Cerebellar ataxia is another rare consequence of cranial trauma, often unexplained but also in cases complicated by cerebral anoxia (causing ataxia with myoclonus) or by a hemorrhage strategically placed in the deep midbrain or cerebellum. When cerebellar ataxia is caused by the trauma itself, it is frequently unilateral and the result of injury to the superior cerebellar peduncle. We have experience with a severely ataxic patient who had only small lesions in the cerebellum after bilateral acute subdural hematomas from an assault with head trauma. An “apraxia” of gait may also reflect the presence of a communicating hydrocephalus (see below and Chap. 29).
Acute traumatic encephalopathy In almost all patients with cerebral concussive injury, there remains a gap in memory (traumatic amnesia) spanning a variable period from before the accident to some point following it as discussed earlier. This gap is permanent and is filled in only by what the patient is told. In addition, as stated in the introduction to this section, some degree of impairment of higher cortical function may persist for weeks (or be permanent) after moderate to severe head injuries, even after the patient has reached the stage of forming continuous memories. During the period of reduced mentation, the memory disorder is the most prominent feature; in that respect, the state resembles the alcoholic form of the Korsakoff amnesic state and has some resemblance to the state of transient global amnesia (see Chap. 20).
With more careful testing, other cognitive disorders are usually evident. Concussed patients, during the period of posttraumatic amnesia, rarely confabulate. Apart from disorientation in place and time, the head-injured patient also shows defects in attention, as well as showing distractibility, perseveration, and an inability to synthesize perceptual data. Judgment and executive function may be mildly impaired, rarely severely, during the amnestic epoch. A perseverative tendency interferes with both action and thought. Leininger and associates, for example, found that most of their 53 patients who suffered minor head injury in traffic accidents performed less well than controls on psychologic tests (category test, auditory verbal learning, copying of complex figures). The fact that those who were merely dazed did as poorly as those who were concussed and that litigation was involved in some cases would lead one to question these results. Perhaps most affected, and most evident to high-functional individuals, is a problem with overall planning and coherence that is attributable to a defect in frontal lobe executive functioning.
As a general rule, the lower the score on the Glasgow Coma Scale immediately after injury (see Table 34-1) and the longer the posttraumatic gap in the formation of new memories (anterograde amnesia), the more likely the patient is to suffer some permanent cognitive and personality changes. According to Jennett and Bond, patients with good recovery achieved their maximum degree of improvement within 6 months. Others have found that detailed and repeated psychologic testing over a prolonged period, even in patients with relatively minor cerebral injuries, discloses measurable improvement for as long as 12 to 18 months.