Concussion and skull fractures

• Concussion is a traumatically induced functional brain disturbance, graded clinically as a mild traumatic brain injury with a Glasgow Coma Scale (GCS) score of 13 to 15, without a structural lesion that needs surgery. ^[1][3]
• It shows four symptom groups - somatic, cognitive, affective and sleep - and most children recover within a few weeks, with 70 to 80% back to baseline within 3 months.^[3]
• The injured brain enters a transient "energy crisis": metabolic recovery can take 7 to 10 days in adults, which is why another blow during that window carries the greatest risk of further injury.^[4]
• A suspected concussion means immediate removal from play; the athlete returns to contact sport only when asymptomatic off medication, graded step by step.^[2]
• Skull fractures are classified by morphology: linear non-displaced fractures are often observed, depressed fractures may need surgical elevation, and basal skull fractures declare themselves by CSF leak and periorbital or post-auricular bruising.^[1][6]

By the end of this page you should be able to:

1. Explain why a concussion behaves as a functional, rather than structural, brain injury, including the ionic flux and metabolic energy crisis.
2. Recognise the early features of concussion, choose appropriate side-line and clinical assessment tools, and interpret their limits.
3. Apply current guidance on rest, return to school and return to sport, and know when prolonged symptoms need referral.
4. Classify skull fractures, recognise basal skull fracture signs and decide when computed tomography is needed.
5. Recognise, investigate and manage cerebrospinal fluid leak, including when to operate.
6. Counsel athletes, children, older adults and patients in low-resource settings.

Head injuries span a spectrum from a trivial bump to an emergency with raised intracranial pressure. Concussion sits at the mild, functional end: consciousness may be lost for seconds or minutes, and imaging is normal, yet symptoms can persist for weeks.^[4][1] Skull fractures are structural. A linear fracture without displacement may be found only incidentally on imaging, whereas a depressed fracture drives bone fragments inward and a basal fracture tears the dura, creating a leak of cerebrospinal fluid and a route for meningitis.^[1][6] This page covers both, because the two often present together, and because the first hours of assessment and the instructions given at discharge decide how well a patient does.

NICE grades severity by GCS: 13 to 15 is mild, 9 to 12 moderate, and 8 or less severe traumatic brain injury.^[1] The American Academy of Neurology and the Centers for Disease Control and Prevention define mild traumatic brain injury inclusively as GCS 13 to 15 with or without intracranial injury on imaging, and regardless of whether admission or neurosurgery is required.^[2][3]

Skull fractures are classified by morphology rather than by severity alone:

• Linear (simple) fracture: a single fracture line without displacement. NICE defines an isolated simple linear non-displaced fracture as one line that neither displaces inward nor outward, is not multiple, and does not cross a suture.^[1]
• Depressed fracture: a segment of bone driven inward relative to the inner table of the skull. It can be simple (no dural tear) or compound, with a scalp wound exposing bone, air or dura.
• Basal skull fracture: a fracture of the base of the skull, often radiographically subtle, diagnosed by clinical signs and by the consequences of a dural tear.
• Growing skull fracture: a rare complication of skull fracture in infants and young children, in which a dural tear allows arachnoid herniation and gradual enlargement of the fracture.^[6]

Sports-related mild traumatic brain injury affects between 1.6 and 3.8 million people each year in the United States, many of whom never seek care.^[2] Primary head injury is usually mild: most traumatic brain injuries present with GCS 13 to 15, and the large majority recover, although a minority have prolonged symptoms.^[3]

Childhood data show a faster, but still variable, course. Most children with mild traumatic brain injury recover within a few weeks; 70 to 80% are back to baseline by 3 months.^[3] The injury spans gender and mechanism, with sport, falls and road traffic common causes. Repeated mild injuries are more common in contact sports and are the starting point for concern about long-term neurodegeneration.

Growing skull fractures occur in roughly 0.05 to 1.6% of skull fractures in children, and more than 90% occur in children under 3 years of age, most often in the parietal bone.^[6] Traumatic cerebrospinal fluid leak has been reported in roughly 2% of pediatric traumatic brain injury, although case series and population data range from about 1% to 3% of closed head or skull-fracture admissions (about 1.5% of paediatric skull-fracture admissions in one large cohort).^[6] It occurs in 12 to 30% of skull base fractures.

Concussion follows translational, rotational, or angular brain acceleration from a blow to the head or an impact to the body transmitted to the head.^[3] Risk is greater in female soccer and basketball players than in their male counterparts, and highest in sports such as American football and rugby; the risk is lowest in baseball, softball, volleyball and gymnastics.^[2] Body checking in ice hockey increases risk, as does a mass index above 27 kg per square metre or training fewer than 3 hours weekly.^[2]

A prior concussion is a highly probable risk factor for a recurrence, and the risk is greatest in the first 10 days after the first injury.^[2][4] Younger athletes and those in high school recover more slowly than collegiate or professional athletes and should be managed more conservatively.^[2] Premorbid migraine, fatigue, early amnesia, early headache and prior headaches also predict a prolonged recovery.^[2]

Skull fractures reflect the mechanism and the skull's regional strength. Basal fractures usually follow high-energy blunt trauma to the front of the head, side or posterior skull base. Linear fractures are more common where force is spread across a broad area, whereas depressed fractures usually follow a focal blow from an object smaller than the skull's curvature.

The single most important idea in concussion is that macroscopic damage is absent, yet cellular function is profoundly disturbed.^[4] The neurometabolic cascade proceeds as follows:

1. Ionic flux. Biomechanical stretch opens cell membranes and creates sublethal defects. Potassium leaves cells, sodium and calcium enter, and there is indiscriminate release of glutamate. The result is a spreading-depression-like ionic wave, linked to the migraine-like symptoms, photophobia and phonophobia seen soon after injury.^[4]
2. Energy crisis. Membrane pumps work to restore the ionic gradients, consuming ATP. Cells shift into hyperglycolysis and then depletion of energy reserves, and mitochondria worsen the crisis by sequestering calcium. Early on, demand outstrips supply, because cerebral blood flow is normal or reduced.^[4]
3. Axonal dysfunction. Axons are especially vulnerable to stretch. Mechanoporation, microtubule disruption and impaired axonal transport slow neurotransmission, producing slowed processing and reaction time.^[4]
4. Metabolic recovery. In animal models, the hypometabolic period lasts up to 7 to 10 days in adults and about 3 days in younger subjects.^[4] Loss of N-acetylaspartate after injury recovers by about 30 days, but only by 45 days where a second concussion occurred in the interim.^[4]

Because metabolic recovery lags behind apparent clinical recovery, a second blow during that window produces a greater ionic and metabolic insult. This biological vulnerability is the reason for immediate removal from play, which is supported by human studies of repeat concussion risk in the first 10 days.^[4][2]

Post-mortem and imaging evidence suggest a separate, much rarer pathway: repeated concussive injury may progressively activate proteases, alter protein homeostasis and produce chronic traumatic encephalopathy.^[4]

Concussion symptoms fall into four groups: somatic, cognitive, affective and sleep.^[3] Typical examples are shown in the table.

Loss of consciousness is not required. Amnesia for events before or after the injury, confusion lasting seconds, minutes or occasionally a few hours, and a non-displaced or minimally displaced linear skull fracture may be present.^[1] A GCS score of 13 to 15 is consistent with mild traumatic brain injury; a combined score of 8 or less is regarded as coma.^[1]

Examination is normal in a pure concussion: pupils are equal and reactive, power and sensation are intact, and there are no focal neurological deficits. Signs of a basal or more serious skull fracture, cervical spine tenderness, or any deterioration in GCS change the pathway entirely. Younger children show behavioural change, feeding or sleep changes, listlessness or loss of interest.^[1]

A linear fracture may cause only a headache and point tenderness at the fracture site, or no symptoms at all, and is identified on imaging done for another indication. A depressed fracture may be palpable as a step in the skull and can produce local tenderness, a scalp laceration, or neurological deficit if the fragment presses on the brain. A compound fracture adds an overlying scalp wound, with risk of infection.

Basal skull fractures produce characteristic signs that can appear minutes to hours after injury.^[1][6]

NICE lists signs of a basal, open or depressed skull fracture as clear fluid from the ears or nose, a black eye with no direct injury to the orbit, bleeding from one or both ears, bruising behind one or both ears, penetrating injury signs, and visible trauma of concern.^[1]

The tear that vents cerebrospinal fluid allows brain tissue to herniate slightly and fluid to leak from the nose (rhinorrhoea) or ear (otorrhoea). CSF leak occurs in 12 to 30% of skull base fractures and in roughly 2% of pediatric traumatic brain injury by older review estimates (contemporary cohorts report 1 to 3% of closed head injuries).^[6] The frontal and ethmoid sinuses are the most common sites; the ethmoid plate is thin and fractures with minor trauma.^[6]

Timing is variable: many leaks present in the first 48 hours (about 55% in one paediatric review), and most are evident within the first 1 to 2 weeks; 10 to 20% begin months or years later.^[6] Most leaks stop without intervention: one paediatric review reported closure in 20 to 30% within a week, 70% within a few months and the large majority within 6 months, but other series only confirm that a high proportion close spontaneously, without giving identical intervals.^[6] Diagnosis rests on bedside and laboratory tests (beta2-transferrin or beta-trace protein in the fluid) and on high-resolution computed tomography in axial, coronal and sagittal planes; magnetic resonance imaging helps distinguish pooled fluid from mucus.^[6] Meningitis complicates an estimated 1% to 30% of untreated CSF leaks (older paediatric reviews commonly quote about 24%), most often from Streptococcus pneumoniae, with gram-negative bacilli predominating in some series.^[6]

• CSF rhinorrhoea or otorrhoea
• Haemotympanum or bleeding from the external ear canal
• Battle sign: mastoid ecchymosis
• Raccoon eyes: periorbital ecchymosis
• Anosmia, hearing loss, or facial nerve weakness

In a patient with confusion after a blow, exclude structural lesions and systemic causes before diagnosing concussion.

For a basal skull fracture, the main differential is facial injury without skull fracture. For prolonged symptoms, consider migraine, vestibular dysfunction, and psychological factors alongside post-concussion syndrome.

A normal examination does not exclude concussion; equally, imaging is not diagnostic of concussion.

NICE recommends computed tomography of the head within 1 hour of identifying any of the following risk factors in a person aged 16 or over: GCS 12 or less on initial assessment, GCS less than 15 at 2 hours after the injury, suspected open or depressed skull fracture, any sign of basal skull fracture (haemotympanum, panda eyes, cerebrospinal fluid leak from the ear or nose, Battle sign), post-traumatic seizure, focal neurological deficit, or more than one episode of vomiting.^[1] With loss of consciousness or amnesia and additional risk factors (age 65 or over, bleeding or clotting disorder, dangerous mechanism, more than 30 minutes of retrograde amnesia), scanning should be undertaken within 8 hours of injury.^[1]

For children, NICE gives age-specific criteria that include GCS thresholds, bruising larger than 5 cm in babies under 1 year, tense fontanelle, and additional risk factors.^[1]

Computed tomography should not be used routinely to diagnose concussion. The American Academy of Neurology reserves imaging for ruling out serious traumatic brain injury where there is loss of consciousness, post-traumatic amnesia, persistently altered mental status with GCS less than 15, focal neurological deficit, evidence of skull fracture on examination, or clinical deterioration.^[2]

Plain skull radiographs are not used to diagnose traumatic brain injury, and computed tomography rather than plain radiograph is the first study in significant head trauma. Where cervical spine injury is suspected, the cervical spine should also be imaged.^[1]

No tool diagnoses concussion on its own. Standardised checklists and side-line tests are adjuncts to a clinical examination and should be used by those trained in their administration.^[2]

Imaging is normal in concussion. Advanced imaging and electrophysiological techniques are research tools rather than routine care.

Concussion is a clinical syndrome without a single diagnostic test. Modern definitions require an external force, an acute alteration in brain function affecting memory, orientation, or consciousness, and standard imaging that is normal or does not explain the symptoms.^[2][3] Severity is graded by GCS: 13 to 15 mild, 9 to 12 moderate, 3 to 8 severe.^[1]

Post-concussion syndrome is not limited to mild injuries and is under-recognised in them. It describes a cluster of somatic, cognitive and emotional symptoms that persist after a head injury, and NICE lists headache, dizziness, nausea, visual changes, fatigue, hyperacusis, photophobia, sleep disturbance, cognitive difficulties, executive dysfunction, amnesia, and mood symptoms including depression and anxiety.^[1] Children under 5 show behavioural change, feeding or sleep change, listlessness or reduced interest.^[1]

Follow the principles of advanced trauma life support, prioritising airway with cervical spine protection, breathing and circulation. Treat pain, because pain raises intracranial pressure. Secure the airway early when GCS is 8 or less.^[1] NICE recommends considering a 2 g intravenous bolus of tranexamic acid as soon as possible within 2 hours of injury for people 16 or over with GCS 12 or less and no active extracranial bleeding.^[1]

For suspected open or depressed skull fracture, or a sign of basal fracture, the cranial computed tomography should be done within 1 hour, and neurosurgery should be involved where imaging is surgically significant or a CSF leak exists.^[1]

Removal from play or activity at once after a suspected concussion reduces recovery time and prevents second impact syndrome, a rare but catastrophic brain swelling after a second blow before recovery.^[6]

Guidance on recovery is as follows:

• First 24 hours: a responsible adult should stay with the patient, with verbal and written instructions on warning signs.^[1]
• Rest: a brief period of 24 to 48 hours of physical and cognitive rest after a sports concussion (Concussion in Sport consensus), followed by a gradual and progressive return. NICE and the CDC advise a short period of rest, variously worded as 2 to 3 days (NICE discharge advice) or no more than 1 to 2 days in the current CDC clinician guidance, followed by a gradual return as symptoms allow.^[6][3][1]
• Return to non-sport activities: resume normal, non-contact activities within a few days at an intensity that does not worsen symptoms, with close monitoring. Most children can return to school within 2 to 3 days (CDC/NICE), although some newer guidance emphasises an earlier graded return.^[3]
• Return to contact sport: only after the athlete is symptom-free off medication, and with an individualised, graded plan, supervised by a clinician experienced with concussion.^[2] Athletes of high school age or younger should be managed more conservatively than older athletes.^[2]

The Amsterdam 2022 Concussion in Sport Group consensus (published 2023) produced the recognition and assessment tools CRT6, SCAT6, Child SCAT6, SCOAT6 and Child SCOAT6, and updated the graduated protocols now used in schools and clubs.^[5]

A 2013 American Academy of Neurology review found no intervention with proven benefit to enhance recovery or reduce long-term sequelae after sports concussion, and recommended preparticipation counselling, education, removal from play for suspected concussion, and conservative management in younger athletes.^[2]

Post-concussion symptoms usually benefit from education, reassurance and reattribution, with cognitive restructuring counselling.^[2] Persistent physical symptoms such as headache or vestibular complaints can be treated with targeted therapy; multidisciplinary teams (vestibular, psychological, cognitive and headache specialists) are appropriate for persistent cases.^[6] Avoid narcotic analgesia for post-traumatic headache where possible; simple analgesia used judiciously is preferred.

NICE recommends referring patients with persisting problems to a clinician trained in assessing and managing the consequences of traumatic brain injury, such as a neurologist, neuropsychologist, clinical psychologist, neurosurgeon, endocrinologist, or a multidisciplinary neurorehabilitation team.^[1] Early endocrine review is reasonable for patients with persistent low sodium or blood pressure, since any severity of head injury can cause hypopituitarism, presenting weeks or months later.^[1]

Linear non-displaced fracture requires observation and discharge with head injury advice when neurological examination is normal and there is no CSF leak. NICE notes that an isolated simple linear non-displaced skull fracture is unlikely to be a clinically important abnormality unless the patient is on anticoagulant or antiplatelet drugs.^[1]

Depressed fracture management depends on the degree of depression, contamination, associated haematoma, dural tear, or neurological deficit. In general, compound depressed fractures, fractures with brain or meningeal involvement, or those producing mass effect require operative elevation, debridement and dural repair.

Basal skull fracture is managed by head injury observation plus protection of the airway (prefer orogastric intubation) and management of the CSF leak. No routine intravenous prophylactic antibiotic has clear benefit, and the effectiveness of prophylactic antibiotics remains controversial.^[6] Surgery (intracranial repair or endoscopic repair) is reserved for persistent leakage beyond weeks to months, recurrent meningitis, or a large or displaced defect.

Cerebrospinal fluid leak is managed in a stepwise way: conservative management (head elevation, rest, avoidance of straining) for 7 to 10 days in the first instance; if leakage continues, endoscopic or open surgical closure; treating episodes of meningitis promptly; and correcting the dural defect to prevent recurrence.^[6]

Growing skull fracture in infants is treated surgically with watertight dural closure and cranioplasty.^[6]

• Second impact syndrome: rare, rapid, often malignant cerebral oedema after a second concussion before recovery. Rare but potentially fatal, particularly in children.^[6]
• Concussion recurrence: repeat concussion, with risk greatest in the first 10 days after the first.^[2][4]
• Post-concussion syndrome: prolonged somatic, cognitive and emotional symptoms, seen at all grades of injury.^[1]
• Chronic traumatic encephalopathy: a proposed long-term consequence of cumulative mild brain injury; evidence exists in selected cases.^[4]
• Meningitis: a recognised complication of a persistent CSF leak, affecting about 24% of untreated CSF rhinorrhoea.^[6]
• Pneumocephalus, intracranial abscess and persistent CSF fistula after basal fracture.
• Palpable defect and cranial deformity after an untreated growing skull fracture.
• Hypopituitarism after any severity of head injury, presenting weeks or months later.

Most people recover from concussion: many within days, and 70 to 80% of children within 3 months.^[3] A minority have prolonged symptoms influenced by prior head injury, lower cognitive ability, an intracranial lesion, neurologic or psychiatric disorder, learning difficulties, pre-injury symptoms and family or social stressors.^[3] Younger athletes and those with prior concussion recover more slowly and are at higher risk of recurrence.^[2]

Skull fractures generally heal without lasting effects unless complicated by intracranial injury, persistent CSF leak, or an infected depressed fracture. Growing skull fractures, if untreated, progressively enlarge over months.

Prevention of concussion rests on sport-specific risk reduction: education, rule changes, enforcement against dangerous play (for example body checking rules in ice hockey), headgear in rugby, and individual baseline assessments with standardised tools.^[2] Protective equipment: rugby headgear probably reduces incidence; mouth guards do not clearly prevent concussion.^[2]

Inform athletes and parents of the risks of concussion, the second impact syndrome and the reasons for removal from play.^[2] Athletes with a history of multiple concussions and subjective persistent impairment should be referred for neurological and neuropsychological assessment, particularly for retirement decisions.^[2]

There is no screening test for skull fracture or CSF leak outside the context of acute trauma.

• Children: smaller neck muscles, larger heads and less myelinated neurons make the pediatric brain more susceptible, and cranial fractures behave differently. Most recover within weeks. Rule out child protection concerns when the history is unclear.^[1][6]
• Women: concussion risk is higher in female soccer and basketball players than in the corresponding male athletes.^[2]
• Older adults: falls dominate, anticoagulation raises haemorrhage risk, and fracture lines may be subtle. Fractures that are radiologically trivial may matter more clinically.
• Anticoagulated patients: should usually have brain imaging after head injury, even when other criteria are mild, and highlight any bleeding or clotting disorder.^[1]
• Pregnancy and tumour contexts do not routinely change skull fracture management; maternity input is added for pregnant patients.

• Clinical recognition of red flags is more useful than imaging. Where computed tomography is unavailable, observe, reassess, and provide clear written return precautions and follow-up.
• Airway protection, C-spine control, blood pressure and oxygenation matter more than advanced monitoring.
• Basal skull fracture signs, especially CSF leak, are clinical diagnoses made at the bedside.
• Most CSF leaks stop with conservative care (head elevation, rest, avoiding straining); arrange referral for persistent leaks or meningitis.
• Rugby or football clubs in resource-limited settings can implement simple protocols: remove any player with suspected concussion, no same-day return, 24 to 48 hours of rest, then gradual staged return under supervision.
• Seek neurosurgical transfer early for depressed, open or basal fractures with leaks.

Traumatic brain injury and severity grading; raised intracranial pressure and herniation; subdural and epidural haematoma; cervical spine injury and clearance; antiplatelet and anticoagulant reversal in head injury; chronic subdural haematoma; concussion and sports-related return to play; basilar skull (base of skull) fractures.