Incidence and Costs of TBI

TBI is the leading cause of death and disability among children and young adults in the United States (CDC, 1998). An estimated 56,000 lives are lost in the United States each year to TBI (Kraus and McArthur, 1996). Motor vehicle accidents, followed by injuries due to firearms and falls, are the leading causes of death from TBI (Sosin, Sniezek, and Waxweiler, 1995). Males are 3.4 times as likely as females to die of TBI (National Institute of Neurological Disorders and Stroke). About 50 percent of people who sustain TBI are intoxicated at the time of injury (Ruff, Marshall, Klauber, et al., 1990; Kreutzer, Doherty, Harris, et al., 1990).

In a recent analysis based on hospital discharge data and vital statistics, the annual incidence of TBI in the United States was estimated as 102.8 per 100,000 (CDC, 1997). Figure 1 shows TBI incidence rates by age group and sex. In males, the incidence peaks between the ages of 15 and 24 (248.3 per 100,000) and again above 75 years of age (243.4 per 100,000). The incidence in females peaks in the same age range, but the absolute rates are lower (101.6 and 154.9, respectively). These rates may underestimate the true incidence of head trauma because people with milder symptoms at the time of injury are usually not hospitalized.

Figure

Figure 1. Incidence of traumatic brain injury per 100,000 U.S. population. Source: MMWR - Morbidity and Mortality Weekly Report. 46(1):8-11, 1997 Jan 10.

About three-quarters of traumatic brain injuries that require hospitalization are nonfatal. Each year, about 80,000 survivors of TBI will incur some disability or require increased medical care (Kraus and Sorenson, 1994). From an economic viewpoint, the problem posed by survivors of TBI is how much to invest in their rehabilitation after it becomes clear they will survive. The type, intensity, and duration of rehabilitation services affect the total economic impact associated with TBI. For example, investing in rehabilitation services to help a survivor become independent or return to work may reduce the lifetime economic burden of illness. To date, no study has comprehensively examined the lifetime costs of TBI. As shown in Table 1, the total economic impact includes many types of costs besides direct medical costs. A starting point for estimating these costs would be information about the prevalence of chronic TBI in the general population, but such data are lacking.

Table

Table 1. Direct medical care and rehabilitation costs.

Although it is difficult to precisely quantify costs, useful information can be gleaned by studying charge data from published studies in various settings. The total cost of traumatic brain injuries in the United States is estimated to be $48.3 billion annually. Hospitalization accounts for an estimated $31.7 billion, whereas fatal brain injuries cost the Nation approximately $16.6 billion (Lewin, 1992).

In recent years, LOS and inpatient costs for rehabilitation have decreased. In the years 1988-1992, reports of average LOS for the initial admission for inpatient rehabilitation range from 40 to 165 days (Blackerby, 1990; Carey, Seibert, and Posavac, 1988; Giacino, Kezmarsky, DeLuca, et al., 1991; Mackay, Bernstein, Chapman, et al., 1992; McMordie and Barker, 1988; Rappaport, Herrero-Backe, Rappaport, et al., 1989). In one older multicenter study (the Model Systems study), the average rehabilitation length of stay (LOS) was 61 days, and the average charge was $64,648 exclusive of physician fees. Total charges averaged $154,256 (Lehmkulh, Hall, Mann, et al., 1993). In more recent studies performed in the early 1990s, rehabilitation LOS and charges were lower, ranging from 19 days and $24,000 for patients with milder injuries to 27 days and $38,000 for those with severe injuries (Cowen, Meythaler, DeVivo, et al., 1995). In the Medicare population in 1994, mean charges for patients admitted for brain injury (excluding stroke) were $42,056 (Chan, Koepsell, Deyo, et al., 1997).

Conceptual Model of the Lifetime Burden of Illness

To focus attention on important questions, we characterized the life of a person with TBI in terms of five phases, as presented in Figure 2. The first phase is "pre-injury." "Medical treatment" is divided into the acute (or immediate) treatment phase, and the intensive treatment phase, lasting days to weeks. The "rehabilitation" phase may last months to years. The "survivor" phase signifies the remaining life of the person with TBI and involves continual development and adjustment. This division into phases clarifies the three challenges to assessing the efficacy of rehabilitation discussed above. Patient populations are defined generally in terms of the phases, and interventions and outcomes must be specific to the phase being evaluated.

Figure

Figure 2. The career of a TBI survivor.

Mechanisms of Brain Injury

In TBI, the disease process begins at the moment of impact and extends thereafter for a protracted period of time. In strictly biological aspects, the brain injury disease process can be divided into primary and secondary insults. The primary insult initiates with the physical trauma to the brain. The secondary insults occur thereafter and, in many cases, are the primary determinants of outcome.

Beginning at impact and continuing for a generally brief period, primary insults to the brain include formation of intracranial hematomas (subdural or epidural), intracerebral hematoma, cerebral parenchymal contusions, cerebral swelling, and/or diffuse axonal injury. Intracranial hematomas such as subdurals and epidurals occur outside of the brain parenchyma and exert much of their pathological effects via increasing pressure on the brain (elevation of intracranial pressure [ICP]). Particularly with respect to epidural hematomas, if this pressure is avoided or rapidly reversed through expedient surgery, there may be no damage to the underlying brain and no residual effects of the hematoma. When there is a period of protracted intracranial hypertension, the ICP elevation may result in herniation of the brain tissue through orifices of the skull and/or cerebral ischemia due to interference with cerebral blood flow. Depending on magnitude and duration, such insults can produce deficits that vary from subtle to mortal.

Subdural hematomas also can cause significant intracranial hypertension and have a high likelihood of damaging underlying brain. This damage is often the primary determinant of long-term recovery.

Similar concerns about ICP are also relevant to cerebral swelling. Intracranial processes such as increased extracellular or intracellular fluid or elevated intracranial blood volume can raise ICP and impair adequate blood flow to the brain. In addition, some of these processes can cause primary cellular damage or ischemia by interfering with oxygen transport between vessels and cells.

Injuries such as intracerebral hematomas and cerebral contusions result in blood intermixed with brain. In the case of contusions, the pathology includes primary damage to neuronal cells. In both instances, the presence of blood within brain tissue appears to have significant toxic effects which can produce profound secondary insults to the injured tissue.

Diffuse axonal injury is a somewhat different disease entity. In this injury type, the physical forces the brain sustains during an injury characteristically consist of linear as well as angular acceleration or deceleration. These forces disrupt axons within the cerebral white matter, and these are called shear injuries. In this injury type, there may be no herniation or intracranial hypertension and, indeed, computer tomographic (CT) studies often may be normal or remarkably benign in appearance. Unfortunately, the widespread damage to the white matter will produce a recovery that is characteristically slow and incomplete.

Primary brain injuries occur at the time of injury and, by definition, must be treated post hoc. Secondary brain injuries are initiated sometime after injury and are often due to systemic factors. Their generally delayed onset allows them to be treated when they occur and also to be forestalled. This aspect of prevention has stimulated many of our trauma protocols and drives significant ongoing pharmaceutical research efforts.

The best known and possibly most devastating secondary brain insult is that of cerebral ischemia due to systemic hypotension. Systemic hypotension is extremely common, occurring in about one-third of patients with TBI during the period of injury through the end of resuscitation. A single hypotensive episode is associated with a doubling of mortality (Chesnut, Marshall, Klauber et al., 1993). Systemic hypotension illustrates the profound influence secondary brain insults can have on recovery and strongly supports the potential benefits of optimal trauma care.

Secondary brain insults may be due to intracranial processes that are initiated by:

1. Primary brain injury.
2. Secondary systemic insults such as hypoxia or hypotension.
3. Injuries to extracranial organ systems.
4. Systemic complications directly or indirectly related to the initial traumatic incident.

Secondary brain insults arising from the initial trauma include a number of toxic cellular and subcellular biologic processes, including:

1. Cerebral edema.
2. Alterations in intracranial ionic homeostasis (e.g., calcium, chloride).
3. Free radical formation.
4. Alterations at the molecular biology level.

These processes may result in ongoing and self-perpetuating brain injury. Cerebral edema will interfere with transport of nutrients, oxygen, and waste products and cause injuries to cells surrounding the area of primary injury as well as impair the healing of the initially damaged cells. Alterations in ionic homeostasis will disrupt the transmission properties of the neuronal and neighboring cells. Free radical formation can initiate a self-perpetuating cascade of toxic elements that may damage cells initially untouched by the injury. Finally, alterations at the molecular biology level will interfere with the primary genetic cellular control processes.

Secondary brain insults due to hypoxia or hypotension have become very well recognized over the past two decades and are a primary target of resuscitation protocols. The magnitude of importance of these insults is illustrated by the data on hypotension. Because we now have several tools to effectively recognize and treat such insults that are so devastating, intense interest is currently focused on managing them. Secondary insults also may occur from systemic trauma to extracranial organ systems. Although much of the influence of such extracranial trauma is mediated through hypoxia or hypotension, some aspects are unique to the individual organ system. For instance, long bone fractures may produce fat emboli to cerebral vessels that interfere with cerebral circulation. Alterations in timing and techniques of managing such fractures may improve cerebral outcome by decreasing the risk of embolism.

Finally, cerebral injury can be influenced by systemic complications occurring during the acute phase of management. The most well established of these complications as determinants of outcome include hypotension, pneumonia, sepsis, and coagulopathy. The importance of such factors in determining outcome supports the necessity of excellent critical care in managing patients with TBI.

The biologic aspects of repair or recovery are of primary importance during the early postinjury period, while the cognitive, psychological, and behavioral issues become increasingly predominant over time. The primary processes involved in biologic neuronal recovery are (1) reparative and (2) adaptive or plastic processes. Scientists believe that, except under extremely unusual circumstances, new neurons are not formed in the mature human brain, and thus when a neuron dies, its contribution to brain function is irreparably lost. Since neuronal death apparently can be induced not only by direct trauma but also by traumatic activation of inherent biological processes of programmed cell death (apoptosis), the question of cessation or reversal of such processes is an active focus of research.

Neurons have somewhat limited capabilities of self-repair, but the physiologic underpinnings of this regeneration are not completely understood. Although some clinical evidence suggests that neuronal repair can be facilitated pharmacologically in the injured spinal cord, no clinical evidence suggests that we can favorably influence such processes in the brain.

Research in animals suggests that there are critical periods during recovery wherein interventions may be particularly beneficial. The existence of similar periods has been postulated for the injured human brain, both for biological and behavioral interventions. To date, however, no clinical evidence supports the existence of such critical periods in the human.

Another biologic recovery mechanism is adaptation. In a biologic sense, this involves the formation of new circuitry to replace that lost from trauma. There is a great deal of plasticity in the nervous system, some of which continues throughout the organism's life--for example, learning of new information. At the more macroscopic level of altering neuronal circuits to directly replace those lost, however, abilities seem to be significantly limited in the adult human brain. In the immature nervous system, such plasticity is commonplace. A primary example is the alteration of laterality of language function resulting from very early injury to the left cerebral hemisphere. Unfortunately, the ability to make adaptations of such magnitude is lost early in life and the degree to which plasticity of lesser magnitude persists or can be induced in a more mature brain remains unclear. The question of such plasticity is fundamental to the concept of restorative cognitive therapy as well as to the concept of critical periods.

Memory

Brain injury can cause deficits in memory that range from mild, intermittent forgetfulness to profound inability to recall anything from the past or to integrate new information. Cognitive scientists and clinicians have made distinctions in mechanisms of memory that reflect modes of memory loss. Implicit memory records information that occurs nonconsciously; explicit memory is a function of active work such as repetition. Some brain injury depletes implicit memory but not explicit or vice versa. Semantic memory allows for understanding of the meaning of words; episodic memory records time- and place-specific experiences. Procedural memory is reflected in behavioral routines; declarative memory is reflected in the ability to explicitly report.

The burden of illness with respect to memory loss depends on the scope and degree of deficit and is also context-specific. For example, loss of procedural memory may result in devastating occupational consequences to a person whose work tasks are routine. However, if that is the only affected mechanism, other intact modes of memory may substitute for the deficit, and the person may be able to learn a new skill and regain independence.

The inability to integrate new information can result in global loss of independence, especially when accompanied by intact premorbid memory. The individual clearly remembers profession, life circumstances, and family from before the injury but nothing thereafter. Because they do not remember, they do not know that they do not remember, which leads them to insist on a daily and sometimes hourly basis that they are who they used to be. A reminder of the injury may last a minute or a day but will fade with other postmorbid information. These people cannot work, and the burden of their illness is evidenced in the consequences to family and caregivers.

Mobility and Independence

Limitations in mobility and independence may result in the inability to drive or ride a bus, work and earn a living, balance a checkbook, or prepare meals. Mobility also will be affected by physical impairment and independence by degree of memory deficit. The burden is also affected by the individual's social milieu. For example, for one person the presence of family to facilitate mobility may mediate the impact of the trauma; for someone else, dependence on family may be abhorred and may compound the burden of illness.

Organization and Productivity

Many survivors of brain injury exhibit an obsession for orderliness. Some are capable of servicing the obsession to varying degrees. For example, one person's home may be cluttered and disorganized, with one room (a computer room or tool shop) in meticulous order. The burden of illness can be observed in the amount of time and energy devoted to the orderly space and the confusion and lack of productivity experienced in the disorderly environments. Often, on a daily basis, a person never disconnects from the obsessional tasks in order to engage in other productive activities.

Physical Limitations

Physical deficits include difficulty with ambulation, hearing, vision, speaking, fatigue, and use of the hands. Such deficits may result from injuries sustained at the same time as, but distinct from, the head injury, or they may result directly from brain and spinal column nerve damage.

Inappropriate Behavior

People with traumatic brain injury often lose the ability to monitor and control behavior (Lezak, 1995). They may say whatever comes to their minds, even at inappropriate times. They may misunderstand the meaning of a situation or conversation and respond according to their misunderstanding. This problem can have profound effects on a person's life, resulting in loss of work, friends, and family.

Practice Settings

The following are practice settings. Although they are presented separately here, they often overlap to varying degrees.

• (Coma) treatment centers--A small number of people with head injuries will remain in a minimally responsive state for months or longer after injury. A few centers will accept such individuals once they are medically stable and attempt to achieve improvement by the use of various stimulation techniques. Skilled nursing care and physical therapy are also important elements of these programs.
• Acute rehabilitation programs are prepared to treat patients as soon as they are medically stable and are discharged from the acute hospital. Most of these are located in rehabilitation hospitals. Their primary emphasis is to provide intensive physical and mental restorative services in the early months after injury. Many will have specialized head injury units with an interdisciplinary team composed of physicians, nurses, speech and occupational therapists, and neuropsychologists. These programs are relatively short term, but longer stays may occur.
• Long-term rehabilitation programs provide extended rehabilitation and management services. They may provide a full range of rehabilitation services for the person with brain injury who is in need of a structured environment and is making slow improvements. Such programs generally are not for permanent placements, although they may have this service available. Usually a person may remain in the program as long as there continues to be some improvement.
• Transitional living programs--The goal of a transitional program is to prepare individuals for maximum independence, teach the skills necessary for community interaction, and work on prevocational and vocational training. Specialized programs stressing cognitive, memory, speech, and behavioral therapies are usually structured to the needs of the individual. Programs of this type are being established in a variety of settings--small group homes, special educational institutions--as part of a continuum of care in rehabilitation centers.
• Behavior management programs--Severe maladaptive or aggressive behavior will limit an individual's participation in most rehabilitation settings. While these programs treat the common behavioral problems following head injury, many of them cannot handle destructive behavior to self or others (e.g., sexual aggression).
• Day treatment programs are nonresidential facilities that emphasize services to upgrade functional skills. These services are similar to those described above under transitional living programs. Some offer day-care (supervision) services for those unable to benefit from an active program.
• Extended intensive rehabilitation--the more seriously injured person may require extended therapies in a structured program that has all the elements found in the acute rehabilitation center. Emphasis will usually be on cognitive and memory retraining, speech therapy, activities of daily living (ADLs), restructuring lost social behaviors, and continuing physical therapy. Prevocational and vocational training, recreational therapy, and community reentry are usually part of each program. Patients will remain in these programs as long as progress is being made--usually 6 to 12 months.
• Late rehabilitation--After discharge from the acute rehabilitation center, many people with head injury will need extended rehabilitation either in a residential or inpatient setting or in an outpatient program. Admission requirements may vary and be defined by a specific time after head injury.
• Independent living programs (ILPs) are community-based services that assist people with severe disabilities living in their own homes to increase personal self-determination and independence. ILPs provide both direct and indirect services ranging from residential/transitional programs to resource referral.
• Life-long residential programs--For those individuals unable to live at home or independently, a residential program may be the only alternative. There are very few programs of this type specifically set up for people with head injuries. Some facilities that have had experience with other disabled populations are beginning to explore this possibility.
• The home--For some, the home environment provides the most productive setting for therapy. In addition to in-home nursing care, rehabilitation professionals may come to the client's home on a routine basis to conduct therapy sessions.
• TBI social clubs--Although not necessarily a setting for formal rehabilitation, social clubs provide an environment in which people with TBI can associate with each other, form friendships, and instruct each other in how to manage life with a disability.

Techniques

Therapies discussed here may be provided on an individual basis or in group settings.

• Physical therapy comprises treatment designed to restore normal physical function: walking, use of hands, use of arms, and so forth. A physiatrist may specify the course of treatment, integrating physical therapy with other programs.
• Therapeutic recreation focuses on resuming leisure activities, community skills, and social skills.
• Speech and language therapy--Language disruption is common with TBI and is specifically addressed in speech therapy. Speech therapy encompasses relearning appropriate methods of communication, verbal and nonverbal, as well as relearning communication of abstract thought.
• Cognitive therapy offers retraining in the ability to think, use judgment, and make decisions. The focus is on correcting deficits in memory, concentration and attention, perception, learning, planning, sequencing, and judgment. A neuropsychologist, aided by other specialists (for example, occupational therapists [OTs], speech and language pathologists [SLPs]) may be asked to evaluate the level and kind of cognitive dysfunction following TBI, and they may reassess the individual over time to measure recovery.
• Occupational therapy offers retraining to enable the person with TBI to cope with the routine demands of a work environment. Often the occupational tasks are at a level below that of preinjury status.
• Behavioral therapy involves modification of maladjusted, asocial, or socially inappropriate behaviors.
• Psychotherapy targets emotional issues, social adaptation, and self-awareness. Group psychotherapy is useful for feedback, support, and confrontation by peers. Family members may participate in therapy to help them cope with the stress of being a caregiver and to build their ability to provide appropriate in-home support.
• Social skills training may be provided as a separate program, or it may be integrated into any of the methods described above.

Pupils

The status of the pupils (an indicator of intracranial pressure or herniation) helps predict outcome (Marshall, Gautille, Klauber, et al., 1991).

Age

Age is usually (Jennett, Teasdale, Galbraith, et al., 1979; Vollmer, Torner, Jane, et al., 1991; Waxman, Sundine, and Young, 1991; Braakman, Gelpke, Habbema, et al., 1980; Choi, Narayan, Anderson, et al., 1988) but not always (Reeder, Rosenthal, Lichtenberg, et al., 1996) found to predict GOS and function (FIM) after rehabilitation. Age appears to be a primary predictor independent of age-related factors such as systemic illnesses (Vollmer, Torner, Jane, et al., 1991).

Systemic Hypotension

The presence of severe systemic injuries is also correlated with worse outcome (Bowers and Marshall, 1980; Klauber, Marshall, Luerssen, et al., 1989; Mayer, Walker, Shasha, et al., 1981). However, when systemic hypotension occurring during the period between injury and the end of resuscitation is controlled, the influence of systemic trauma drops out (Chesnut, Marshall, Klauber, et al., 1993). This suggests that the influence of injuries to extracranial organ systems on outcomes from TBI is primarily mediated by the associated hypotension.

Intracranial Computer Tomographic (CT) Diagnosis

It would seem logical that the location, extent, and severity of damage to the brain would be predictive of outcome from TBI. Although prediction studies have correlated outcome with various parameters consistent with severity of brain injury such as skull fracture, intracranial hematoma, or presence of surgical mass lesions (Bergman, Rockswold, Haines, et al., 1987; Braakman, Gelpke, Habbema, et al., 1980; Jennett, Teasdale, Galbraith, et al., 1979; Waxman, Sundine, and Young, 1991), no one has yet demonstrated the expected degree of anatomic specificity in predicting recovery or residual deficits. This may be largely a question of defining the extent of brain injury based on the rather limited technology of computed tomography and magnetic resonance imaging. To date, the Traumatic Coma Data Bank classification of the CT imaging of the brain during the acute-care course is the most promising method of incorporating the anatomical nature of the brain injury into a predictive model (Marshall, Bowers-Marshall, Klauber, et al., 1991).

Other Variables

Other variables that have been suggested as predictive of outcome, as measured by GOS, include mechanism of injury (Waxman, Sundine, and Young, 1991), brainstem reflexes (Born, Albert, Hans, et al., 1985), evoked potentials (Anderson, Bundlie, and Rockswold, 1984), cerebrospinal fluid (CSF) catecholamines (Woolf, Hamill, Lee, et al., 1987), degree and severity of intracranial hypertension (Alberico, Ward, Choi, et al., 1987; Jones, Andrews, Midgley, et al., 1994; Marmarou, Anderson, Ward, et al., 1991), jugular venous desaturation (Gopinath, Robertson, Contant, et al., 1994; Jones, Andrews, Midgley, et al., 1994; Robertson, Contant, Gokaslan, et al., 1992), cerebral perfusion pressure (Gopinath, Robertson, Contant, et al., 1994; Jones, Andrews, Midgley, et al., 1994; Robertson, Contant, Gokaslan, et al., 1992), fever (Jones, Andrews, Midgley, et al., 1994), and in-hospital hypotension (Chesnut, Marshall, Piek, et al., 1993; Jones, Andrews, Midgley, et al., 1994). The statistical independence of these various factors remains to be clearly delineated. It cannot be suggested at this time that they be included as potential injury severity confounding variables in rehabilitation studies. When planning such investigations, however, the present state of the literature must be assessed since some of these indexes, or variations thereof, may develop as mandated covariables.

Two other indexes, duration of PTA and coma, are frequently used in quasiexperimental studies to adjust for severity of injury. Both of these are determined at some time following the injury.

The use of PTA originated with Russell and colleagues in the 1930s (Russell, 1932; Russell, 1935; Russell, 1971; Russell and Nathan, 1946; Russell and Smith, 1961). Russell classified injuries with PTA < 5 minutes as very mild; 5 to 60 minutes as mild; 1 to 14 hours as moderate; > 24 hours as severe; > 1 week as very severe; and > 4 weeks as extremely severe. In a study of 1,766 patients, Russell and Smith (1961) found the duration of PTA to be the single best predictor of neurological outcome.

In many studies, PTA is measured retrospectively by reviewing patient charts. Unfortunately, retrospective PTA is unreliable (Gronwall and Wrightson, 1980). PTA is best determined prospectively using as an index the attainment of a criterion score (e.g., 85 percent) on the Galveston Orientation and Amnesia Test (GOAT) (Levin, O'Donnell, and Grossman, 1979).

It is difficult to reconcile PTA with the more commonly used GCS score as an index of TBI severity. Using a PTA of > 24 hours as their criterion for the diagnosis of severe TBI, Bishara and colleagues found that 81 percent of such patients attained a good outcome (GOS 4-5) at 1 year (Bishara, Partridge, Godfrey, et al., 1992). This contrasts with only 43 percent of patients achieving such an outcome in the Traumatic Coma Data Bank (TCDB), where severe head injury was defined as a postresuscitation GCS = 8 (Marshall, Gautille, Klauber, et al., 1991). Such a discrepancy suggests that these two indexes cannot be used interchangeably as they will be predictive of markedly different courses of recovery.

Duration of coma has been used to quantify the severity of brain injury and to predict outcome. Patients in coma for < 20 days frequently regain independence in functional activities, whereas those who remain in coma > 20 days are usually profoundly disabled (Jones, 1981; Pazzaglia, Frank, Frank, et al., 1975). Like the PTA, duration of coma is unreliable when determined retrospectively, and it is not interchangeable with the GCS score. In addition, its determination can be confounded by the use of medications which are commonly administered during treatment of TBI patients.

Average LOS in acute care after TBI has been used as a gross indicator of the "sickness" of the patient during the immediate, posttraumatic period. More recent studies have reported acute care stays ranging from 20 to 60 days (Lehmkulh, Hall, Mann, et al., 1993; Mackay, Bernstein, Chapman, et al., 1992; Sakata, Ostby, and Leung, 1991; Sparadeo and Gill, 1989). Unfortunately, this variable is sensitive to socioeconomic issues, which may be difficult to control when using it as an indicator of trauma severity.

The above considerations reveal that the prediction of outcome based on physiologic indicators of TBI remains in a state of active development. At present, a credible attempt to control for (or match on) severity of illness should include the five best physiologic indicators described above. Older studies frequently do not use these indicators, the importance of which was not clearly established until recently.

Even today, retrospective analyses are hampered by the lack of reliability and absence of the necessary data in patient charts. Properly approaching this problem in the future will require a coordinated effort in data collection beginning at admission and continuing through rehabilitation wherein common definitions are used throughout.