Head injury is usually characterized as mild, moderate, or severe and is measured by a number of methods, including loss of consciousness (LOC), posttraumatic amnesia (PTA), and magnetic resonance imaging (MRI) or computed tomography (CT). The length of LOC at the time of injury is often related to severity; however, it is now well established that brain injury can occur without complete LOC (2). Alteration of consciousness (AOC) or mental status (i.e., being dazed, disoriented, or confused) following head trauma is considered the minimal grade of concussion or cerebral injury (61). The Glasgow Coma Scale (GCS) (77) quantifies level of consciousness, ranging from alert to comatose, with scores of 13 to 15 (of a maximum score of 15) considered mild injury, scores of 9 to 12 considered moderate injury, and scores of 8 or less considered severe injury. PTA presupposes that the patient is alert and functioning and has recovered from the comatose state but has persistent, severe deficits in retaining new information and processing new memories (2). It is generally accepted that the greater the length of PTA, the greater the severity of the head injury. Moreover, patients with injuries classified as mild by GCS, LOC/AOC, or PTA but with evidence of intracranial pathology on neuroimaging are considered to have moderate injuries, although the term complicated mild TBI is also used.

Studies of young TBI patients have demonstrated that these severity markers (GCS score and duration of AOC/LOC and PTA) are related to both the initial degree of cognitive and behavioral deficits and to the level of recovery (44). However, the clinical utility of these severity markers to predict outcome in older adults may be more variable. Goldstein and Levin (24) demonstrated that GCS and the presence of intracranial pathology were more strongly related to outcome than duration of LOC or PTA in older adults. The authors suggest that these results may reflect measurement issues because older adults are more likely to be injured in low-velocity falls and have delayed complications where LOC/PTA may not occur and/or be very brief or may be difficult to assess by the time the older individual gets medical attention. The differential clinical presentation of older adults with head trauma is discussed later in this chapter.

Structural neuroimaging techniques (MRI or CT) can provide additional information to help in the estimation of injury severity. Neuroradiographic evidence
of abnormality (i.e., edema, hemorrhage, and any other structural lesion) can suggest a greater level of severity of injury than indicated by PTA or LOC alone (2). Functional neuroimaging methods, including single photon emission CT (SPECT) and positron emission tomography (PET), may be more sensitive to cerebral dysfunction after TBI and identify areas of abnormality that appear intact with structural imaging. McAllister et al. (55) reviewed the literature on neuroimaging and mild TBI and noted that SPECT is more sensitive than structural imaging for the identification of cerebral dysfunction. Similarly, PET may have increased sensitivity over CT or structural MRI. Therefore, it is important to realize that no one neuroimaging technique can identify all of the neuropathophysiologic processes of TBI.

A large body of evidence indicates that neuropathologic changes occur with even mild head injury. Mild head injury represents the low end of a spectrum where pathologic changes increase as the severity of injury increases (10). In all head injuries, mechanical force to the head, either through direct impact or acceleration-deceleration motion, leads to a rapid displacement of the skull, which, if sufficiently severe, can cause differential motion between the brain and skull. The path of head motion, the anatomic surfaces surrounding the brain, and the violence of the motion determine the severity of displacement. Deformation of brain tissue is a result of such displacement and is thought to be the primary factor in traumatic brain damage. Cerebral deformation can result in structural alterations of neurons such as axonal and cytoskeletal injury, vascular changes (e.g., contusions and hemorrhage), generation of oxygen radicals, and excessive neural depolarization causing abnormal neurochemical agonist-receptor interactions related to excitotoxic processes (10). Evidence suggests that changes in muscarinic, nicotinic, and N-methyl-D-aspartic acid (NMDA) glutamate receptors are involved (34,82). Such neurochemical alterations may play a role in the behavioral changes associated with head injury.

Diffuse axonal injury has been demonstrated in clinical and laboratory studies of head injury and seems to be a consistent feature of all injuries, regardless of severity, with the distribution and number of axons involved increasing with injury severity (66). Povlishock et al. (65) found that axonal changes occurred without the presence of focal parenchymal or vascular damage even in mild head injuries. The traditional notion held that axons are physically torn at the time of injury. However, it appears that this is not true in most cases, except in severe injuries with high physical stress (19,67). It is now known that focal alteration of the axon membrane occurs after TBI. This membrane alteration results in progressive changes that disrupt axonal transport, subsequently leading to focal swelling. This swelling then leads to the collapse and detachment of the axon at the point of swelling and can take from several hours to several days after trauma. Moreover, impaired axonal transport leads to the production and accumulation of toxic proteins, peptides, and their aggregates, some of which have been implicated in the pathology of neurodegenerative disorders including Alzheimer’s disease (AD). In particular, the accumulation of amyloid precursor protein (APP) and beta-amyloid peptides found in AD has been observed in damaged axons after TBI in animals and in human brain tissue (74).

Orbitofrontal and anterior temporal regions are particularly vulnerable to contusions, lacerations, abrasions, hematomas, and intercerebral hemorrhages caused by forceful contact with the rough bony surface of the skull in these areas during head injury (47,51,80). In addition, diffuse axonal damage can disrupt frontal pathways to other cortical and subcortical regions, including the limbic system. Damage to these regions has been linked to deficits in complex neurocognitive functioning, including attention, memory, and emotional changes (51).

With aging, a greater risk exists for postinjury neurologic changes, including subdural hematomas, intracranial hemorrhage, and posttraumatic infections. Older adults are at increased risk for subdural hematoma because brain atrophy increases the distance between the brain surface and the venous sinuses. Bridging veins are more vulnerable to rupture, increasing the risk of subdural bleeds, even with less severe or seemingly trivial injuries (1,8,39). Subdural hematomas are also common consequences of falls (12), the most common cause of TBI for those aged 65 years and older. Older adults with head injuries may have a delayed presentation for medical care, even hours to days or weeks to months after a TBI. Acute subdural hematomas (clinically evident within 72 hours) usually occur in younger adults, whereas chronic subdural hematomas (>20 days old) usually occur in older adults, with a peak incidence in the sixth and seventh decades of life (39).

The clinical presentation of older individuals with head trauma can differ from that of younger adults because of differences in demography (e.g., live alone, no close family or friends), etiology, and prevalence of comorbidity (15). The course of the geriatric patient
can be further complicated by comorbid medical or neurologic disease (e.g., cardiovascular disease, dementia, diabetes, or chronic obstructive pulmonary disease). Falls are a major cause of morbidity and mortality in older individuals (79). Moreover, falls themselves are often the result of comorbid medical conditions. Coronado et al. (7) found that older adults hospitalized for a TBI-related fall had a greater number of comorbid medical conditions than those with TBI secondary to motor vehicle crashes. Falls were more likely in individuals with gait disturbance, dizziness, history of stroke, decreased visual acuity, cognitive impairment, and postural hypotension. In addition, polypharmacy, which is common in older adults, and medications with psychotropic effects also put individuals at greater risk for falls.

In contrast to younger patients, an older person may fall, lose consciousness, and not be brought for medical treatment until they are found unconscious or confused or they recover enough to call for help themselves. Alternatively, an older patient may gradually develop a subdural hematoma after a relatively minor injury. Such a patient may present as much as 3 months after the onset of mental status changes and even longer after the injury (35,81). As Flanagan et al. (14) noted, clinicians should keep an “index of suspicion” regarding TBI when seeing an older patient with a history of cognitive changes that have occurred over a period of weeks to months. In addition, urgent orthopaedic or other medical problems may supersede or even prevent recognition of the TBI. Common situations include hip fractures with head trauma or head trauma from a fall precipitated by a medical problem such as syncope. Even when head trauma is recognized, severity can be difficult to assess because the medical problems may contribute to the altered mental status. Finally, older individuals may present with a chronic progressive cognitive impairment and disability; for example, an older patient with pre-existing dementia may be brought to medical attention by family or friends because of a rapid change in their ability to perform day-to-day activities. Although evidence of physical trauma may be seen, the patient may be unable to provide details. In such a case, head trauma should be suspected as contributing to or exacerbating the patient’s pre-existing cognitive difficulties (e.g., dementia) (15).

In general, both injury severity and the patient’s age at the time of injury influence the cognitive outcome following head injury. With increasing age is seen increasing risk of negative outcome as well as greater risk for mortality (63,68,69,79). The cognitive effects of a closed head injury emerge after resolution of PTA and have been well documented in younger patients (47,54). Although the deficits observed vary with injury severity, they generally include problems with executive and attention functions (e.g., concentration, speed of information processing, mental flexibility, problem solving), memory, and aspects of language such as naming. These cognitive deficits are found within the overall context of diffuse cerebral injury and, in particular, injury to frontal and temporal areas. Each of the cognitive domains and associated functions is discussed in the following sections.