impact damage

Last reviewed 01/2018

Two impact pathologies are recognised, which may co-exist.

Cortical contusions and lacerations are often multiple, and may be bilateral. They result from direct linear impact without rotation and are due to the deceleration of moving brain tissue by non-compliant structures within the cranium - falx and tentorium cerebelli, and the sphenoid wing and petrous temporal bones. Coup and contracoup lesions are typical, e.g. parietal lesion accompanied by a contracoup contusion in the opposite temporal lobe. Lesser injuries may manifest as small surface contusions on the summits of the convexity of the gyri.

Consciousness is usually preserved except when bleeding produces a space occupying haematoma. Common causes include direct puncture, bullet wounds and crush injuries.

Diffuse white matter lesions are caused by rotational acceleration. Mechanical shearing results from different resistances in different regions of the brain. It is maximal in the cortical and immediate sub-cortical areas due to a combination of both physical distance from the rotational centre, and from differences in compliance between grey and white matter. This mechanism is the principal cause of damage in cases of closed brain injury. The brain stem is affected in only more severe rotational injury.

Nerve fibre damage is accompanied by intracranial haematoma. Road traffic accidents are the most common cause. Deterioration of consciousness is usual.

Microscopically, axonal tearing may be evident by retraction balls of axoplasm in the shearing plane. These disappear after about 2 weeks. Clusters of hypertrophied microglia may be seen scattered diffusely throughout the white matter. After about 5 weeks, Wallerian degeneration may be demonstrated using the Marchi stain.