Cerebral oedema and CSF disorders
CSF flow disorders, blood-brain barrier and cerebral oedema
The brain sits in a closed box, so any extra fluid, blood or tissue raises pressure. CPSP asks how CSF is made and absorbed, types of hydrocephalus, the barriers and what crosses them, the four kinds of cerebral oedema and the herniation syndromes, with their CT and MRI appearances.
CSF production and flow
- Made mainly by the choroid plexus of the lateral, third and fourth ventricles at about 500 mL/day; total volume about 150 mL, so it turns over three to four times a day.
- Path: lateral ventricles, foramina of Monro, third ventricle, aqueduct, fourth ventricle, foramina of Luschka and Magendie, subarachnoid space, arachnoid granulations into the dural venous sinuses.
- Arachnoid granulations can appear as round CSF-density filling defects in the transverse sinus on venography.
- The dural sac ends at S2; the cord ends at L1–L2 in adults and about L3 at birth.
- Normal lumbar opening pressure (lying relaxed on the side) is about 10–20 cmH₂O.
Hydrocephalus
| Type | Cause | Imaging |
|---|---|---|
| Obstructive (non-communicating) | Aqueduct stenosis, posterior fossa mass, colloid cyst | Ventricles dilated above the block only |
| Communicating | Failed absorption: after meningitis (especially TB basal exudate), subarachnoid haemorrhage | All four ventricles dilated |
| Overproduction | Choroid plexus papilloma (infants, trigone of lateral ventricle) | All ventricles dilated, enhancing mass |
| Normal pressure | Elderly; gait disturbance, incontinence, dementia | Large ventricles out of proportion to sulci |
- Acute hydrocephalus: rounded frontal horns, dilated temporal horns, periventricular low density (transependymal CSF), effaced sulci.
- Atrophy (ex vacuo) enlarges ventricles and sulci equally; do not call it hydrocephalus.
- Infant hydrocephalus: enlarging head, bulging fontanelle, setting-sun eyes from pressure on the pretectal dorsal midbrain.
- Shunt overdrainage collapses the ventricles and tears bridging veins: slit ventricles with subdural collections.
- Lumbar puncture is dangerous in obstructive hydrocephalus or with a mass (herniation), but not in communicating hydrocephalus.
CSF findings
| Condition | Cells | Protein | Glucose |
|---|---|---|---|
| Normal | <5 lymphocytes | 0.15–0.45 g/L (15–45 mg/dL) | >60% of blood |
| Bacterial | Neutrophils, high | High | Low |
| Viral | Lymphocytes | Mildly high | Normal |
| Tuberculous | Lymphocytes | Very high | Low |
- Froin syndrome: yellow, protein-rich CSF that clots, below a complete spinal block.
- CSF rhinorrhoea after frontal injury comes through the cribriform plate; it brings meningitis risk and loss of smell.
Blood–brain and blood–CSF barriers
- Blood–brain barrier: tight junctions of capillary endothelium, with basement membrane and astrocyte foot processes. Absent in circumventricular organs (area postrema, pituitary, pineal).
- Blood–CSF barrier: choroid capillaries are fenestrated; tight junctions of the choroid plexus epithelium keep solutes out. So the plexus enhances with gadolinium but CSF stays dark.
- Lipid-soluble, small, uncharged drugs cross; quaternary amines do not (glycopyrronium, neostigmine), whereas atropine and physostigmine do.
- Levodopa crosses on the large neutral amino acid transporter (protein meals compete); carbidopa does not cross, so it blocks peripheral conversion only.
- Inflamed meninges loosen the barrier, letting penicillin reach CSF in meningitis.
- Contrast enhancement in the brain parenchyma means barrier breakdown (tumour, abscess, active MS plaque, subacute infarct).
Cerebral oedema
| Type | Mechanism | Example | Imaging | Steroids |
|---|---|---|---|---|
| Cytotoxic | Na⁺/K⁺ pump failure, cell swelling | Ischaemia, head injury, status epilepticus | Grey and white matter, restricted diffusion | No |
| Vasogenic | Barrier leak, extracellular fluid | Tumour, abscess | Finger-like white matter low density, grey matter spared | Yes |
| Interstitial | CSF forced across ependyma | Hydrocephalus | Periventricular low density | No |
| Osmotic | Plasma becomes hypo-osmolar relative to brain | Rapid fall of glucose in DKA, rapid sodium correction | Diffuse swelling | No |
- Acute liver failure: ammonia is turned into glutamine in astrocytes, which swell; this does not happen in chronic liver failure.
- PRES: vasogenic oedema in the parieto-occipital white matter (hypertension, eclampsia, tacrolimus); posterior vessels have sparse sympathetic supply.
- Mannitol works only where the barrier is intact; it may worsen swelling in damaged areas.
Intracranial pressure and herniation
- Monro–Kellie: brain, blood and CSF share a fixed volume.
- Cerebral perfusion pressure = mean arterial pressure − intracranial pressure (MAP 80, ICP 30: CPP 50 mmHg).
- Autoregulation keeps flow constant between a MAP of about 50 and 150 mmHg; it shifts upwards in chronic hypertension.
- Idiopathic intracranial hypertension: obese young women, tetracyclines (doxycycline), pregnancy; papilloedema with normal or small ventricles, empty sella, flattened posterior globes, transverse sinus narrowing; vision is at risk.
| Herniation | Structure compressed | Result |
|---|---|---|
| Subfalcine | Anterior cerebral artery | Leg weakness, ACA infarct |
| Uncal (transtentorial) | Oculomotor nerve, posterior cerebral artery, midbrain | Fixed dilated pupil, occipital infarct, Kernohan notch (false localising hemiparesis), Duret haemorrhage |
| Tonsillar | Medulla at foramen magnum | Respiratory arrest |
| Upward | Vermis through tentorium | After rapid ventricular drainage with a posterior fossa mass |
Remember Steroids help oedema around a tumour, not oedema after a stroke or head injury.
Exam trap Large ventricles with large sulci mean atrophy; large ventricles with small sulci mean hydrocephalus.
Exam trap Calculate perfusion pressure with the mean arterial pressure, not the systolic.
Test yourself on this topic
5 of the 29 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
At autopsy of an 80-year-old woman with Alzheimer disease, the brain weighs 950 g, the gyri are narrow, the sulci are widened and the lateral ventricles are enlarged. What best explains the ventricular enlargement?
Answer: Generalised cerebral atrophy
When brain tissue is lost, as in Alzheimer disease or ageing, the ventricles and sulci enlarge together to fill the space: hydrocephalus ex vacuo. CSF pressure and flow are normal. True hydrocephalus enlarges the ventricles out of proportion to the sulci, which are compressed rather than widened. Aqueductal stenosis dilates the lateral and third ventricles only, and normal pressure hydrocephalus shows ventricles larger than expected for the sulci.
Atrophy vs hydrocephalus
- Atrophy: ventricles and sulci both large
- Ex vacuo: normal CSF pressure
- Hydrocephalus: ventricles out of proportion
- Hydrocephalus: tight sulci
Remember Big ventricles with big sulci means lost brain, not trapped CSF.
Exam trap Do not call every large ventricle hydrocephalus; compare with the sulci.
Why the other options are wrong
- Normal pressure hydrocephalus Ventricles would be disproportionately large compared with the sulci.
- Aqueductal stenosis Would dilate the lateral and third ventricles with a normal fourth and tight sulci.
- Obstruction at the foramina of Monro Would dilate the lateral ventricles only.
- Choroid plexus overproduction Rare, usually from a papilloma in a child.
A woman with suspected meningitis has a lumbar puncture lying relaxed on her side. What is the normal range of CSF opening pressure?
Answer: About 10 to 20 cm of water
Normal adult CSF opening pressure measured with a manometer in the relaxed lateral decubitus position is about 10 to 20 cm H2O (roughly 7 to 15 mmHg); up to 25 cm H2O may be normal in obese people. Values above this suggest raised intracranial pressure, as in idiopathic intracranial hypertension, cryptococcal meningitis or venous sinus thrombosis. Measurements in the sitting position, or with the patient tense and straining, are falsely high.
CSF opening pressure
- Normal: 10-20 cm H2O
- Measure lateral, relaxed
- Sitting or straining: falsely high
- Raised in IIH, cryptococcus
Remember Ten to twenty centimetres of water is normal.
Exam trap Measure with the legs relaxed; flexed, tense patients give falsely high readings.
Why the other options are wrong
- About 30 to 40 cm of water Raised, as seen in idiopathic intracranial hypertension.
- About 1 to 3 cm of water Too low; suggests a CSF leak or intracranial hypotension.
- About 50 to 60 cm of water Markedly raised.
- About 80 to 100 cm of water Far above physiological pressure.
After a frontal head injury, a 28-year-old man has lost his sense of smell and has clear watery nasal discharge that increases on bending forward. Why is he at risk of recurrent meningitis?
Answer: Torn dura links subarachnoid space to nose
The cribriform plate is the thinnest part of the anterior skull base, perforated by olfactory nerve filaments, and the dura is tightly attached to it. A fracture here tears the dura and arachnoid together, so the subarachnoid space opens directly into the nasal cavity. CSF leaks out (rhinorrhoea), and nasal bacteria, especially Streptococcus pneumoniae, can ascend into the meninges, causing recurrent meningitis until the defect heals or is repaired. Loss of smell supports damage at this site.
CSF rhinorrhoea
- Commonest site: cribriform plate
- Dura tightly adherent, tears with bone
- Subarachnoid space open to the nose
- Recurrent pneumococcal meningitis
Remember Clear nasal drip after a frontal blow: the meninges are open to the nose.
Exam trap Loss of smell after the injury supports a cribriform plate fracture.
Why the other options are wrong
- Olfactory axons carry bacteria to the cortex The route is the dural tear, not axonal transport.
- Frontal sinus now drains into the ventricles The frontal sinus does not drain into the ventricles.
- Leaking CSF loses its antibacterial glucose CSF glucose is not an antibacterial defence of this kind.
- Nasal mucosa loses its lymphatic drainage Not the mechanism; the problem is a direct open route.
In a healthy adult about 500 mL of CSF is produced each day, yet the volume stays at about 150 mL. Through which structures does most CSF return to the blood?
Answer: Arachnoid granulations in dural sinuses
Arachnoid granulations (villi) are outpouchings of arachnoid that project through the dura into the dural venous sinuses, especially the superior sagittal sinus. CSF passes through them into venous blood in one direction, driven by the pressure difference between CSF and venous blood, so the whole volume is turned over three to four times a day. Some CSF also drains along cranial and spinal nerve sheaths to lymphatics. Blocked granulations, as after meningitis or haemorrhage, cause communicating hydrocephalus.
CSF absorption
- Made: 500 mL a day
- Volume about 150 mL
- Absorbed by arachnoid granulations
- Into dural venous sinuses
Remember CSF goes home through the arachnoid granulations into the sinuses.
Exam trap Blocked granulations cause communicating, not obstructive, hydrocephalus.
Why the other options are wrong
- Choroid plexus of the lateral ventricles Produces CSF rather than absorbing it.
- Ependymal lining of the third ventricle Lines the ventricles; not the main absorption site.
- Capillaries of the pia mater Not the main route of CSF return.
- Central canal of the spinal cord A tiny channel that does not absorb CSF.
In a healthy adult, over roughly which range of mean arterial pressure does cerebral autoregulation keep blood flow almost constant?
Answer: About 50 to 150 mmHg
Cerebral autoregulation keeps blood flow fairly constant at about 50 mL/100 g/min across a mean arterial pressure of roughly 50 to 150 mmHg, through myogenic and metabolic adjustment of arteriolar diameter. Below the lower limit flow falls and ischaemia threatens; above the upper limit the vessels are forced open, the barrier fails and oedema follows, as in hypertensive encephalopathy. In chronic hypertension the curve shifts to the right, so lowering blood pressure too quickly can cause ischaemia.
Cerebral autoregulation
- Constant flow at MAP 50-150 mmHg
- Below: ischaemia
- Above: barrier breakdown, oedema
- Chronic hypertension: curve shifts right
Remember The brain holds its flow steady between 50 and 150.
Exam trap Rapidly lowering pressure in a chronic hypertensive can drop flow below its shifted limit.
Why the other options are wrong
- About 20 to 60 mmHg Too low; flow would fall below about 50 mmHg.
- About 150 to 250 mmHg Too high; autoregulation breaks down above about 150 mmHg.
- About 90 to 110 mmHg only The range is much wider than this.
- Over all physiological pressures Autoregulation has clear upper and lower limits.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Nervous system disorders, CSF flow disorders, blood-brain barrier and cerebral oedema
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