Intracranial pressure

Intracranial pressure

Before considering coma and unconsciousness it is useful to understand intracranial pressure and brain herniation. The intracranial compartment is a fixed box containing brain, blood and CSF. The dynamics of CSF flow are illustrated in Figure 1. Pressure may be increased by:

intracranial masses, either intrinsic (e.g. glioma) or extrinsic (e.g. extradural haematoma)

diffuse brain swelling following severe hypoxia, liver failure or hypertensive encephalopathy

impaired circulation or absorption of CSF.

Fig. 1 CSF production and flow.

Hydrocephalus and ventricular dilatation occur if CSF is under increased pressure relative to the surrounding brain. This may be due to blocked flow (obstructive) or failure of reabsorption (communicating). Excess CSF production due to a tumour of the CSF-producing choroid plexus is a rare cause of communicating hydrocephalus.

There are two semi-rigid sheets, the falx cerebri and the tentorium cerebelli, which almost divide the brain into separate compartments with relatively small apertures between them (Fig. 2). When the pressure rises in one compartment, the brain may herniate through the apertures into adjacent compartments. The cerebellar tonsils and fourth ventricle may also be forced down through the foramen magnum. These are life-threatening complications that further block CSF flow, causing a vicious circle of rising intracranial pressure, resulting in coma (see below).

Fig. 2 Tentorial herniation.

Failure of CSF reabsorption may occur because of thrombosis in the sagittal sinus, increased venous pressure reducing the pressure gradient across the arachnoid villi, or because the function of the arachnoid villi is damaged by the contents of the CSF: excessive cellularity (chronic meningitis), subarachnoid haemorrhage or very high protein content (some tumours and inflammatory conditions).

In some circumstances, such as idiopathic intracranial hypertension (IIH), previously called benign intracranial hypertension (BIH), no cause may be found (p. 40).

Raised intracranial pressure

Raised intracranial pressure is a medical emergency. It causes headache, ataxia, confusion, drowsiness and coma. Papilloedema is usually present if the raised pressure has been longstanding, but because it takes time to develop, may be absent. Sixth nerve palsy is a common false localizing sign due to compression of the 6th nerve as it passes over the petrous ridge. Other signs include 3rd nerve palsy in temporal lobe herniation, failure of upgaze, due to midbrain compression, a rise in systolic blood pressure and a fall in pulse due to medullary involvement.

Intermittent obstruction of CSF flow can cause sudden headache with loss of consciousness. For example, intraventricular tumours may block CSF flow on sudden manoeuvres such as coughing or straining.

In children who develop raised intracranial pressure, usually a result of hydrocephalus, before closure of the skull sutures, presentation may be with a rapidly enlarging head size and minimal neurological compromise.

Low intracranial pressure

Reduced CSF pressure is usually due to CSF leakage through torn meninges. The most common causes are trauma, iatrogenic (neurosurgery, lumbar puncture and inadvertent puncture of the subarachnoid during epidural anaesthesia) and tumours. In these circumstances, patients may present with headache on standing or with CSF rhinorrhoea. Leakage from the nose is especially associated with recurrent meningitis.

Spontaneous intracranial hypotension is being recognized increasingly. Patients present with generalized headaches, that at least initially are posturally triggered, getting worse on standing and improving on lying flat. They may develop false localizing signs such as 6th nerve palsies. MRI scanning with gadolinium demonstrates marked dural enhancement reflecting engorged normal veins (Fig. 3). The CSF volume is reduced so the veins enlarge and the skull is a a fixed volume ‘box’. The condition is often self-limiting, but may improve with blood patching (p. 39).

Fig 3. Spontaneous intracranial hypotension. A coronal T1 MRI before (a) and after (b) gadolinium enhancement showing marked dural enhancement (arrows).

Herniation

There are two major sites of cerebral herniation.

The tentorium

Here the brain herniates through the space between the cerebrum and the cerebellum surrounded by the tentorium cerebri (see Fig. 2). This can be symmetrical or asymmetrical. Asymmetrical is more common. The uncus of the temporal lobe is squeezed through this space. This compresses:

the 3rd nerve, leading to unilateral 3rd nerve palsy involving the pupils

the midbrain, leading to coma and pupillary changes bilaterally with a tetraparesis

the posterior cerebral artery, leading to occipital infarction, increasing supratentorial pressure and increasing the herniation.

Symmetrical herniation produces compression of the whole of the midbrain as it is forced through the tentorium cerebri, producing bilaterally dilated pupils, coma and tetraparesis.

Foramen magnum herniation

This is rarer and the syndrome results from compression of the reticular formation, respiratory centres and motor tracts. This leads to severe neck pain, erratic breathing, progressing tetraparesis and coma.

Both of these processes progress to death if uninterrupted.

Treatment

Treatment will depend on the cause. There may be readily treatable surgical causes, such as subdural (Fig. 4) or extradural haematoma, or hydrocephalus (Fig. 5). These would be treated with drainage or shunting.

Fig. 4 An isodense right-sided subdural (arrows) haematoma which presented with symptoms and signs of raised intracranial pressure.

Fig. 5 Acute hydrocephalus with enlarged lateral and 3rd ventricles.

In patients with brain swelling, mannitol, the osmotic diuretic, will briefly reduce the intracranial pressure. However, this is only short lived and is thus of limited use. Steroids will reduce cerebral oedema, though usually not cytotoxic oedema (brain swelling resulting from swelling of dying cells). Hyperventilation of ventilated patients will reduce intracranial pressure. In some clinical circumstances, surgical decompression can be used.

Intracranial pressure

Increased intracranial pressure occurs with space-occupying lesions, diffuse brain swelling or abnormal CSF circulation or reabsorption.

Raised intracranial pressure is a medical emergency, presenting with progressive headache, ataxia and drowsiness.

Herniation of the brain through the tentorium cerebelli or the foramen magnum leads to brain stem and cranial nerve compression that is fatal if untreated.