Several studies in adults have given broad guidance in choosing which patients to image (“New Orleans Criteria” and “Canadian CT Head Rule”; Table 34-2). They include features that are sensitive but not specific for intracranial injury, such as age above 60 years, intoxication, more than 30 min of retrograde amnesia, suspected skull fracture, seizure, anticoagulation, and dangerous mechanism of injury (see Smits et al and Stiell et al). These two validated schemes for assisting in the determination of need for CT scanning in the emergency department are included for the reader’s reference but they should be viewed as guidelines with fairly high sensitivity for important lesions on the CT, but low specificity so that most CT scans done under these advisories can be expected to be normal. These issues were addressed in a review by Ropper and Gorson.
Minor and seemingly trivial head injuries may sometimes be followed by a number of puzzling and worrisome clinical phenomena, some insignificant, others serious and indicative of a pathologic process other than concussion. The latter are described below. When they occur, a neurologic or neurosurgical evaluation is indicated.
Drowsiness, headache, and confusion These symptoms occur most often in children, who, minutes or hours after a concussive head injury, seem not to be themselves. They lie down, are drowsy, complain of headache, and may vomit—symptoms that suggest the presence of an intracranial hemorrhage. Mild focal edema near the point of impact may be seen on MRI. There is usually no skull fracture but, as Nee and colleagues point out, vomiting is associated with an increase in the incidence of skull fracture and the New Orleans and Canadian CT rules found vomiting to be a factor associated with intracranial bleeding (see Table 34-2). The symptoms subside after a few hours, attesting to the benign nature of the condition in most cases but some form of cerebral imaging is required.
Transient paraplegia, blindness, and migrainous phenomena With falls or blows on top of the head, both legs may become temporarily weak and numb, with wavering bilateral Babinski signs and sometimes with sphincteric incontinence. Impact over the occiput may cause temporary blindness. The symptoms disappear after a few hours. It seems possible that these transient symptoms represent a direct localized concussive effect, caused either by indentation of the skull or by impact on these parts of the brain against the inner table of the skull, but a vascular mechanism cannot be excluded. The blindness and paraplegia are usually followed by a throbbing, vascular type of headache. Transient migrainous visual phenomena, aphasia, or hemiparesis, followed by a headache, are observed sometimes after minimal concussion in athletes who participate in contact sports. Possibly all of these phenomena are the result of an attack of migraine induced by a blow to the head. These focal syndromes can be perplexing and very worrisome for a few hours, especially if it is the first such attack of migraine in a child. Possibilities to be remembered, particularly in cases of acute quadriplegia, is traumatic cord compression or the rarer cartilaginous embolism of the cervical cord (see “Fibrocartilaginous Embolism” in Chap. 42). A concussion of the cervical portion of the spinal cord is another potential mechanism of transient paraplegia.
Episodes of transient global amnesia (TGA) after minor head injury have been described by Haas and Ross, as mentioned in Chap. 20 but the difficulty differentiating concussive amnesia from TGA has been mentioned. They share the sign of repetitive stereotyped questioning regarding orientation that is common to both processes. A duration of 2 to 24 h for TGA and the feature of repetitive querying were suggested by Haas and Ross as differentiating the two conditions but the separation on this basis is not compelling.