By MRCSA in MRCS Part A — 04 Jul 2026

20 HEAD INJURY

# 21 HEAD INJURY

Head injury is one of the highest-yield topics in MRCS Part A — expect three to five questions per paper. Questions are predictable in shape: a GCS calculation, a NICE-criteria triage question, a CT image pattern (lens vs crescent), and a physiology question on intracranial pressure or the Cushing reflex. Master five blocks and you cover almost everything the examiners can throw at you: GCS and airway thresholds, NICE CT criteria, the Monro–Kellie doctrine and cerebral perfusion pressure, the three classic haemorrhage patterns, and base of skull fracture signs.

Primary versus secondary brain injury

The single concept that ties this whole topic together is the distinction between primary and secondary injury.

Primary injury happens at the moment of impact — neuronal disruption, contusion, diffuse axonal injury, vascular tear. Nothing the surgeon does changes the primary injury. It is fixed by the time the patient reaches you.

Secondary injury evolves over the minutes, hours and days that follow. It is caused by hypoxia, hypotension, hypercapnia, raised intracranial pressure (ICP), seizures and pyrexia. Every intervention in head injury management — airway, ventilation, fluids, ICP control, surgical evacuation — exists to prevent secondary injury.

> Pearl: A single episode of hypotension (SBP <90) or hypoxia (SaO₂ <90%) doubles mortality in severe TBI. The mantra is "normal everything" — normotension, normoxia, normocapnia, normoglycaemia, normothermia.

The Monro–Kellie doctrine

The cranial vault is a rigid box of fixed volume containing three compartments: brain (~80%), blood (~10%) and CSF (~10%). The Monro–Kellie doctrine states that the total volume is constant, so an increase in any one component must be matched by a decrease in another, or ICP will rise.

When an extradural haematoma expands, CSF is first displaced into the spinal subarachnoid space and venous blood is squeezed out. Once these reserves are exhausted, even a small additional increase in volume produces a steep, exponential rise in ICP — this is why patients can be relatively stable, then deteriorate catastrophically over minutes.

Normal ICP in an adult is 7–15 mmHg. Treatment is generally triggered above 20–22 mmHg.

Cerebral perfusion pressure

This is the equation every examiner expects you to know:

CPP = MAP − ICP

Target CPP in TBI is >60 mmHg. Below this, the brain becomes ischaemic. This is why hypotension is so dangerous — it drops MAP, which drops CPP. It is also why raised ICP is so dangerous — for any given MAP, a rising ICP eats into CPP.

This is also why Cushing's reflex exists. The brainstem senses falling CPP and triggers a massive sympathetic surge to drive MAP up and restore perfusion. The classic triad is the result.

Cushing's reflex and triad

Cushing's triad = Hypertension + Bradycardia + Irregular respirations.

The mechanism is a sequence, not three independent events:

1. Rising ICP compresses the brainstem.

2. Brainstem ischaemia triggers a massive sympathetic outflow.

3. MAP rises sharply (to maintain CPP).

4. Aortic and carotid baroreceptors detect the high BP and increase their firing.

5. Afferents to the nucleus tractus solitarius drive increased vagal output to the heart → reflex bradycardia.

6. Direct compression of the medullary respiratory centre causes irregular or depressed respirations (Cheyne–Stokes, ataxic breathing).

Cushing's response is a pre-terminal sign. It means herniation is imminent.

Glasgow Coma Scale

GCS scores three domains: Eye (E1–4), Verbal (V1–5), Motor (M1–6). Maximum 15, minimum 3.

Score	Eye opening	Verbal response	Motor response
6	—	—	Obeys commands
5	—	Oriented	Localises pain
4	Spontaneous	Confused	Withdraws from pain
3	To voice	Inappropriate words	Abnormal flexion (decorticate)
2	To pain	Incomprehensible sounds	Extension (decerebrate)
1	None	None	None

Motor mnemonic (M1–6): None, Extends, Flexes abnormally, Withdraws, Localises, Obeys.

👩‍⚕️ The single most testable threshold: GCS ≤ 8 = intubate. The patient cannot protect their airway. "GCS less than 8, don't wait — intubate."

👩‍⚕️ Don't confuse abnormal flexion (decorticate, M3) with withdrawal (M4). Decorticate posturing involves arm flexion and adduction at the elbow with the wrist flexed across the chest — it is stereotyped and pathological. Withdrawal is purposeful movement away from the stimulus.

NICE criteria for CT head

Two windows: within 1 hour (high-risk) and within 8 hours (intermediate-risk).

CT within 1 hour

- GCS <13 on initial assessment

- GCS <15 at 2 hours post-injury

- Suspected open or depressed skull fracture

- Any sign of basal skull fracture (raccoon eyes, Battle's sign, CSF rhinorrhoea/otorrhoea, haemotympanum)

- Post-traumatic seizure

- Focal neurological deficit

- More than one episode of vomiting

CT within 8 hours

- Age ≥65 with any LOC or amnesia

- Anticoagulation (warfarin, DOACs such as rivaroxaban/apixaban, antiplatelets if symptomatic)

- Dangerous mechanism (pedestrian struck, fall >1 m or 5 stairs, ejection from vehicle)

- Retrograde amnesia >30 minutes

👩‍⚕️ Anticoagulation alone — even with no symptoms and GCS 15 — mandates CT within 8 hours. This is a favourite SBA trap.

ICP management ladder

Step up only as needed; revisit the lower steps continuously.

1. Head elevation 15–30° — promotes venous drainage via jugular veins.

2. Sedation and analgesia — reduces metabolic demand and prevents cough/strain spikes.

3. Hyperventilation to PaCO₂ 4.0–4.5 kPa — cerebral arteriolar vasoconstriction. Works in seconds in an intubated patient but is a temporising bridge only — prolonged hypocapnia causes ischaemia.

4. Osmotherapy: mannitol (0.25–1 g/kg) or hypertonic saline — osmotic gradient pulls water out of brain parenchyma.

5. CSF drainage via external ventricular drain (EVD).

6. Decompressive craniectomy — last resort.

> Pearl: Dexamethasone is contraindicated in TBI. It works for vasogenic oedema around tumours and abscesses, but the CRASH trial showed increased mortality when given for traumatic brain injury. Hypothermia is not a sustainable measure — it causes coagulopathy, arrhythmias and rebound ICP elevation on rewarming.

Cerebral blood flow is exquisitely PaCO₂-sensitive: a 1 kPa change in PaCO₂ alters CBF by roughly 30%. PaO₂ has little effect within the normal range — only profound hypoxia (<8 kPa) causes vasodilation.

Coup and contre-coup injury

A coup injury sits beneath the point of impact — the brain bruises against the skull as the skull is driven inward.

A contre-coup injury sits diametrically opposite — as the head decelerates suddenly, the brain continues to move and strikes the inside of the skull on the far side. The classic example is a fall backwards onto the occiput producing bifrontal contusions as the frontal lobes strike the rough floor of the anterior cranial fossa.

Diffuse axonal injury

DAI is caused by rotational acceleration–deceleration forces (typically high-speed RTAs). Shearing forces tear axons at grey/white matter interfaces, the corpus callosum and the dorsolateral midbrain.

Two clinical fingerprints:

- Severe deficit out of proportion to imaging — patients are often deeply comatose from the moment of injury yet the initial CT looks normal or shows only subtle petechial haemorrhages.

- MRI (especially GRE/SWI sequences) is much more sensitive than CT.

There is no surgical treatment for DAI — management is supportive ICU care to prevent secondary injury.

Intracranial haemorrhages

The three patterns examiners want you to recognise instantly:

Feature	Extradural (EDH)	Acute Subdural (SDH)	Subarachnoid (SAH)
Vessel	Middle meningeal artery	Bridging veins	Berry aneurysm (Circle of Willis)
Typical mechanism	Pterion fracture (temporal blow)	Acceleration–deceleration; cerebral atrophy	Spontaneous; exertion; trauma
CT shape	Biconvex / lens-shaped	Crescent-shaped	Blood in sulci, fissures, cisterns
Crosses suture lines?	No (dura tightly adherent at sutures)	Yes (but not midline — falx stops it)	N/A — follows CSF spaces
Classic history	Lucid interval → rapid deterioration	Elderly, alcoholic, anticoagulated; insidious	Thunderclap headache, neck stiffness
Age group	Young adults (dura less adherent in elderly)	Elderly, alcoholics	40–60; younger if APKD/coarctation

Extradural haematoma

The middle meningeal artery is the first branch of the maxillary artery (itself a terminal branch of the external carotid). It enters the skull through the foramen spinosum and runs on the inner surface of the squamous temporal bone — directly beneath the pterion, the thinnest part of the skull, where the frontal, parietal, temporal and sphenoid bones meet.

A temporal blow fractures the pterion and tears the artery. Blood accumulates under arterial pressure between the dura and the inner table of the skull. Because the dura is tightly adherent to the skull at suture lines, the haematoma is contained — giving the characteristic biconvex (lens) shape on CT.

The lucid interval is the classic — though not universal — history: brief LOC at impact, then apparent recovery, then progressive headache, deteriorating GCS, contralateral hemiparesis and finally an ipsilateral fixed dilated pupil from uncal herniation compressing CN III.

EDH is a neurosurgical emergency. Definitive treatment is craniotomy and clot evacuation.

👩‍⚕️ "Middle Meningeal from Maxillary" — both start with M. "Spinosum = sphenoid Spine = middle meningeal Speeds through."

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Subdural haematoma

Bridging veins drain from the cortical surface through the subdural space into the dural venous sinuses. Sudden acceleration–deceleration stretches and tears them. In elderly and alcoholic patients, cerebral atrophy lengthens these veins and they tear with trivial trauma.

Blood accumulates under low (venous) pressure, conforms to the brain surface and crosses suture lines, giving the crescent shape on CT. The falx cerebri prevents crossing the midline.

- Acute SDH (hyperdense, <3 days): high-velocity trauma, young patients, often with underlying contusions. High mortality.

- Chronic SDH (hypodense, weeks–months): elderly, alcoholic, anticoagulated; insidious onset of headache, confusion, falls. The "great mimic" — easily mistaken for dementia or stroke.

The "talk-and-deteriorate" patient — initially well, deteriorating hours to days later — is classic for an evolving (subacute) SDH.

Subarachnoid haemorrhage

Spontaneous SAH is almost always due to rupture of a saccular ("berry") aneurysm at branch points of the Circle of Willis. By frequency:

1. Anterior communicating artery (junction with ACA) — most common

2. Posterior communicating artery (junction with ICA) — classically causes a painful CN III palsy with a fixed dilated pupil before rupture

3. MCA bifurcation

Associations: adult polycystic kidney disease, coarctation of the aorta, Ehlers–Danlos, smoking, hypertension, family history.

Presentation: thunderclap headache ("worst headache of my life"), often during exertion or straining, with neck stiffness, photophobia and vomiting. Sudden collapse and death in a young adult during exercise is a classic SAH vignette.

Investigation: non-contrast CT within 6 hours is >95% sensitive. If CT is negative and clinical suspicion remains high, perform LP at 12 hours looking for xanthochromia — yellow discoloration of the CSF supernatant caused by bilirubin from breakdown of red cells, distinguishing true SAH from a traumatic tap.

Definitive treatment is endovascular coiling (preferred) or surgical clipping. Nimodipine is given to reduce vasospasm.

Uncal herniation and the blown pupil

An expanding supratentorial mass pushes the medial temporal lobe (uncus) through the tentorial notch. The herniating uncus compresses the ipsilateral CN III against the tentorial edge.

CN III carries parasympathetic fibres on its outer surface (to the sphincter pupillae). These superficial fibres are crushed first, before the somatic motor fibres. The result is:

- Loss of parasympathetic tone to the pupil → unopposed sympathetic action via the long ciliary nerves → ipsilateral fixed dilated pupil ("blown pupil").

- Followed by contralateral hemiparesis (corticospinal tract compression at the cerebral peduncle) and eventually third nerve motor signs (ptosis, "down and out" eye).

👩‍⚕️ The blown pupil is ipsilateral to the lesion. If a patient has bilateral haematomas and one dilated pupil, operate on the side of the dilated pupil first — that is the side that is herniating.

Skull fractures

Type	Key features
Linear	Single fracture line; uncomplicated unless overlying middle meningeal artery or venous sinus
Depressed	Inner table driven >1 thickness; risk of dural tear and underlying contusion; surgical elevation often needed; CT within 1 hour
Diastatic	Fracture along a suture line (children)
Basal skull	Anterior or middle/posterior cranial fossa; recognised clinically rather than radiologically

Signs of basal skull fracture

- Raccoon eyes (periorbital ecchymosis) — anterior cranial fossa

- Battle's sign (retroauricular bruising over the mastoid) — middle cranial fossa, develops over 24–48 h

- Haemotympanum — blood behind an intact tympanic membrane

- CSF rhinorrhoea (cribriform plate fracture) or CSF otorrhoea (petrous temporal fracture through the tegmen tympani — the bony roof of the middle ear)

- Halo (target) sign — central blood with peripheral clear ring on filter paper or bed linen — suggestive but not confirmatory

- Beta-2 transferrin is the gold-standard confirmatory test for CSF leak (found almost exclusively in CSF, perilymph and aqueous humour)

👩‍⚕️ Any one of these signs = NICE criterion for CT within 1 hour.

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Test yourself

A man is intubated in ICU with severe head injury. CT shows multiple intracerebral bleeds with no midline shift. Pupils are dilated and sluggish. HR 50, BP 170/110, RR 10. The rising BP is due to?

((Aortic and carotid baroreceptor stimulation::Baroreceptors detect the high BP — they don't drive it. They are the feedback, not the trigger.))
((Cortisol-mediated stress response::Too slow — cortisol acts over hours via fluid retention.))
((Activation of the renin-angiotensin-aldosterone system::RAAS acts over hours to days, not seconds.))
((Sympathetic stimulation secondary to blood loss::Blood loss gives tachycardia and hypotension — the opposite picture.))
((Sympathetic stimulation related to raised intracranial pressure::☑️ Cushing response — brainstem ischaemia triggers sympathetic surge to maintain CPP.))

👩‍⚕️ "The brain is being Crushed, so it Cushings." Triad = HTN + bradycardia + irregular respirations.

A head injury patient is hypertensive and bradycardic. What are the changes in baroreceptor firing and parasympathetic activity?

((Decreased baroreceptor firing, decreased parasympathetic activity::This is the shock pattern — low BP, sympathetic surge.))
((Increased baroreceptor firing, increased parasympathetic activity::☑️ Baroreceptors stretch with high BP → vagal output up → reflex bradycardia.))
((Decreased baroreceptor firing, increased parasympathetic activity::Physiologically inconsistent — low firing doesn't trigger vagal activation.))
((Increased baroreceptor firing, decreased parasympathetic activity::Wrong direction — the reflex INCREASES vagal tone in response to high BP.))

In raised ICP, what is the pattern seen in Cushing's triad?

((High BP, low HR, low RR::☑️ Sympathetic surge raises BP; baroreceptor-mediated vagal response drops HR; brainstem compression depresses respirations.))
((Low BP, high HR, low RR::Haemorrhagic shock pattern — not raised ICP.))
((High BP, low HR, high RR::Respirations are depressed, not elevated, when the brainstem is compressed.))
((High BP, high HR, low RR::A tachycardic patient hasn't engaged the vagal reflex — not Cushing's.))
((Normal BP, normal HR, low RR::Isolated respiratory depression suggests opioid toxicity, not raised ICP.))

Which is NOT a sustainable measure to decrease ICP?

((Raise head of bed 15–30°::Promotes jugular venous drainage — simple, effective, sustainable.))
((Hypothermia::☑️ Transient effect only; causes coagulopathy, arrhythmias and rebound ICP on rewarming.))
((Mannitol::Standard osmotic agent — sustainable as bolus therapy.))
((Controlled hypocapnia via hyperventilation::Useful as a bridge, though prolonged use risks ischaemia.))
((Sedation and analgesia::Reduces metabolic demand — core part of the ladder.))

A patient has elevated ICP. Which intervention would lower ICP?

((Increase PCO₂::Hypercapnia causes vasodilation — raises ICP further.))
((Decrease PCO₂::☑️ Hyperventilation → cerebral vasoconstriction → ↓ blood volume → ↓ ICP within seconds.))
((Increase PO₂::PO₂ has minimal effect on vessel calibre in the normal range.))
((Decrease PO₂::Hypoxia causes compensatory vasodilation — raises ICP.))
((Administer hypotonic saline::Drives water into brain tissue — worsens oedema.))

👩‍⚕️ A 1 kPa change in PaCO₂ alters cerebral blood flow by ~30%.

A patient has GCS 8, BP 190/100, HR 40. What is the immediate method to decrease ICP?

((Dexamethasone::Worsens outcomes in TBI (CRASH trial); only useful for tumour oedema.))
((Decompressive hemicraniectomy::Definitive but not immediate — needs theatre.))
((Burr hole drainage::Indicated for specific clots, not generic ICP reduction.))
((Hypertonic saline infusion::Effective but takes longer to prepare and infuse.))
((Hyperventilation::☑️ In an intubated patient, just turn up the rate — works in seconds as a bridge.))

An RTA patient has a CT showing cerebral oedema. What is the best management?

((Mannitol::☑️ Osmotic diuretic (0.25–1 g/kg) — first-line for traumatic cerebral oedema.))
((Dexamethasone::Contraindicated in TBI; CRASH trial showed increased mortality.))
((Hypotonic solution::Drives water into the brain — worsens oedema.))
((Normal saline::Maintenance fluid only — doesn't create an osmotic gradient.))

A patient opens eyes spontaneously, localises pain, and says inappropriate words. What is the GCS?

((10::Components add up to more than 10.))
((11::Would require M4 (withdrawal), but the patient localises (M5).))
((12::☑️ E4 + V3 + M5 = 12.))
((13::Would need V4 (confused), but inappropriate words = V3.))

A patient opens eyes to pain, makes incomprehensible sounds, and shows abnormal flexion. What is the GCS?

((6::E2 not E1 — they do open eyes to pain.))
((7::☑️ E2 + V2 + M3 (decorticate) = 7.))
((8::Abnormal flexion is M3, not M4 (withdrawal).))
((9::Overestimates each component.))

👩‍⚕️ GCS 7 is below the intubation threshold — secure the airway.

A patient opens eyes spontaneously, is confused in speech, and obeys commands. What is the GCS?

((13::Confused = V4, not V3 (inappropriate words).))
((14::☑️ E4 + V4 + M6 = 14.))
((15::Would require V5 (oriented).))
((12::Underscores — all components are at the higher end.))

A patient opens eyes to pain, makes incomprehensible sounds, and localises pain. What is the GCS?

((7::Would require M3 (abnormal flexion); patient localises (M5).))
((8::Localising is M5, not M4.))
((9::☑️ E2 + V2 + M5 = 9.))
((10::Would need E3 (to voice); patient opens to pain only.))

A patient has GCS 14 which drops to 7 after vomiting. What is the next step?

((Call the neurosurgical team::Inform them, but the airway is the immediate priority.))
((Intubate the patient::☑️ GCS ≤8 plus vomiting = aspiration risk — secure the airway now.))
((Urgent CT brain::Essential, but only after the airway is protected.))
((Administer IV mannitol::ICP treatment cannot precede airway protection.))

👩‍⚕️ "GCS less than 8, don't wait — intubate."

An elderly man is found outside a pub, smells of alcohol, has a small scalp laceration and no neurological deficits. He lives alone. What is the next step?

((Admit for observation::☑️ Intoxication makes GCS unreliable, and no responsible adult at home — NICE mandates admission.))
((Discharge with head injury advice sheet::Safe discharge requires reliable exam AND a responsible adult — neither is present.))
((CT head and discharge if normal::A normal CT doesn't exclude delayed deterioration; supervision still needed.))
((Suture the laceration and discharge::Addresses the wound but ignores the occult brain injury risk.))

A patient is struck by a ball and has a depressed skull fracture with no vomiting or loss of consciousness. What is the next step?

((CT within 8 hours::Depressed fractures fall under the 1-hour criteria regardless of symptoms.))
((CT within 1 hour::☑️ Depressed skull fracture is a NICE 1-hour indication — risk of dural tear and underlying brain injury.))
((Skull X-ray::Plain films cannot assess underlying brain or quantify depression.))
((Observation and discharge if stable::Imaging is mandatory regardless of clinical appearance.))

Which of the following is an indication for urgent CT head under NICE guidelines?

((Single episode of vomiting::NICE requires MORE than one episode.))
((GCS of 14 at 2 hours post-injury::GCS <15 at 2 hours triggers CT, but GCS 14 initially does not.))
((Retroauricular bruising::☑️ Battle's sign = basal skull fracture = CT within 1 hour.))
((Scalp haematoma in an adult::Not an independent NICE criterion in adults (different rules in infants).))
((Headache following head injury::Very common and non-specific — not a standalone criterion.))

A patient on rivaroxaban falls and feels fine. What is the next step?

((Discharge with head injury advice::Anticoagulation hugely increases bleeding risk — cannot discharge without imaging.))
((Observe for 4 hours then discharge::Delayed haemorrhage may not declare itself clinically until catastrophic.))
((CT head::☑️ Anticoagulation (including DOACs) is a NICE indication for CT within 8 hours, regardless of symptoms.))
((Check coagulation studies only::Anti-Xa levels don't replace imaging.))

A patient has 15 seconds of loss of consciousness, is now GCS 15 with no risk factors. What is the next step?

((CT within 1 hour::No 1-hour criteria met — GCS 15, no focal signs, no basal skull signs.))
((CT within 8 hours::No 8-hour criteria — not anticoagulated, no dangerous mechanism, no prolonged amnesia.))
((Provide written head injury instructions and discharge with a responsible adult::☑️ Brief LOC with full recovery and no risk factors = safe for discharge with adult supervision.))
((Admit for 24-hour neurological observation::Disproportionate for a low-risk presentation.))

What is the best indicator for confirming a CSF leak?

((Glucose testing of fluid::Non-specific — nasal secretions and tears also contain glucose.))
((Halo or ring sign on bed linen::Suggestive but not confirmatory.))
((Beta-2 transferrin::☑️ Found almost exclusively in CSF, perilymph and aqueous humour — gold standard.))
((Protein electrophoresis::Lacks specificity for clinical use.))
((Chloride concentration::CSF chloride is higher than serum, but specificity is poor.))

A patient has a temporal bone fracture with CSF otorrhoea. Which structure is damaged?

((Internal auditory meatus::Contains CN VII/VIII — damage causes facial palsy and hearing loss, not CSF leak.))
((Tympanic membrane::Must be ruptured for CSF to exit, but isn't the source of the leak.))
((Tegmen tympani::☑️ Thin bony roof of the middle ear — its fracture lets CSF drain from the middle cranial fossa into the middle ear.))
((Eustachian tube::Connects to the nasopharynx — not the intracranial space.))
((Mastoid air cells::Often involved in temporal fractures, but the tegmen tympani is the specific leak conduit.))

An alcoholic patient presents after a fall with lateralising neurological signs. What is the most likely diagnosis?

((Extradural haematoma::EDH is arterial, occurs in younger patients after temporal trauma, with a lucid interval.))
((Subdural haematoma::☑️ Cerebral atrophy in alcoholism stretches bridging veins — they tear with minor trauma. Crescent-shaped on CT.))
((Subarachnoid haemorrhage::Thunderclap headache, meningism — not insidious lateralising signs.))
((Intracerebral haemorrhage::Possible, but SDH is the classic answer for this risk profile.))

👩‍⚕️ SDH risk factors: elderly, alcoholics, anticoagulated, repeated minor trauma.

A footballer sustains a head injury, is briefly unconscious, continues playing, then collapses the next day. What is the diagnosis?

((Acute subdural haematoma::Acute SDH usually presents within hours, not the next day.))
((Subarachnoid haemorrhage::SAH is acute thunderclap, not delayed collapse after recovery.))
((Chronic subdural haematoma::☑️ Classic "talk-and-deteriorate" pattern from slow bridging-vein bleeding.))
((Extradural haematoma::EDH's lucid interval is hours, not the next day — arterial bleeding deteriorates faster.))
((Diffuse axonal injury::DAI causes immediate prolonged coma — no lucid interval.))

In an extradural haematoma with a lucid interval, the involved middle meningeal artery is a branch of which artery?

((Superficial temporal artery::Terminal branch of external carotid — runs superficial to the temporal fascia.))
((Internal carotid artery::Supplies the brain itself via ACA/MCA — not the meninges.))
((Vertebral artery::Supplies the posterior circulation; no relation to MMA.))
((Maxillary artery::☑️ MMA is the first branch of the maxillary, itself a terminal branch of the external carotid.))

👩‍⚕️ "Middle Meningeal from Maxillary" — both start with M.

The middle meningeal artery passes through which foramen?

((Foramen spinosum::☑️ In the greater wing of the sphenoid — MMA enters the middle cranial fossa here.))
((Foramen rotundum::Transmits CN V2 (maxillary nerve).))
((Foramen ovale::Transmits CN V3 and the accessory meningeal artery — not the MMA.))
((Foramen lacerum::Filled with cartilage in life; ICA passes over, not through it.))
((Carotid canal::Transmits the ICA and sympathetic plexus.))

👩‍⚕️ "Spinosum = sphenoid Spine = MMA Speeds through."

An extradural haematoma most commonly occurs at which anatomical location?

((Frontal bone::Possible via anterior meningeal artery, but far less common.))
((Pterion::☑️ Thinnest part of the skull where frontal, parietal, temporal and sphenoid meet — directly over the MMA.))
((Occipital bone::Posterior fossa EDH is rare and usually involves the transverse sinus.))
((Vertex::Vertex injuries cause sagittal sinus injury and SDH, not classic EDH.))

A patient is struck on the left temporal region and develops an extradural haematoma. Which bone is most likely fractured?

((Mastoid process of temporal bone::Thick and posterior — not the typical fracture site.))
((Occipital bone::At the back of the skull — not affected by a lateral blow.))
((Parietal bone::☑️ The parietal contribution to the pterion is the thinnest part — fractures here tear the underlying MMA.))
((Zygomatic bone::Forms the cheek — inferior to the pterion, unrelated to EDH.))

A patient develops a right fixed dilated pupil after head trauma, then deteriorates. What is the cause?

((Left extradural haematoma::A left lesion would cause LEFT uncal herniation and a LEFT blown pupil.))
((Right extradural haematoma::☑️ Right-sided mass → right uncal herniation → right CN III compression → right ipsilateral mydriasis.))
((Right acute subdural haematoma::Possible, but lucid interval + rapid deterioration is the classic EDH story.))
((Subarachnoid haemorrhage::SAH rarely causes isolated unilateral pupil dilation post-trauma.))
((Diffuse cerebral oedema::Would cause bilateral, not unilateral, pupil changes.))

👩‍⚕️ The blown pupil is ipsilateral to the lesion — parasympathetic fibres on the surface of CN III are crushed first.

A patient has bilateral extradural haematomas and one dilated pupil. Which side should be operated on first?

((Ipsilateral to the dilated pupil::☑️ That is the side that is herniating — decompress it first to prevent brainstem death.))
((Contralateral to the dilated pupil::Leaves the herniating side untreated — fatal.))
((The side with the larger haematoma on CT::Clinical signs of herniation trump radiological size.))
((Both sides simultaneously with two surgical teams::Not standard practice — prioritise the herniating side.))

A head injury patient has GCS 15 that then develops a blown pupil. What is the diagnosis?

((Acute hydrocephalus::Causes bilateral papilloedema, not a unilateral blown pupil.))
((Transtentorial herniation::☑️ Expanding mass pushes uncus through tentorial notch → CN III compression → ipsilateral mydriasis.))
((CN VI palsy from raised ICP::Causes lateral rectus palsy and diplopia — not pupil dilation.))
((Direct traumatic optic neuropathy::Causes an afferent (Marcus Gunn) defect, not a fixed dilated pupil.))

A patient has a fixed dilated pupil after head injury. What is the cause of the dilation?

((Unopposed sympathetic activity::☑️ CN III parasympathetic fibres are crushed during uncal herniation; sympathetic supply to dilator pupillae is unopposed → mydriasis.))
((Unopposed parasympathetic activity::Would cause miosis (constriction), not mydriasis.))
((Direct sympathetic stimulation from raised ICP::The mechanism is loss of parasympathetic input, not extra sympathetic drive.))
((Traumatic iris sphincter damage::Requires direct ocular trauma — not the mechanism in raised ICP.))

A 21-year-old collapses while running a marathon and dies. Post-mortem shows intracranial haemorrhage. What is the most likely site?

((Extradural::EDH requires trauma — none described here.))
((Intracerebral::Rare in young patients without hypertension or AVM.))
((Intraventricular::Primary IVH is rare; usually neonatal or secondary.))
((Subarachnoid::☑️ Spontaneous SAH in a young adult during exertion = ruptured berry aneurysm at the Circle of Willis.))
((Subdural::Bridging vein rupture requires trauma or cerebral atrophy — neither applies.))

👩‍⚕️ Most common berry aneurysm site: anterior communicating artery. Associations: APKD, coarctation of the aorta, Ehlers–Danlos.

Revision summary

Primary vs secondary injury — primary is fixed at impact; secondary (hypoxia, hypotension, raised ICP) is what surgery prevents.

Monro–Kellie: brain + blood + CSF = constant. CPP = MAP − ICP (target >60).

Cushing's triad = HTN + bradycardia + irregular respirations. Pre-terminal sign of brainstem compression.

GCS: E4 V5 M6 = 15. Motor: None, Extends, Flexes abnormally, Withdraws, Localises, Obeys. GCS ≤8 = intubate.

NICE CT <1 h: GCS <13 initial / <15 at 2 h, depressed or open #, basal skull # signs, seizure, focal deficit, >1 vomit.

NICE CT <8 h: age ≥65, anticoagulants/DOACs, dangerous mechanism, retrograde amnesia >30 min.

ICP ladder: head up → sedate → hyperventilate (bridge only) → mannitol/hypertonic saline → EVD → craniectomy. No steroids. No hypothermia.

EDH: middle meningeal artery (branch of maxillary, through foramen spinosum), pterion, biconvex, doesn't cross sutures, lucid interval, blown pupil ipsilateral.

SDH: bridging veins, crescent, crosses sutures not midline, elderly/alcoholic/anticoagulated, "talk-and-deteriorate".

SAH: berry aneurysm, AComm > PComm > MCA bifurcation, thunderclap headache, xanthochromia on LP at 12 h, APKD/coarctation.

DAI: rotational deceleration; CT often normal; MRI sensitive; supportive care only.

Basal skull #: raccoon eyes (ACF), Battle's sign (MCF), CSF rhino/otorrhoea (cribriform / tegmen tympani), halo sign suggestive, beta-2 transferrin confirmatory.

Blown pupil = ipsilateral uncal herniation → operate that side first.