Review of the Literature


The Brain



Briefly, the brain is a soft mass with a custard-like consistency. The brain mass floats in a bath of cerebral spinal fluid and is shielded and held in place by membranes called meninges. The brain basically consists of nerve cells called neurons and supporting cells called glia. It has from 10 to 100 billion nerve cells and a far greater number of glia.

The cerebral cortex, a thin layer of nerve cell bodies, forms the one-quarter inch outermost part of the brain. At the center of the brain are four cerebrospinal fluid-filled spaces called ventricles. Other major parts of the brain include the brain stem, the cerebellum, and the cerebrum. The brain stem, which includes the midbrain, pons, and medulla oblongata, lies at the base of the brain and extends into the spinal cord. It is evolutionarily the oldest part of the brain and is responsible for such basic and vital functions as heartbeat, breathing, alertness, arousal, and basic orientation. The cerebellum sits on the back of the brain stem and coordinates smooth motor movements and balance. The cerebrum, evolutionarily the newest part of the brain, is responsible for higher intellectual functioning. It includes the telencephalon (gray cerebral cortex, subcortical white matter, and basal ganglia) and diencephalon (thalamus and hypothalamus).

The cerebrum is divided into two hemispheres, the left cerebral hemisphere and the right cerebral hemisphere. The two hemispheres are divided by a large groove (fissure). The hemispheres are connected by bundles of nerve fiber tracts (commissures), the largest of which is called the corpus callosum.

There are four lobes in each hemisphere: the frontal, temporal, occipital, and parietal. The frontal lobes are the most recently developed section of the cerebral cortex and perform many higher forms of abstract thinking and executive operations such as planning and organizing. The temporal lobes receive incoming auditory sensations. Deep within the temporal lobes are the hippocampus, important for memory encoding, and the limbic system, which deals with emotions and drives such as hunger, thirst, anger, fear, and sexual drives. Pieper (1991) reported that:

Because of rough bones at the skull base and the typical site of injury, the temporal and frontal lobes of the cortex are most vulnerable to injury. Damage to these cortical areas accounts for disturbance in behavior, affect, emotion, attention, and memory typifying traumatic brain injury. (p. 3)

The occipital lobes are responsible for many vision-related activities such as reception and analysis. The parietal lobes are involved with somatosensory and tactile functions and spatial abilities; for example, with one’s awareness of where one is in space and where body parts are in relationship to one another.

Many sections of the brain interrelate to perform functions. For example, areas responsible for memory processing include the medial temporal lobes, hippocampus, limbic system, thalamus, diencephalon, and basal forebrain (Bondy, 1994). According to Segalowitz (1983), older research indicated that language functions involved the Broca (expressive) and the Wernicke (receptive) areas and the interconnecting fibers between the two. But new research indicated more areas are involved (Bigler, 1988), especially in the temporal, parietal, and frontal lobes of the left hemisphere (Bondy, 1994).


Lateralization of function.

The left and right hemispheres of the brain do not have identical purposes. A division of functions exists between the two hemispheres which is called lateralization. For example, for 99% of right-handed and 70% of left-handed individuals the left hemisphere is strongly dominant for speech (Kalat, 1995). As a result, the left hemisphere has been called the dominant hemisphere because of its importance in language functioning. Both the Broca and Wernicke areas are on the left side of the brain. The left hemisphere controls motor activity on the right side of the body. Damage on the left side often may result in an acute emotional anxiety reaction called the catastrophic reaction (Lezak, 1976). Individuals injured on the left side are often more sensitive to their impairments.

The right hemisphere is more responsible for visual and spatial processes (deGroot, 1991; Kolb & Whishaw, 1990, Segalowitz, 1983). The right hemisphere controls motor movements on the left side of the body. It deals with unverbalizable patterns and whole forms and stores in a nonverbal, visual, spatial, auditory, or musical configuration (Lezak, 1976). The right hemisphere may underestimate or ignore damage. Persons with right-sided cortical involvement may make light of or even be unaware of their deficits (Lezak, 1976).

More evidence of lateralization of brain function was provided by Soderbock and Ekholm in 1992. They noted a relationship between lesions in the right hemisphere and disturbed activity in personal care, housework, gardening, and temporal adaptation. Lesions in the right hemisphere were more related to these disruptions than lesions in the left hemisphere. However, this study showed no significant difference in intellectual functioning between survivors with left brain lesions and survivors with right brain lesions. In the study, 188 survivors in three age groups answered a post-TBI questionnaire. The authors acknowledged some weaknesses with regard to validity and reliability in the use of a questionnaire, but concluded that, notwithstanding these problems, their research was consistent with earlier research.


Brain mapping research.

Current brain mapping research being conducted by various hospitals and universities should shed further light on the brain’s delegation of functions. Positron emission tomography (PET) scans in which blood flow levels are measured are now being used to identify correlations between function and anatomy in the brain. At the First International Conference on Functional Mapping of the Human Brain (held in Paris in June, 1995), the latest developments in the field were addressed. New databases to help discover structural and functional correlations of the brain were heralded. Examples of innovations included BrainMap and Brain Image Database (BRAID). BrainMap, being developed at the Research Imaging Center in San Antonio, Texas, is meant to serve as a community database of brain function neuroanatomic information (Fox, Lancaster, Davis, & Mikiten, 1995). Data regarding psychological and cognitive testing, neurological examination, and other patient variables are also being input on the database. Other brain mapping projects are also being conducted at universities such as the University of California at Los Angeles.


Traumatic Brain Injury


According to the National Head Injury Foundation (NHIF), the leading causes of traumatic brain injury are motor vehicle crashes, falls, violence, and sports and recreation accidents. Child abuse accounts for many injuries. An estimated 64% of head injuries among infants are caused by child abuse (Gelman, 1990). Most injuries in preschool years are caused by falls or abuse. Children under age 14 are most often injured in sports-related, pedestrian, and bicycle accidents. Persons over the age of 14 are most often injured in vehicular accidents (Waaland & Cockrell, 1990). Violent causes of TBI include gunshot wounds, stab wounds, and suicide attempts. Other injuries are the result of falling objects and agricultural and equestrian accidents (Colombani, Buck, Dudgeon, Miller, & Haller, 1985).

A generation ago most individuals who had sustained a severe head injury perished as a result of it, but in the 1990’s advances in medical treatment, such as the computed tomographic (CT) scans, the computerized axial tomographic (CAT) scan, and the magnetic resonance imaging (MRI) have brought the survival rate close to 90% (Gelman, 1990). These diagnostic tools allow doctors to look inside of the skull to discover the physiological nature, location and extent of brain injury. Other improvements in medical interventions such as intensive care management, intracranial pressure monitoring, and surgical intervention have also decreased the death rate (Farley, 1990). Although medical advances have reduced the mortality rate, the numbers of persons who have survived with some type of permanent cognitive, physical, or other impairment has increased dramatically.


The Neuropathologies of a Traumatic Brain Injury


Mechanism of injury.

TBI occurs when the brain mass is shaken and bounced around against the skull in a violent and unnatural way. A stationary head may be struck by an object, for example, a baseball bat or steel pipe. A moving head may strike an object such as a windshield or the cement pavement. Or a violent motion can occur without the head being struck, as happens with a whiplash or when a baby is shaken. In all of these scenarios, the brain will slam against the inside of the skull at the point of impact, causing damage. The brain will also bounce off the site opposite the impact, causing contrecoup damage. As the brain mass pulls, shakes, and rotates during the event, brain cells are stretched and often torn (Levin, Benton & Grossman, 1982). This type of injury is called diffuse injury because it occurs widely throughout the brain (Waaland & Cockrell, 1990; Lezak, 1983). As the brain rubs against the sharp, bony protrusions that make up part of the inner surface of the skull, further bleeding and contusions often occur (Mira & Siantz Tyler, 1991). 



Secondary damage and delayed brain injury.

Secondary damage may occur due to oxygen or blood deprivation, infection, raised intracranial pressure, or brain swelling (edema) (Mira & Siantz Tyler, 1991; Pang, 1985). A hemorrhage or the formation of a hematoma (a sac filled with blood) may also occur (Falvo, 1991).

The diagnosis of delayed brain injury is not uncommon. In 1993 Stein, Spettell, Young, and Ross reviewed a trauma hospital’s records for severe head trauma admissions. Three thousand were admitted for head trauma in a three year period (1986 to 1989). Nine-hundred-eighty were considered to have severe or moderate head injury. All received cranial CT scans at admission. Most recovered quickly, but 337 did not improve and required a second CT scan within 72 hours of admission. Where new lesions or an increase in lesions from the initial CT scan was found, a diagnosis of delayed brain injury was made. Forty-four and one-half percent (149 out of the 337) exhibited delayed cerebral injury. This diagnosis was most likely in patients who had the severest head injuries (acute subdural hematoma, coagulopathy, low Glasgow Coma scores), and other system injuries (major chest trauma, shock, cardiac arrest).


Posttraumatic amnesia.

Standard medical opinion requires that all head injuries producing a period of unconsciousness should be attended to by a physician, and a head injured person showing disorientation should be hospitalized. Unfortunately, this often is not the case. It is also not uncommon for a person to be oriented (aware as to time, surroundings, etc.) and free of focal signs shortly after a head injury. The person may not remember what occurred. Therefore, witnesses should make sure the person see a doctor. Patterson, Brown, Salassi-Scotter, and Middaugh (1992) addressed this issue with regard to children:

Many children experience posttraumatic amnesia, forgetting events immediately before and after the injury. After a blow to the head, the child may regain consciousness rapidly, complain of pain, and remember nothing about the incident. Upon arrival at the emergency department, the child of any age will know something has happened, but will be unable to describe it. The young child often cannot communicate feelings and fears surrounding the incident. (p. 23)


Minor, Moderate, and Severe Brain Injuries

The neurological pathologies of a brain injury trauma are varied depending on the severity of the trauma, other system involvement, and secondary factors. There may be a focal point of injury and/or diffuse injury throughout the brain. Certain areas may be badly damaged and other areas spared. Because of the wide variety of sequelae, traumas are now being broken down into different classifications.

Unfortunately, there is no one uniform system in place to gauge the severity of TBI (Mira & Siantz Tyler, 1991). This is a big problem because various studies define brain traumas in different ways, and therefore results can be difficult to interpret across studies. For example, a person having entered the hospital with a Glasgow Coma Scale (GCS) rating of 13 might be classified as having a moderate head trauma in some studies and a mild head trauma in other studies. The names of categories for brain trauma are not consistent: labels of minor and mild, severe and serious are used in different ways in different studies.

In addition, the symptoms in categories are not always consistent. Sometimes symptoms or ranges of symptoms are placed in different categories. For example, skull fractures that would be classified as severe in some studies are classified as moderate in others. This makes the interpretation or results inconsistent across studies.


Classification and terminology.

There are some frequently cited systems. For example, Klonoff, Low, and Clark (1977) divided TBI into minor, mild, moderate, severe, and serious classifications. A minor injury occurred when there was no evidence of concussion. Common bumps on the head may have been the result. A doctor often did not see this type of insult. A mild head injury arose if there were symptoms such as vomiting, lethargy, and/or lack of recall of the injury. There may or may not have been a brief loss of consciousness. Moderate injury occurred if there is a loss of consciousness for less than five minutes and/or evidence of a concussion. If there was a concussion or skull fracture and a loss of consciousness that lasted from five to thirty minutes, this indicated a severe injury. Finally, under this system a serious injury arose if the loss of consciousness was sustained for more than 30 minutes, there was a concussion or skull fracture, or there were other notable neurological sequela.

The Glasgow Coma Scale (GCS) is usually cited in the classification of brain injury severity. The GCS was initially developed by Teasdale and Jennet (1974) to measure the depth and duration of coma. The GCS is a thirteen point scale (3-15) which measures three categories of neurological responsiveness: eye opening, verbal responses, and motor responses. The GCS scale assesses admission brain injury as follows:

near fatal
moderately severe

Siegal, Gens, Mamantov, Geisler,
Goodarzi and MacKenzie (1991)

Rimel, Giordani, Barth, and Jane (1982) utilized the GCS as an indicator in their injury severity scale. Under this medical system a GCS of 13 to 15 with hospitalization for less than 48 hours and unconsciousness for less than 20 minutes was a minor trauma. A GCS of 9 to 12 (at six hours after admission) was a moderate trauma, and a GCS of 8 or less was a severe injury. In this and many other studies the term serious has been replaced with severe.

In some more recent studies, the term minor was replaced by mild. Englander, Hall, Stimpson and Chaffin (1992) assigned a mild traumatic brain injury (MTBI) classification to any person admitted to the hospital with a 13-15 GCS or a period of confusion or amnesia at any time postinjury. Jones, Viola, LaBan, Schynoll, and Krome (1992) assigned a MTBI to any one visiting the emergency room of a hospital with evidence of head trauma, a +12 GCS but a normal CAT scan study.

The use of concussion (from the Latin, concussio, meaning to shake violently) as a severity indicator for TBI is also common even though there is no universal agreement on how to use it in the grading of TBI severity. Concussion has been defined by the Committee of Head Injury Nomenclature of the Congress of Neurological Surgeons as “a clinical syndrome characterized by immediate and transient post-traumatic impairment of neural functions, such as alteration of consciousness, disturbance of vision, equilibrium, etc. due to brain stem involvement” (LeBlanc, 1994, p. 802). It is important to note that the definition does not require that a loss of consciousness have been sustained in order for a concussion to have occurred.

A clarification of the classifications, terminology, and symptoms in this field would greatly aid further research efforts. It is the intention of this researcher to utilize the mild, moderate, and severe classifications throughout this report.


Mild traumatic brain injury (MTBI).

A working definition for mild traumatic brain injury (MTBI) was provided by Kay (1986). MTBI is:

…trauma in which the head is struck, or moves violently, resulting in a transient alternation of consciousness, for which the patient is hospitalized for a relatively brief period of time (usually a few days, but often not at all) followed by discharge directly home with no prescription for formal rehabilitation (p. 2)

MTBI is sometimes overlooked because dramatic events, such as a coma, unconsciousness, or a hospital admission, may not occur (Pieper, 1991). Also CAT Scans, EEGs and MRIs may not show any neurological damage, because the injuries are so minute. However, significant neural damage can result from MTBI. This has been demonstrated by microscopic analysis of the tissues during autopsy (Kay, 1984).

MTBI can significantly reduce the capacity to process information rapidly (Gronwall & Wrightson, 1975). MTBI can produce significantly poorer memory performance (Hall & Bornstein, 1991). In the Jones et al. study, 21% of MTBI survivors were still reporting symptoms 2 to 6 months after their initial emergency room visit. Of the 14 individuals who were reporting residual symptoms, only 3 had been admitted to the hospital at the time of the MTBI. In the Englander study, 26% of individuals with MTBI continued to report problems 1 to 3 months postinjury. Eighty-eight percent had returned to work with symptoms, but returning to work after mild TBI is not unusual.

Blows to the head sustained in sporting contests can result in damage that would be classified as MTBI. It has been reported that 250,000 concussions and eight deaths occur yearly in the U.S. from football alone (Kelly, Nichols, Filley, Lillehei, Rubenstein, & Kleinschmidt-DeMasters, 1991). In a study of former professional soccer players, it was reported that almost all had signs of MTBI, such as intellectual and memory impairment (Tysvaer & Lochen, 1991). LeBlanc (1994) asserted that it was especially important to guard against second-impact syndrome in sports. In this syndrome, individuals who are symptomatic from concussion, even without loss of consciousness, are at risk for developing diffuse brain swelling after a second, even very minor, blow to the head. And second-impact syndrome can kill. LeBlanc provided guidelines regarding concussions during sporting contests.


Moderate traumatic brain injury.

Some studies have created a moderate head injury classification along the continuum between mild and severe head injuries. Whereas some medical studies utilize this classification, it is less common in educational studies.

In one study Rimel, Giordani, Barth, and Jane (1982) classified a group of people who had substantially worse outcomes than a minor TBI group as a moderate TBI group. In this study the researchers divided 1248 patients into three categories based on the GCS. They classified all persons with a GCS of 8 or less as having severe head injuries. Persons diagnosed with a GCS of 9 through 12 were classified in the study as having sustained a moderate head injury. Individuals who had received a GCS 13 to 15 in the hospital were placed in the minor head injury category. This study presented the findings regarding the moderate injury group. The moderate injury individuals were more likely to have sustained a skull fracture or to have undergone a surgical procedure such as craniotomy (e.g., to relieve brain hematoma) than the MTBI population. Three months after their injuries, 93% had persistent headaches and 90% had memory problems.

The group was also rated on the Glasgow Outcome Scale (GOS) (Jennett & Bond, 1975) three months postinjury. The GOS is a four-level medical outcome scale. The basic categories of the scale are persistent vegetative state, severe disability, moderate disability, and good recovery. Only 38% had made a good recovery. Even within this group, only 4% were asymptomatic. Unlike reports about mild TBI survivors at three months postinjury, most (69%) of the moderate TBI group had not gone back to work. From this study it can be inferred that moderate TBI symptoms will be more severe and of longer duration than mild TBI. If this classification is to be acknowledged and utilized across domains, then even more precise symptomatology attributable to the category will need to be formulated.


Severe traumatic brain injury.

Englander et al. (1992) reported that 25% of all TBI resulted in death or severe neurological injury. Indicators of a severe or serious traumatic brain injury include hospital admission, a concussion or skull fracture, and a loss of consciousness. (Time frames for loss of consciousness often commence at over five, ten, or thirty minutes in this category.) Other indictors usually mentioned include coma, abnormal CT or MRI, focal neurological deficit, posttraumatic amnesia, and GCS 3 to 7, 8 or 9 (depending on the citing authority). More severe neurologic dysfunction occurs in patients with a neurologic dysfunction of GCS 8 or less, including spastic paraplegia and vegetative state. In some studies the term persistent vegetative state, indicating those who do not regain consciousness, has been replaced by the designation prolonged unawareness (Levin, 1992; Sazbon, 1991). A possibility is locked-in syndrome in which the survivor is alert in mind, but unable to interact or even blink. “Severe head injury may be accompanied by extensive neurologic and sensorimotor impairments ranging from seizures, sleep disorders and visual/hearing deficits to motor paresis or spasticity” (Waaland et al., 1994, p. 3). The more severe the head injury, the higher the mortality rate (Colombani, Buck, Dudgeon, Miller, and Haller, 1985).


The Stages of Recovery from a Brain Injury


In the area of recovery from TBI, there are several parallel systems in usage. The Rancho Los Amigos Rehabilitation Center Levels of Cognitive Functioning (RLAL) is an eight-stage protocol used by rehabilitators to monitor recovery from moderate or severe head injuries. The scale rates functional levels in areas of awareness, orientation, memory, social appropriateness, and independence.

According to Henry (1984), early recovery (RLAL 1-3) from severe head injury started at the end of a coma. Patients could be confused, disoriented, agitated, incoherent, and bizarre. Dysphasia (an impairment of receptive and expressive language) was reported to be common during this phase (Stern, Grosswasser, Alis, Geva, Hochberg, Stern, & Yardeni, 1985). On the other hand, motor functions and communication skills were reported to often be the first to improve (Mira & Siantz Tyler, 1991).

Another possibility during this stage is posttraumatic amnesia (PTA). The survivor may be unable to acquired or retain even the most fundamental information. The duration of PTA was shown to also have an impact on memory ability later (Geffen, Encel, & Forrester, 1991).

During middle recovery from severe head injury (RLAL 4-6), the survivor is capable of some responsiveness and interaction. Henry (1984) reported that during this phase the survivor moved from simple to more complex tasks and from passive to more active interaction. Schwartz-Cowlet and Stepanik (1989) catalogued other symptoms including disorganization, disorientation, disinhibition, agitation, and circumlocution (speaking in roundabout or indirect ways).

Cognitive and behavioral aspects are often the focus of the late recovery phase (RLAL 6-8). Stern et al. (1985) found cognitive and behavioral aspects to be slower to recover. Attention and memory (Levin, Benton, & Grossman, 1982) and language processing, word finding, judgment, reasoning, sequential outputs, and executive functions were also found to take longer to recover (Ylvisaker, 1986).

What is clear is that recovery from TBI is a long-term process. Jennet and Bond asserted in 1975 that most restoration of function will be determined within the first few months after TBI. More recent studies (Sbordone & Liter, 1995; Stern et al., 1985; Klonoff et al., 1977) have acknowledged that improvement can occur even after a period of years.

Sbordone, Liter, and Pettler-Jennings (1995) studied twenty individuals who had sustained severe closed head TBI (coma of at least six hours and PTA of at least 24 hours) at least five years earlier and an average of 10.3 years earlier. The main conclusion of the researchers was that individuals with severe head injuries were continuing to make significant improvements in functioning at least 10 years post-TBI. The results were based on retrospective observations of the TBI survivors and their significant others.

Thirty-two factors collapsed to fourteen categories were analyzed. Significant improvements were found over 1 to 5 years and 1 to 10.3 years post-TBI in the following categories: behavioral response to environment, cognitive functioning, language-communication, initiative-independence, motor-functioning, social-interpersonal, and work-leisure. No significant changes over time and/or low incidence were reported in the categories of epilepsy, legal problems, perceptual functioning (auditory and visual), psychotic behaviors (delusions, paranoia), school education (attendance), and substance abuse. Actually, substance abuse had declined over time. Improvements were also broken down by other time frames. For example, cognitive functioning, language-communication, motor functioning, and work-leisure were also reported to have improved between 1 and 2 years. Another finding of the study was that family involvement had declined over time. Although not enunciated by the study, the authors probably meant that many survivors’ needs for extensive care-giving by their families had declined over time.


Predictors Affecting TBI Outcome (Recovery)


According to a study by Levin, Benton, and Grossman (1982), “Outcome is the global term used to indicate the adequacy with which a patient’s life-style is resumed, including the efficiency with which he performs the activities of daily life” (p. 63). Research is currently focused on which variables have an impact on the outcome of a brain trauma. Some factors that have been addressed are severity of brain injury, existence of secondary injuries, age at time of injury, and level of education. Research has also asked whether scale measurements, such as the GCS and the PTA, are good predictors of outcome.

Waaland and Cockrell (1990) reported that measures of severity of injury, such as unresponsiveness, coma, and posttraumatic amnesia, correlated with degree of functional outcome. However, the exact relationship of these factors and cognitive outcome is not yet understood. Geffen, Encel, and Forrester (1991) studied 19 patients and found a connection between severity of injury and length of PTA. They concluded that the longer the PTA, the poorer the performance one month postrecovery from PTA on a test of memory function.

The existence of secondary injuries (organ or skeletal injury) in addition to the brain injury has been shown to have a deleterious effect on the brain injury itself (Siegal, et al., 1991). Additional system injuries of the heart; spine; liver; bowel; pelvis; and long, great vessels; and also femur fractures, were cited. In the Siegal et al. study of 1709 persons who had sustained documented brain injuries, the addition of an organic or skeletal injury to a brain injury increased the mortality rate, especially in the moderate brain injury category. Even femoral fractures increased the mortality rate. The survivors were analyzed one year postinjury. Eighty-seven percent of the isolated mild-to-moderate brain injury group were found to have no limitations on daily living or mobility. Only 42% of mild-to-moderate brain injury survivors with secondary injuries had no limitations on daily living or mobility.

In the Klonoff, Clark, and Klonoff (1993) study, long-term outcome from mild head injury in childhood was studied.  This was a 23-year follow-up on an older study. One hundred and seventy-five of 231 individuals in the earlier study were traced and, of these, 159 (a 91% response rate) participated in the 1993 study. The study concluded that severity of the head injury was the primary contributing factor to outcome. There was an absence of relationship between age, gender, and individual differences in disposition. IQ recorded in the post-acute phase was found to be a reliable indicator of long-term outcome.

Unconsciousness at the time of the injury was shown to have only limited predictive value and taking an EEG at the time of injury was shown to have no predictive value. CT and MRI’s were not available to factor into the original study results. In future longitudinal studies, CT and MR will certainly be assessed for their value as predictors of outcome. In conclusion, Klonoff et al. found that a composite model, taking into account many variables (neurologic, seizures, fractures, unconsciousness, etc.), best discriminated the long-term outcome of survivors.

Sbordone, Liter, and Pettler-Jennings 91995) also found that severity of TBI affected recovery. Their analysis demonstrated a relationship between duration of coma and problem severity. TBI survivors who had spent more time in coma were consistently rated by their significant others as having more severe problems regardless of time postinjury. In contrast to Klonoff et al, which found no relationship between age and outcome, Sbordone et al. found age at time of injury to be an important outcome factor. Their results showed that return to work was related to age at time of injury with age becoming a statistically significant factor at age 35.

Sbordone et al. also detected that one subgroup in their study did not show significant improvements over time. This group had sustained significant hypoxia (oxygen deprivation to the brain) at the time of injury. Further studies on the predictive value of a diagnosis of hypoxia need to be undertaken.

In the current study the medical records of the participants could not be accessed. However, there was still an interest in determining what factors indicated in the previous discussion affected the outcomes of this study’s participants. Therefore, for the purpose of this study, outcome was defined operationally as either working or not-working. The research question asked became, “How did known medical predictors of recovery, (e.g., length of unconsciousness) affect outcome as measured by work status?”


Evaluation of Capacity following TBI


Formal testing.

Many instruments are used to assess functional capacity post-TBI, such as the Halstead-Reitan Battery (HRB) and the Wechsler Intelligence Scales (WAIS-R and WISC-R). According to Brazil (1992), the HRB is a comprehensive assessment that recognizes the complexity of neurological dysfunction. It assesses attention, memory, language, visual spatial abilities, and perceptual-motor skills. But many tests do not do an accurate job of assessing TBI. Standard psychological or academic tests generally underestimate true cognitive deficits (Waaland & Cockrell, 1990). Intelligence (IQ) tests are “largely insensitive” to the subtler deficits of minor head injury and may fail to detect cognitive problems altogether (Kay, 1986). Tests may not be sensitive enough to detect late-state recovery deficits (Milton, 1988). IQ scores within normal range may only indicate what is retained of pre-TBI learned information (Mira & Siantz Tyler, 1991).

Sohlberg and Mateer (1989a) described how a formal neuropsychological test might not reflect a TBI survivor’s functional state. A survivor might score in the average range on such an assessment, they said, and yet be unable to complete such simple tasks as making a cup of tea or getting dressed. On the other hand, a survivor showing profound impairments on a standard measure might have been able to function safely in an independent living situation.

Formal tests may not show difficulty in processing new information or functioning in an unstructured atmosphere. IQ tests and other standardized tests utilize brief, structured tasks performed one at a time, whereas the ability of survivors to handle more than one tasks at a time or to juggle tasks is not measured (Kay, 1986). Another problem is that most of the formal and standardized tests have not been normed for the TBI population (Seiters & Jackson, 1986). Keeping these limitations in mind, the following are some of the test instruments currently used to assess survivors of TBI: (See also Appendix B.)


Brain damage in general

Halstead-Reitan Battery (HRB) (Reitan & Wolfson, 1993)
Mini Inventory of Right Brain Injury (MIRBI) (Pimental & Kingsbury, 1989)
Multidimensional Aptitude Battery (MAB) (D. N. Jackson, 1986)
Wechsler Intelligence Scales (WIS) (D. Wechsler 1955, 1981)
Woodcock-Johnson PsychoEducational Battery-Revied (WJ-R) (Woodcock & Johnson, 1989)



Boston Diagnostic Aphasia Examination (BDAE) (Goodglass & Kaplan, 1983a,b)
Five clinical scales on the Luria-Nebraska Neuropsychological Battery (LNNB)
Multilingual Aphasia Examination (MAE) (Benton & Hamsher, 1989)
Neurosensory Center Comprehensive Examination for Aphasia
(NCCEA) (Spreen & Benton, 19677)
Revised Token Test (RTT) (McNeil & Prescott, 1978)
Sklar Aphasia Scale (SAS) (Sklar, 1983)
Western Aphasia Battery (Kertesz, 1982)



New England Pantomime Tests (R. J. Duffy & Duffy, 1984)


Attention and orientation

Digit Span Forward and Backward
Good Samaritan Hospital Orientation Test (Sohlberg & Mateer, 1989)
Letter Cancellation and Scanning Tests
Luria-Nebraska Neuropsychological Battery (LNNB)
Paced Auditory Serial Addition Test (PASAT) (Gronwall, 1977;
Gronwall & Wrightson, 1974)
Symbol Digit Modalities Test (SDMT) (A. Smith, 1982)
Trail-Making Test of the HRB


Auditory processing

Seashore Rhythm Test of the HRB
Seashore Tonal Memory Test (Seashore et al., 1960)
Rhythm Test on the LNNB


Cognitive function

Cognitive Assessment Procedures (Center for Cognitive Rehabilitation, Sohlberg & Mateer, 1989)
Halstead-Reitan (HRB) Neuropsychological Battery
Wisconsin Cardsorting Test (Grant & Berg, 1948)


Concept formation

Abstraction subtest, Shipley Institute of Living Scale (Shipley, 1946; Zachary, 1986)
California Proverbs Test (CPT) (Delis, Kramer, Kaplan, 1983, 1987, no date)
California Verbal Learning Text: Adult Version (Delis, Kramer, Kaplan & Ober, 1987)
Modified Vygotsky Concept Formation Test (MVCFT) (P. L. Wang, 1984)



Developmental Test of Visual-Motor Integration (Beery VMI) (Beery& Buktenica, 1989)
Symmetry Drawing Test (Hanninen & Lindstrom, 1979)


Discourse language

The Test of Language Competence-Expanded Ed. (Wiig & Secord, 1989)


Executive function

Halstead Category Test (Halstead, 1947)
Porteus Maze Test (Porteus, 1959)
Tinkertoy Test (TTT) (Lezak, 1983)
Tower of London Puzzle (Shallice, 1982)



Benton Visual Retention Test (BVRT) (Benton, 1974; Sivan, 1992)
Luria-Nebraska Neuropsychological Battery (LNNB) Memory Scale
Logical Memory (LM-O, LM-R) (D. Wechsler, 1987)
Memory Assessment Scales (MAS) (J. M. Williams, 1991)
Recognition Memory Test (Goldman, Fristoe & Woodcock, 1974)
WAIS Digit Span subscale
Wechsler Memory Scale-Revised (WMS-R) (D. Wechsler, 1987)


Reading skills

Gates-MacGinitie Reading Tests, 2nd Ed. (MacGinitie, 1987)
National Adult Reading Test (NART) (H.E. Nelson, 1982)
Stroop Test (Talland, 1975)
Wide Range Achievement Test-Revised (WRAT-R) (Jastak & Wilkinson, 1984)
Woodcock-Johnson PsychoEducational Tests-Revised (WJ-R) (1989)
Woodcock Reading Mastery Tests



Spelling subtest of the Wide Range Achievement Test-Revised
(WRAT-R) (Jastak & Wilkinson, 1984)
John Hopkins University Dysgraphia Battery (Goodman & Caramazza, 1985)


Tactility and kinetics

Finger Tapping Test (FTT) (Halstead, 1947, Reitan & Wolfson, 1993)
Grooved Pegboard (Klove, 1963; Matthews & Klove, 1964)
Halstead-Reitan Battery (HRB)
Luria-Nebraska Neuropsychological Battery (LNNB)
Purdue Pegboard Test (Purdue Research Foundation, no date)


Verbal skills

Boston Naming Test (BNT) (E. F. Kaplan, Goodglass, & Weintraub, 1983)
Peabody Picture Vocabulary Test (PPVT_R) (Dunn & Dunn, 1981)
The Set Test (Isaacs & Kennie, 1973)


Visual skills

Copying figures
Recognizing a face
Reconstructing and copying simple puzzle


As in any testing situation, evaluation may be difficult due to many factors. Repeated examination using the same tests can be misleading due to practice effects. External and internal factors such as fatigue, depression, anxiety, distraction, noise, interruptions, faulty materials, lighting, and room temperature must also be taken into account. Many of these factors can particularly influence the performance of the survivor of TBI. Therefore, it is especially important to eliminate any negative external factors from the formal testing experience. 


Alternative evaluations.

In addition to formal testing, Sohlberg and Mateer (1989b) recommended that evaluations be made of the functional capabilities of the survivor of TBI in natural settings. They called this naturalistic functioning (p. 19) assessment. This involved assessing the survivor in a variety of structured and unstructured settings, utilizing interviews and questionnaires, and making actual observations of the survivor’s behaviors. They stated that there were some particular areas amenable to functional assessment. These matters included safety, response in emergencies, money management, community access, use of transportation, and meal planning capabilities. Neuropsychological assessments are also being used to describe functional impact on a person’s everyday behavior.

Milton (1988) applauded vocational assessments. An example of a vocational analysis for an employed person was to do a job analysis. This could include both an analysis of the job’s requirements (including a task analysis of each work assignment) and an analysis of the person’s performance on the job. Brazil (1992) advised that a TBI assessment be created that will include medical, psychological, vocational, and sociocultural perspectives.


Neuropsychological assessment.

Neuropsychology is the study of the brain and the behaviors that result from normal and altered brain function. A neuropsychologist is a psychologist who specializes in brain behavior relationships. Neuropsychologists study the brain’s cognitive functioning. They also explore the relationship between brain anatomy and physiology and brain function, including neurotransmitters, biochemical, and bioelectrical factors (Pieper, 1991).

The neuropsychologist focuses on the ability of the client to learn and on the specific strengths and weaknesses of his or her brain function. The neuropsychologist will be versed in the nature of cognitive, executive, behavioral, and psychological deficits. Neuropsychologists can identify specific intact systems, areas of weakness, and compensatory strategies to overcome deficits (Schuyler, 1991).

Traditional psychological evaluations may not always identify brain trauma problems, especially for minor head injuries (Kay, 1986). Therefore, an evaluation by a neuropsychologist or a psychologist trained in neuropsychology is an important step in meeting the challenge of TBI. A neuropsychological assessment should be in-depth and systematic (Schuyler, 1991). Evaluations should be made in areas of cognitive functioning such as verbal comprehension and reasoning, memory and learning, visual and spatial domains, and problem solving. Assessments will also be made of tactile, auditory, and visual perception; motor abilities; and emotional functioning (Schuyler, 1991).

According to Bondy (1994): “A typical neuropsychological evaluation report contains information regarding the presence or absence of brain damage, data about the extent and severity of impairment, laterialization and localization information….” (p. 26). The report also contains an analysis of the survivor’s intact abilities, impaired systems, and the potentiality for using the preserved abilities to remediate, manage, and compensate for evident or likely problems (Pieper, 1991; Diller, 1987).

Patients who are released from the hospital a short time after their brain injury often have not received a neuropsychological evaluation. (Stern et al., 1985). It is essential that they receive such an assessment to advise, prepare, and inform them of acute or subtle cognitive and behavioral disabilities that may surface after they leave the hospital. Children who have been out of school due to a TBI should receive an assessment performed by a neuropsychologist that is made part of the school record.

Machine tests, such as CT scans, X-rays, or EKGs are not yet available to test cognitive function, but Cytowic, Stump, and Larned (1988) argued that pen and paper tests are as instructive as medical diagnostic tests. In their study of 178 nonhospitalized, closed head, TBI survivors they were able to characterize individuals as normal, symptomatic or impaired based on a medical and neuropsychological battery which included the following tests:

Computerized Tomography (CT) Scan
Goldmann Visual Perimetry
Beck Depression Scale
Halstead-Reitan Battery
Wechsler Adult Intelligence Scale-Revised
Wechsler Memory Scale
Aphasia Screening Test
Drawings on Command
Trail Making
Reitan-Klove Sensory Perceptual Exam
Form Board
Finger Tapping
Grip Dynamometry
Minnesota Multiphasic Personality Inventory (MMPI)

They argued that symptoms not verifiable by medical diagnostic tools were often ignored by medical professionals. “Patients are being denied treatment for want of an abnormal image” (p. 254). They made an impassioned plea for medical professionals to look to and accept psychological tests of patient symptomology.

This study sought to find out if survivors of traumatic brain injury were receiving the types of cognitive assessments documented in the above discussion. Survivors would not necessarily have a memory of specific assessments, or recall the names of particular assessment instruments (if they were ever told), but it was assumed that they would at least have some memory of psychological or neuropsychological testing. Since this type of testing is essential after a head trauma, the question became whether or not individuals were receiving such testing.  Hence, this study asked, “Were cognitive and other assessments (e. g., neuropsychological) performed to evaluate the traumatic brain injury?”


Deficits after Injury


Cognitive Deficits.

Cognitive impairments can be in the areas of attention, memory, concentration, problem-solving, initiating, organizing, sequencing, and conceptual thinking. (Waaland & Cockrell, 1990; Ewing-Cobbs & Fletcher, 1987).  Processing time may be slowed. Judgment, for example in the area of basic safety awareness, may be compromised. Cognition problems may also manifest as disorientation, confusion, forgetfulness, amnesias, dysphasia, perseveration, and distractibility (Whitman, 1991). Individuals may be unable to understand time concepts and/or estimate the passage of time (Seiters & Jackson, 1986).

In any kind of brain injury from mild to severe, the most common deficits are in the areas of impaired attention and memory (Gronwall, 1987).  When looking at attention, one asks how long, how well, and how selectively the survivor of TBI can attend (Henry, 1984). The survivor may not be able to screen out unimportant information or easily shift attention from one event, task, or person to another. Attention may be easily diverted. Melamed, Stern, Rahmani, Grosswasser, and Najenson (1985) have noted an attention capacity limitation. The deficit is that one cannot perform tasks that require simultaneous attention and response to two sources of stimulation. Pieper (1991) reported that concentration on and vigilance to the task at hand may also be impaired. Kolb and Whishaw (1990) emphasized that attention ability is required to activate higher cognitive areas such as memory, speech, and executive functions.

Attentional deficits are likely from lesions scattered throughout the brain and may or may not involve the frontal lobes (Gronwall, 1980). DeGroot (1991) reported that the areas of the brain involved in attention were all sites of sensory processing, the reticular formation, the thalamus, and the cortical association areas of the parietal and frontal lobes. In a key finding, Reid and Kelly (1993) stated: “Patients who are suffering from closed-head injuries may therefore ‘register’ information through attention-focusing components of perception, but not consolidate this information to memory storage” (p. 252). This is because the areas of the brain responsible for attending and memory are different.

Memory problems after head trauma can involve encoding (input), storage, consolidation, or retrieval problems (Kay, 1984). DeGroot (1991) described three stages of memory: immediate recall, short-term memory, and long-term memory. Kolb and Whishaw (1990) and other psychological literature distinguished between declarative and procedural memory (Bondy, 1994). Declarative memory involved the acquisition of learned facts and information by sensory organs and is dependent on an intact medial temporal region. Procedural memory was the ability to learn rule-based or automatic behavioral sequences (motor skills, conditioned responses). Sohlberg and Mateer (1989b) asserted that declarative memory is the type of memory more often impaired in TBI.

Reid and Kelly (1993) compared the memory performance of closed-head injury individuals and non-head injured controls and found that the closed-head injury population evidenced greater memory problems, especially in the area of the delayed-recall-of-information memory component.

Mateer and Sohlberg (1988) surveyed 178 TBI survivors and a non-injured control group (157) regarding the nature of their forgetting experiences. Their analysis yielded four separate memory factors. These were attentional memory or prospective memory, retrograde memory, anterograde memory, and historical or overlearned memory. Both groups reported the most forgetting experiences involved their prospective memory. Mateer and Sohlberg defined prospective memory as “the ability to remember to perform future actions” (p. 204). Examples were remembering to keep an appointment or return a phone call. They also suggested that individuals are more concerned with their ability to remember to perform future actions than their ability to recall using other types of memory.

For both the TBI and control group, historical or overlearned memory was the lease problematic. For controls and non-coma TBI survivors, anterograde (new memorizing) and retrograde (memories from before injury) problems were intermediate. For TBI survivors who had sustained coma (121 out of the 178), recalling anterograde memories was more difficult than recalling retrograde memories.

Similar to the declarative and procedural memories discussed by Mateer and Sohlberg were effortful and automatic memory processing related by Goldstein and Levin (1988), and Hasher and Zacks (1984, 1979). Under their model, the basic amount of information that can be processed and stored fluctuated. This process, called capacity, varied depending on factors such as age, intelligence, the difficulty of the data, and familiarity with the data. Encoding operations in memory could be effortful; for example, memorizing a telephone number or a name. These required deliberate strategies and were capacity-limited, and were a drain on the attentional system. Automatic processing, on the other hand, went on without active encoding and did not drain on the capacity system. Automatic processes included temporal and spatial order and frequency of events. As described by Goldstein and Levin, Hirst (1982) first speculated that more capacity was required by head injured persons to encode automatic data, thus leaving less capacity for effortful memorization.

Goldstein and Levin conducted a series of tests of TBI survivors and controls and found that the head-injured population had deficits in both effortful and automatic processing abilities. They found that severe TBI disrupted automatic basic encoding ability and active, effortful processing.

DeGroot (1991) reported that the hippocampus was involved in converting short-term memory (up to sixty minutes) to long-term memory (several days or more). Bilateral (both sides) destruction of the hippocampus or diencephalic midline resulted in anterograde amnesia, the failure to retain any new memories, but pre-destruction memories were retained.

Shimamura, Janowsky, and Squire (1991) reported that frontal lobe lesions were related to prospective memory deficits. They included in this category metamemory (knowledge about strategies one can employ to aid memory), source memory (how, where and when one acquired memory), short term memory, and free recall. Shimamura et al. also reported that anterograde learning was relatively controlled in individuals only displaying frontal lobe lesions.


Language Disturbances.

Dennis (1992) demonstrated that even mild injuries sometimes resulted in language impairments. Potential communication deficits cited by the Colorado State Department of Education (1991) included initiating, sustaining, discriminating information, processing verbal information, articulating, voicing sounds, sequencing, formulating ideas, and understanding and producing written and spoken communication.

The Colorado State Department of Education stated that the survivor could have a tendency to confabulate (to unintentionally fill in memory gaps with detailed accounts of fictitious events) or perseverate (spontaneous or uncontrolled repetition of words or phrases). Word retrieval (anomia) problems were common. The survivor might have had difficulty naming physical or mental objects or producing appropriate words in context. On the other hand, the survivor might have exhibited good communication and language skills on the surface, but have been unable to formulate in-depth, detailed, complex explanations. Dennis (1992) reported the possibility of problems understanding ambiguous words or getting the point of figurative expressions.

One specific language disorder is aphasia. Nonfluent (Broca’s or motor) aphasia is characterized by telegraphic, sparse, articulation (Bondy, 1994). Fluent (Wernicke’s or sensory) aphasia is characterized by semantic jargon. Speech will be grammatically correct, but will be nonsensical. Nonfluent (Broca’s) aphasia appears to be associated with the motor speech area of the frontal lobe and fluent (Wernicke’s) aphasia is associated with the sensory speech area of the temporal lobe (Davis, 1983). However, according to Schwartz-Cowlet and Stepanik (1989), aphasia was rarely a linguistic deficit of TBI. Levin, Benton and Grossman (1982) reported a 2% aphasia rate after blunt head injury.

Geschwind (1964) (as cited in Levin et al., 1982) reported subclinical aphasia or nonaphasic disorders of speech to be more common after closed head injury, especially in early stages of recovery. Confusion and memory disorder problems could interfere with language processing. Forms of nonaphasic disorder of speech included dysarthria, mutism, stuttering, and rarely, echolalia and palilalia. TBI survivors commonly had trouble with visual naming of familiar objects (Levin, Grossman, & Kelly, 1976).

Dennis and Barnes (1990) reported impairment of discourse language in some children and adolescents following closed head injury. Successful production or comprehension of discourse was impeded in some way for 80% of their study participants well into the chronic state (postmedical recovery stage). Areas that presented problems for some included knowing alternative meanings of ambiguous words in context, understanding metaphors or figurative speech, making inferences from stereotyped social situations, and producing speech acts.

Although mainly associated with the left cerebral hemisphere, research has shown that right hemisphere postnatal lesions also have an impact on verbal memory and language skills (Vargha-Khadem & Isaacs, 1985).  Segalowitz (1983) reported that right hemisphere damage may result in intonation of speech (pitch, loudness, emotional tone) problems, including a flattening of intonation. Right hemisphere damage could also result in an inability to properly interpret speech acts. With this disability, the survivor was less likely to choose the implication of a speech act and more likely to choose the literal meaning. For example, hearing the statement, “Where’s the salt?” the survivor might say, “It’s next to the plate,” instead of passing the salt to the requestor. Segalowitz also found that right hemisphere damage may result in the survivor’s inability to understand metaphors (example: loud tie, hard heart) and humor, drawing morals from a story, interpreting motivations and feelings of story characters, or utilizing imagery.

Joanette, Goulet, and Hannequin (1990) reported that some right-brain damaged survivors are impaired in their use of language in context (pragmatics), as evidenced by problems interpreting indirect speech acts, humor, and metaphors (sarcasm or irony).


Emotional and Behavioral Issues.

Behavior disorders were frequently reported and, behavioral problems, unlike cognitive deficits, tended to increase the first several years postinjury (Waaland & Cockrell, 1990). There was no typical pattern except perhaps inappropriate or uninhibited behavior after a severe injury. In early recovery stages agitation, confusion, impulsiveness, and noncompliance with treatment were frequently reported (Mira & Siantz Tyler, 1991). Other common behavioral sequelae were hyperactivity, impulsivity, and irritability. Emotional lability (instability) was often reported (Golden, Smith, & Golden, 1993; Waaland & Cockrell, 1990). The survivor could fluctuate between alertness and lethargy, euphoria and depression, aggression and passivity. Examples of poor impulse control included talking out of turn, interrupting others or interjecting nonrelevant information into conversations (Pieper, 1991).

Damage can be caused to centers of the brain which control impulses and emotions. Secondary social and emotional problems surface because of frustrations with and failures in dealing with the TBI. The TBI survivor may remember how he or she used to be able to do things, but now can’t function in the same way. The survivor may react with anger, withdrawal, or depression.

Pettersen (1991) reported that the survivor could also have problems perceiving, using, and evaluating social cues. Motivation and self-esteem could suffer. Golden, Smith, and Golden (1993) cited other problem areas which could surface, including inability to control behavior in social situations, substance abuse, and inability to control sexual inhibition.

Lezak and O’Brien (1988) found that emotional, psychosocial and personality disturbances were more disabling than cognitive and physical disabilities. Forty-two white male volunteers were surveyed. The sample consisted of 17 participants who were unconscious for less than two weeks and 25 participants who were unconscious more than two weeks. The researchers did not break down their results based on these two subsets, but they did state that more than one-third were still showing temperament and behavioral problems in the fifth year postinjury. Forty percent still reported anger problems in the fifth year. The only exception to this pattern were the members of the milder injury subset, a group of eight men in the study who at the time of their injury were unconscious fewer than 24 hours, if at all.

Interestingly, anxiety and depression levels had increased in the first 12 to 24 months postinjury and then improved in years 3 and 4. Lezak and O’Brien speculated that this probably reflected the participants’ realization of their situation and new limitations during months 12 to 24. They concurred with Prigatano (1986) that many survivors initially underestimated their deficits. Often they attempted to return to work and other previous activities too soon. They became frustrated and were unable to cope. They then tended to withdraw to a safer environment. Often this led to social isolation and diminished social contacts. Indeed, this scenario was playing out in many of the study participants as long as five years postinjury.

Levin, Benton, and Grossman (1982) also reported a reduction in social contacts and a withdrawal to isolated activities for many TBI survivors. Disruptions of marriage, a decline in the number of close friends, a rise in loneliness, and disturbed social functioning also sometimes occurred after TBI. Gronwall speculated in 1976 that “residual impairment in capacity for information processing, particularly in situations with multiple speakers and conversations, might contribute to the social retreat in many patients” (p. 71).

Another possible outcome from brain trauma is posttraumatic stress disorder (PTSD). PTSD is characterized by recurrent nightmares, thoughts, or flashbacks about the traumatic event. Other sequelae such as phobic behavior, hypervigilance, or generalized apathy may occur. Figley, Scrignar, and Smith (1992) indicated that if these symptoms persisted more than one month, PTDS was indicated. The person who experienced the symptoms might also have persistently avoided stimuli associated with the traumatic event.

There is a debate raging in psychological circles as to whether or not PTSD can coexist with head trauma. According to Henry (1983) some authorities say that, if there was a loss of consciousness from the TBI, there can be no PTDS; and, if there was no loss of consciousness, PTSD may have occurred, but not TBI. This argument in and of itself is fallacious because TBI’s can occur in situations where consciousness is not lost. Henry (1983) posited that, even if consciousness is lost, PTSD and TBI can coexist.

Sbordone and Liter (1995) argued that PTSD and mild traumatic brain injury (MTBI) are mutually incompatible disorders. In their study of 70 individuals, they found that all PTSD sufferers gave an emotionally charged recollection of the stressing event and that all MTBI survivors had no recollection of the traumatic event. The study was based on self-report and subjective recollections of the participants. In the study 0% of the PTSD individuals reported a loss of consciousness or amnesia, but 85.7% of MTBI individuals reported loss of consciousness and 96.4% reported amnesia. All of the PTSD individuals were emotional or upset when recalling the events leading up to the trauma. MTBI individuals could not provide highly detailed memories of events leading up to the trauma and were not upset or anxious when discussing this information.

The study had some weaknesses. Apparently, the participants were already labeled as MTBI or PTSD prior to initiation of the study, but criteria was not indicated. If the criteria were the same as the study criteria, it could be concluded that the 100% or 0% conclusions were more reflective of proper labeling (based on their criteria of PTSD versus MTBI) of individuals than analysis of the conditions. In other words, anyone with an emotionally charged recollection of the events had been classified PTSD. This would not in and of itself eliminate MTBI as a diagnosis.

Nothing in the study was presented regarding the participants’ medical records, scans, etc. From these records one might have extrapolated whether the individuals involved had displayed any concussional symptoms at the time of injury which might have signified MTBI. In order to eliminate a concomitant diagnosis, at a minimum, one would have had to analyze the medical records from the time of injury to rule out any symptomology that was attributable to TBI or concussion. The authors made the assumption that anyone recalling the event in an emotional or anxious way had PTSD, but no MTBI. Other authors have not seen the two categories as mutually exclusive.

Another interesting slant on behavioral sequel is that of Persinger (1994). He reported that a sense of presence often accompanied head injury. The survivor sensed that he was now sharing his mind with another entity who spoke to him or put thoughts into his or her mind. His hypothesis was that this was an intrusion of awareness of the right hemispheric equivalent of the left hemispheric sense of self. Persinger posited that mild neuropsychological dysfunction in the prefrontal and temporoparietal lobes would account for the anomaly. He speculated that increased or decreased activity in one area led to a sensed presence. One side of the brain was intruding on or talking to the other side of the brain. A left side presence seemed to be associated with anxiety, fear, or apprehension. A right side presence was generally more pleasant, for example, voices attributed to angels or God.


Physical Impairments.

Symptoms of severe head injury may include extensive neurological and sensorimotor impairments. Acute stage disorders include thromboembolism, increased intracranial pressure, infection, and shock. Sleep disorders, visual and hearing problems, olfactory sensation problems, motor paresis, paralysis, seizures, and spasticity are also possible. Specific disorders include contractures, dysarthria, dysphagia, dyspraxia, hemiparesis, incontinence, and paresthesia. These terms are defined in the glossary.

Patterson, Brown, Salassi-Scotter, and Middaugh (1992) and Flint (1988) reported on cranial nerve damage. Cranial nerve I (olfactory) damage can result in a loss of smell. Cranial nerve II (vision) damage can result in a loss of sight or blurry vision. Cranial nerve III damage (oculomotor) can result in impairments of eye movement (squinting or a fixed dilated pupil). Cranial nerve VII (facial) damage can lead to partial facial paralysis or paresis. Damage to Cranial nerve VIII (auditory) can lead to balance disturbances or hearing loss.

More specific vision problems include double vision, failure to compensate for reduced visual acuity, and visual field neglect (physical vision is adequate, but the survivor ignores objects in the visual field) (Seiters & Jackson, 1986). Survivors may be totally unaware of one part of their environment (one-sided neglect). Hemi-Spatial Neglect Syndrome refers to the loss of awareness of one side of the environment or of one side of the body (Segalowitz, 1983).

Apraxia involves disturbances in the coordination of movements. For example, dressing apraxia is diagnosed if the TBI survivor (who does not appear clumsy in other respects) can’t orient and place clothing appropriately on his body (Segalowitz, 1983).

Seizures are sustained by about 5% of all children who have a TBI (Mira & Tyler, 1991). This figure is substantially higher for those who sustain a severe TBI. The seizure activity may begin immediately after injury or as long as a year later. For this reason in the past doctors often automatically placed survivors of a severe TBI on anticonvulsant medication (phenytoin) for one year. Recent findings (Levin, 1992) showed that such medication adversely affected the cognitive performance of severely-injured patients one month postinjury. There was also a greater improvement in cognitive function after the year on seizure medication had ended for the formerly medicated group over the placebo group. Since seizure medicine is required by some individuals, but does show adverse cognitive effects, determining who is most at risk to sustain a seizure is an important research question. A research study on the issue has just begun at the Santa Clara Valley Medical Center in California, (G. Moreci, personal communication, April 24, 1995) and should shed light on the issue in several years, when the results are reported.

DeGroot (1991) explained that temporal lobe epilepsy, a particular kind of seizure activity, sometimes arose after brain trauma. “The temporal lobe (especially the hippocampus and the amygdala) has a lower threshold for epileptic seizure activity than do the other cortical areas. These seizures, called psychomotor (temporal lobe) seizures, differ from the Jacksonian seizures that originate in or near the motor cortex” (p. 191). He hypothesized that the temporal lobe seizures may be triggered by glial scar formation to the temporal lobe(s) after a brain trauma. Temporal lobe epilepsy, also called uncinate fit, may be characterized by abnormal sensation, repeated involuntary movements, such as chewing, swallowing, lip smacking, hallucinations, and temporary loss of consciousness, memory, and recall.


Executive Dysfunction.

In 1983 Lezak reported on survivor problems in such areas as planning, organizing, and judgment. Luria had also pioneered discussion of this area in the 1940’s. Ylvisaker and Szekeres (1989) created a conceptual framework in which to group these interrelated mental functions. These skills, all necessary to formulate and carry out goals, were part of the executive system. The system also included such functions as goal-setting and initiating. A key concept was that it was a self-engendered system. Self-direction, inhibition, monitoring, evaluation, and correction were all important components of this framework. When survivors had problems in these areas, it was called an executive disorder.

Executive disorder can involve cognitive, behavioral, and emotional issues. Survivors may engender goals, but be unable to take the steps necessary to reach them. They may be unable to formulate the steps to reach the goal, organize, or follow through (Pieper, 1991).

Survivors may have little knowledge of their own strengths and weaknesses. They may be cognitively unable to sequence tasks or to think flexibly and creatively. Initiating spontaneous activity may be difficult. Survivors may not be able to self-question or accept feedback (Sohlberg & Mateer, 1989b). Individuals may also display poor self-awareness, which interferes with planning and initiating (Prigatano, 1991).

Behavioral impairments such as the demonstration of socially inappropriate behavior may also be described as deficits in the executive system because the self-inhibiting, monitoring, and correcting functions are not operating.

Impaired executive functions are usually associated with frontal and temporal lobe damage (Luria, 1973), especially the orbital region of the prefrontal lobe areas. They are also associated with damage to the subcortical limbic system (Lezak, 1983). Frontal and temporal brain injury are very common sequelae of mild, moderate, and severe brain injuries.


PostConcussion Syndrome.

PostConcussion Syndrome (PCS) refers to a collection of symptoms which may present weeks or months after a mild to moderate head injury (Long & Williams, 1988). PostConcussional symptoms were reported in 40 to 60% of all head injury patients (Long & Williams, 1988). The collection of symptoms included headache, visual problems, dizziness, attention and concentration difficulties, fatigue, irritability, language disturbances, tinnitus, depression, social isolation, sleep disturbances, and alcohol intolerance. In other words, the symptoms were quite wide-ranging. PCS was most likely in impaired individuals who attempted to resume their pre-injury life style and duties. Apparently, their already impaired systems were taxed beyond limits by an attempted resumption of pre-injury level of functioning (Gronwall & Wrightson, 1975).

Cytowic, Stump, and Larned (1988) reported the following symptoms when identifying one particular type of PostConcussional patient:

These patients are most distinct. They prefer dark, quiet isolation as if overloaded by sensory stimuli. They startle at environmental sounds, such as television, closing doors, clanking dishes, or shouting children, complain that the radio or television is too loud, frequently find more than one person talking at a time unpleasant and sometimes confusing, are astonished at the uncharacteristic ease and lability of their temper, and abhor sexual relations. Quite a few wore sunglasses. The sonophobia was unassuaged by most medications; relief was sometimes obtained with industrial earplugs. (p. 231)

In the past, PostConcussion Syndrome was considered by some authorities to be an emotional reaction (Levin et al., 1982). However, more authors are seeing it as an organically-based disorder. For example, Waddell and Gronwall’s 1984 study of minor closed-head-injury patients did not support a psychogenic explanation of PCS. For example, Waddell and Gronwall’s 1984 study of minor closed-head-injury patients did not support a psychogenic explanation of PCS. Their study demonstrated that the patients were more hypersensitive to light than controls and tolerated less sound intensity than controls. Light tolerance was measured using a floodlight luminance condition. Sound tolerance was ascertained using a pure tone audiometer. Intensities were gradually increased using an incremental step system until the stimulus became uncomfortable for the participant at which time he signaled for cessation. A peripheral finding was that the patients’ own estimations of their light and sound sensitivity did not significantly relate to the objective measurement. Some individuals had underestimated their sensitivity to light or noise. None of the individuals had sustained a skull fracture, PTA for more than one hour, or loss of consciousness for more than a few minutes.

Even Posttraumatic Neurosis, a more severe disorder than PostConcussion Syndrome, although considered to be an emotional reaction, is being looked at as an organic condition caused by changes in the nervous system (Long & Williams, 1988). Posttraumatic Neurosis occurs when individuals who are unable to meet the demands of their environment take a cautious, defensive posture to cope with it.

One purpose of the current study was to explore some of the cognitive, emotional, behavioral, physical, executive, and perceptual motor deficits resulting from TBI. In an attempted replication of the above-listed study results, the current study asked general questions regarding deficits of the survey participants to record whether or not their symptomology was consistent with earlier reported findings.


Emotional Reactions to Traumatic Brain Injury


Waaland and Cockrell reported in 1990 that personality changes, impairments and dependencies created by the TBI were difficult for both the survivor and the family. The initial reaction was usually one of shock, followed by grief. Survivors and their families often went through a stage in which they were hopeful and overly optimistic that everything would be just fine. When problems continued to exist or arise, this was replaced by anxiety, guilt, depression, and even embarrassment. Withdrawal and anger were also possible. Frustrated survivors often developed avoiding and isolating strategies.

The reported findings tended to focus on the survivors’ emotional reactions after TBI. The present study addressed survivors’ feelings at the time of injury about the TBI itself. To see what kind of emotional adjustment had been made later, even many years later, this study also addressed a second issue as to the kinds of emotions and feelings currently reported by survivors about TBI.

A corollary to emotional response and adjustment is emotional support. Research data in which survivors rated potential providers of emotional support was not found. Finding out what sources of support have been available and most supportive to survivors to deal with the emotional problems subsequent to a head injury appears to be a valid research issue. Consequently, in this research study the following question was also posed: “How did survivors rate providers of emotional support?”


Rehabilitative Issues


Rehabilitative placements.

The aftermath of a severe TBI is often the requirement that a survivor spend some time in a rehabilitation setting. There are acute rehabilitation activities commencing even in the intensive care or general unit of a hospital. When ready, an individual will then move to an acute rehabilitation center within the hospital or a residential rehabilitation program. The next transition is to an outpatient rehabilitation program. There are hundreds of rehabilitation facilities in the United States. Whitman (1991) wrote that a good rehabilitation program will provide sophisticated, interdisciplinary care in the health, physical, cognitive, behavioral, and psychosocial domains. Prigatano et al. (1986) saw the need to design affective programs that would be able to cope with both depressed, unmotivated TBI survivors and paranoid or temperamental TBI survivors.

Henry (1983) stated that, whereas rehabilitative research previously stressed diagnostic considerations, there has been a shift now to improving treatment models. The emphasis on late-term treatment is shifting to a functional standard. Whitman recommended that treatment tasks seen in the rehabilitation environment be relevant to the real world. The desired and model outcome is that the performances achieved by the survivor in the rehabilitation center can be replicated and maintained in the outside world.

In one study (Lam, Priddy, & Johnson, 1991), the average stay in a rehabilitation facility was found to be six months. Another study touted the usefulness of outpatient rehabilitation centers, and recommended that the therapeutic process for severe TBI routinely be extended to three to four years (Stern et al., 1985). Further longitudinal studies regarding the necessity for long-term rehabilitative placements are warranted.


Compensatory versus restorative rehabilitation.

Rehabilitators often see rehabilitation efforts in terms of restoration or compensation (Levin, 1992; Sohlberg & Mateer, 1989a, 1989b; Pieper, 1991; Goldstein, 1987). Restoration involves the retraining and enhancement of that which has been damaged. Restorative processes focus on what has been damaged and hope for a reorganization or restoration of cortical function. Compensation models identify and concentrate on activities that won’t be affected by the deficit areas. Compensation models circumvent the damaged systems. “Compensatory strategies require reliance on intact skills, division of tasks into steps, and use of external and internal cues” (Milton, 1988 p. 5). Well-known examples of compensation include the use of memory notebooks and spontaneous actions such as writing down information to be remembered (Sohlberg & Mateer, 1989a, 1989b).

Sohlberg & Mateer (1989a) recommended a two-pronged approach in which both compensation and restoration were employed. Pieper asked: “To retrain, remediate, compensate: is that the question?” (p.8). In her opinion, no. Don’t rely on one or the other. She recommended using whatever works.

Geffen et al. (1991) found that survivors of brain injury initially often manifested prolonged disorientation and were unable to acquired new information and retain it for twenty-four hours. They demonstrated that, after a severe brain trauma, the recovery of rudimentary memory went through progressive stages involving both registration and retrieval ability. They defined rudimentary memory as basic orientation to person (name, marital status, number of dependents, occupation), rough time of day, and place. They found that the survivors first regained their ability to recognize new information by prompt. Secondly, they regained their ability to recognize new information without prompt. Once they were able to utilize recognition skills they moved to a recovery of their ability to retrieve information. First they retrieved by cued recall. The final step was to be able to retrieve information by free recall.

Usually the first step to improving cognition was to improve attention and memory function (Prigatano, 1987; Sohlberg & Mateer, 1987). Gliskey and Schacter (1988) speculated that brain-injured individuals suffering from severe memory problems might be able to memorize domain-specific data using a system of vanishing cues. The assumption was that although the individuals had severe problems with declarative, conscious memory, they might be able to memorize procedurally using a method of vanishing cues. The study established that four amnesic individuals were able to acquire new facts even though they had no conscious recollection of learning the facts. The facts, 20 to 30 new vocabulary items, were learned utilizing the vanishing cues methodology. Gliskey and Schacter also reported that the participants’ learning was hyperspecific (utilizable only in the training situation) as opposed to generalizable. The individuals also learned the facts at a much slower rate than that of controls. Lastly, the learning was found to be durable over a 6 week period.

Mateer and Sohlberg (1988) stated that memory and attention must be addressed before other forms of higher thinking, such as problem solving and abstract thinking, might be rehabilitated. They found restorative-based computer programs to be ineffective in improving memory (1989b). They devised attention process training (APT), prospective memory process training (PROMPT), and memory notebook training as compensatory techniques in rehabilitation of attention and memory (1989a, 1989b; 1988). Their preliminary research results have shown that these techniques assisted in compensating for attention and memory deficits (1989b).

Clearly several types of rehabilitation are available in theory. This study sought to determine what kinds of rehabilitation, if any, survivors are actually receiving. A related question was whether or not survivors were satisfied with the degree of coordination and cooperation which they perceived to exist between care-giving professionals and institutions.

Other studies also have not addressed the satisfaction level that survivors have had with the types of treatment and information that they have received. Measurement of consumer satisfaction for services provided is a legitimate concern in any business relationship. Therefore, the survivor participants were also asked how satisfied they were with the type of treatments they have received.


Resumption of Activities


Accommodations and modifications.

After a traumatic brain injury, survivors may require accommodations so that they may be able to resume function in society, at work, or at school. For example, in the school setting the Colorado State Department of Education (CDSE) (1991) reported utilizing accommodations such as reducing the length of the class day, altering the types of classes taken, and providing home schooling. Pieper (1991) found that using special materials such as computer software, logs, and audiotapes was useful in working with survivors of TBI. Modifications often seen in work settings include reducing work hours or assigning a job coach to the survivor.

Many modifications are mentioned as potentialities, but the question remains as to whether or not survivors of TBI are being afforded modifications upon their return to work or school. Consequently, a research question of this study was what kinds of modifications or accommodations, if any, were the survivors receiving at school and work?


Spontaneous accommodations.

Kay (1986) used the term spontaneous accommodation to describe what happens when the survivor of TBI has long-term cognitive impairments, but recognizes his or her deficits and lives in such a way as to get around it. The TBI survivor “spontaneously compensates for his deficits by making common sense changes in his environment” (p. 8). It appeared that an investigation of strategies and types of spontaneous accommodation would be worthy of further study.

Therefore, in the present study strategies utilized by survivors were identified. Survivors might find accommodations reported by others in a similar situation to be useful. For example, since executive dysfunction is a common problem for many survivors, it was hoped that they would gain comfort and inspiration from the report of self-initiated strategies employed by other survivors. Perhaps even professionals, studying rehabilitation in cognitive functioning and in other areas, might find certain strategies noteworthy of further investigation. Therefore, with the theoretical basis of spontaneous accommodation in mind, the final research question of this study was, “What devices did the survivors find to be most useful in coping with their TBI-engendered deficit areas?”

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