Head Injury


Microglial clusters (hyper-' trophied microglia) are :.<• found diffusely throughout the white matter

Diffuse axonal injury (contd)

Microscopic evidence of neuronal damage depends on the duration of survival and on the severity of the injury. After a few days, retraction balls and microglial clusters are seen in the white matter.

Retraction balls reflect axonal damage. Note only axons in plane are involved, indicating the direction of the 'shear'

If the patient survives 5 weeks or more after injury then appropriate staining demonstrates Wallerian degeneration of the long tracts and white matter of the cerebral hemispheres. Even a minor injury causing a transient loss of consciousness produces some neuronal damage. Since neuronal regeneration is limited, the effects of repeated minor injury are cumulative.

SECONDARY BRAIN DAMAGE: may occur at any time after the initial impact. Impact damage is unavoidable, but secondary brain damage caused by haematoma, brain swelling, brain shift, ischaemia and infection may be preventable and this must be the aim of head injury management.

1. Intracranial haematoma

Intracranial bleeding may occur either outside (extradural) or within the dura (intradural).

Intradural lesions usually consist of a mixture of both subdural and intracerebral haematomas although pure subdurals occur in a proportion. Brain damage is caused directly or indirectly as a result of tentorial or tonsillar herniation.

Incidence of haematoma:

Extradural - 27%


Pure subdural - 26%



A skull fracture tearing the middle meningeal vessels bleeds into the extradural space. This usually occurs in the temporal or temporoparietal region. Occasionally extradural haematomas are caused by a ruptured sagittal or transverse sinus.

Intracerebral ± subdural (burst lobe)

Contusions in the frontal and temporal lobes often lead to bleeding into the brain substance, usually associated with an overlying subdural haematoma.

'Burst lobe' is a term sometimes used to describe the appearance of intracerebral haematoma mixed with necrotic brain tissue, rupturing out into the subdural space.



In some patients impact may rupture bridging veins from the cortical surface to the venous sinuses producing a pure subdural haematoma with no evidence of underlying cortical contusion or laceration.

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