What is Head Trauma?

There are two principal types of cerebral traumatic lesions: primary lesions, that result from a direct traumatic impact (head trauma); and secondary lesions that occur subsequent to the direct impact or as sequelae of the primary injury (Table 1).

Neuronal injuries

In the field of primary neuronal injuries, diffuse axonal injuries (DAI) is the most common type of primary traumatic lesion.

Cortical contusion is the second most common type of primary intra-axial lesion. It is limited to the superficial grey matter of the brain with relative sparing of the underlying white matter, apart from more severe contusions that can involve the subjacent white matter. It is frequently haemorrhagic, ranging from microhaemorrhagic petechiae to real haematoma. Contusions tend to be bilateral and multiple, and they mostly involve the frontal and temporal lobes. Frontal lesions tend to be located near the cribriform plate, the orbit or the planum sphenoidale, whereas temporal lesions mostly occur just above the petrous bone or behind the greater sphenoid wing. Other parts of the brain can also be involved, though much less frequently, and the most frequent zones are the parietal and occipital lobes and the cerebellum.

Cerebral contusions tend to be associated with clinical impairment; only when the contusions are very large will the consciousness be seriously impaired.

Subcortical grey matter injury is a particular entity characterized by multiple petechial haemorrhages primarily located in the mesencephalon, basal ganglia, thalamus and hypothalamus. These lesions are typical in very severe head trauma and in patients who often die within few days after injury.

Primary and secondary brain stem injuries are lesions that could be haemorrhagic or not, depending on when the injury occurs. Their radiological aspects derive from the mechanism of trauma which can be divided into precise categories:

  • hypoxia/ischaemia;
  • haemorrhage or secondary injury to the brain stem perforating vessels;
  • direct impact/ penetrating injury;
  • tearing forces; and
  • tearing of the pontomedullary junction.

MR is the method of choice for study of these injuries and shows focal T2 hyperintense lesions if there are no haemorrhagic components or T2 shortening if there is haemosiderin consequent on haemorrhagic components.


Epidural haematomas are most frequently of arterial origin, resulting from direct laceration or tearing of meningeal arteries (typically the middle meningeal artery) by skull fracture. They are typical of temporal or temporoparietal regions.

Venous epidural haematomas are much less common than those of arterial origin. They are usually related to a dural sinus laceration caused by occipital, parietal or sphenoid bone fractures.

They are located mostly in the posterior fossa as a result from laceration of the transverse or sigmoid sinus in the middle fossa as a result of sphenoparietal sinus injury or in the parasagittal area as a result of superior sagittal sinus laceration.


Subdural haematomas are caused by tearing of bridging veins that run through the subdural space and are very sensitive to rotational or linear acceleration. The clinical presentation is variable, ranging from impairment of consciousness to a general headhache.

They are usually located in the supratentorial convexity although they can also be in the posterior fossa, along the tentorium and the falx. These latter two locations are most common in children and in victims of nonaccidental injuries (battered child syndrome), but they are not specific for child abuse.

CT scan is very sensitive to acute or chronic bleeding, but not so much to subacute haematoma, so that in fact CT detects only about 50 - 60% of subdural haematomas.

MR offers many advantages over CT: MR is superior in locating lesions because the posterior fossa, tentorium and inner table of the skull are well visualized with no artefacts and with a sensitivity of 1-2mm; MR can also easily stage haemorrhage in different stages of evolution. For this reason MR is very helpful in subacute subdural haematomas that are CT isodense, because MR is sensitive to the presence of free methaemoglobin in solution, subacute subdural haematomas having a high intensity on T2 and T1 sequences. Contrast-enhanced CT is no longer necessary for confirmation of this diagnosis. Finally, MR is also very helpful also because of its intrinsic capacity to visualize lesions in three dimensions; this is often useful in determining the severity of mass effects of the haematoma, and the consequent therapeutic choice (conservative or surgical).

Intracerebral haematomas are focal collections of blood that mostly arise from rotationally induced shearstrain injury to intraparenchymal veins or arteries, or sometimes from direct penetrating injury to a vessel. Intracerebral haematomas are usually located in the frontotemporal white matter or basal ganglia and are frequently associated with calvarian fractures. The clinical course is mild, with no loss of consciousness; sometimes a headache is present.

They may vary in dimension from a few mm to several cm.

Sometimes it is difficult to differentiate intracerebral haematomas from haemorrhagic contusions or DAI. The difference is that intracerebral haematomas expand between relatively normal neurons, while haemorrhagic contusions are located in simultaneously injured and oedematous brain.

Intraventricular haemorrhage is due to rotationally induced tearing of subependymal veins on the ventral surface of the corpus callosum and along the septum pellucidum or fornix.

subarachnoid haemorrhage is very frequent in head trauma, even in mild trauma. CT is the imaging method of choice as MR is not as sensitive in the acute phase (although better for detecting subacute subarahcnoid haemorrhage).

Head trauma, Table 1.

Primary lesions
neuronal injuries:
diffuse axonal injury (DAI)
cortical contusion
subcortical grey matter injury
primary brain stem injury
epidural haematoma
subdural haematoma
intracerebral haematoma
intraventricular haemorrhage
subarachnoid haemorrhage
vascular injuries
carotid cavernous fistula
arterial pseudoaneurysm
dural sinus laceration/occlusion
cranial nerve injuries
subdural hygromas
Secondary lesions
infarction of terminal zone
diffuse hypoxic injury
diffuse brain swelling/oedema
brain stem injury
fat embolism


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Last Updated: Feb 10, 2010

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