Brain swelling and raised intracranial pressure

Intracranial pressure increases as a consequence of a rapidly developing intracranial mass lesion, hypoxia, hypercarbia, during an epileptic seizure, and in acute hydrocephalus. Brain oedema is defined as an increase in brain volume due to increase in brain water content. Klatzo defined it as "vasogenic"8 because of disruption of the blood-brain barrier and escape of water and plasma into the extracellular compartment, in contrast to "cytotoxic oedema" in which a noxious factor produces intracellular swelling without increased vascular permeability.9,10 The oedema around a contusion or haematoma was initially thought to be vasogenic; protein rich fluid leaking into the extracellular space, increasing the water and sodium in the brain to produce "mass effect". Marmarou, however, has shown that most of the water in areas of brain contusion is in fact intracellular and represents "cellular" oedema, caused by ischaemia.11 This in turn produces astrocytic swelling and increased release of excitatory amino acids and a consequent failure of membrane ion pumps and cellular ionic homoeostasis. This is recognisable radiographically as an increase in the signal on T2 weighted MRI and as radiolucent areas on CT.

Alternatively, brain injury may lead to cerebrovascular congestion and an excess cerebral blood volume, resulting in cerebral hyperaemia, that is, an absolute or relative increase in the cerebral blood flow in relation to cerebral metabolic demand.

The consequence of raised intracranial pressure is the development of pressure gradients across the midline, between supratentorial and infratentorial compartments, and between the cranial and spinal compartments across the foramen magnum. In 1965 Langfitt showed how raised supratentorial pressure produces a rise in infratentorial pressure which subsequently plateaus and falls as the cisterna ambiens becomes blocked by tentorial herniation. The brain is shifted away from the region of higher pressure, so midline structures are pushed laterally, causing the cingulate gyrus to herniate under the fixed free edge of the falx. This distorts the pericallosal arteries, and may occlude the foramen of Munro. The cerebrospinal fluid (CSF) drainage of the contralateral ventricle is obstructed, so the ventricle dilates; the ipsilateral ventricle may become compressed, giving characteristic features suggesting raised intracranial pressure (ICP) on cross-sectional imaging. Further increases in ICP produce tentorial herniation, with a temporal or parietal lesion compression of the ipsilateral oculomotor nerve and midbrain. Further distortion leads to posterior cerebral artery compression. Bilateral or frontal lesions produce posterior herniation, compressing the tectal plate, resulting in failure of upward gaze and bilateral pupillary abnormalities. Infratentorial masses or further herniation of a supratentorial mass results in herniation through the foramen magnum. As the medulla and cerebellar tonsils are pushed interiorly, distortion of the vasomotor and respiratory centres leads to circulatory collapse and respiratory arrest.

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