Intracranial pressure

What it normally does

• The adult skull is a rigid container of roughly 1700 mL holding three things: brain tissue (about 1400 g), blood (about 150 mL) and cerebrospinal fluid (about 150 mL). Their volumes must add up to the same total at all times, so if one grows, another must shrink (the Monro-Kellie doctrine). Normal intracranial pressure in a supine adult is about 7-15 mmHg. Measured at lumbar puncture in the lateral decubitus position, normal opening pressure is about 6-20 cm H2O; 20-25 cm H2O is borderline and 25 cm H2O or more is accepted as raised (this is the threshold used in the diagnostic criteria for idiopathic intracranial hypertension).

  any new volume inside the skull — a tumour, a bleed, swollen brain, dammed-up CSF, congested veins — is a volume problem before it is a pressure problem, and the pressure only rises once the box has nothing left to give up.

• The give comes from two things that can be pushed out: CSF, squeezed down into the spinal sac and reabsorbed faster, and venous blood, drained out of the compliant cerebral veins and sinuses. Those buffers are small and they run out. Plot pressure against volume and the line is nearly flat at first, then it turns a corner and goes almost vertical: the same extra millilitre that did nothing early raises pressure enormously late (falling compliance).

  a patient with a slowly growing mass can look well for weeks and then crash over hours — and once past the corner, small insults that add a few millilitres of blood volume (a cough, a seizure, a rising CO2, lying flat, a tight cervical collar obstructing jugular drainage) cause a dangerous pressure spike.

• The brain has no fuel reserve and needs continuous flow. What drives that flow is cerebral perfusion pressure = mean arterial pressure − intracranial pressure (CPP = MAP − ICP), with roughly 60-70 mmHg the usual target. Arterioles autoregulate flow across a MAP of about 50-150 mmHg, and they are exquisitely sensitive to carbon dioxide: a rising PaCO2 dilates them and adds blood volume, a falling PaCO2 constricts them and takes blood volume away.

  rising ICP eats into perfusion pressure and starves the brain, which explains both the brainstem's violent blood-pressure response (Cushing reflex) and why hypercapnia in a drowsy head-injured patient is disastrous while short-term hyperventilation temporarily buys pressure back.

• The box is subdivided by stiff dural sheets — the falx between the hemispheres, the tentorium between cerebrum and cerebellum — and has one true exit, the foramen magnum. Vital structures run along those edges: the oculomotor nerve (CN III) passes forward beside the free edge of the tentorium with its pupil-constricting parasympathetic fibres running superficially, on the outside of the nerve, the midbrain sits in the tentorial notch, and the posterior cerebral artery crosses the same edge. The subarachnoid space also runs forward around each optic nerve as a blind cul-de-sac. CN VI is tethered as it climbs the clivus and bends sharply over the petrous ridge into Dorello canal, so any downward displacement of the brainstem stretches it.

  pressure does not rise evenly — brain gets pushed from a full compartment into an emptier one and jams against these edges (herniation), which is why a blown pupil, a hemiparesis and papilloedema are pressure signs, and why a sixth nerve palsy can be produced by raised pressure alone rather than by disease at that spot (a false localising sign).

What goes wrong

• Raised intracranial pressure — the box is full← from “The adult skull is a rigid container of roughl…”

  Something adds volume: a tumour or abscess with the oedematous brain around it, a haematoma, infarcted brain swelling at 2-5 days, CSF that cannot drain or be reabsorbed (hydrocephalus), or blocked venous outflow such as cerebral venous sinus thrombosis. CSF is displaced into the spinal sac and venous blood is squeezed out of the sinuses, so pressure stays near normal while the mass grows. When those buffers are spent, pressure climbs steeply, perfusion pressure falls, and the brain begins to shift toward the tentorial notch and foramen magnum.

  In Australia the common causes seen in practice are traumatic brain injury (road trauma and assault in young men, falls in people over 65) and tumour; Aboriginal and Torres Strait Islander people are hospitalised with head injury at roughly two to three times the rate of other Australians, higher again in remote communities, so the threshold for imaging should reflect that. Non-contrast CT head is the first test. Sustained ICP above about 22 mmHg is the usual treatment threshold. Nurse head-up 30 degrees, keep the neck straight and the collar loose, treat pain, fever and seizures — all of these work by removing volume or demand, not by magic.

  You would find: Headache that is worse lying flat, worse in the early morning, and worse with anything that raises venous pressure — coughing, straining, bending. Vomiting, often without much nausea. Papilloedema: pressure tracks along the optic nerve sheath and swells the disc, so the disc margins blur and, as the swelling progresses, the cup fills; vision stays normal at first apart from an enlarged blind spot. Papilloedema takes hours to days to appear, so its absence never excludes acutely raised pressure. A sixth nerve palsy with horizontal double vision that localises nowhere. Then the important one — a falling conscious state (drop in GCS), which is the sign that matters most and the one people notice last.

• Decompensation — the extradural haematoma and its lucid interval← from “The give comes from two things that can be pus…”

  A blow to the temple fractures the thin squamous temporal bone and tears the middle meningeal artery. Arterial blood strips dura off the inner table of the skull and collects as a lens-shaped clot that does not cross suture lines. Early, the bleed sits on the flat part of the pressure-volume curve: CSF and venous blood are displaced and the patient is buffered, so after the initial knock they wake up and talk. Then the buffers are gone, the curve turns vertical, and the same rate of bleeding now produces a steep rise in pressure with herniation within minutes to an hour.

  A patient who talks and then dies. Young brains have less atrophy and therefore less spare space, so they buffer for a while and then crash later and harder. The treatment is a neurosurgical drill and evacuation, and time to theatre is what determines outcome; drugs only buy transport time. Contrast with a subdural haematoma — torn bridging veins, crescent shaped, crosses sutures but not the midline, common in older people and heavy drinkers and those on anticoagulants, and often a slow story of confusion over weeks.

  You would find: Head strike, brief loss of consciousness, then a period of being awake and coherent (the lucid interval), then rapid deterioration: worsening headache, vomiting, a dilated pupil on the side of the clot, weakness on the other side, and a plummeting GCS. Battle sign or bruising around the eyes points to a base of skull fracture, though both take hours to appear. On CT the clot is biconvex and hyperdense, stopping at the sutures, with midline shift.

• Cushing reflex — the brainstem's last resort← from “The brain has no fuel reserve and needs contin…”

  ICP rises until cerebral perfusion pressure (MAP − ICP) drops far enough to make the brainstem ischaemic. The medulla responds with a massive sympathetic discharge that raises systemic blood pressure, forcing perfusion pressure back above intracranial pressure. That high pressure is then sensed by the carotid sinus baroreceptors, which increase vagal outflow and slow the heart. Direct pressure on the brainstem breaks up the respiratory rhythm.

  Hypertension plus bradycardia in a head injury is raised ICP until proven otherwise — never treat that blood pressure down, because it is the only thing perfusing the brain. Do the opposite: lower the ICP and protect the airway. Bradycardia with hypotension is a different animal — think spinal cord injury and neurogenic shock.

  You would find: The Cushing triad: hypertension with a widening pulse pressure, bradycardia, and irregular breathing (Cheyne-Stokes, then central neurogenic hyperventilation or apneustic gasping, then ataxic breathing). Together with a falling GCS and a dilated pupil this is a pre-terminal emergency, not a warning shot.

• Herniation — brain forced through the gaps← from “The box is subdivided by stiff dural sheets — …”

  Pressure is never uniform, so brain moves down a pressure gradient into an emptier compartment. In uncal (transtentorial) herniation the medial temporal lobe slips over the free edge of the tentorium: it first squashes CN III, whose parasympathetic fibres lie on the outside of the nerve and fail first, then it compresses the midbrain's cerebral peduncle, then the posterior cerebral artery. If the shift pushes the opposite peduncle against the far tentorial edge, the weakness appears on the same side as the lesion (Kernohan notch, a false localising sign). If pressure keeps climbing, the cerebellar tonsils are forced down through the foramen magnum onto the medulla (tonsillar herniation, coning).

  A unilateral blown pupil in a deteriorating head injury is uncal herniation on that side until proven otherwise, and it means theatre or decompression now. This is also why you image before you tap: doing a lumbar puncture in someone with focal signs, papilloedema, seizures or a reduced GCS can pull the tonsils through the foramen magnum. Fever and neck stiffness without those features, and without significant immunocompromise, is meningitis and does not need a CT before the LP — but never delay antibiotics for imaging.

  You would find: Uncal: a fixed, dilated pupil on the side of the lesion, then ptosis and an eye that sits down and out, weakness on the opposite side, drowsiness, and an occipital infarct with a homonymous field loss if the PCA is caught. Tonsillar: neck stiffness with a tilted head, then Cushing signs, then irregular breathing and apnoea, then death.

• Idiopathic intracranial hypertension← from “The adult skull is a rigid container of roughl…”

  CSF is produced normally but leaves too slowly, so the fluid compartment expands and pressure rises with no mass, no hydrocephalus and no thrombosis to explain it. Raised venous sinus pressure in obesity and impaired reabsorption are the leading explanations. Pressure tracks along the optic nerve sheaths into that blind cul-de-sac around each optic nerve and swells both discs; sustained swelling strangles axons and destroys vision permanently.

  Rising in Australia with obesity, and the sight-threatening part is silent — visual acuity is preserved until late, so formal perimetry, not the Snellen chart, is what follows the patient. Check the medication list: vitamin A derivatives (isotretinoin), tetracyclines such as doxycycline, and withdrawal of long-term corticosteroids can all cause it. Sustained weight loss (of the order of 5-10 per cent of body weight) is the definitive treatment; drugs and, if vision is failing, shunting or optic nerve sheath fenestration buy the eyes time.

  You would find: A young woman with obesity, daily headache worse lying flat, transient greying of vision for seconds when she stands or bends (transient visual obscurations), whooshing pulsatile tinnitus, and horizontal diplopia from a sixth nerve palsy. Fundoscopy shows bilateral papilloedema. MRI with venography excludes a mass, hydrocephalus and venous sinus thrombosis, and may show only an empty sella, flattened posterior globes, distended optic nerve sheaths or transverse sinus stenosis; CSF opening pressure is 25 cm H2O or more with completely normal CSF constituents.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.