Delayed hemiplegia The main causes of delayed hemiplegia are a late-evolving epidural or subdural hematoma and, in more severe injuries, an intracerebral hemorrhage. Most of these are associated with a diminution in the level of consciousness from the outset but there are exceptions.
Dissection of the internal carotid artery should also be considered in cases of delayed hemiplegia. The dissection may occur in the extracranial or the intracranial portion of the carotid artery and should be sought by vascular imaging study if the hemiparesis has no other explanation. In other instances, the hemiplegia has no clear explanation other than the blow to the head, perhaps related to the migraine phenomenon described earlier.
This group is smaller than the other two but is of importance because it includes a disproportionate number of patients who are in urgent need of surgical treatment. The initial loss of consciousness from concussion may have lasted only a few minutes or, exceptionally, there may have been no period of unresponsiveness at all, in which instance one might wrongly conclude that there was no concussion and little possibility of traumatic hemorrhage or other type of brain injury. Patients who display this sequence of events, in the past referred to vividly as “talk and die” by Marshall and associates (1983), have late deterioration because of the expansion of a subdural hematoma, worsening brain edema around a contusion, or the delayed appearance of an epidural clot. Among 34 such patients in the Traumatic Coma Data Bank who had this type of lucid interval, the majority showed substantial degrees of midline shift on the initial CT scan, reflecting the presence of early brain edema and contusion (Marshall et al, 1983). A somewhat related condition of delayed intracerebral hematoma (spät apoplexie), discussed further on, is a feature of a more severe initial head injury that usually produces coma from the onset. The problem of cerebral fat embolism, mentioned earlier, should be considered in these cases of delayed deterioration, especially if there is interposed respiratory failure.
Patients Who Remain Comatose From the Time of Head Injury
Here, the central problem, set forth by Symonds, is the relationship between concussion and contusion and other forms of persisting structural brain damage. Because consciousness is abolished at the moment of injury, one can hardly doubt the existence of concussion in such cases; but when hours pass without consciousness being regained, the second half of the usual definition of concussion—that the disruption of cerebral function be transitory—is not satisfied. Pathologic examination of such cases usually discloses evidence of increased ICP and of cerebral contusions, subarachnoid hemorrhage, zones of infarction, and scattered intracerebral hemorrhages both at the point of injury (coup) and on the opposite side (contrecoup), in the corpus callosum, and between these points, along the line of force of the impact. In some patients, the diffuse axonal type of injury is prominent or, as mentioned, there are separate but strategically placed ischemic and hemorrhagic lesions in the upper midbrain and lower thalamic region. Varying amounts of blood in the subarachnoid and subdural spaces are present. Displacement of the thalamus and midbrain may be present, with compression of the opposite cerebral peduncle against the free margin of the tentorium as well as secondary midbrain hemorrhages and zones of necrosis; in some cases, there is transtentorial herniation.
Severe head injury is often associated with an immediate arrest of respiration and sometimes with bradyarrhythmia and cardiac arrest. The immediate effects on the brain of these systemic changes may in themselves be sufficiently profound to cause coma. Intracranial pressure is almost always elevated and imaging of the brain shows various degrees of brain swelling, ventricular compression, and displacement of midline structure. Also, head injury often complicates alcohol and drug ingestion, so the possibility of a toxic or metabolic encephalopathy as the cause (or a contributing cause) of stupor must always be considered.