Intracranial Haemorrhage & Neuroanatomy

Part IIntracranial haemorrhage

Epidural · Subdural · Subarachnoid · Intracerebral

Four lesions, four planes. Each type of intracranial haemorrhage is named for the compartment it occupies, and almost every difference in shape, speed and behaviour follows from that compartment and from the pressure in the vessel that fills it. Learn the geometry once and the rest stops being a list.

1.1Epidural haematoma

Blood between the inner table and the outer, periosteal layer of the dura. It is nearly always traumatic, and the classic source is the middle meningeal artery, a branch of the maxillary artery that runs in a groove on the inner surface of the temporal squama, under the pterion where the bone is thinnest. Because the source is arterial, the collection expands under systemic pressure, and that single fact explains almost everything else.

Why the shape follows from the space

The extradural space is potential. Dura is bonded to the inner table, most tightly at the sutures, where the periosteal layer becomes continuous with the outer periosteum. An arterial jet has to strip dura off bone to make room, and it does so until it reaches a suture and stops. The result is the biconvex lens: sharply marginated, tall in the middle where the pressure head is applied.

The mirror-image rule is more useful than either half of it. Epidural blood does not cross sutures but can cross the midline; subdural blood crosses sutures but is stopped at the falx and tentorium. Hold that pair and you rarely need the shape.

The lucid interval

A minority of patients — series report 20–50% — show the classic sequence: brief unconsciousness from the impact, apparent recovery, then rapid secondary deterioration. The recovery is real. The patient is compensating on the flat part of the pressure–volume curve (Figure 4) while CSF is displaced into the spinal sac; deterioration is abrupt because the curve has a knee, not because anything new has happened to the bleed.

The temporal location puts the clot beside the uncus. Uncal herniation compresses the third nerve (an ipsilateral fixed, dilated pupil) and the cerebral peduncle (contralateral hemiparesis). Sometimes the shift presses the opposite peduncle against the tentorial edge and gives an ipsilateral hemiparesis — Kernohan's notch, a false-localising sign that has sent more than one patient to theatre on the wrong side.

On the scan

• Hyperdense (about 60–90 HU) biconvex collection against the inner table, usually temporal or temporoparietal.
• A hypodense swirl inside the clot is unclotted blood — active bleeding, and an argument against watchful waiting.
• An overlying fracture in most adults; its absence in a child, whose skull deforms, does not exclude the diagnosis.

1.2Subdural haematoma

Blood between dura and arachnoid, usually from rupture of the cortical bridging veins that cross from the brain surface to the superior sagittal sinus, tethered at both ends. They carry blood at 5–10 mmHg, so bleeding is slow, the course is variable, and the presentation is often nothing like the textbook trauma case.

Table 1.2 Severe anaemia lowers attenuation and can make acute blood look isodense.

Why older people

Atrophy lengthens the unsupported course of the bridging veins and lets the brain move inside the vault, so a trivial mechanism — a fall from standing, sometimes nothing remembered — tears them. The same atrophy leaves room for a large collection before anything localising appears, which is why chronic subdural haematoma presents as gait disturbance, apathy or confusion far more often than as hemiparesis. Anticoagulants, antiplatelets, alcohol and thrombocytopenia all raise the risk.

1.3Subarachnoid haemorrhage

Bleeding into the CSF between arachnoid and pia. About 85% of spontaneous cases come from a ruptured saccular aneurysm, usually at a bifurcation on or near the circle of Willis; perimesencephalic non-aneurysmal haemorrhage and other causes make up the rest. Because the blood enters flowing CSF, it spreads within seconds through the basal cisterns, over the convexities and down the spinal canal — and disrupts CSF handling for weeks.

The headache

A headache maximal within seconds to a minute. Two mechanisms combine: an abrupt rise in ICP at rupture, and chemical irritation of the pain-sensitive meninges. Meningism develops over hours, so a supple neck early on is not reassuring. A sizeable minority describe a sentinel headache days or weeks earlier; recognising and investigating it is one of the few genuinely life-saving acts in this disease.

Imaging, and when the lumbar puncture is still needed

Non-contrast CT on a modern scanner, read by an experienced radiologist, is close to 100% sensitive within six hours of onset. Sensitivity falls after that as blood is cleared. If CT is negative and the story is convincing, lumbar puncture at least 12 hours after onset remains the standard next step. Xanthochromia comes from bilirubin made in vivo from oxyhaemoglobin by haem oxygenase — which is why it takes hours to appear and why it distinguishes true haemorrhage from a traumatic tap; spectrophotometry beats inspection. CT angiography is an alternative where expertise allows, at the cost of finding incidental aneurysms.

The later complications

• Delayed cerebral ischaemia peaks between days 4 and 14. Oxyhaemoglobin drives endothelin release and scavenges nitric oxide, narrowing large arteries — but delayed ischaemia and angiographic vasospasm are not the same thing. Clazosentan largely abolished vasospasm without improving outcome, the clearest demonstration that microvascular failure, microthrombosis and spreading depolarisation matter too. Treat the patient, not the angiogram.
• Nimodipine 60 mg orally every 4 hours for 21 days is the only drug with an outcome benefit; start on admission. Triple-H therapy is abandoned: keep euvolaemia, and induce hypertension when a new deficit appears; endovascular rescue for refractory cases.
• Hydrocephalus — early obstructive from intraventricular clot, later communicating as breakdown products block absorption. A falling conscious level, sometimes impaired upgaze. External drain acutely; a shunt in the minority who stay dependent.
• Systemic complications — neurogenic stunned myocardium, neurogenic pulmonary oedema, hyponatraemia (cerebral salt wasting more often than SIADH, so fluid restriction is harmful) and fever. These kill patients who survived the aneurysm.

1.4Intracerebral haemorrhage

Bleeding into the brain itself. It causes 10–15% of strokes in high-income settings but about a quarter worldwide, with a higher share across sub-Saharan Africa and Asia, and 30-day mortality of 30–50% that has barely moved in decades. The dominant cause is hypertensive small-vessel disease: lipohyalinosis and fibrinoid necrosis of penetrating arteries, with Charcot–Bouchard microaneurysms. In older patients with lobar bleeds, cerebral amyloid angiopathy is the other major cause.

Table 1.4 Ranges across series; they do not sum to 100.

Haematoma expansion is the treatable enemy

About a third of patients have meaningful growth, most of it within the first 3–6 hours; each 10% increase in volume adds roughly 5% to mortality. The window in which anything you do can change the outcome is open when the patient arrives. The CT angiographic spot sign marks active extravasation — good specificity, modest sensitivity; useful for prognosis, not for triage.

Estimate volume with ABC/2: A, the largest diameter on the slice with the biggest clot; B, the diameter perpendicular to it; C, the number of slices with clot multiplied by slice thickness. It approximates an ellipsoid and over-estimates irregular clots.

Surgery, reconsidered

• Cerebellar haemorrhage over 3 cm, or with deteriorating consciousness, brainstem compression or hydrocephalus, is evacuated urgently. A ventricular drain alone is not enough for a compressing posterior fossa clot.
• Supratentorial haemorrhage has a long record of neutral trials of open craniotomy (STICH, STICH II). ENRICH (2024) changed the picture for a defined group: minimally invasive trans-sulcal parafascicular evacuation within 24 hours of onset improved outcome, driven by lobar haemorrhages of 30–80 mL; deep bleeds did not show the same benefit.
• Decompressive craniectomy without evacuation was tested in SWITCH (2024) for severe deep haemorrhage: the result favoured surgery but missed conventional significance. A rescue option, not a standard.
• No prophylactic antiseizure drugs. Treat clinical seizures, and electrographic seizures found on EEG when consciousness is depressed out of proportion.

When it is not hypertensive

Attributing every bleed to hypertension is the commonest diagnostic error in this disease. Suspect a secondary cause in patients under 55 or without hypertension, and when the haematoma is lobar, purely intraventricular, oddly shaped, multiple, surrounded by disproportionate oedema, or accompanied by subarachnoid blood.

• Vascular malformation — arteriovenous malformation, cavernoma, dural fistula. The commonest secondary cause in the young.
• Aneurysm — especially with subarachnoid blood, or a frontal or temporal clot next to the circle of Willis.
• Venous sinus thrombosis — haemorrhagic venous infarction that ignores arterial territories, often parasagittal or temporal, with disproportionate oedema. The treatment is anticoagulation — the opposite of the reflex.
• Tumour — melanoma, renal, thyroid, choriocarcinoma and lung metastases bleed; so does glioblastoma.
• Drugs and coagulopathy — sympathomimetics, anticoagulants, thrombolysis, and haemorrhagic transformation of an infarct.
• Vasculopathy — RCVS, vasculitis, moyamoya; consider them in recurrent or multifocal bleeds.

1.5Master comparison

Table 1.5 Almost every difference traces to two variables: the pressure in the bleeding vessel and the plane the blood is forced into.

Part IIMeningeal architecture

The layers · The dural venous sinuses · The blood–brain barrier

2.1The meningeal layers

Dura mater

A dense fibrous membrane in two layers: the outer periosteal layer, which is the periosteum of the inner table, and the inner meningeal layer, which continues as the spinal dura. They are fused everywhere except where they part to enclose the venous sinuses. The meningeal layer folds inward as the falx cerebri, tentorium cerebelli and falx cerebelli. The tentorial notch, through which the midbrain passes, is the choke point in uncal herniation — the reason a supratentorial mass kills through a brainstem it never touches.

The dura is the main pain-sensitive covering of the brain. Above the tentorium it is supplied by the trigeminal nerve; below, by the upper cervical roots and branches of the vagus and glossopharyngeal nerves. Supratentorial pathology refers pain to the front of the head; posterior fossa pathology to the occiput and neck.

Arachnoid mater

Thin, avascular, held against the dura by CSF pressure. It bridges over the sulci rather than following them, creating the cisterns wherever the brain surface falls away. Fine trabeculae cross the subarachnoid space to the pia. The arachnoid granulations project into the venous sinuses and act as one-way valves, opening when CSF pressure exceeds sinus pressure by a few mmHg.

Pia mater

The innermost layer, adherent to every gyrus and sulcus. As an artery dives into the parenchyma it carries a sleeve of pia, forming the perivascular (Virchow–Robin) space — the anatomical substrate of glymphatic exchange.

2.2The dural venous sinuses

Valveless, rigid channels between the two dural layers that receive cerebral venous blood and CSF. Their rigidity is the point: they do not collapse when ICP rises, which keeps venous outflow possible until pressures become extreme.

• Superior sagittal sinus — along the attached margin of the falx to the torcular; the main recipient of arachnoid granulations; usually drains preferentially to the right transverse sinus. Thrombosis gives bilateral parasagittal venous infarcts, often haemorrhagic, and can cause convexity subarachnoid haemorrhage.
• Transverse and sigmoid sinuses — with the superior sagittal sinus, the commonest sites of venous thrombosis. A hypoplastic left transverse sinus is a normal variant and a frequent source of false-positive reports.
• Cavernous sinuses — either side of the sella. The oculomotor and trochlear nerves and the ophthalmic and maxillary divisions run in the lateral wall; the abducens nerve runs free within the sinus beside the internal carotid artery, so an isolated sixth nerve palsy can be the first sign of cavernous sinus disease. Septic thrombosis from mid-facial infection gives painful ophthalmoplegia, proptosis and chemosis.
• Straight sinus — draining the vein of Galen and so the deep white matter, basal ganglia and thalami. Deep venous thrombosis gives bilateral thalamic oedema and a falling conscious level — an easily missed and treatable cause of coma.

2.3The blood–brain barrier

Tight junctions between specialised endothelial cells — claudins and occludin anchored by zonula occludens proteins — supported by pericytes, a basal lamina and astrocytic end-feet. It excludes most hydrophilic molecules, ions and proteins, including most drugs.

In haemorrhage the barrier fails locally. Thrombin, complement and iron released from degrading haemoglobin drive perihaematomal oedema, which peaks around days 3–5 and can exceed the volume of the clot. This secondary injury is the most attractive therapeutic target in the disease and, so far, the least successfully hit.

Part IIICSF dynamics

Production · Circulation · Absorption and clearance · Reference values

3.1Production

CSF is secreted by the choroid plexus: a sealed epithelium over leaky, fenestrated capillaries — the reverse of the usual arrangement, which puts the blood–CSF barrier at the epithelium. Secretion is active: basolateral Na⁺/K⁺-ATPase sets the gradient, carbonic anhydrase supplies bicarbonate and protons, aquaporin-1 provides the water route. Because it is active, production is largely independent of pressure — which is why a blocked pathway causes relentless hydrocephalus.

• About 500 mL a day from a standing volume of about 150 mL: three to four turnovers daily, about 0.35 mL a minute.
• Most is made in the lateral ventricles; the rest in the third and fourth ventricles, with an extrachoroidal contribution.
• Acetazolamide reduces production modestly — the basis of its use in idiopathic intracranial hypertension.

3.2Circulation

From the lateral ventricles CSF passes through the foramina of Monro into the third ventricle, then through the aqueduct of Sylvius — narrow and the most stenosis-prone segment of the pathway. Aqueductal stenosis, pineal tumours and tectal gliomas obstruct here. The fourth ventricle empties through the paired foramina of Luschka and the midline foramen of Magendie. Obstruction at this level — posterior fossa tumour, cerebellar haematoma, Chiari malformation — is dangerous out of proportion to its size, because the compartment has no room and the medulla is next door. Beyond, CSF flows through the cisterns, over the convexities and into the spinal subarachnoid space, the compliant reservoir that buys time when intracranial volume rises.

3.3Absorption and clearance

The classical account gives all absorption to the arachnoid granulations. That model is correct but incomplete.

• Glymphatic exchange — aquaporin-4-dependent movement of CSF along perivascular spaces into the interstitium and out again, carrying solutes such as amyloid-β. In mice it rises sharply in sleep, when the interstitial space expands by about 60% (Xie et al., 2013).
• Meningeal lymphatics — described in 2015, running along the dural sinuses to the deep cervical nodes.
• Cribriform plate and nerve sheaths — CSF tracks along olfactory and spinal nerve sheaths into lymphatics, proportionally more in the young.

3.4Reference values

Table 3.4 Adult values; use your laboratory's ranges where they differ.

Part IVIntracranial pressure

Monro–Kellie · Compliance and waveforms · High- and low-pressure headache

4.1The Monro–Kellie doctrine

After the sutures fuse, the skull is a rigid box holding three effectively incompressible contents: brain (about 1,400 mL), blood (about 150 mL) and CSF (about 150 mL). An increase in one must be matched by a decrease in another or pressure rises. Normal ICP in a supine adult is 5–15 mmHg.

The doctrine's real value is that it explains timing. Compensation is finite and is spent in order: CSF is displaced into the spinal sac (the largest, fastest buffer), CSF absorption rises, venous blood is squeezed out, and production falls slightly. Once that reserve is used, each further millilitre costs disproportionate pressure.

4.2Waveforms and plateau waves

A monitored ICP trace is pulsatile, synchronous with the heartbeat and modulated by breathing. Three peaks are described: P1, the percussion wave of the arterial pulse; P2, the tidal wave, which reflects intracranial compliance; and P3, the dicrotic wave after aortic valve closure. Normally P1 > P2 > P3. As compliance falls, P2 rises above P1 — often before the mean ICP moves, which makes it one of the few early warnings available.

• Lundberg A (plateau) waves — sustained rises to 50–100 mmHg for 5–20 minutes, then abrupt return. They reflect exhausted compliance with intact but overwhelmed autoregulation, and are an emergency.
• Lundberg B waves — rhythmic oscillations at 0.5–2 per minute, marking reduced compliance.
• Lundberg C waves — 4–8 per minute, linked to systemic arterial (Traube–Hering–Mayer) waves; of little significance.

4.3High-pressure headache and its treatment

Sustained raised pressure produces headache by distending and pulling on the pain-sensitive dura, sinuses and proximal arteries; the parenchyma has no nociceptors.

• Worse in the morning and lying flat — recumbency impedes venous drainage, and mild nocturnal hypoventilation raises PaCO₂ and cerebral blood volume.
• Worse with Valsalva — coughing, straining and bending obstruct jugular outflow.
• Papilloedema takes days to develop; its absence never excludes acutely raised pressure.
• Sixth nerve palsy — the classic false-localising sign.
• Vomiting, often without much nausea; Cushing's response — hypertension, bradycardia, irregular breathing — late and pre-terminal.

4.4Low-pressure headache

Intracranial hypotension is usually a CSF leak — after lumbar puncture, spontaneously through a spinal dural tear or CSF–venous fistula, or after trauma or surgery. An opening pressure below 6 cmH₂O supports it, but many patients with proven leaks have normal pressures.

The brain weighs about 1,400 g in air and about 50 g floating in CSF. Lose the buoyancy and it sags on standing, pulling on the bridging veins, dura and pain-sensitive nerves. Monro–Kellie demands compensation for the lost volume, delivered as venous engorgement — which produces the MRI picture: smooth pachymeningeal enhancement, subdural collections, engorged sinuses, pituitary swelling and brain sag with tonsillar descent that can be mistaken for Chiari I.

Part VSynthesis

Rates and pressures · Herniation · CT chronology · Prognosis

5.1Why the epidural kills faster than the subdural

The answer is hydraulic. The middle meningeal artery delivers blood at systemic pressure; bridging veins at 5–10 mmHg. Flow through a breach scales with the pressure gradient, so an epidural collection fills many times faster and decompensation arrives in minutes to hours rather than days to weeks. Location compounds it: an epidural haematoma sits over the temporal squama, directly lateral to the uncus. And the brains differ: the young brain that suffers an epidural has no atrophic reserve; the atrophic brain that develops a chronic subdural has room to spare.

5.2Subarachnoid haemorrhage — sabotage of the drainage system

Subarachnoid haemorrhage is the only one of the four that attacks CSF handling directly. Fibrin and blood products obstruct the arachnoid granulations and provoke fibrosis, so absorption stays impaired long after the aneurysm is secured. Meanwhile the cisternal blood narrows large arteries and disturbs the microcirculation. Four waves arrive in sequence — the ictus, rebleeding, delayed ischaemia from day 4 to 14, and hydrocephalus that may take weeks — each with its own window and its own intervention.

5.3Herniation syndromes

5.4CT chronology of blood

Table 5.4 Severe anaemia (haemoglobin below about 8–9 g/dL) and coagulopathy lower attenuation throughout.

5.5Prognosis, and the trap inside it

The ICH score (Hemphill, 2001) estimates 30-day mortality in seconds and makes handovers precise.

AppendixAbbreviations and sources

For checking

AAbbreviations

ABC/2

bedside haematoma volume formula

CAA

cerebral amyloid angiopathy

CPP

cerebral perfusion pressure

CTA

CT angiography

DCI

delayed cerebral ischaemia

EDH

epidural (extradural) haematoma

EVD

external ventricular drain

ICH

intracerebral haemorrhage

ICP

intracranial pressure

ISF

interstitial fluid

MAP

mean arterial pressure

MMA

middle meningeal artery

PCC

prothrombin complex concentrate

SAH

subarachnoid haemorrhage

SDH

subdural haematoma

SIBICC

Seattle International Severe Traumatic Brain Injury Consensus Conference

WFNS

World Federation of Neurosurgical Societies

BSources

Guidelines and consensus

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Trials

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17. Macdonald RL, Higashida RT, Keller E, et al. (CONSCIOUS-2). Clazosentan in patients with aneurysmal subarachnoid haemorrhage undergoing surgical clipping. Lancet Neurol 2011;10:618–625.
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19. Perry JJ, Stiell IG, Sivilotti MLA, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage. BMJ 2011;343:d4277.

Anatomy and physiology

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