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This group is smaller than the other two but is of great importance because it includes a disproportionate number of patients who are in urgent need of surgical treatment The initial coma may have lasted only a few minutes or, exceptionally, there may have been none at all in which instance one might wrongly conclude that since there was no concussion, there is no possibility of traumatic hemorrhage or other type of brain injury Patients who display this sequence of events, referred to as talk and die by Marshall and associates, deteriorate because of the delayed expansion of a small subdural hematoma, worsening brain edema, or occasionally the late appearance of an epidural clot Among 34 such patients in the Traumatic Coma Data Bank, the majority showed substantial degrees of midline shift on the initial CT scan, re ecting the presence of early brain edema and contusion (Marshall et al) A similar condition of delayed intracerebral hematoma, discussed further on (Spatapoplexie), is a feature of a more severe initial head injury that engenders coma from the onset

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SPECIFIC TRAUMATIC CRANIAL LESIONS (Table 35-2)

The following conditions must be considered in all cases of these delayed types but occur as often with serious initial injury

As a rule, this arises with a temporal or parietal fracture and laceration of the middle meningeal artery or vein Less often, there is a tear in a dural venous sinus The injury, even when it fractures the skull, may not have produced coma initially, or it may be part

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The problems created by acute and chronic subdural hematomas are so different that they must be discussed separately In acute subdural hematoma, which may be unilateral or bilateral, there may be a brief lucid interval between the blow to the head and the advent of coma Or, more often, the patient is comatose from the time of the injury and the coma deepens progressively Frequently the acute subdural hematoma is combined with epidural hemorrhage, cerebral contusion, or laceration The clinical effects of these several lesions are dif cult to distinguish; there are some patients in whom it is impossible to state before operation whether the clot is epidural or subdural in location Subdural clots more than 5 mm thick can be accurately visualized by the CT scan in more than 90 percent of cases (Fig 35-9) A large acute clot causes a pineal shift as well as marked compression of one lateral ventricle; but if the clots are bilateral, there may be no shift and the ventricles appear symmetrical Acute, rapidly evolving subdural hematomas are due to tearing of bridging veins, and symptoms are caused by compression of the brain by an expanding clot of fresh blood Unlike epidural arterial hemorrhage, which is steadily progressive, venous bleeding is usually arrested by the rising intracranial pressure Exceptionally, the subdural hematoma forms in the posterior fossa and gives rise to headache, vomiting, pupillary inequality, dysphagia, cranial nerve palsies, and, rarely, stiff neck and ataxia of the trunk and gait if the patient is well enough to be tested for these functions Because of their apposition to bone or their axial orientation along the tentorial dura, posterior fossa clots are more likely than clots over the cerebral convexities to be missed in CT scans In chronic subdural hematoma, the traumatic etiology is often

Figure 35-8 Acute epidural hematoma; unenhanced CT scan showing a typical lens-shaped frontal epidural clot

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