3 to 8 — coma, from the Greek kōma for deep sleep — moderate 9 to 12, mild 13 to 15; about 80, 10, and 10 percent. Record it serially. The classic trap: a single GCS is a snapshot; a fall of 2 or more points is an emergency.[1]

An intubated patient cannot speak — record the verbal as V1t (best possible 10t). Always chart pupils and lateralised motor response beside the GCS. Together they localise the lesion and catch herniation before it becomes irreversible.[1]

Mechanism and morphology

By mechanism, TBI is blunt (the overwhelming majority — falls, road traffic accidents, assaults) or penetrating (gunshot, shrapnel, stab — different management, higher epilepsy risk). It is closed (dura intact) or open (skull fracture with dural tear and CSF leak — a portal for infection needing antibiotics and repair). By morphology, injury is focal (fracture, contusion, extradural/subdural/intracerebral haematoma — a discrete CT lesion) or diffuse (concussion, diffuse axonal injury, swelling — dysfunction out of proportion to the scan).[1]

But the division examiners hammer is primary versus secondary — and it is the one you must never blur.[1][4]

[1] [4]

Herniation syndromes — where the brain goes when ICP rises

When a mass or oedema raises ICP, brain tissue shifts compartment — and each shift is an emergency. Learn the clinical signature of each.[1]

Cushing's triad — hypertension, bradycardia, irregular respiration — is the pre-terminal sign of markedly raised ICP. It means the medulla is being compressed. When you see it, the patient is herniating or about to; lower the ICP now.[1]

Epidemiology & Risk Factors — who bleeds after a trivial knock

TBI is a leading global cause of death and disability — 50 to 60 million people a year — and the leading killer under 45. It accounts for roughly 30 to 50 percent of trauma deaths. The burden is not shared equally: low- and middle-income countries carry a disproportionate share, because motorisation has outrun road-safety and trauma systems.[1]

[1]

The leading causes are road traffic accidents (dominant in young adults globally), falls (the leader in the over-65s and in young children), assault (including non-accidental injury in children), sport (concussion), and blast in military populations. The aetiology shifts predictably with age — and examiners test the shift.[1]

Know the patients who bleed after a seemingly trivial knock — they are your lower threshold for CT. The elderly (cerebral atrophy stretches the bridging veins, so subdurals form from trivial trauma), the anticoagulated or antiplateleted (warfarin, DOACs, aspirin, clopidogrel — reverse urgently), alcoholics (atrophy, falls, coagulopathy), and anyone with previous neurosurgery. Contact and collision sports (rugby, boxing, American football, ice hockey), cycling and equestrian activities, and military service carry the highest concussion risk. Repeated concussions are cumulative — longer recovery each time, and a rising risk of second-impact syndrome (rare, catastrophic cerebral oedema when a second hit lands before the first has settled) and chronic traumatic encephalopathy (a progressive tauopathy of retired contact-sport athletes and veterans).[2][9]

Pathophysiology — primary you cannot undo; secondary you must prevent

TBI injures the brain in two waves. Primary injury is the mechanical event at impact — fracture, contusion (the coup at the impact site, the contrecoup at the opposite pole as the brain accelerates inside the skull), laceration, axonal shearing, and the torn vessels that make the named haematomas. It is fixed and irreversible. Nothing you do un-stretches a torn axon or un-crushes a contused cortex. Secondary injury unfolds over minutes to days and is preventable — and that one word organises every intervention you will make.[1][4]

The primary mechanical event

The insult works through three mechanisms. Contact forces at the impact point make the fracture, laceration, and local contusion (the coup). Inertial (acceleration–deceleration) forces — especially rotational and angular acceleration — shear axons where grey and white matter differ in density: the grey–white junction, the corpus callosum, and the dorsolateral brainstem. That is diffuse axonal injury (DAI). The same forces tear the cortical bridging veins as they cross the subdural space to the venous sinuses — the subdural haematoma. A fracture of the squamous temporal bone tears the middle meningeal artery — the extradural haematoma. Etymology pins the picture in memory: contrecoup is French contre- (against) plus coup (blow) — the brain striking the skull opposite the hit.[1]

The secondary-injury cascade

After impact, a biochemical cascade unfolds — and it is the target of every ICU intervention in TBI. Hypoxia (SaO2 under 90) and hypotension (SBP under 90) are the two most preventable insults, and each drives cellular energy failure: ATP depletion, pump failure, and excitotoxicity as dying neurons release glutamate. Glutamate opens NMDA receptors; calcium floods in, activating calpains and generating free radicals that wreck mitochondria — apoptosis and necrosis follow. The same pump failure traps sodium and water intracellularly (cytotoxic oedema), and the damaged blood–brain barrier leaks (vasogenic oedema). Oedema raises ICP, CPP falls, perfusion drops, more ischaemia, more oedema — a vicious spiral into herniation.[1][4]

Meet the patient

A 22-year-old cricketer is struck on the right temporal region by a fast delivery. He drops, is unconscious for 30 seconds, then sits up talking and refuses to leave the field. Twenty minutes later the nurse finds him drowsy and confused, with a right pupil that is sluggish. By the time you reach him the right pupil is fixed and dilated and he is no longer obeying commands.[1]

Two questions, and they are the highest-yield stem in head injury: which lesion, and what do you do now? The answer is an expanding extradural haematoma — the lucid interval was your warning, and the ipsilateral fixed pupil is uncal herniation. You do not wait. Protect the airway (his GCS is falling — intubate), keep him oxygenated and perfused (SaO2 at least 94 percent, SBP over 110), and get an immediate CT with neurosurgery activated. Say the mantra as you run: primary injury is fixed; secondary injury is preventable — and is the target of all treatment. His primary injury is done; everything you do now is secondary-injury prevention.[1][4]

Why the secondary cascade kills

Because autoregulation is lost, cerebral blood flow is pressure-passive — the brain can no longer defend itself against a falling blood pressure. A single hypotensive episode (SBP under 90) in severe TBI doubles mortality; a single hypoxic episode (SaO2 under 90, or apnoea) does the same. As ICP climbs, CPP falls, ischaemia deepens, oedema grows, ICP climbs further — the spiral ends in herniation and the Cushing response. Hyperglycaemia, fever, seizures, and anaemia each independently worsen outcome by the same route: more metabolic demand or less oxygen delivery. This is why every move in severe TBI — intubation, oxygenation, blood-pressure support, ICP control, normoglycaemia, anticonvulsants — exists for one reason: to prevent secondary injury.[1][4]

Clinical Presentation — what you meet at 3am

The presentation tracks the severity grade — but examiners probe the atypical, especially in the elderly, the anticoagulated, and after seemingly minor trauma.[1][2]

Mild TBI (concussion)

Concussion is a cluster of symptoms, not signs: headache (commonest), dizziness, nausea and vomiting, confusion or a "foggy" feeling, amnesia (retrograde before impact, anterograde after), photophobia and phonophobia, poor concentration and memory, fatigue, irritability, sleep disturbance, and intolerance of alcohol and exertion. LOC happens in only a minority — its absence does not exclude concussion. Most resolve over days to weeks; in 10 to 20 percent symptoms persist beyond a month as post-concussion syndrome. The SCAT5 and newer SCAT6 (Amsterdam 2022) standardise the sideline assessment — symptom checklist, cognition (orientation, immediate memory, concentration, delayed recall), and a neurological screen.[9][10]

Moderate and severe TBI

As severity deepens, symptoms become objective signs of structural injury: a falling GCS, focal deficits (hemiparesis, aphasia, visual field cut), pupil asymmetry or a fixed dilated pupil (uncal herniation), seizures, and Cushing's triad (hypertension, bradycardia, irregular respiration) signalling dangerously raised ICP. Decorticate posturing (M3, flexion — lesion above the midbrain) and decerebrate posturing (M2, extension — brainstem or midbrain) localise the level. Post-traumatic amnesia (injury to recovery of continuous memory) longer than 30 minutes marks more significant injury than simple concussion.[1]

Lens vs crescent — the two neurosurgical emergencies

The two neurosurgical emergencies every student must separate produce a stereotyped picture — and examiners reward it.[1]

Extradural (epidural) haematoma. A young patient takes a low-velocity blow to the temporal region (a cricket ball, a falling object, a punch). The sequence is brief loss of consciousness, then a lucid interval — the patient walks, talks, refuses help — then rapid deterioration as the expanding biconvex haematoma compresses the temporal lobe. The full triad on the side of impact: an ipsilateral fixed dilated pupil (CN III compression from uncal herniation) and contralateral hemiparesis (cerebral peduncle). The lucid interval is the warning that deterioration is coming — and the single most testable stem in head injury. Source: the middle meningeal artery, torn by a squamous temporal fracture.[1]

Subdural haematoma. An elderly, alcoholic, or anticoagulated patient — often after trivial or forgotten trauma — presents with fluctuating consciousness, headache, and a progressive focal deficit over days to weeks. The culprit is a torn cortical bridging vein; the haematoma spreads diffusely over the convexity. On CT it is crescent-shaped, crosses suture lines, and does not cross the midline (it sits under the falx). A chronic subdural can present weeks after the forgotten injury as cognitive decline mistaken for dementia, or as seizures.[1]

Diffuse axonal injury. A patient from a high-speed rotational mechanism (motorcycle crash, high fall) is comatose from the moment of impact, often with a normal or near-normal early CT — the classic "coma out of proportion to the CT". Small petechial haemorrhages at the grey–white junction, in the corpus callosum, or in the dorsolateral brainstem may show on CT; MRI gradient-echo or susceptibility-weighted imaging (SWI) reveals the microbleeds.[1]

[1]

Skull fractures

A linear fracture is usually silent but raises the risk of an extradural — especially across the middle meningeal groove. A depressed fracture (a palpable bony step) carries a high risk of cortical laceration, late epilepsy, and infection — elevate it if depressed more than the skull thickness, if there is a dural tear, or if an underlying haematoma sits beneath. A basal skull fracture shows the peri-orbital and mastoid signs: raccoon eyes (periorbital bruising, bilateral, confined to the orbital margins — distinct from direct trauma), Battle's sign (mastoid bruising, appearing hours later), CSF rhinorrhoea or otorrhoea, haemotympanum, and CN VII or VIII signs. The trap here: do not instrument the nose — no NG tube, no nasotracheal intubation in a suspected basal fracture.[1]

Differential Diagnosis

In any reduced-GCS patient after head injury, always include the non-intracranial causes — which is why every head-injured patient gets a glucose and a temperature at the bedside. The mnemonic AEIOU-TIPs frames the search: Alcohol or drug abuse, Endocrine or encephalopathy, Insulin (hypoglycaemia), Oxygen lack, Uraemia or electrolytes; Trauma, Infection, Poisoning, Seizure or post-ictal.[1]

[1] [3]

The cervical spine is the special case. About 10 percent of significant head injuries carry a co-existing cervical spine injury, and an unrecognised C-spine fracture can turn a stable patient quadriplegic. Everyone forgets the neck. Assume a C-spine injury until cleared — by clinical criteria (Canadian C-spine rule or NEXUS) or by CT — and hold manual in-line stabilisation through the primary survey and intubation.[1]

A drunk patient with a head injury has a GCS of 12 — is the alcohol enough to explain the score?

No. Alcohol alone, even at high levels, rarely drops the GCS below 13. A reduced GCS in an intoxicated head-injured patient is presumed intracranial injury until CT proves otherwise. And check the glucose — alcohol intoxication causes hypoglycaemia, especially in children and the malnourished.[1]

Clinical & Bedside Assessment

The focused head-injury examination has three layers: the ATLS primary survey (ABCDE) with cervical spine control, a neurological assessment (GCS, pupils, limb power), and a search for the external signs of skull fracture. Record the GCS at first contact and repeat it every 15 to 30 minutes — the trend is more important than any single value, and a fall of 2 or more points is an emergency mandating urgent CT.[1]

Airway with cervical spine control comes first: the neck is immobilised in a hard collar, sandbags, and tape (or by manual in-line stabilisation during intubation) until cleared. Breathing is assessed for rate, oxygen saturation (target 94 percent or above), and chest movement — TBI frequently co-exists with chest trauma. Circulation hunts for external bleeding and the shock pattern — and the trap here: shock is rarely caused by isolated head injury in adults. If the patient is shocked, find the thoracic, abdominal, pelvic, or long-bone source. Disability records the GCS, pupils (size, symmetry, reactivity), and a capillary glucose — hypoglycaemia is the rapidly reversible mimic, so the finger-prick glucose is non-negotiable in every reduced-GCS patient.[1]

Pupillary examination is the single most useful focal sign. A unilaterally dilated, poorly reactive pupil in a comatose patient is ipsilateral CN III compression from uncal herniation until proven otherwise — an expanding mass on that side. Bilateral small pupils suggest a pontine (opiate) lesion; bilateral fixed dilated pupils are a grave sign of brainstem failure. Test the motor response to a central painful stimulus (supraorbital pressure or trapezius squeeze): obeys commands (M6), localises (M5), withdraws (M4), abnormal flexion or decorticate (M3), abnormal extension or decerebrate (M2), none (M1). Lateralised weakness points to a contralateral hemisphere lesion.[1]

Seek the external signs of a basal skull fracture in every significant head injury: raccoon eyes, Battle's sign, CSF leak (test any clear nasal or ear discharge), haemotympanum, and CN VII or VIII signs. A palpable bony step suggests a depressed fracture; a boggy scalp swelling may overlie a fracture line. Inspect and palpate the scalp for lacerations — a scalp laceration can bleed enough to shock a patient on its own.[1]

Neurological observations (GCS, pupils, vital signs) are recorded every 15 minutes initially, then less often as the patient stabilises. Continuous pulse oximetry, ECG, and blood-pressure monitoring are mandatory. The whole point of the observation is to catch secondary deterioration — an expanding extradural, a rising ICP, a delayed haematoma — before it does irreversible harm.[1]

Investigations

First test — non-contrast CT brain

The non-contrast CT brain is the first and most important investigation in a significant head injury. It identifies acute blood (extradural lens, subdural crescent, intracerebral contusion, intraventricular and subarachnoid blood), mass effect and midline shift, skull fractures, pneumocephalus (an open fracture), hydrocephalus, and cerebral oedema (effaced basal cisterns, loss of grey–white differentiation). The CT decides who needs neurosurgery, who needs ICP monitoring, and who can go home.[1]

Because CT carries a small radiation dose and most head-injured patients have no intracranial injury, clinical decision rules were built to pick out who actually needs one. The two best validated are the Canadian CT Head Rule (CCHR), reproduced here, and the NICE criteria used in the UK. Both are highly sensitive — designed to rule out clinically important injury — and examiners expect the components stated exactly.[3]

MRI brain — for diffuse axonal injury

An MRI brain is indicated when the CT is normal but the clinical picture says significant injury — most often suspected diffuse axonal injury in a comatose patient after high-speed rotational trauma, persistent unexplained symptoms after concussion, or suspected non-accidental injury in children. Gradient-echo (GRE) and susceptibility-weighted imaging (SWI) sequences show the microbleeds of DAI at the grey–white junction, in the corpus callosum, and in the brainstem. MRI may also reveal small ischaemic strokes, contusions below the resolution of CT, and the diffuse oedema of second-impact syndrome. MRI is not a first-line test in the unstable patient.[1]

ICP monitoring

An intracranial pressure (ICP) monitor — an intraventricular catheter (external ventricular drain, EVD) or an intraparenchymal sensor — is indicated in severe TBI (GCS 3 to 8) with an abnormal CT (haematoma, contusion, oedema, compressed cisterns), or a normal CT with two or more of age over 40, motor posturing, or SBP under 90. The Brain Trauma Foundation 4th edition target is ICP under 22 mmHg (lowering above this threshold improves outcome) and CPP 60 to 70 mmHg. The ICP waveform, the pressure–volume index, and the relationship between ICP and MAP guide therapy.[4][7]

Bloods and adjuncts

Blood tests in every significant head injury: glucose (exclude hypoglycaemia — the rapidly reversible mimic), full blood count, urea and electrolytes, coagulation or INR (a coagulopathy may develop after injury and dramatically worsen a haematoma), blood group and crossmatch (for surgery), alcohol and drug levels, beta-hCG in women of childbearing age, and a trauma panel (amylase or lipase, lactate, venous blood gas). Add CT angiography if a vascular injury (carotid or vertebral dissection) is suspected. CT cervical spine is part of the trauma pan-scan in all high-risk patients. Skull X-rays are now rarely indicated — CT is more sensitive for both fractures and intracranial injury.[1]

Management — Resuscitation: the four numbers mantra

Resuscitation is the ATLS primary survey (ABCDE) with cervical spine control, run on a single overriding principle: the brain cannot tolerate hypoxia or hypotension, and one episode of either doubles mortality in severe TBI. The discipline is to secure the airway early, oxygenate aggressively, and hold the blood pressure — all while not missing a co-existing cervical spine injury. Repeat the mantra as you work: primary injury is fixed; secondary injury is preventable — and is the target of all treatment.[1][4]

[1] [4]

Blood pressure is held with isotonic crystalloid or blood products; avoid hypotonic fluids (they lower serum osmolarity and worsen cerebral oedema). Add a vasopressor (noradrenaline) if fluids alone miss the MAP target. Reverse anticoagulation urgently: warfarin with vitamin K plus prothrombin complex concentrate; dabigatran with idarucizumab; anti-Xa DOACs with andexanet alfa; antiplatelets discussed with neurosurgery. Terminate seizures with IV lorazepam 0.1 mg/kg (or IV diazepam), then load an anticonvulsant. Correct hypoglycaemia with IV dextrose. The principle throughout is resuscitate before you image — an unstable patient does not go to the CT scanner.[1]

Management — Definitive & Stepwise

Definitive management splits cleanly into concussion (mild TBI) on one side and moderate-to-severe TBI on the other. The concussion pathway is a graded return to activity; the moderate-to-severe pathway is neurocritical care aimed at preventing secondary injury and evacuating mass lesions.[4][9]

Concussion — the graded-return pathway

Concussion is managed conservatively — there is no role for routine CT in the asymptomatic patient who meets no high-risk criterion (per the Canadian CT Head Rule). Management has three components.[9][10]

1. Immediate removal from play. Any athlete with suspected concussion comes off and does not return the same day — "when in doubt, sit them out". Same-day return is the single behaviour that precipitates second-impact syndrome, a rare but catastrophic diffuse cerebral oedema that strikes when a second concussion lands before the first has resolved. The SCAT6 (Amsterdam 2022) is the recognised sideline tool.[9]

2. Physical and cognitive rest for 24 to 48 hours. Strict rest beyond 48 hours is no longer recommended — prolonged rest delays recovery, deconditions the patient, and worsens mood. After the initial rest, the patient resumes light activity below symptom threshold.[10]

3. Graduated return to school, work, and sport. The Concussion in Sport Group (Amsterdam 2022) six-stage protocol moves through symptom-limited activity, light aerobic exercise, sport-specific exercise, non-contact training drills, full-contact practice, and return to sport, spending a minimum of 24 hours at each stage and progressing only if symptom-free. The minimum time before return to full-contact sport is about one week. If symptoms recur at any stage, drop back to the previous asymptomatic level for 24 hours. Medical clearance is required before return to contact sport.[9][10]

Moderate-to-severe TBI — the neurocritical-care bundle

The moderate-to-severe pathway builds on resuscitation with five pillars: ICP control, surgical evacuation, seizure prophylaxis, hyperosmolar therapy, and supportive ICU care. The Brain Trauma Foundation 4th edition (2017, Carney) is the international benchmark.[4]

1. ICP control. Elevate the head of bed to 30 degrees and keep it midline to optimise venous drainage. Sedation and analgesia (propofol and fentanyl infusions) cut metabolic demand and the coughing or straining that raises ICP. Hold normocapnia (PaCO2 4.5 to 5.0 kPa) — avoid prophylactic hyperventilation, which constricts cerebral vessels and causes ischaemia; brief hyperventilation is reserved as a bridge to surgery in impending herniation. Place an ICP monitor for severe TBI with an abnormal CT, targeting ICP under 22 mmHg and CPP 60 to 70 mmHg.[4][7]

2. Hyperosmolar therapy. For acutely raised ICP or impending herniation, osmotic agents draw water out of the brain and into the vascular space.[4]

[1] [4] [4]

3. Surgical evacuation. Neurosurgical evacuation is indicated for an extradural or subdural haematoma over 30 mL in volume or with midline shift over 5 mm (lower thresholds in the posterior fossa), for any deteriorating patient with a mass lesion, for a depressed skull fracture depressed more than the skull thickness or with an underlying injury, and for a large contusion with mass effect. The Bullock surgical guidelines frame it: an acute subdural over 10 mm thick or with midline shift over 5 mm is evacuated within 4 hours if the GCS is deteriorating; an extradural over 30 mL is evacuated regardless of GCS; a decompressive craniectomy is considered for refractory raised ICP.[1][4]

4. Decompressive craniectomy for refractory raised ICP. When medical therapy fails, a decompressive craniectomy (removing a large bone flap, often with a duraplasty) makes room for the swollen brain and lowers ICP. Read the two trials carefully — they point in opposite directions. The DECRA trial (Cooper 2011) showed that early bifrontal craniectomy for diffuse injury was associated with worse neurological outcome at 6 months — cautioning against early prophylactic craniectomy. The RESCUEicp trial (Hutchinson 2016) showed that craniectomy as a last-tier therapy for refractory intracranial hypertension lowered mortality compared with medical management, but at the cost of higher rates of vegetative state and severe disability in survivors. The mantra: DECRA early worsens, RESCUEicp last-tier saves — heavily dependent — lives.[6][8]

5. Seizure prophylaxis. Early post-traumatic seizures (within 7 days) are prevented with a short course of an anticonvulsant — phenytoin or levetiracetam — in severe TBI, started within 24 hours and continued for 7 days. The Temkin 1990 randomised trial established that phenytoin reduces early seizures but does not prevent late epilepsy. Late post-traumatic epilepsy (after 7 days) is not prevented by prophylaxis and is treated as any other epilepsy if it develops. Prophylaxis is not indicated for mild TBI.[5]

[5]

6. Supportive ICU care. The general ICU bundle keeps the brain out of trouble while it recovers. Hold normoglycaemia (an insulin sliding scale for hyperglycaemia, which worsens outcome; avoid hypoglycaemia more strictly), normothermia (paracetamol and cooling for fever — every 1 degree rise in temperature raises cerebral metabolic demand by up to 10 percent), and treat anaemia (transfusion threshold generally a haemoglobin of 70 to 80 g/L). Begin venous thromboembolism prophylaxis with mechanical compression immediately, adding low-molecular-weight heparin after 48 hours once bleeding is controlled. Add early enteral nutrition, stress-ulcer prophylaxis, glycaemic control, and infection surveillance.[4]

Steroids are contraindicated

The MRC CRASH trial (Edwards 2005) is the single most important negative trial in TBI: high-dose corticosteroids increase mortality after significant head injury and must not be used. This is one of the most heavily tested facts in the subject.[11]

Specific Subtypes & Scenarios

Each named lesion has its own management pathway.[1]

[1]

Chronic subdural haematoma

The chronic subdural is a subtype of its own. It presents weeks to months after a forgotten or trivial head injury in an elderly, alcoholic, or anticoagulated patient, with a fluctuating level of consciousness, headache, focal deficit, cognitive decline (mistaken for dementia), or seizures. The CT shows a crescentic collection that may be iso- or hypodense relative to cortex (subacute or chronic blood). Management is burr-hole drainage for symptomatic collections; small asymptomatic collections may be managed conservatively. Reverse anticoagulation before surgery. Outcomes are generally good, but recurrence is common.[1]

Sport-related concussion

Sport-related concussion deserves special attention because of the risk of second-impact syndrome and the cumulative brain damage of repeated concussions. Management is immediate and permanent removal from play ("when in doubt, sit them out"), no return the same day, and a graduated return-to-sport (CISG 6-stage protocol, minimum 24 hours per stage, symptom-free before progression, minimum about one week before full contact, medical clearance). The Amsterdam 2022 (6th) consensus refined the protocol to emphasise early light activity rather than prolonged strict rest, the SCAT6 in adults and Child SCAT6 in children, and an individualised return-to-school before return-to-sport.[9][10]

Complications & Pitfalls

The complications of TBI follow a predictable timeline from the moment of injury, and recognising each is a core skill.[1][2]

Second-impact syndrome deserves special emphasis. A second concussion sustained before the first has fully resolved triggers catastrophic, often fatal, diffuse cerebral oedema within minutes, typically in young male athletes. It is rare but devastating — and entirely preventable by enforced rest and graduated return. That is the rationale for the strict "no return to play the same day" rule.[9]

Post-concussion syndrome — persistent headache, dizziness, poor concentration, irritability, fatigue, and sleep disturbance beyond 4 weeks — affects roughly 10 to 20 percent of patients after concussion. Risk factors include female sex, previous concussion, migraine, and a high symptom burden at presentation. Management is reassurance (most cases resolve within 3 months), graded aerobic rehabilitation (sub-symptom-threshold exercise), and targeted treatment of headache, vestibular symptoms, and mood. Cervicogenic headache and vestibular dysfunction are common, treatable contributors.[2]

Post-traumatic epilepsy divides into early (within 7 days) and late (after 7 days). Early seizures are prevented by a 7-day course of phenytoin or levetiracetam (Temkin 1990); late epilepsy is not prevented by prophylaxis and is treated as chronic epilepsy if it develops. Features that raise the risk of late epilepsy: a penetrating injury, depressed skull fracture, intracerebral haematoma, early seizure, traumatic SAH, and a GCS under 10.[5]

Cranial nerve injuries (olfactory anosmia, facial nerve palsy from temporal bone fracture, vestibulocochlear hearing loss), CSF leak and meningitis, hydrocephalus (communicating from subarachnoid blood, or obstructive from intraventricular clot), and vascular injury (carotid or vertebral dissection, traumatic pseudoaneurysm) are further recognised complications.[1]

Prognosis & Disposition

Prognosis tracks the severity grade, modified by age, the depth and duration of coma, the pupillary response, hypotension or hypoxia, and the CT findings. The IMPACT and CRASH prognostic models combine these variables to give calibrated 6-month outcome predictions.[1]

Mild TBI (concussion) recovers fully in most within days to weeks. About 10 to 20 percent develop post-concussion syndrome. Repeat injuries raise the risk of cumulative damage and chronic traumatic encephalopathy; the brain is more vulnerable to a second concussion for several weeks after the first — hence the second-impact syndrome risk.[2]

Moderate TBI leaves a significant minority with residual cognitive disability, fatigue, mood disturbance, and (in some) post-traumatic epilepsy.[1]

Severe TBI carries a mortality of 20 to 40 percent; of survivors, many have permanent cognitive, physical, and behavioural disability. The key prognostic factors are age, the initial GCS and its trend, pupillary reactivity (bilaterally fixed dilated pupils are a grave sign), the presence of hypotension or hypoxia, and the CT findings — midline shift, compressed or absent basal cisterns, traumatic SAH, and a mass lesion all predict worse outcome. The motor response of the GCS carries the most prognostic weight of any single component.[1]

[1]

Disposition follows severity. Mild TBI with a normal CT, normal GCS, and a responsible adult at home is discharged with written head-injury advice ("return immediately if persistent or worsening headache, repeated vomiting, increasing drowsiness, weakness, seizures, or visual disturbance"). Moderate TBI is admitted for observation and CT. Severe TBI goes to a neurocritical-care ICU with ICP monitoring and surgical evacuation as needed, followed by early multidisciplinary rehabilitation (physiotherapy, occupational therapy, speech and language therapy, neuropsychology). Driving is restricted for a period after concussion; alcohol is avoided; return to work and sport is graduated. Structured outpatient follow-up detects post-concussion syndrome early.[1]

Special Populations

Sport-related concussion — the priority is immediate removal from play, no return the same day, and a graduated return-to-sport over a minimum of about one week (CISG Amsterdam 2022). The SCAT6 is used for adults and the Child SCAT6 for children aged 8 to 12. Prolonged strict rest is no longer recommended — early sub-symptom-threshold light activity aids recovery. The diagnosis remains clinical; imaging is normal.[9][10]

Elderly and anticoagulated patients have a lower threshold for CT (the Canadian CT Head Rule and NICE criteria both include age 65 or older and anticoagulant use as high-risk), a high risk of subdural haematoma even from trivial trauma, and worse outcomes. Reverse anticoagulation urgently: warfarin with vitamin K and prothrombin complex concentrate, dabigatran with idarucizumab, anti-Xa DOACs with andexanet alfa, and antiplatelets discussed with neurosurgery. The chronic subdural may present weeks after a forgotten injury with cognitive decline.[3][1]

Paediatric head injury uses a modified GCS (the verbal component is replaced by age-appropriate interactions in young children), wider CT indications (the PECARN paediatric criteria), and a lower threshold for admission. Non-accidental injury (NAI) must be considered in any infant with an unexplained head injury, an inconsistent history, retinal haemorrhages, or multiple injuries of different ages — and safeguarding procedures activated. A growing skull fracture (a diastatic fracture that enlarges as the brain pulsates through it) is a complication unique to children.[1]

Pregnant trauma patient — the mother is resuscitated first (the best resuscitation of the fetus is the optimal resuscitation of the mother). A left lateral tilt avoids aortocaval compression; beta-hCG is checked; imaging decisions balance radiation against risk (CT of the head is safe — the radiation dose to the fetus from a head CT is negligible). Multidisciplinary care with obstetrics is essential.[1]

Military or blast TBI is increasingly recognised. The mechanism includes the primary blast over-pressure wave (transmitted through the skull), and is associated with higher rates of PTSD, post-concussion syndrome, and chronic traumatic encephalopathy. The management principles are the same.[2]

Evidence, Guidelines & Regional Differences

The evidence base for TBI is anchored by a handful of landmark trials and authoritative guidelines — and examiners reward knowing them.[4]

The CRASH trial (Edwards 2005) is the single most important negative trial in TBI — it established that high-dose corticosteroids increase mortality and are contraindicated. The Temkin (1990) trial established that phenytoin prevents early post-traumatic seizures but not late epilepsy. The DECRA (2011) and RESCUEicp (2016) trials redefined the role of decompressive craniectomy — DECRA showed early prophylactic craniectomy worsens outcome, while RESCUEicp showed last-tier craniectomy for refractory ICP lowers mortality at the cost of higher disability. The BEST-TRIP (Chesnut 2012) trial showed that ICP-monitoring-guided therapy in a protocolised bundle was equivalent to imaging-and-examination-guided therapy in a region with limited neurocritical-care resources — widely misread as "monitoring does not matter".[5][6][7][8][11]

The Brain Trauma Foundation 4th edition (Carney 2017) is the current international benchmark for severe TBI. It targets ICP under 22 mmHg (a tightening from the 3rd edition's 20 mmHg on the basis of outcome data), CPP 60 to 70 mmHg, decompressive craniectomy for refractory raised ICP (not prophylactic), prophylactic anticonvulsant for 7 days, and no corticosteroids.[4]

Prevention is the highest-yield intervention of all. Bicycle and motorcycle helmets reduce head injury by up to 85 percent; seatbelts and airbags reduce mortality in road traffic accidents; fall prevention in the elderly (home safety assessments, medication review); sport-specific rule changes (head-high tackles, concussion substitution rules); and drink-driving legislation all act upstream of the emergency department.[1]

Ward-round test

Stem 1 — the cricketer. A young cricketer is struck on the temporal region, blacks out briefly, then walks and talks — and 20 minutes later is drowsy with a dilated right pupil. Which lesion, and what is your first move? [1]

Stem 1 — answer

An expanding extradural haematoma — the lucid interval was the warning, the ipsilateral fixed pupil is uncal herniation, and the source is the torn middle meningeal artery. First move: protect the airway (intubate — the GCS is falling), oxygenate (SaO2 at least 94 percent), hold the SBP over 110, and get an immediate CT with neurosurgery activated. The mantra: primary injury is fixed; secondary injury is preventable — and is the target of all treatment.[1]

Stem 2 — the four numbers. A severe TBI patient has an ICP of 28 mmHg. What is the target, and which two drugs do you reach for? [4]

Stem 2 — answer

Target ICP under 22 mmHg, CPP 60 to 70 mmHg. Reach for mannitol 0.25 to 1 g/kg IV or 3% hypertonic saline 250 mL IV bolus — and keep the head up 30 degrees and midline, sedated, normocapnic. Hold the four numbers: GCS 8 or lower means intubate; SaO2 at least 94 percent; SBP over 110; ICP under 22.[4]

Stem 3 — the trap. Your registrar suggests IV dexamethasone for cerebral oedema in a severe TBI. What do you say? [11]

Stem 3 — answer

No. The MRC CRASH trial (2005) showed that high-dose corticosteroids increase mortality after significant head injury (2-week mortality 21 vs 18 percent). Never give corticosteroids in TBI — it is the single most important drug class NOT to give.[11]

Stem 4 — the trend. A patient's GCS is recorded as 12, then 9 thirty minutes later. What does this mean, and what do you do? [1]

Stem 4 — answer

A fall of 2 or more points is an emergency — the trend matters more than any single value. Reassess the airway (intubate if GCS is now 8 or lower), repeat the CT urgently, and call neurosurgery. Assume a co-existing cervical spine injury until cleared, and check a finger-prick glucose.[1]

Exam Pearls

[1] [4] [1] [4] [5]

Exam application bank (NEET-PG / INICET)

One-line answer

Traumatic brain injury (TBI) is a disruption of brain function from external mechanical force, graded by the Glasgow Coma Scale (GCS) into mild (GCS 13 to 15, about 80 percent — concussion), moderate (GCS 9 to 12, about 10 percent) and severe (GCS 3 to 8, about 10 percent). Injury is divided into primary (mechanical, instantaneous, largely irreversible) and secondary (delayed, PREVENTABLE — hypoxia, hypotension, raised ICP, ischaemia, infection); preventing secondary injury is the target of all treatment. Hold the four numbers: GCS 8 or lower means intubate; SaO2 at least 94 percent; SBP over 110; ICP under 22 mmHg (CPP 60 to 70). Extradural (lucid interval, lens, middle meningeal artery) and subdural (crescent, bridging veins, elderly) are the two neurosurgical emergencies; the GCS trend beats any single score. Never give corticosteroids (CRASH).[1][4][11]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. [1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [4]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [3]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. [9]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps[1]

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Concussion and Traumatic Brain Injury.[1]

References

1. [1]Maas AI, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults Lancet Neurol, 2008.PMID 18635021
2. [2]Zetterberg H, Smith DH, Blennow K. Biomarkers of mild traumatic brain injury in cerebrospinal fluid and blood Nat Rev Neurol, 2013.PMID 23399646
3. [3]Stiell IG, Wells GA, Vandemheen K, et al. The Canadian CT Head Rule for patients with minor head injury Lancet, 2001.PMID 11356436
4. [4]Carney N, Totten AM, O'Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition Neurosurgery, 2017.PMID 27654000
5. [5]Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures N Engl J Med, 1990.PMID 2115976
6. [6]Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury N Engl J Med, 2011.PMID 21434843
7. [7]Chesnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure monitoring in traumatic brain injury N Engl J Med, 2012.PMID 23234472
8. [8]Hutchinson PJ, Kolias AG, Timofeev IS, et al. Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension N Engl J Med, 2016.PMID 27602507
9. [9]McCrory P, Meeuwisse W, Dvořák J, et al. Consensus statement on concussion in sport-the 5(th) international conference on concussion in sport held in Berlin, October 2016 Br J Sports Med, 2017.PMID 28446457
10. [10]Patricios JS, Schneider KJ, Dvorak J, et al. Consensus statement on concussion in sport: the 6th International Conference on Concussion in Sport-Amsterdam, October 2022 Br J Sports Med, 2023.PMID 37316210
11. [11]Edwards P, Arango M, Balica L, et al. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months Lancet, 2005.PMID 15936423