The contused cortex is diffusely swollen and hemorrhagic, most of the blood being found around parenchymal vessels. On CT, the lesions appear as edematous regions of cortex and subcortical white matter admixed with areas of increased density representing leaked blood (Fig. 34-6). The bleeding points may coalesce and give the appearance of a unitary clot in the cortex and immediately adjacent white matter. The predilection of these lesions for the crowns of convolutions attests to their traumatic origin (being thrown against the overlying skull) and distinguishes them from cerebrovascular and other types of cerebral lesions. There may be ball hemorrhages within the hemispheres that are independent of contusions as discussed below. Not surprisingly, such deep areas of bleeding are common in patients receiving anticoagulant or antiplatelet medications.
Of equal importance are axonal lesions that occur at the time of impact or evolve soon afterward. Strich (1961) described the neuropathologic findings in patients who died months after severe closed head injuries that had caused immediate and protracted coma. In all of her cases, in which there were no signs of skull fracture, raised ICP, or gross subarachnoid hemorrhage, she observed an uneven but diffuse degeneration of the cerebral white matter that has become the basis of all subsequent work on diffuse axonal shearing (diffuse axonal injury, DAI). In cases of shorter survival (up to 6 weeks), she observed ballooning and interruption of axis cylinders. These findings were subsequently confirmed and expanded by Nevin, by Adams and colleagues (1982), and by Gennarelli and coworkers, the last of these groups also working with monkeys.
The extension of Strich’s concept, that postulates diffuse axonal injury throughout the cerebral white matter as the main cause of persistent unconsciousness, has been widely adopted. In relation to concussion, shearing lesions are also seen in the midbrain and lower thalamus in severe injury, providing some evidence for neuronal dysfunction in these regions as the cause of concussion rather than diffuse white matter injury as commented below. The matter has not been settled and the two types of injury can occur together.
In most cases of severe head injury, there is damage to the corpus callosum by impact with the falx; necrosis and hemorrhage are sometimes visible by CT and can be seen to spread bilaterally to adjacent white matter (Fig. 34-7). There may also be scattered hemorrhages in the white matter along lines of force from the point of impact to the contralateral side. The degeneration of white matter from diffuse axonal injury can be remarkably diffuse, with no apparent relationship to focal destructive lesions, although differentiating it from secondary wallerian change that originates in a surface or callosal contusion can be difficult. Investigations using MRI, such as the series by Kampfl and colleagues, suggest that diffuse axonal injury may be the substrate of the persistent vegetative state. However, in most cases of severe cranial injury and protracted coma, there have been major sites of injury in the midbrain and subthalamus, that is, in the zones subjected to the greatest torque, and these latter lesions may be the critical ones in persistent coma and vegetative state (Adams et al, 2000; Ropper and Miller). This was true of the cases of persistent coma described by Jellinger and Seitelberger. Notable, again, was that these deep lesions coincided with the postulated locus of reversible concussive paralysis.
Primary brainstem hemorrhages due to torsion and tearing of tissue at the time of impact are distinguished from the secondary hemorrhages that are a result of the effects of downward displacement of the brainstem. Duret originally emphasized the medullary location of these secondary hemorrhages, but the term “Duret hemorrhage” has come to signify all brainstem hemorrhages when there is mass effect that distorts the brainstem.