Epidemiology of Traumatic Brain Injury

Consequences of Traumatic Brain Injury

Mechanisms Underlying Functional Recovery Following Traumatic Brain Injury

Effectiveness of Rehabilitation Interventions to Address Cognitive, Behavioral, and Emotional Consequences of Brain Injury

Models of Comprehensive Rehabilitation for Traumatic Brain Injury

Definitions of Traumatic Brain Injury

No single, concise, universally accepted definition of traumatic brain injury (TBI) exists. According to Lehmkuhl (1996), TBI is defined as "damage to living brain tissue caused by an external, mechanical force. It is ... characterized by a period of altered consciousness (amnesia or coma) that can be very brief (minutes) or very long (months/indefinitely). The specific disabling condition(s) may be orthopedic, visual, aural, neurologic, perceptive/cognitive, or mental/emotional in nature. The term does not include brain injuries that are caused by insufficient blood supply, toxic substances, malignancy, disease-producing organisms, congenital disorders, birth trauma, or degenerative processes." The Centers for Disease Control and Prevention (Thurman et al., 1995) defines TBI as either "an occurrence of injury to the head that is documented in a medical record with one or more of the following conditions attributed to head injury:

• observed or self-reported decreased level of consciousness
• amnesia
• skull fracture
• objective neurological or neuropsychological abnormality
• diagnosed intracranial lesion

or as an occurrence of death resulting from trauma, with head injury listed on the death certificate, autopsy report, or medical examiner’s report in the sequence of conditions that resulted in death."

The severity of TBI has been classified as mild, moderate, and severe. These levels are differentiated clinically. The classification must be made immediately after the injury (Alexander, 1995).

Mild Traumatic Brain Injury

Mild TBI is a very common injury, resulting in 290,000 hospital admissions each year (Whyte, in press). Many more people sustain mild TBIs that do not require hospitalization. About 80 percent of people admitted to a hospital with the diagnosis of TBI have mild TBI (Kraus et al., 1994). In a review article by Kraus and McArthur (1996), mild TBIs accounted for between 60 percent and 90 percent of the samples of selected epidemiological studies of TBI. The most common cause of mild TBI is a motor vehicle crash (Kraus et al., 1994).

According to Whyte (in press), the three symptom clusters characteristic of mild TBI are cognitive symptoms (e.g., attention and concentration difficulties, memory impairments); affective symptoms (e.g., irritability, depression, anxiety); and somatic symptoms (e.g., headache, dizziness, insomnia, fatigue, and sensory impairments). The literature suggests that mild TBI does not typically cause prolonged impairments and that recovery is expected to occur within 3 months of the injury (Kibby, Long, 1996). However, Kraus (1991) summarizes recent studies that suggest persistent unfavorable outcomes following mild TBI, including physical complaints, cognitive changes, and behavioral problems. These persistent symptoms are termed post-concussion syndrome (PCS). Similarly, Alexander (1995) notes that 15 percent of individuals who suffer mild TBI still have disabling symptoms after 1 year.

The definition of mild TBI has provoked a great deal of controversy in the clinical and research literature. This is because the lower limit of the injury (i.e., the most mild TBI) is difficult to detect and define.

Before 1991, mild TBI was defined as "an injury with an initial Glasgow Coma Scale score of 13 to 15, post-traumatic amnesia (PTA) of less than 24 hours, and a loss of consciousness (LOC) of less than 20 minutes" (Esselman, Uomoto, 1995). One disputed aspect of this definition was that it included only those persons whose injuries resulted in a LOC. This restriction is problematic because some mild TBIs can occur without LOC.

In 1991, the Mild Traumatic Brain Injury Committee of the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine (Kay et al., 1993) provided the following definition of mild TBI:

"A patient with mild traumatic brain injury is a person who has had a traumatically induced physiological disruption of brain function, as manifested by at least one of the following:

1. any period of LOC.
2. any loss of memory for events immediately before or after the accident.
3. any alteration in mental state at the time of the accident (e.g., feeling dazed, disoriented, or confused).
4. focal neurological deficit(s) that may or may not be transient, but where the severity of the injury does not exceed the following:

• posttraumatic amnesia not greater than 24 hours.
• after 30 minutes, an initial Glasgow Coma Scale of 13–15.
• LOC of approximately 30 minutes or less."

As compared with the previous definition, this definition of mild TBI includes a wider range of people, ranging from those who are only dazed to those who are hospitalized, require rehabilitation, and have permanent neurological deficits (Esselman, Uomoto, 1995). In addition, this new definition resulted in an increase in the number of persons diagnosed as having TBI because it adds those who do not have LOC. The problematic aspect of this definition, according to Kibby and Long (1996) and Kraus and colleagues (1994) is that it could include a person with normal performance on the Glasgow Coma Scale (GCS) (i.e., a score of 15) who had sustained a minor blow to the head with little or no evidence that the brain had been injured. They assert that nearly every child or adult at some point experiences an event which would be classifiable as mild TBI, as a result of a fall or sports injury, and therefore, there is a need to differentiate a superficial injury to the head from mild TBI. Kraus and colleagues (1994) questioned the use of the GCS in determining mild TBI, because "its use at the upper end of the scale lacks both validity and sensitivity in distinguishing among milder injuries."

One modification of the definition of mild TBI offered by Dicker (1989) is the additional criteria of symptoms (e.g., headache) or services (e.g., seeking medical care within 24 hours of the injury) that would more reliably and validly separate persons with mild TBI from those with superficial injuries to the head. Kibby and Long (1996) offer a different suggestion, namely requiring two or more of the four criteria in the American Congress of Rehabilitation definition of mild TBI instead of one. A study by Williams and colleagues (1990) demonstrated that persons with mild TBI and radiographic evidence of a focal brain lesion and/or depressed skull fracture had significantly worse outcomes than those who had mild TBI without complications. Hence, there may be a need to further differentiate the heterogeneous category of mild TBI.

Esselman and Uomoto (1995) offer a classification of concussions, which is a term often used interchangeably with mild TBI, based on Ommaya’s (1985) conceptualization:

• Grade I concussions result in confusion only.
• Grade II concussions result in amnesia, PTA, or retrograde (RGA) without LOC.
• Grade III concussions involve LOC for up to 6 hours. (Note that a Grade III concussion would exceed the definition of a mild TBI.)

The Quality Standards Subcommittee of the American Academy of Neurology (1997) published a grading system of concussions which differs from the Ommaya (1985) classification. In the American Academy of Neurology three-grade system, Grades 1 and 2 are defined by transient confusion but no LOC. In Grade 1 injuries, the concussion symptoms and mental status abnormalities are resolved in less than 15 minutes, whereas in Grade 2 injuries, the symptoms and abnormalities last longer than 15 minutes. Grade 3 concussions involve LOC for any period of time.

Moderate Traumatic Brain Injury

There is no clearly demarcated clinical transition from mild to moderate TBI (Alexander, 1995). According to Kibby and Long (1996), moderate TBI is defined as a GCS of 9–12 during the first 24 hours after the injury and post-traumatic amnesia lasting from 1 to 24 hours. In research conducted by Thurman and others (1996) in Utah, the definition of moderate TBI was expanded to include not only those with a GCS of 9–12 but also those with intracranial lesions or focal neurological deficits and a GCS of 9 or higher. However, there is no formal definition of moderate TBI as there is for mild TBI, and the demarcation between mild and moderate TBI is unclear.

In the Kraus and McArthur (1996) summary of epidemiological studies in the United States, between 10 and 30 percent of TBIs are classified as moderate TBIs. Unpublished data by Kraus suggest that 93 percent of those persons who suffer moderate TBI are discharged from the hospital alive. Recovery of cognitive functions following moderate TBI is expected in about 1 year, and 80 percent of adults are likely to have returned to work by that point (Kibby, Long, 1996). The cognitive impairments in persons with moderate TBI are more significant than in those with mild TBI (Williams et al., 1990). They have a longer duration of impaired consciousness, more impaired verbal memory shortly after the injury, and a lower likelihood of achieving a good recovery within 6 months (Williams et al., 1990).

Severe Traumatic Brain Injury

Severe TBI is defined as a GCS score of 8 or less (comatose) during the first 24 hours after the injury (Thurman et al., 1996). Jennett and colleagues (1977, 1979) defined severe TBI by loss of consciousness (a coma) for 6 hours or longer, either immediately after the injury or after an intervening period of lucidity. The incidence of severe TBI is lower than mild or moderate. Whyte (in press) reported that between 50,000 and 75,000 people suffer severe TBI each year in the United States; of these between one-third and one-half die. Kraus and McArthur (1996) noted that the incidence of severe TBI is between 5 and 25 percent of all cases with TBI. In an epidemiological study of TBIs that led to hospital admission or death in Utah over a 3-year period, 16 percent of the hospitalized cases were considered to have severe TBI and another 13 percent died before hospital admission (Thurman et al., 1996).

Individuals who suffer severe TBI are at risk for long-term disability. Their behavior can be disinhibited, egocentric, and, at times, disregarding of social conventions (Whyte, in press). As a result, they often have difficulty remaining employed, maintaining pre-injury relationships, and establishing new social contacts. Thomsen (1992) studied 31 individuals with severe TBI over a 20-year period. Fully 61 percent had no friends. Many followup studies report depression for years after the injury in the individual who sustains severe TBI (Whyte, in press).

Penetrating and Nonpenetrating Injuries

There are two types of TBI: penetrating and nonpenetrating. Penetrating TBIs, or open head injuries, occur when an object lacerates the scalp, fractures the skull, and enters the brain. The injury results from destruction of nerve cells in the path of the penetrating object. Sources of penetrating injuries include gunshot wounds, knife wounds, and accidents.

Nonpenetrating TBIs, also known as closed head injuries, involve the collision of the head with another surface. Brain damage results even though no object penetrates the brain. This is because the brain is hurled against the inside of the skull, resulting in focal damage (e.g., contusions, lacerations, hematomas, raised intracranial pressure) or diffuse lesions (e.g., ischemic brain injury, diffuse axonal injuries) that are the result of acceleration/deceleration effects (McIntosh et al., 1996). Focal injuries are more likely to be the consequence of a fall, whereas motor vehicle accidents are the most prominent cause of more diffuse acceleration/deceleration type injuries.

Reporting Mechanisms

Adequacy of Current Data

Until the recent emergence of State registries and surveillance systems, few population-based studies were available from which to draw conclusions about the absolute numbers of TBIs and the incidence of TBI in the United States. Most studies relied on hospital discharge data. These studies do not include TBI cases that are mild and do not require medical care, nor do they include persons with TBI who are treated in emergency departments or on an outpatient basis. Many studies exclude cases who die at the scene of the injury or in the emergency department. However, some studies based on hospital discharge information use death records to augment their cases with those who have died from TBI. Studies vary according to differences in the clinical definition used for diagnosis, in coding of hospital admissions, and in the external causes of injuries included in the study. Prior studies have often been confined to small geographic areas and have focused on short time intervals, precluding the assessment of time trends. These limitations make it difficult to get an accurate assessment of factors related to TBI on a national basis or to allow geographic comparisons.

Registries and Surveillance Systems

Surveillance systems are just beginning to document the incidence of TBI in the United States. These systems will also characterize the persons injured and the external causes of TBI. The Centers for Disease Control and Prevention (CDC) under Public Law 104-166 has been funding the collection of uniform data by States and has been designated as the lead Federal agency to coordinate and plan central nervous system (CNS) injury prevention programs. CDC has published guidelines for surveillance of CNS injury (CDC, 1995). This manual sets forth standards and recommendations for the uniform collection of data across the United States. As of 1993, 16 States had TBI surveillance systems in place or were in the process of developing a system. However, as of 1998, only a few of these States have published data from their systems. Important to the success of these systems is the enactment of reporting laws in each State legislature. Along with the reporting laws, it is also necessary for State legislatures to provide the resources for the staffing of these registries.

The Traumatic Brain Injury Model Systems of Care database is a multicenter project funded by the National Institute on Disability and Rehabilitation Research (NIDRR) of the U.S. Department of Education. This prospective, longitudinal, multicenter study examines the course of recovery and outcomes of persons with TBI. Although one goal of the project is to create a database for research, from an epidemiologic perspective it is limited in assessing the demographic characteristics of persons with TBI and the causes and severity of TBI. This limitation is the result of the marked selection bias of the population who participates in this program.

Epidemiology

Incidence and Absolute Numbers of TBI Cases in the United States

Using national data from available sources, Kraus estimated that in 1990 in the United States 75,000 deaths, 366,000 hospitalizations, and 1,975,000 medically attended cases of TBI of any severity occurred at a rate of 145 of 100,000 persons per year (Kraus, 1993). This rate was consistent with the U.S. rate of 136 of 100,000 estimated by Fife (1987) using data from the National Health Interview Survey (NHIS) (National Center for Health Statistics, 1985). Alternatively, Kraus (1993) used composite data from all U.S. studies published before 1990 to develop an overall estimate of incidence of 200 of 100,000 TBI cases per year, age-adjusted to the 1990 U.S. population. This rate of 200 of 100,000 per year eliminates studies with the highest and lowest rate of TBI and is the most widely accepted rate of TBI, corresponding to 500,000 cases per year. More recently, an analysis of the 1993 National Hospital Discharge Survey (NHDS) data estimated a rate of 102 TBI-related hospitalizations per 100,000 population (CDC, 1997a).

Incidence rates in TBI have been calculated in a number of defined geographic regions in the United States (Table 1). The rates reported vary from 98 of 100,000 in Oklahoma (CDC, 1997a) to 367 of 100,000 in the intercity Chicago area (Whitman et al., 1984). More recently, reported rates from State Surveillance Systems appear to be somewhat lower than those reported for the 1970s and early 1980s. This possible decline in the incidence of TBI is thought to reflect successful injury prevention efforts but may merely reflect changes in definitions and criteria for admitting individuals to hospitals (CDC, 1997a). The CDC estimates the number of serious brain injuries that occur each year in the United States to be 250,000 (CDC, 1997a).

Table 1. Brain injury incidence from selected reports from various geographical areas within the United States, 1980–1993*

* Updated from Kraus, 1993
** PAS - Professional Activities Study
*** DOA - Dead on Arrival

Mortality

Sosin (1995) estimates that on average, 52,000 U.S. residents die from TBI each year. The 1992 U.S. death rate due to TBI was 19.3 per 100,000 U.S. residents. This rate showed a 22 percent decline from 24.6 per 100,000 U.S. residents in 1979. Sosin (1995) attributed this decline to successful efforts to prevent TBI caused by motor vehicle crashes. Other estimates of fatality rates due to TBI range from 22 to 30 of 100,000 per year (Kraus, 1993). Surveillance studies in four U.S. States from 1990 to 1993 found that 23 percent of the 13,978 TBI cases reported in those States were fatal (CDC, 1997a).

Severity

An accurate U.S. distribution of TBI by severity is difficult to determine because studies vary by the clinical definitions to classify systems of severity. The proportion of brain injuries that were classified as severe varied from 5 to 27 percent in the studies that have reported severity (Table 2). It is likely that the methods of case ascertainment in the reported studies also have a strong effect on the distribution of TBI by severity level.

Characteristics of TBI Cases

Age. In most reports, the incidence of TBI is highest among young people, with a peak at age 15 to 24 (Kraus et al., 1990). Secondary peaks occur in the elderly at ages 65 or older and in children ages five and younger (Kraus et al., 1990; CDC, 1997a; Kraus 1993; Thurman et al. 1996; Jagger et al., 1984; Fife et al., 1986; LeMier et al., 1994). The data from the surveillance systems in Colorado, Missouri, Oklahoma, and Utah demonstrate this pattern (Table 3, CDC, 1997a). Mortality from TBI is highest among the elderly, followed by those who sustain an injury at age 15 to 24 (LeMier et al., 1994; Kraus et al., 1984; Sosin et al., 1989).

Table 2. Severity of traumatic brain injury in the United States—selected reports*

	Severity
Study Location	Mild	Moderate	Severe			Comments
Olmsted County, MN	63	29	7	Severity based on symptoms, diagnosis, and loss of consciousness.
San Diego County, CA	91		9	Severity distribution based on GCS** for a nonrandom sample of individuals admitted with head injury to 10 of 30 county hospitals.
North Central Virginia	49	26	25
San Diego County, CA	82	9	9	Severity based on GCS.**
Chicago, IL	86	9	5	Severity based on symptoms, diagnosis, and length of loss of consciousness.
Maryland	70	17	13	Severity based on ICD:*** AIS**** 1,2 = mild AIS 3 = moderate AIS 4.5 = severe
Utah†	33	35	27	Cases that led to hospital admission or death only. Severity based on GCS.** If no GCS** was available, severity was based on awake, obtunded, or comatose.
University of Virginia Hospital (Rimel et al.)	55	34	21	Based on 1,248 individuals with head injury admitted to U.V. Hospital. Severity measured by GCS.**

* Adapted from Kraus, 1993 in Cooper PR (ed.). Head Injury. 3rd edition.
** GCS - Glasgow Coma Scale
*** ICD - International Classification of Diseases
**** AIS - Abbreviated Injury Score
^†   3.5% had no classification.

Table 3. Rate* of traumatic brain injury^†, by age group and sex—Colorado, Missouri,
Oklahoma, and Utah, 1990–1993^‡

* Per 100,000 persons.
^† International Classification of Diseases, Ninth Revision, Clinical Modification, codes 800.0-801.9, 803.0-804.9, and 850.0-854.1.
^‡ Information was collected for 1991–1993 in Colorado, 1992–1993 in Missouri and Oklahoma, and 1990–1993 in Utah (CDC, 1997a).

Gender. In all studies, TBI is more common in males of all ages than females (Kraus, 1993; LeMier et al., 1994; CDC, 1997a) (Table 3). Overall, men have twice as many brain injuries as women, but the ratio varies by age. For children ages 5 and younger and the elderly ages 75 and older, the ratio of the rates is less than 2, with a higher absolute number of TBI cases among women 75 and older (Thurman et al., 1996). This reflects the larger number of older women than older men in our population. The mortality rate for males is higher at all ages (Kraus, 1993; Klauber et al., 1981).

Race. When information on race is available, black and other nonwhite races have higher rates of TBI (Sosin et al., 1996; Kraus et al., 1990; Jagger et al., 1984; Whitman et al., 1984). The age-adjusted incidence of TBI in the Bronx, New York, from March 1980 to February 1981 was 209 of 100,000 for white residents, 278 of 100,000 for black residents, and 261 of 100,000 for Hispanic residents (Cooper et al., 1983). TBI mortality rates followed a similar pattern, with 18.7 of 100,000 for white residents, 34.2 of 100,000 for black residents, and 28.7 of 100,000 for Hispanic residents. They speculated that these racial differences reflected underlying patterns of socioeconomic or environmental factors in the Bronx. Cooper noted that the excess TBI in the black and Hispanic populations was due to violence. In contrast, when Sosin and colleagues (1996) used a nationally representative household sample (1991 NHIS) to determine the incidence of self-reported medically attended mild and moderate TBI by race, they found that incidence varied little between white, black, and Hispanic respondents. MacKenzie and colleagues (1989) also found little difference in white TBI rates compared with nonwhite rates overall or by severity level. Kraus (1993) cautioned that most studies that addressed TBI incidence rates by race did not adjust for socioeconomic status or other potentially important community characteristics.

Urban/Rural. Gabella and colleagues (1997) compared the epidemiology of rural and nonrural TBI in Colorado, using the statewide population-based TBI surveillance system. They found that the overall ratio of the incidence of TBI in rural areas versus the metropolitan Denver-Boulder area was 1.8 to 1. This ratio was similar for males and females. The mortality rates were not different for women by urban/rural residence, but the mortality rates for males were more than doubled in the rural areas, particularly for suicide and causes other than motor vehicle crashes, falls, and assault/homicide.

Sosin and colleagues (1996) used the NHIS data base to assess the incidence rates of self-reported medically attended TBIs (mild to moderate) by urbanization. They did not find any differences in the incidence rates of city, suburban, or rural residence for these less severe injuries.

Le Mier and colleagues (1994) found that the five counties in Washington State with the highest TBI rates were counties that are considered predominately rural. The reason for this geographical distribution was not clear; however, it was speculated that these counties had proportionately higher numbers of high-risk populations, such as males 15 to 24 years of age, the elderly, and minorities.

Education/income. Sosin and colleagues (1996) reported on self-reported medically attended mild and moderate TBI by level of education and income using the 1991 NHIS. The incidence was 633 per 100,000 for the population with yearly household incomes less than $20,000, whereas the incidence was 395 per 100,000 for the population with yearly household incomes equal to or greater than $20,000. Although the differences in incidence rates were not as great by education, the TBI rate of the population with some college education, 416 per 100,000, was somewhat lower than that of the population with education less than high school, 476 per 100,000, or that of high school graduates, 536 per 100,000. Fife and colleagues (1986) examined the Rhode Island population for the incidence of TBI, excluding fatally injured persons and those who were never hospitalized, by income and population density. They reported that the incidence rates of TBI for the census tracts in the lowest decile of median income were twice those for the census tracts in the highest decile. In general, incidence rates in cities increased with increasing population density.

Seasonality. A number of studies have examined the distribution of TBI by month or season of occurrence (Klauber et al., 1981; Whitman et al., 1984; Cooper et al., 1983; Diamond, 1996; Kraus, 1980). Most of these studies found peak incidence during the late spring and summer months.

Work-related TBI. There is a dearth of information on work-related TBI. Annegers and colleagues (1980), using the Olmsted County, Minnesota, population, found that the rate of occupation-related TBI was 11 of 100,000. The events occurred most frequently among men, particularly those in the farming and construction occupations. Heyer and colleagues (1994) used the Washington State Workers’ Compensation System from 1988 through 1990 to estimate the incidence of TBI. They calculated an incidence rate of hospitalized occupation-related TBI of 9.4 of 100,000 per year. The highest relative risks of TBI were found among loggers, followed by roofers, garbage collectors, and road construction workers. He found a large proportion of injuries clustered in a few industries, offering opportunities for prevention.

Other Risk Factors

Alcohol. Alcohol intoxication is often a contributing factor in the occurrence of traumatic brain injury. It is well known that alcohol is frequently associated with motor vehicle crashes (CDC, 1997b; American Medical Association Council on Scientific Affairs, 1986). Studies that have specifically evaluated the relationship of alcohol use to TBI in the United States found 9 percent (Klauber et al., 1981), 49 percent (Gale et al., 1983), and 72 percent (Rimel, 1981) of TBI cases had alcohol as a contributing cause. Kraus (1990), in a study of persons with TBI in San Diego, found that among the 26 percent ages 15 to 19 years who were given blood tests, 51 percent had a measurable blood alcohol content. It is likely, however, that this was not a random sample of persons with TBI in this age group. Goodman and Englander (1992) reviewed the literature on TBI in the elderly. They noted chronic use of alcohol as an important factor in this age group for both motor vehicle and fall-related TBI. Braakman and colleagues (1980) found alcohol to be related to 30 percent of TBI cases in a study of elderly persons with a mean age of 74.8 at the time of the event. Hartshorne and colleagues (1997) analyzed 75 cases of fatal TBI that occurred as a result of ground-level falls and that were autopsied in King County, Washington, over a 48-month period. Postmortem toxicology reports or clinical records of alcohol analysis were available on 48 of the cases. Of those tested, ethyl alcohol was present in 48 percent. It is clear from the available studies that the testing for alcohol in persons with TBI has not been done in a consistent or unbiased manner.

TBI as a risk factor for TBI. Many persons who recover (or think they have recovered) from TBI return to the activities that may have led to the initial episode. Most of the research and reports on recurrent TBI have focused on sports-related injuries that involve repeated blows to the head, such as boxing and football (CDC, 1997c; Enzenauer et al., 1989; Sortland et al., 1989; Saunders et al., 1984). Of importance is that even mild TBI, if repeated within a short timespan, can result in high mortality and morbidity (Hilton, 1994). Annegers and colleagues (1980), in their Olmsted County, Minnesota, study estimated the risk of a second TBI among those with previous TBI to be threefold the risk among those without TBI. They attributed this high risk to "behavioral characteristics such as use of alcohol."

External Causes

In the majority of studies, transportation-related incidents account for approximately 50 percent of TBI (Kraus, 1993; CDC, 1997a). This proportion is highly weighted by the high rate of transportation-related injuries in the 15 to 24 year age group, the age group of highest TBI incidence (Table 4). Falls are the second leading cause of TBI, accounting for a little over 20 percent of the incidence of TBI. In contrast with transportation-related injuries, the age groups most affected by falls are children younger than age 5 and the elderly, ages 75 and older. Firearms and nonfirearm assaults account for close to 20 percent of the incidence, with the remainder accounted for by sports/recreation and other causes.

Prevention

Beyond the fetal and newborn period, TBI is the result of potentially preventable incidents and intentional injuries (Daemon, Leviton, 1997; Thurman et al., 1995; Sosin et al., 1995; Kraus, 1993). Unintentional injuries can be separated into those resulting from motor vehicle crashes, occupational mishaps, falls, organized and individual sports, and other recreation. Intentional injuries are the result of violence: child abuse, domestic violence, crime, street violence, and military actions or war. Alcohol and other consciousness-altering drugs also deserve special consideration in attempts to prevent TBI.

Table 4. Rate* of traumatic brain injury,^† by external cause of injury^‡ and age group—
Colorado, Missouri, Oklahoma, and Utah, 1990-1993.^¶

* Per 100,000 persons.
^† International Classification of Diseases, Ninth Revision, Clinical Modification, codes 800.0-801.9, 803.0-804.9, and 850.0-854.1.
^‡ Information obtained from all cases reported in Missouri and Oklahoma and random samples of cases reviewed in Colorado (13% sample) and Utah (10% sample). Estimated mean annual numbers of cases by cause were 6,597 transportation-related, 3,186 fall-related, 1,346 firearm-related, 1,191 nonfirearm assault-related, and 353 sports- and recreational-related. An estimated mean of 727 and 579 cases for each year was related to other and unknown causes, respectively.
^¶ Information was collected for 1991-1993 in Colorado, 1992-1993 in Missouri and Oklahoma, and 1990-1993 in Utah (CDC, 1997a).

Unintentional Injuries

Preventive strategies target both the prevention of events that can lead to injury and the prevention of TBI when these events do occur. Most strategies fall into one of three categories: improved technology development and dissemination, consumer education, and legislative actions and mandates. Motor vehicle injury prevention is a good example of the different strategies and targets. Seatbelts, shoulder harnesses, infant and child car seats, airbags, and their legislatively mandated use are all aimed primarily at the prevention of traumatic brain and spinal cord injury when motor vehicle crashes occur. Changes in speed limits, road design, and traffic control measures are aimed at the prevention of the crashes themselves (Jagger, 1987 and 1992; U.S. Department of Transportation, 1980).

Motorcycle and bicycle helmet laws are aimed at prevention of TBI, but do little if anything to affect the risk of spinal cord injury. Bicycle helmets have been shown to decrease both the occurrence and severity of TBI in cyclists (Thompson et al., 1989; Rodgers et al., 1994). Attempts to mandate helmet use, especially for adults, have met with opposition in many States. The rules governing driving of watercraft, snowmobiles, and all-terrain and three- and four-wheel off-road vehicles have received significantly less attention.

Attempts to reduce sports-related TBI include the modification and development of newer sports equipment such as better helmets for football, hockey, bicycling (Thompson et al., 1989), and horseback riding (Lantis, 1994; Nelson et al., 1992; American Academy of Pediatrics, 1992) and posterior neck pads or rolls for football players. Rule changes which prevent amateur athletes with even the mildest concussion from re-entering a game without physician approval have raised awareness of the risk of TBI in school and community sports and reduced the risk of exacerbation of existing injuries and immediate reinjury (American College of Sports Medicine, 1993; Cantu, 1987; Hugenholtz, Richard, 1982; Kelley et al., 1991). The success of these prevention activities has not been carefully studied (Torg, 1985). However, recent detailed research on the biomechanics of cervical spine and brain injuries offers hope for improved prevention strategies in the areas of better safety equipment, appropriate rules changes to enhance safety, and greater coach, player, and parent awareness (Winkelstein, Myers 1997).

Each new technology or legislative mandate is felt to warrant a careful evaluation. Although considered to be successful in overall injury prevention, some safety devices such as shoulder harnesses and airbags have had unanticipated adverse effects on children. Similarly, consumer education programs must be evaluated, even those that sound reasonable. The National Head and Spinal Cord Injury Prevention Program of the American Association of Neurological Surgeons and Congress of Neurological Surgeons is an educational intervention with teens regarding seatbelt and shoulder belt use. It has been shown to increase knowledge but not modify behavior (Neuwelt et al., 1989; Robertson, 1983).

Appropriate prevention strategies are also age dependent. For example, unintentional injuries in infants reflect their developmental stage and are often the result of falls from walkers, from strollers, down stairs or from shopping carts (Chadwick et al., 1991). Changes in the design of these devices and proper use by parents, including lap straps in shopping carts and gates for stairs, could prevent many of these injuries (Fisher, 1997). In primary school age children, injury prevention should focus on safety in recreational activities, such as bicycling and skate boarding, as well as vehicle passenger safety. In adolescents and young adults, injury concerns include driving and alcohol, sports, recreational activities, and violence.

Occupational injuries are the concern of the Occupational Safety and Health Administration (OSHA). Some of the required occupational injury prevention activities are obvious, such as wearing hardhats at construction sites. Other prevention strategies, such as rules regarding package stacking and storage, are less apparent to most Americans. Mortality and TBI surveillance for all job sites has helped to identify additional safety measures that may be helpful in TBI and spinal cord injury prevention.

Overall, the most effective unintentional injury prevention measures are reported to be legislative and regulatory controls in road, sport, and workplace settings. The ability of educational programs to modify behavior may be enhanced through the use of incentives (Munro et al., 1995; Halperin et al., 1983).

Intentional Injuries

Violence has been recognized as a pandemic (Beauchesne et al., 1997). In the United States, street violence, violent crimes, and child and domestic abuse are all associated with increased mortality and TBI in children and young adults. Since the Vietnam War, U.S. involvement in military actions has been limited to short periods of time or peace-keeping activities and has therefore accounted for a smaller portion of TBIs than in earlier decades.

Prevention of street violence, especially handgun violence, has not been very successful (Hausman et al., 1996; Nadel et al., 1996; Powell et al., 1996; Tolan, Guerra, 1996). Strategies have included both attempts to remove the tools of violence, such as handguns, and establishing programs to identify and modify the causes of violence, through interventions such as youth activity programs, control of illegal drugs, education and work programs, and changes in television network programming and viewing (Durkin et al., 1996; Grossman et al., 1997; Davidson et al., 1994; Finkelhor et al., 1995). Evaluation of most prevention activities has been scant (Powell et al., 1996).

Child abuse continues to be the etiology of thousands of childhood injuries and deaths each year (Committee on Child Abuse and Neglect, 1997; Billmire, Myers, 1985). Shaken baby syndrome results specifically in TBI and spinal cord injuries (Bruce, Zimmerman, 1989; Dykes, 1986; Hahn et al., 1983; Caffey, 1972; Cullen, 1975; Dickson, Leatherman, 1978; Gosnold, Sivaloganathan, 1980). Similarly, domestic violence affects children and adults of both genders. Prevention programs for child abuse and domestic violence are often secondary prevention efforts, attempting to prevent further abuse after a pattern of abusive behavior is recognized (Saltzman, Johnson, 1996). More recently, high schools, hospitals, and community centers have developed educational programs regarding conflict management and parenting, and pre- and postmarriage support groups (U.S. Advisory Board on Child Abuse and Neglect, 1991). Early education and support in high-risk families is often done either in the home of pregnant or new mothers or in community education, public health, or social services centers (Showers, 1992). In early assessment studies, such programs appear to have variable levels of efficacy in preventing abuse (Taal, Edalaar, 1997; Rispens et al., 1997). Legislators have proposed legislated "prevention" (Browne, 1994; Dresser, 1994). This would of course also include prevention of second injuries.

Most researchers agree that prevention of TBI due to violence will require major new programs and perhaps reevaluation of societal values and norms, changes in the judicial system, a reduction in poverty, and expanded educational and adequate employment opportunities for youth, especially inner-city youth and those of African American and Hispanic descent (Beauchesne et al., 1997; Committee on Child Abuse and Neglect, 1997; Taal, Edalaar, 1997; Rispens et al., 1997).

Alcohol and Drug Use

Alcohol and other drugs that alter cognitive abilities and judgement should receive special attention in the prevention of both unintentional and intentional injuries. Alcohol-impaired drivers kill and maim many Americans every day (Cunningham, 1996), and alcohol use is highly associated with physical and sexual abuse of children by parents and relatives (U.S. Advisory Board on Child Abuse and Neglect, 1991). Congress has recently debated strengthening laws that identify alcohol-impaired drivers. In many European countries, driving while drug or alcohol impaired results in immediate loss of license and/or vehicle. Whether it is the tougher laws or social norms, driving while intoxicated appears to result in fewer deaths and TBIs in countries with swift and definitive consequences of this offense (Dresser, 1995; Ross, 1995; Chafetz, 1995; O’Connor, Schottenfeld, 1998).

Prevention of underage drinking may be especially important in the prevention of TBI, since it is the young impaired driver who is most likely to sustain or cause such injuries in passengers or victims (U.S. Department of Transportation, 1989). More strict drinking rules among student athletes and on college campuses have been instituted to curb underage drinking (Carr et al., 1996; Heyman, 1996; Tricker, 1996; Ungerleider, 1996).

Illegal drugs play a large role in street violence, and violent crime, both as mind-altering substances and as the reason for theft, violence, and injury. Attempts to control drug trafficking and the traffickers have met with limited success in the global market. Primary prevention of drug use in children and young adults has also met with limited success (Fawcett et al., 1997; Shope et al., 1996). Programs such as DARE have been used widely and studied little.

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Top

TBI may be classified as mild, moderate, or severe, but no matter the severity, consequences are rarely limited to one set of symptoms, clearly delineated impairments, or a disability that affects only part of a person’s life. Rather, consequences of TBI often affect human functions along a continuum: from altered physiologic functions of cells, through neurological and psychological impairments, to medical problems and disabilities that affect the individual with TBI, family, friends, and community, as well as society in general. Furthermore, the consequences of TBI may be insidious in that early manifestations of impairment with relatively mild symptoms may be overlooked or overshadowed by urgent medical problems related to trauma yet result in subtle impairments. This section reviews the neurological, functional, and medical consequences of TBI, as well as special issues related to TBI in children and the elderly. It also summarizes what is known about the social and economic consequences that TBI may have on the family, the community, and society.

Neurological Consequences

In general, neurological outcomes are directly influenced by the type of TBI and the severity of the neurophysical, neurocognitive, and neurobehavioral complications.

Neurophysical Sequelae

In this report, the term "neurophysical impairment" denotes the noncognitive and nonbehavioral neurological complications of TBI. These neurophysical impairments will have a direct impact on the overall neurological recovery of the individual. Neurophysical impairments that may be encountered after TBI are listed in Table 1.

Headaches represent the most common sequelae of TBI and may occur as a component of the postconcussion syndrome or as a consequence of any type of TBI. Posttraumatic headaches are typically caused by injury to the scalp, cervical spine, or intracranial structures and are more commonly associated with mild TBI than its more severe forms (Packard, Ham, 1994). Posttraumatic headaches may be accompanied by cognitive and somatic symptoms such as memory impairment, difficulty concentrating, dizziness, and fatigue. Although the pathophysiology of posttraumatic headache is poorly understood, most individuals will improve in 6 to 12 months (Packard, Ham, 1994), although persistent headaches may be anticipated in 15 to 20 percent (Speed, 1991).

Posttraumatic seizures are a relatively common complication of TBI and can be classified as early (within the first week) or late (after the first week). Risk factors for early seizures include posttraumatic amnesia lasting longer than 24 hours, depressed skull fracture, and acute intracranial hematoma (Jennett, Bond, 1975). Late seizures tend to be associated with a history of early seizures, depressed skull fracture, and acute intracranial hematoma (Jennett, Bond, 1975).

Motor and sensory impairments are relatively common consequences of moderate and severe TBI. Both have a profound effect on neurological and rehabilitation outcomes. Motor impairment can be present as weakness, ataxia, spasticity, or other forms of movement disorder. Hemiparesis can occur from focal lesions affecting the corticospinal tract in the cerebral hemispheres or brainstem. Spasticity usually emerges in the evolution of recovery from upper motor neuron weakness (Bachman, 1992). Ataxia after severe brain injury may occur secondary to damage to the cerebellum or cerebellocortical pathways (Haggard et al., 1995). Movement disorders encountered after TBI include tremor, dystonia, choreoathetosis, tics, and myoclonus (Goetz, Pappert, 1996).

Posttraumatic ventricular enlargement or hydrocephalus can occur as an acute or chronic complication of TBI. Symptoms of posttraumatic hydrocephalus usually occur within 1 year and include impaired consciousness, ataxia, failure to improve, behavioral changes, incontinence, and/or signs of increased intracranial pressure (Cardoso, Galbraith, 1985). Factors contributing to the development of posttraumatic hydrocephalus include meningitis, traumatic subarachnoid hemorrhage, posterior fossa mass, fibrosis related to craniotomy, and intracranial hematoma (Cardoso, Galbraith, 1985). Early diagnosis and ventricular shunting may improve neurological outcome and prevent further neurological deterioration (Scheffler et al., 1994).

Posttraumatic cerebrospinal fluid (CSF) leaks are associated with skull fractures and can be present as rhinorrhea or otorrhea. Individuals with CSF rhinorrhea usually have sustained a dural tear and a fracture of the ethmoid or sphenoid bone or the orbital plate of the frontal bone (Cooper, 1993).

Otorrhea typically occurs when there is a combination of a fracture of the petrous bone, a tear in the dura mater and arachnoid, and a rupture of the tympanic membrane (Cooper, 1993).

Compressive cranial neuropathies can occur with or without skull fractures. The most commonly injured cranial nerves in TBI include the olfactory, facial, and audio vestibular nerves, whereas the least involved cranial nerves are the trigeminal and lower cranial nerves (Kean, Baloh, 1996). Trauma to the ocular nerve and ocular motor nerves are intermediate in frequency (Keane, Baloh, 1996).

Neuroendocrine dysfunction secondary to posttraumatic hypopituitarism and hypothalamic damage is a relatively uncommon consequence of TBI. Hypothalamic or pituitary damage can occur after any type of head injury but tends to be associated with more severe brain injury. The clinical manifestations of hypopituitarism can be immediate or delayed and can include decreased growth hormone, decreased gonadotrophin, decreased thyrotropin, and/or increased prolactin production (Wyngaarden et al., 1992, p.1229). Other less frequently encountered neurological complications of TBI include arachnoid cysts, arteriovenous malformations, posttraumatic aneurysms, and posttraumatic subdural hygromas.

Neurocognitive Consequences

Several cognitive functions can be affected by TBI (Table 2). In TBI, memory, attention/concentration, executive functioning, and information-processing speed are the most commonly affected functions. Visual-spatial skills and language function are less commonly impaired unless associated with focal or penetrating brain injury. Intelligence, which is the sum of an individual’s knowledge and problem-solving skills (Capruso, Levin, 1996), may also be impaired following severe TBI (Levin et al., 1979b). Levin and colleagues (1979b) noted that

designed to assess cognitive function after TBI. These include the Galveston Orientation and Amnesia Test (GOAT) (Levin et al.,1979a), the Children’s Orientation and Amnesia Test (COAT) (Ewing-Cobbs et al., 1990), and the Levels of Cognitive Functioning Scale (Hagan et al., 1979).

TBI has profound effects on memory function. Memory deficits following TBI include anterograde (impaired memory for events after TBI) and retrograde (impaired memory for events before TBI) amnesia. The period of anterograde or posttraumatic amnesia (PTA) appears to be a reliable predictor of outcome following TBI (Ellenberg et al., 1996). In addition to the acute effects of TBI on memory function, more chronic memory problems such as dementia pugilistica and posttraumatic dementia may be encountered (Jordan, 1998). Dementia pugilistica, which is primarily exhibited by retired boxers, represents the chronic, long-term consequences of repetitive concussive blows to the head and is distinguished from posttraumatic dementia characterized by an individual experiencing long-term memory impairment after a single severe TBI, typically associated with prolonged coma (Jordan, 1998). In addition, TBI has been linked to the pathophysiology of Alzheimer’s disease (Van Duijn, 1996), especially in those harboring the apolipoprotein E allele (Mayeux et al., 1995; Katzman et al., 1996).

Neurobehavioral Sequelae

Problematic behavioral and emotional consequences of TBI are common and varied (Table 3) yet poorly understood. One or more forms of neurobehavioral sequelae are estimated to exist in up to 94 percent of victims. The major problems reported are restlessness, agitation, aggression, withdrawal, emotional outbursts including violence, and a variety of personality changes (Levin et al., 1987; Silver, Lux, 1994; Galski et al., 1994; Volavka, 1995). Individuals with severe TBI, compared with those with mild and moderate TBI, are at greatest risk for developing and sustaining these problems. Disruptive behaviors, for example, agitation, hostility, and verbal and physical aggression, are particularly common and troublesome; they appear early (1 to 3 weeks) and may persist more than 5 years after TBI (Wroblewski et al., 1997; Fugate et al., 1997; Olver et al., 1996; Fowler et al., 1995; Brooke et al., 1992; Dunlop et al., 1991; Levin et al., 1987). There is some suggestion that restlessness (i.e., continuous activity) may be distinguished from agitated behaviors, be time limited, and reflect early recovery (Brooke et al., 1992). An inverse relationship exists between agitation and cognitive function in the early rehabilitation period (Corrigan et al., 1989; 1992). Instruments commonly used to measure problem behaviors include (1) Overall and Gorhams’ Brief Psychiatric Rating Scale, (2) Neurobehavioral Rating Scale, (3) Overt Aggression Scale, and (4) Agitated Behavior Scale. Posttraumatic amnesia confounds agitated states (Sandel, Mysiw, 1996). Agitation often lessens as amnesia clears (Corrigan, 1989). In children with TBI, premorbid behaviors appear highly relevant for understanding posttrauma behavior patterns (Max et al., 1997a; 1997b, 1997c; Bijur et al., 1996). There is some indication that frontal lobe damage impairs inhibitory control over limbic activity leading to a prevailing pattern of agitation, disorganization, and disinhibition. Disinhibition in children has been associated with impulsivity, forgetfulness, and antisocial behavioral. In general, agitation, aggression, emotional lability, and disinhibition are inversely related to cognitive function. There is also a tendency for behaviors and emotions to deteriorate over time (Dunlop et al., 1991; Olver et al., 1996). Although this might be explained by nonadaptive neuroplastic changes, persistent PTA, increased cognitive demands, sensitization through a central fear system, or some combination of these, little definitive evidence exists to explain events or guide therapy.

Mood disorders and psychiatric manifestations are also prevalent after TBI. Following moderate or severe TBI, major and bipolar depression is estimated to occur in anywhere from 4 to 77 percent of individuals; personality changes and major anxiety disorders (panic attacks, phobias, and obsessive-compulsive disorders ) are estimated to occur in 50 to 60 percent of individuals (Rosenthal et al., 1998; Van Reekum et al., 1996; Emilien, Waltregny, 1996; Jorge et al., 1993a; 1994). Apathy is also a frequent symptom and may occur alone or in combination with depression (Kant et al., 1998). The onset of negative affective symptoms may occur early or late. A more extended longitudinal perspective is needed to determine the persistence of mood alterations in moderate- to severe-TBI groups. Jorge and colleagues (1993a) report that depression alone lasts an average of 1.5 months and is associated with left dorsolateral frontal or basal ganglia damage. These authors suggest that when depression is combined with anxiety disorder, the duration of symptoms is almost 8 months and the origin of injury is often the right hemisphere. Mild TBI is also associated with persistent mood disorders and emotional problems. These tend to take the forms of depression (in 26 to 37 percent of subjects studied), general anxiety, and posttraumatic stress disorders (in 50 percent), which may persist for months after injury in both adults and children (Parker, Rosenblum, 1996).

Psychiatric Disorders After Traumatic Brain Injury

Historically, the neurobehavioral psychosocial consequences of TBI have been measured by either neuropsychological (e.g., attentional, executive, or memory impairments), emotional (e.g., personality assessment profiles), or psychosocial (e.g., return to work or school, quantity and quality of interpersonal relationships) variables. Recent research has begun to document specific psychiatric morbidity following TBI. The findings of this research are reviewed below.

Jorge and colleagues (1993a, b) assessed depression and anxiety disorders in a group of 66 adults hospitalized for treatment of TBI. They conducted assessments during the acute hospitalization and at 3, 6, and 12 months postinjury. A total of 28 subjects met criteria for major depression, 17 during the acute stage and 11 (17 percent) during followup. The mean duration of depression was 4.7 months. Seven of the 17 subjects who were depressed during the acute stage also met diagnostic criteria for generalized anxiety disorder with a mean duration of 1.5 months.

Review of a controlled prospective study of mild TBI in children and adolescents (Asarnow et al., 1995), 30 studies involving mild TBI, and the data from the prospective study by Max and colleagues (1997a,b,c) described below suggests that the evidence in support of the pathogenesis of behavior problems as a direct effect of TBI resulting from an accident, or as a long-term secondary effect of the injury, is weak for the group of mild cases as a whole.

There are only three prospective studies available that use standardized psychiatric assessment methods to assess children with moderate or severe TBI. The first was conducted by Sir Michael Rutter’s group in England (Brown et al., 1981). This was a study of 28 children with severe TBI (PTA 1 week), 29 with mild TBI (PTA 1 hour to 1 week), and 28 control subjects, ages 5 to 14 years. Psychiatric assessments were done at 4 months, 1 year, and 2 to 14 years postinjury. Within the severe injury group, 12 psychiatric diagnoses "attributable to brain injury" were made.

Max and colleagues reported on psychiatric disorders in a group of 50 children and adolescents, ages 6 to14 years, at 3 months (Max et al., 1997a), 6 months (Max et al., 1997b) and 2 years (Max et al., 1997c) following TBI. At 3-month followup (n=37; mild = 46 percent; moderate = 24 percent; severe = 30 percent), a "novel" (i.e., post-TBI onset) psychiatric disorder occurred in 17 of 37 subjects (46 percent). The specific diagnoses were "organic personality syndrome" (10; 4 resolved), attention deficit hyperactivity disorder (ADHD) (6), anxiety disorder (6; 3 resolved), major depression (5; all resolved), mania (1), oppositional defiant disorder (ODD) (3), obsessive compulsive disorder (OCD) (1), mania (1), and adjustment disorder (1; resolved). Of note, in a post hoc forward stepwise logistic regression analysis, the variable most likely to predict novel psychiatric disorder was severity of injury (i.e., lowest postresuscitation Glasgow Coma Scale [GCS] score), which correctly predicted 76.7 percent of novel disorders.

At 6-month followup, 10 of 41 subjects had a novel psychiatric disorder (Max et al., 1997b). In seven of the subjects, novel disorders had persisted from the first 3 months of followup; in two subjects the initial novel disorder had been replaced by another; and in one subject the novel disorder had developed during the second 3 months of followup. The specific disorders were organic personality syndrome (5), ADHD (4), ODD (4), anxiety disorder (2), mania (1), hypomania (1), and OCD (1). The post hoc forward stepwise logistic regression analysis revealed that severity of injury (lowest postresuscitation GCS score) predicted 85 percent of the novel disorders.

At 2-year followup, 15 of 42 subjects had a novel psychiatric disorder (Max et al., 1997c). Novel disorders had persisted from the previous (unpublished) 12-month assessment in 11 subjects (3 had developed an additional novel disorder in the interim); the other 4 subjects developed their disorder during this 12-month period. The disorders included ODD (8; 2 resolved), ADHD (6; 1 resolved), organic personality syndrome (4; comorbid with novel ADHD in all cases), anxiety disorder (4; 1 resolved), mania (1), hypomania (1), adjustment disorder (1; resolved), and marijuana dependence (1; resolved). The post hoc forward stepwise logistic regression analysis revealed that global family function, the first variable, predicted 76 percent of novel disorders; severity of injury (lowest postresuscitation GCS score), the second variable, predicted 78.6 percent; and lifetime psychiatric diagnosis, the third variable, predicted 81 percent of the novel disorders.

Gerring and colleagues (1998) studied 99 children, ages 6 to14 years, with moderate (GCS score = 9 to 12) or severe (GCS score = 3 to 8) TBI. Psychopathology, specifically ADHD and OCD, were systematically assessed immediately after injury and at 1-year followup. Premorbid prevalence of ADHD was 20 percent, significantly higher than a reference population (4.5 percent). Fifteen of the remaining 80 children (19 percent) developed ADHD (except for the age-of-onset criterion) by the end of the first year postinjury. Eight of 72 subjects (11 percent) developed "new onset" OCD at the 1-year followup.

Taken together, these followup studies of children with TBI indicate that psychiatric disorders are rare following mild TBI and common following moderate or severe TBI. The most common psychiatric disorders that persist to 1 or 2 years postinjury are ADHD, personality changes, and OCD. Depression appears to resolve during the first year postinjury. Some anxiety disorders and oppositional behavior also persist, but it is difficult to know whether this is a direct consequence of brain injury or the psychosocial sequelae of the injury. Depression and anxiety are also common following TBI in adults. In general, the anxiety resolves over a few months, whereas the depression may persist in a minority of individuals.

Theoretically, neurological outcome measures after TBI document the associated neurological sequelae or impairments. The distinction between impairment and disability is important because neurological impairments do not always translate into functional disabilities. The majority of individuals who exhibit neurological impairments following TBI reach their maximal outcome within 6 months of injury and very few change after 1 year (Jennett et al., 1981).

Functional Consequences of TBI

Attentional processes are commonly affected following TBI and should be carefully assessed before attributing cognitive dysfunction to a specific domain. After TBI, detailed neuropsychological testing can reveal deficits in vigilance (sustained attention), freedom from distraction (focused attention), and the capacity for divided attention (Capruso, Levin, 1996). The inability to attend to incoming information can result in an information-processing deficit that can affect performance in other cognitive domains (Lovell, Franzen, 1994). Slowed information-processing speed is a sensitive and well-documented sequela of TBI (Capruso, Levin, 1996).

Executive dysfunction is a common sequela of TBI because the frontal lobes are particularly susceptible to vectors of TBI. Cognitive functions that are subserved by the frontal lobes that can be affected by TBI include abstraction, planning, mental flexibility, and mental control.

Dysfunction in visual-spatial skills is infrequently encountered following TBI unless associated with a right hemispheric focal lesion. The relative preservation of complex perception reflects the anterocaudal gradient of TBI that results in more involvement of the anterior cortices and less involvement of the posterior cortices (Capruso, Levin, 1996).

Language dysfunction is variably affected after TBI. Language deficits encountered after TBI can include mutism, anomia, impaired comprehension, decreased fluency, impaired repetition, paraphasia, circumlocution, disorganized and impoverished narrative, tangential or socially inappropriate conversation, disturbances in speech intonation, and the loss of speech spontaneity (Lovell and Franzen, 1994; Capruso and Levin, 1996).

Medical Complications of TBI

TBI (even mild TBI) may affect many organ systems of the body and result in both acute and long-term medical problems that hamper return to normal functioning and increase use of health care services. The potential medical complications can be divided between those occurring within the first days to months following injury and those occurring in the postacute phases.

Acute Complications

Severe TBI resulting in loss of consciousness for greater than 12 to 24 hours is often accompanied by a host of extra cerebral manifestations of the stress, polytrauma, hypermetabolic state, neurological insults, and deficits acutely associated with TBI (Cole et al., 1994; Bloomfield, 1989; Groswasser et al., 1990; Clifton et al., 1984; Balzola et al., 1980).

Pulmonary complications (Slack, Shucart, 1994) include neurogenic pulmonary edema (Dettbarn, Davidson, 1989), adult respiratory distress syndrome, pulmonary emboli from fat and blood clots (Sobus et al., 1994), aspiration pneumonia (Klingbeil, 1988; Citta-Pietrolungo et al., 1993; Splaingard et al., 1988), and the effects of unrecognized blunt trauma to the chest (Cole et al., 1994; Baigelman, O’Brien, 1981; Miyashi et al, 1994; Karaaslan et al., 1995).

Erosive gastritis is an almost universal complication of TBI in individuals not receiving prophylactic gastric acid inhibition (Becker et al., 1978; Arseni, Oprescu, 1975; Halloran et al., 1980). This condition may in turn cause bacteria overgrowth in the stomach, thus increasing the risk of aspiration pneumonia. Associated blunt trauma to the abdomen may lead to pancreatitis or small bowel edema and dysfunction. The frequently observed stress-induced hypermetabolic state and glucogenesis may lead to muscle wasting and starvation of other organ systems.

Fluid and electrolyte balance are hampered by the hypermetabolic state, the need to control intracranial pressure, and dysfunction of the pituitary axis hormones. As a result, both a condition known as "Syndrome of Inappropriate Secretion of Antidiuretic Hormone" (SIADH) (Webster, Bell, 1997) and hypothyroidism (Woolf et al., 1988) are often seen in TBI.

With polytrauma, the need for external airway and ventilation management and immune cellular dysfunction makes infection a likely complication in the majority of persons with severe TBI (Groswasser et al., 1990; Lanza et al., 1990; Quattrocci et al., 1991; Melossi et al., 1991). A hyperdynamic cardiovascular state may occur in more than 25 percent of persons with TBI. This condition can be aggravated by unrecognized blunt trauma to the chest and myocardium, which is common in individuals with severe TBI and polytrauma.

Coagulopathies, such as disseminated intravascular coagulation, frequently aggravate general management of the individuals with TBI and exacerbate CNS damage. Unrecognized extracerebral injuries, such as fractures (Sobus et al., 1993), peripheral nerve injuries (Stone, Keenan, 1988; Cosgrove et al., 1989), and secondary deep vein thrombosis (Stone, Keenan, 1992) may lead to unanticipated secondary disabilities from TBI (Stone et al., 1990).

The involvement of primary care providers in the acute phase of care for severe TBI is usually limited to the provision of information on any relevant medical history to the trauma team and perhaps to initial stabilization and transfer of the individual to a trauma center. However, primary care providers usually become responsible for providing and/or coordinating care for persons with TBI, once they return to the community. This is especially the case for persons with mild TBI, who do not require hospitalization. It is therefore important that primary care physicians recognize the many acute and long-term symptoms and complications common in even mild TBI (Browne, 1994). These include headaches, impaired memory, irritability, depression, anxiety, dizziness, hearing loss, insomnia, and fatigue (Jones et al., 1992; Englander et al., 1992; Rosenthal, 1993; Barrett et al., 1994).

Long-term Complications

People who survive a severe TBI face a variety of extra-cerebral medical complications that depend in part on their state of consciousness, ability to ambulate and care for themselves, and the kind of other injuries sustained (Grosswasser et al., 1990; Twyman, Bivins, 1986; Sazbon, Grosswasser, 1991).

Individuals who remain in a vegetative state following TBI may have medical problems associated with almost any organ system ranging from pressure sores of the skin to recurrent bladder infections, often ending with progressive multiple organ system failure (Fleischer et al., 1978; Bevilaqua, Fornaciari, 1975). Individuals who regain consciousness following TBI may have a variety of complications that are associated with the severity of the injury, the duration of impaired consciousness, and the duration of nutritional and ventilatory support received.

More than 50 percent of all people who regain consciousness after severe TBI report chronic pain (usually headaches) that requires some type of therapy (Beetar et al., 1996; Lahz, Bryant, 1996; Jensen et al., 1990; Uomoto, Esselman, 1993). Postural instability, both static and dynamic, may make ambulation, attention to visual tasks, and complex task integration of motor and cognitive functions difficult (Geurtz et al., 1996).

Chronic endocrine problems, usually thyroid or sexual hormone dysfunction, are common (Sandel et al., 1996; Fok et al., 1989; Kreutzer, Zasler, 1989). Sexual dysfunction is most often reported in male TBI survivors, with complaints of both lower sexual drive and erectile dysfunction associated with lowered testosterone levels (Kreutzer, Zasler, 1989; Su-Ching et al., 1994). Precocious puberty is a possible (although uncommon) consequence of TBI in children. However, when it occurs, it may alarm both parents and children (Sockalaski et al., 1987; Blendonohy, Philip, 1991). Fluid and electrolyte imbalance caused by SIADH may require lifelong monitoring in both children and adults following TBI (Anmuth et al., 1993; Webster, Bell, 1997; Fleischer et al., 1978), as may high blood pressure, because the incidence of chronic hypertension appears to be doubled in those surviving severe TBI (Labi, Horn, 1990).

Heterotopic ossification is more frequent in children with TBI than in the general population. It may affect up to 20 percent of all TBI survivors, even those without recognized fractures of long bones. The most common sites affected are the hip, shoulder, and elbow, resulting in pain, decreased mobility, and the potential for peripheral nerve dysfunction (Citta-Pietrolungo et al., 1992; Garland, 1988).

TBI survivors may experience gastroparesis once they progress to oral feeding. This is thought to be caused by vagal or other nerve dysfunction (Jackson, Davidoff, 1989; Altmayer et al., 1996; Haig et al., 1996). Chronic dysphagia is also common and may hamper rehabilitation efforts and the individual’s ability to maintain adequate calorie intake and ideal weight (Cherney, Halper, 1996).

Individuals with limited ambulatory ability are at increased risk of deep venous thrombosis and secondary pulmonary emboli (Baigelman, O’Brien, 1981). Prolonged and severe physical deconditioning may result in chronic dyspnea and tachycardia even with mild exercise (Becker et al., 1978).

Dysfunction of the immune system and impairment of the urinary and reproductive systems, such as neurogenic bowel and bladder problems, and decreased cough reflex can increase the risk for acute infections and sepsis.

Psychological complications after TBI are common, most often depression and posttraumatic stress disorder (Wroblewski et al., 1996; Jorge et al., 1993a). Alcohol and drug abuse are not uncommon after TBI. However, these problems are also common contributing factors to the initial injury, especially in young adult males (Corrigan, 1995; Kramer et al., 1993; Bombardier et al., 1997).

Chronic insomnia and sleep disturbances may last for years after TBI, aggravating the individual’s inability to cope with other