With regard to visible structural lesions, the study of a large number of coma has disclosed 3 types of lesions, each of which directly or indirectly damage the function of the RAS or its projections to the cerebral hemispheres. In the first type, a large mass in one cerebral hemisphere is demonstrable—chiefly a tumor; abscess; massive infarct; or intracerebral, subdural, or epidural hemorrhage. These mass lesions cause coma by secondary compression of the midbrain and central thalamic region of the RAS. Either lateral displacement or direct compression of these structures by the advancing medical temporal lobe which is forced into the tentorial opening may be the proximate cause of compression (see below and also Chap. 30). Likewise, a cerebellar lesion may compress the adjacent upper brainstem reticular region by displacing it forward and upward. A detailed clinical record will show the coma to have coincided with these displacements and herniations as discussed further on.
In the second structural configuration, which occurs less frequently, a destructive lesion is located immediately within the thalamus or midbrain, in which case the neurons of the RAS are damaged directly. This pattern characterize supper brainstem stroke from basilar artery occlusion, thalamic and upper brainstem hemorrhages, and some forms of traumatic damage.
In the third type of structural damage, there is widespread bilateral damage to the cortex and cerebral white matter, the result of traumatic damage (contusions, diffuse axonal injury), bilateral ischemic strokes or hemorrhages, encephalitis, meningitis, hypoxia, or global ischemia. The coma in these cases results from interruption of thalamocortical impulses or from generalized destruction of cortical neurons. It is only if the cerebral lesions are bilateral and extensive that consciousness is impaired. Many of the diseases in this category also cause severe thalamic damage of the type mentioned earlier; contributing to coma by that mechanism.
Thus, the pathologic changes found in cases of coma are compatible with physiologic deductions—namely that the state of coma correlates with lesions of the diencephalic cortical-activating systems. Small and discrete lesions restricted to the upper dorsal brainstem and lower midline thalami are the smallest ones sufficient to produce coma. A study by Parvizi and Damasio, on the basis of 9 cases of restricted dorsal bilateral pontine lesions, suggested that damage at a site caudal to the midbrain RAS may also cause coma. This view expands our conceptions of the areas of the reticular system that are necessary for arousal, but further study is justified. One conceptual explanation for this configuration implicating the pons in coma would be the disruption of noradrenergic input from the locus coeruleus to the reticular system.
However, in the largest group of cases of coma, no structural lesion is revealed by any technique of conventional pathology. Instead, a metabolic or toxic abnormality or generalized electrical discharge (seizure) causes neuronal failure at a subcellular or molecular level.
PATHOANATOMY OF BRAIN DISPLACEMENT AND HERNIATIONS (SEE ALSO CHAP. 30)