Concussion & Traumatic Brain Injury — Viva

Q1: Definition, classification and severity (2 min)

• Define traumatic brain injury: brain damage from an external mechanical force, spanning a spectrum from concussion to fatal diffuse axonal injury.
• Define concussion (mild TBI): a transient disturbance of brain function produced by biomechanical force, with symptoms (headache, dizziness, confusion, amnesia) that may or may not involve loss of consciousness and with no structural injury on standard imaging.
• Classify by GCS severity: mild 13 to 15 (about 80 percent, includes concussion), moderate 9 to 12 (about 10 percent), severe 3 to 8 (about 10 percent).
• Classify by morphology: focal (contusion, extradural, subdural, intracerebral haematoma, skull fracture) vs diffuse (diffuse axonal injury, diffuse swelling); and primary (mechanical, instantaneous) vs secondary (delayed, preventable) injury.

Q2: Pathophysiology — primary vs secondary injury (3 min)

• Primary injury is mechanical and largely irreversible: skull fracture, contusion (coup and contrecoup), laceration, and diffuse axonal injury (rotational/angular acceleration shears axons at the grey-white junction, corpus callosum and brainstem — CT may be normal; MRI gradient-echo/SWI shows microbleeds).
• Secondary injury is delayed (minutes to days) and preventable — it is the main target of treatment. The cascade: hypoxia and hypotension -> energy failure -> excitotoxicity (glutamate, calcium influx) -> cytotoxic and vasogenic oedema -> raised ICP -> reduced cerebral perfusion pressure (CPP = MAP - ICP) -> herniation.
• Cerebral autoregulation is impaired after TBI, so cerebral blood flow becomes pressure-passive — this is why hypotension is so damaging (CPP collapses) and why blood-pressure and oxygenation control is the cornerstone.
• Even a single episode of hypotension (SBP under 90) or hypoxia doubles mortality.

Q3: Clinical features and the key diagnoses (2 min)

• Concussion: headache, dizziness, nausea, confusion, amnesia (retrograde and anterograde), photophobia, poor concentration; loss of consciousness in a minority only.
• Extradural haematoma: temporal impact, middle meningeal artery, lucid interval, ipsilateral fixed dilated pupil (CN III) and contralateral hemiparesis — neurosurgical emergency.
• Subdural haematoma: torn cortical bridging vein; crescentic on CT, crosses sutures; elderly/alcoholic/anticoagulated; fluctuating, subacute course.
• Diffuse axonal injury: coma from high-speed rotational injury with normal or near-normal early CT.
• Skull base fracture: CSF rhinorrhoea/otorrhoea, Battle's sign (mastoid bruising), raccoon eyes (periorbital bruising), cranial nerve VII/VIII palsy.
• Cushing's triad (bradycardia, hypertension, irregular respiration) is a pre-terminal sign of markedly raised ICP.

Q4: Investigations and CT criteria (2 min)

• First investigation: non-contrast CT brain — shows acute blood (extradural lens, subdural crescent, contusion, traumatic SAH), midline shift, fractures, pneumocephalus.
• NICE adult CT indications (memorise): GCS under 13 on assessment; GCS under 15 at 2 hours; suspected open/depressed/skull-base fracture; sign of skull fracture; post-traumatic seizure; focal neurology; more than one episode of vomiting; dangerous mechanism; coagulopathy/anticoagulant; age 65 or over; amnesia of events more than 30 minutes before impact; previous brain surgery.
• MRI for suspected diffuse axonal injury (gradient-echo/SWI microbleeds) or persistent unexplained symptoms.
• CT cervical spine in all high-risk patients; clear clinically by Canadian C-spine rule / NEXUS criteria.
• Always check glucose, coagulation/INR, alcohol level, and beta-hCG in women.

Q5: Management — resuscitation, definitive and the post-concussion pathway (3 min)

• Resuscitation (ATLS): Airway with C-spine control — intubate if GCS 8 or under; Breathing — keep SaO2 at least 94 percent; Circulation — keep SBP over 110 / MAP over 80; Disability — GCS trend, pupils, glucose.
• Severe TBI / raised ICP: head-up 30 degrees, sedation/analgesia, normocapnia (avoid prophylactic hyperventilation), ICP monitoring (target under 22 mmHg), CPP 60-70 mmHg, osmolar therapy (mannitol or 3 percent hypertonic saline), decompressive craniectomy for refractory raised ICP; seizure prophylaxis (phenytoin/levetiracetam 7 days for early seizures).
• Neurosurgical evacuation for extradural/subdural haematoma over 10 mm, midline shift over 5 mm, or any deteriorating patient.
• Concussion: 24-48 hours physical and cognitive rest, then graduated return (CISG 6-stage protocol, minimum 24 h per stage, symptom-free before progression; no same-day return to play; minimum ~1 week before full contact) — this prevents second-impact syndrome.
• Post-concussion syndrome (symptoms beyond 4 weeks): reassurance, graded rehabilitation, treat headache/vestibular/mood symptoms; refer if persistent.

Q6: Complications, prognosis and an emergency (2 min)

• Emergencies: extradural haematoma with a lucid interval (urgent CT + evacuation); refractory raised ICP and herniation (osmolar therapy + decompressive craniectomy); second-impact syndrome (prevent by enforced rest after concussion).
• Complications: secondary brain injury, post-traumatic epilepsy, post-concussion syndrome, cognitive/behavioural/psychiatric sequelae, CSF leak and meningitis, chronic traumatic encephalopathy.
• Prognosis: mild TBI recovers fully in most within days-weeks (10-20 percent develop post-concussion syndrome); severe TBI mortality 20-40 percent, many survivors with permanent disability. Key prognostic factors: age, initial GCS, pupillary response, hypoxia/hypotension, CT findings (midline shift, traumatic SAH).
• Discharge advice: graduated return to activity, no alcohol, no driving until symptom-free, written head-injury advice ('return immediately if…'), and structured follow-up.