Self-knowledge of deficits and self-concept following severe closed head injury

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Self-knowledge of deficits and self-concept following severe closed head injury
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Self Concept   ( mesh )
Head Injuries, Closed   ( mesh )
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Thesis:
Thesis (Ph. D.)--University of Florida, 1995.
Bibliography:
Includes bibliographical references (leaves 190-206).
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by Russell R. Addeo.
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Typescript.
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Vita.

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SELF-KNOWLEDGE OF DEFICITS AND SELF-CONCEPT FOLLOWING SEVERE
CLOSED HEAD INJURY











By

RUSSELL R. ADDEO



















A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE
UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE
REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY


UNIVERSITY OF FLORIDA


1995













ACKNOWLEDGEMENTS

This project would not have been possible had it not been

for a large number of people generous enough to assist in my

efforts. I would like to thank my chairperson, Bruce Crosson,

Ph.D., for his consistent theoretical, editorial, and personal

support during this project. He provided an integrated model

of an astute and sensitive clinician combined with the skill,

rigor and clarity of an adept investigator. These qualities

and their integration are those that I seek to emulate. I

would also like to thank all of my other committee members

(Russell Bauer, Ph.D., Cynthia Beaulieu, Ph.D., Walter

Cunningham, Ph.D., Eileen Fennell, Ph.D., Anthony Greene,

Ph.D., Michael Crary, Ph.D.) for their time and thoughtful

conceptual, methodological, and statistical advice.

I would also like to thank the staff of Memorial

Rehabilitation Hospital (currently Genesis Rehabilitation

Hospital). The foremost acknowledgement should go to Cynthia

Beaulieu, Ph.D. Without her unfailing support and significant

investment of time in this study, it would not have been

completed. Her dedication to this project and in my

professional development are deeply appreciated. Special

thanks should go to the Occupational therapists who completed

the questionnaires and to the psychology staff who assisted in








the data collection. Those that also contributed their time

were Charles Schauer, Ph.D, and Travis White, Ph.D.

I would like to thank the staff of Transitions of Long

Island and Long Island Jewish Medical Center in New York. I

would like to specifically thank Deborah Benson, Ph.D., Jack

Rattock, Ph.D., and William Barr, Ph.D. for allowing access to

the patients. I would also like to thank the life skill

trainers for completing the questionnaires.

A project of this scope is not possible without the help

of loved ones. Therefore, I would like to thank Lisa

Barbarette and my family for their understanding and emotional

support during the course of this project.

Special thanks should go to the patients that were

willing to participate in this study. I admire their courage

and determination in the face of the many obstacles they

confront. I hope that this study will ultimately help them in

their struggle.









TABLE OF CONTENTS
page
ACKNOWLEDGEMENTS............................................ ii

ABSTRACT..... ........... .................................vii

INTRODUCTION.................................................. 1
Neuropathophysiological Mechanisms.......................2
Cognitive and Psychosocial Consequences of CHI............5

REVIEW OF THE LITERATURE.................................12
Awareness of Deficits After Brain Injury ................12
Psychological Denial...................................17
Awareness Deficits.................................. 19
Awareness Deficits Theories ...........................51
Summary................................................69

Self-Concept after Closed Head Injury ...................71
Self-Concept and Self-Esteem Defined..................74
The Dynamic Self-Concept ............................. 76

Self-Concept, Denial and Awareness Deficits..............79

Psychological Distress Following Closed Head Injury.....83

RATIONALE FOR THE STUDY ...................................87
Statement of Problem...................................87
Hypotheses .............................................93

METHODS ....................... .................. ..... 96
Subjects and Selection Criterion.......................96
Demographics .......................................... 98
Group Differences .................................... 100
Procedures............................................102
Measurement Instruments...............................103
Severity measures..................................103
Cognitive deficit measures ..........................106
Denial measures.....................................116
Comparative self-knowledge measures ................. 121
Self-concept/self-esteem measures...................125

Statistical Analyses................................ 128
Validity and Reliability of Cognitive Self-Concept.128
Path Analyses ...................................... 129

RESULTS. .................................................135
Group Differences......................................135
Validity and Reliability of Cognitive Self-Concept.....137
Path Analyses ..........................................139
Cognitive Self-Concept/Self-Esteem..................141
Social Self-Concept/Self-Esteem.....................143

iv








Physical Self-Concept/Self-Esteem .................... 146
Post-hoc Analyses. ............................. .....152

DISCUSSION...............................................158
Major Findings.......................................... 158
Limitations and Future Directions...................... 174
Implications for Rehabilitation .........................180

REFERENCES ................................ ............. 190

APPENDICES ............................................... 207
1 THE ADULT GENERAL SELF-CONCEPT INVENTORY........... 207
2 THE PATIENT COMPETENCY RATING SCALE................. 210
3 THE ROSENBERG SELF-ESTEEM SCALE .....................212








BIOGRAPHICAL SKETCH


Russell R. Addeo was born on November 26, 1962, in

Queens, New York. He obtained his Bachelors degree in

Psychology from Florida Atlantic University in May, 1989. He

entered the University of Florida in August, 1989, as a

graduate student in the Department of Clinical and Health

Psychology. He obtained his Masters degree in December, 1991.

His masters thesis investigated the construct validity of a

self-esteem measure. Following graduation in August, 1995, he

will be employed as a neuropsychologist at Genesis

Rehabilitation Hospital in Jacksonville, Florida.








Abstract of Dissertation Presented to the Graduate School of
the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Doctor of Philosophy

SELF-KNOWLEDGE OF DEFICITS AND SELF-CONCEPT FOLLOWING SEVERE
CLOSED HEAD INJURY

By

Russell R. Addeo

August, 1995

Chairperson: Bruce Crosson, Ph.D.
Major Department: Clinical and Health Psychology



People that suffer severe closed head injury (CHI)

demonstrate a number of deficits, such as unawareness of

deficits, denial, low self-esteem, and psychological distress,

which ultimately affects their ability to function during

rehabilitation and after discharge. Investigators suggest

that as patients become more aware of their deficits, self-

esteem decreases, and psychological distress increases. The

purpose of the current investigation is the experimental

analyses of some of these assumptions.

A path model is proposed which specifies the relationship

between cognitive deficits (CD) thought to underlie awareness

deficits, denial, comparative self-knowledge (CSK), current

and premorbid self-concept/self-esteem (SCSE), and

psychological distress. From this larger model the

experimental path analysis model investigated the relationship

between CD, denial, CSK and three different dimensions of SCSE

(cognitive, social and physical).


vii








Fifty-seven severe CHI patients undergoing rehabilitation

were studied. Hierarchical multiple regression was used to

calculate the path coefficients. Path analysis modeling was

utilized to test the model predictions. Results confirmed the

prediction that CSK would have a direct effect upon each of

the dimensions of the SCSE (cognitive, social, and physical;

path coefficients were -.49, -.34, and -.35, respectively).

Greater CSK resulted in lower SCSE. Also confirmed was the

prediction that CD would be unrelated to denial. The

predictions that CD and denial would have independent and

direct effects on CSK were not met. The results for the

social and physical SCSE were similar. There were significant

and direct effects from CSK to social and physical SCSE.

Therefore, increased knowledge of deficits is associated with

reduced perceptions of their social competence, physical

abilities and appearance. Analysis of the cognitive SCSE

model found that CSK and CD had direct effects upon cognitive

SCSE, with possibly additive or opposing influences. This

suggests that greater CD and greater CSK result in lower

cognitive SCSE.

A major thesis of this study, that the level of CSK

influences patient SCSE, was confirmed. Suggestions for how

to increase CSK while maintaining self-esteem are discussed

along with the limitations, future directions and implications

for rehabilitation of the current study.


viii













INTRODUCTION

During treatment for closed head injury, rehabilitation

therapists are faced with different degrees of patient non-

compliance with treatment and psychological distress.

Frequently, noncompliance and the presence or absence of

distress are related to how aware the patients are of their

deficits, which can be due to neurologically mediated

awareness deficits or psychological denial. However, the

individual contributions of each of these conditions is often

not known. Psychological distress is most often expressed in

anxiety, depression, and anger. Therapists must often walk a

fine line between helping head injury patients become more

aware of their deficits, which may negatively impact self-

esteem, and trying to maintain self-esteem at a high enough

level that patients have the confidence to accept the

psychological risks inherent in rehabilitation (Deaton, 1986).

On the one hand, if patients do not recognize their deficits,

they will be unable to compensate for them and may not be

motivated for rehabilitation at all. On the other hand,

lowered self-esteem can increase vulnerability to

psychological distress, which can emotionally immobilize the

patient and thwart rehabilitation efforts. Because there is

such a delicate balance between awareness, self-esteem, and







2

psychological distress, it is critical to understand these

variables in the head-injury rehabilitation environment

(Bergquist, & Jacket, 1993; Deaton, 1986).

The purpose of the current investigation is to provide a

model which describes the relationship between awareness,

self-concept, and psychological distress. Experimental

hypotheses will be made for the portion of the model which is

concerned with cognitive deficits (indirectly awareness

deficits), denial, comparative self-knowledge, and self-

concept. However, in order to understand how the patients

responds to their deficits, we must first understand the

nature and cause of their deficits, particularly some of the

neurological, cognitive, and psychosocial consequences of

closed head injury.


Neuropathophvsiological Mechanisms

Closed head injury (CHI), one form of traumatic brain

injury, refers to nonmissile impact of either a moving object

on a relatively stationary head or the head being decelerated

by a relatively stationary object (Levin, Benton, & Grossman,

1982). Levin et al. (1982) outline several primary and

secondary injuries which result from CHI. Among the primary

injuries which result from the immediate impact are

macroscopic and microscopic lesions.

Macroscopic lesions include contusion to the underlying

site of impact, coup and contrecoup lesions (which often occur








3
to the ventral portions of the frontal and temporal poles;

Adams, & Victor, 1989; Lezak, 1983; Prigatano, 1991), and

possible laceration from depressed skull fractures. Other

common sites of macroscopic lesions include the corpus

callosum and superior cerebellar peduncles which are

frequently the site of hemorrhagic lesions.

Widespread shearing/stretching of nerve fibers causes

diffuse microscopic lesions which primarily result in axonal

damage and impaired axonal metabolism (e.g. retraction balls

and axonal swelling; Povlishock, & Coburn, 1989). Shear

strains are usually the result of rotational acceleration of

the brain on its axis (Holbourn, 1943). Other types of focal

injuries include lesions to the cranial nerves which result in

specific sensory-motor losses or hypothalamic-pituitary

lesions which can result in diabetes insipidus, depression,

psychomotor retardation, and diminished sexual functioning.

Intracranial space is occupied by blood, brain and

cerebrospinal fluid. Some of the secondary mechanisms which

can result in injury such as intracranial hemorrhaging, edema

(increased tissue fluid volume) and diffuse brain swelling,

compression ischemia, raised intracranial pressure, and

herniation are related to the physics of intracranial space.

Hemorrhage is the result of ruptured blood vessels and may

result in epidural, subdural, or intracranial hematomas. The

presence of blood in the neuronal extracellular fluid inhibits

neuronal metabolism and results in neuronal death. Subdural








4

and epidural hematoma cause increased pressure on the

underlying tissue, which may cause compression ischemia.

Intracranial hematomas frequently occur in orbital frontal and

temporal lobe regions (Jennett & Teasdale, 1981). Cerebral

edema refers to the increased tissue fluid volume, which may

be the result of either vasogenic or cytotoxic factors.

Studies suggest that as cerebral edema resolves, large areas

of lesioned cerebral white matter are found due to the

destruction of myelinated axon sheaths. Ischemia may result

directly from decreased blood flow due to raised intracranial

pressure, ruptured arteries, and pulmonary and cardiac

insufficiency. Increased intracranial pressure may result

from hematoma or generalized swelling and high levels are

usually associated with brain herniation. Herniation occurs

when intracranial pressure exceeds the buffering capacity of

cerebrospinal fluid. The most common site of herniation is

transtentorial or uncal herniation. This occurs when a

supratentorial mass exerts a downward force on the uncus and

parahippocampal gyrus on to the tentorium, third nerve,

cerebral peduncle and midbrain reticular activating system.

Symptoms typically include third nerve palsy, hemiparesis and

loss of consciousness.

In addition to the primary and secondary causes of

injury, there are delayed effects which impair brain function.

Post-traumatic hydrocephalus (abnormal increase in amount of

cerebrospinal fluid) may result from obstruction of








5

cerebrospinal fluid (communicating or obstructive

hydrocephalus), or atrophy of white matter (ex vacuo

hydrocephalus; Levin et al., 1982). The etiology of normal

pressure hydrocephalus is as yet unknown but the results are

often progressive dementia, impaired gait, and incontinence

(Reitan & Wolfson, 1986). Posttraumatic epilepsy may also

occur following head-injury, and usually occurs around areas

of the brain that have scars, cysts, abscesses, and other

pathological sequelae of trauma.

From the preceding review one can surmise that

heterogeneity of brain injury is the rule rather than the

exception. However, certain types of impairments are

particularly common. Mechanical shearing of nerve fibers and

blood vessels are the most common mechanisms of diffuse brain

injury followed by contusion, swelling, and hemorrhaging. The

foregoing damage frequently results in loss of consciousness

and coma, post-traumatic amnesia, residual deficits in memory,

attention, awareness, executive functioning, and paresis.

Some investigators have suggested a possible relationship

between the preponderance of frontotemporal lesions in CHI

patients and the incidence of awareness deficits (e.g.

Prigatano, 1991).



Cognitive and Psvchosocial Consequences of CHI

Head injuries are increasingly being recognized as a

major health problem in the United States, due to the number








6
of injuries as well as to the costs involved in medical and

rehabilitative care. Estimates run as high as eight million

head injuries recorded annually in the United States (Conboy,

Barth, & Boll, 1986). Of these approximately one million

suffer head injuries severe enough to warrant hospitalization,

approximately 15,000 of which are Floridians (National Head

Injury Foundation, 1991). Statistics reveal that head

injuries are most common for those 10-30 years of age, with

males outnumbering females by more than 2:1 (Bond, 1986).

Due to the advances of modern medical science and

technology, increasing numbers of head injury patients survive

(Adams, & Victor, 1989; Kreutzer, & Wehman, 1991). However,

with survival the patient (and family) must face drastic and

often devastating alterations of their lives, including

changes in cognition, personality, social and familial

relations, physical functioning, and occupational prospects

(Crosson, 1987; Lezak, 1988; Adamovich, 1991; Kreutzer,

Devany, Myers, & Marwitz, 1991; Dikmen, Machamer, Winn,

Temkin, 1995; Dikmen, Ross, Machamer, & Temkin, 1995).

Prigatano (1987) suggests that the interaction between

the cognitive and affective sequelae of CHI is an area that

deserves greater analysis because their combined impact is

perhaps the most devastating consequence of CHI (Armstrong,

1991). For example, several investigators (Bond, 1986;

Jennett, & Teasdale, 1981) reviewed studies which indicate

that personality and intellectual impairments are more








7

strongly related to long term outcome than severity of

neurological damage.

Common cognitive deficits following CHI include impaired

intellectual abilities, memory, attention, executive

functions, awareness, abstract reasoning, communication, and

visuospatial functions (Adamovich, 1991; Bergquist, & Jacket,

1993; Bond, 1986; Conboy, Barth, & Boll, 1986; Dikmen,

Machamer, Winn, Temkin, 1995; Lezak, 1983).

Approximately 60-72% of severe CHI patients also suffer

emotional/personality changes as a result of CHI (Jennett, &

Teasdale, 1981; Crosson, 1987; Lishman, 1978). Common

personality changes include depression and anxiety (Hinkeldey,

& Corrigan, 1990; Tyerman, & Humphrey, 1984), anger and

aggressiveness (Gans, 1983), impulse control deficits

(Crosson, 1987), irritability (Hinkeldey, & Corrigan, 1990;

McKinley, Brooks, Bond, Martinage, & Marshall, 1981), denial

(Crosson, 1987; Deaton, 1986), and low self-esteem (Johnson,

& Newton, 1987; Klonoff, & Lage, 1991; Lewis, & Rosenberg,

1990; Tyerman, & Humphrey, 1984). Far from being a random

sample of the population, CHI patients have a higher incidence

of premorbid mood disorders, alcoholism, disturbed family

life, antisocial practices, and learning disabilities

(Jennett, & Teasdale, 1981; Kreutzer, & Wehman, 1991). Since

there is greater premorbid psychopathology, one should expect

greater personality problems during head injury

rehabilitation.








8
Interest in awareness after brain injury has increased in

the past 10 years (Hibbard, Gordon, Stein, Grober, &

Sliwinski, 1992; Prigatano, & Schacter, 1991). Many studies

suggest that self-esteem and self-concept are impaired

following CHI (e.g. Tyerman, & Humphrey, 1984) and emotional

distress is common (e.g. Crosson, 1987). As mentioned

previously there is often a fine balance between self-esteem,

denial, and psychological distress following CHI, which leaves

the rehabilitation therapist to make sense out of these

cognitive and emotional disturbances following CHI. Some

investigators have provided valuable insights regarding the

relationship between awareness of deficits, self-concept, and

psychological distress following CHI (e.g. Code, 1986; Deaton,

1986; Fordyce, & Roueche, 1986; McGlynn, & Schacter, 1989;

Newton, & Johnson, 1985; Prigatano, & Schacter, 1991; Tyerman,

& Humphrey 1984). However, these constructs have not been

evaluated systematically, and a theory relating them is

lacking (Kihlstrom, & Tobias, 1991). This leaves many

questions unanswered. For example, what is the relationship

between unawareness and the self-concept?

The primary focus of the current investigation is to

understand how awareness of cognitive, emotional, and physical

deficits during rehabilitation is related to different facets

of the patient's self-concept. The benefit of gaining a

greater understanding of awareness and self-concept following

CHI is the potential impact it has for the patients' emotional









status and their involvement in acute rehabilitation (Crosson,

1987; Deaton, 1986; Jennett, & Teasdale, 1981). In addition,

it may also allow clinicians to understand when to discontinue

treatment, which has important financial ramifications. If a

patient is unwilling to engage in rehabilitation, attempts at

persuasion usually fail. For example, if a once successful

businessman has a severe anterograde memory deficit following

a car accident, he may refuse to participate in cognitive

rehabilitation for several reasons. He may simply be unaware

that he has a memory problem due to the neurological

impairment or he is attempting to avoid psychological distress

inherent in recognition of deficits. The latter explanation,

however, only scratches the surface regarding psychological

denial and provides an incomplete understanding of the

psychological status. In particular, the individual's self-

concept and its impact upon his estimates of his ability must

be considered. Perhaps, engaging in cognitive rehabilitation

does not match his prior self-concept which described him as

having an excellent ability to recall information. In fact,

he may have been particularly impressed with his ability to

speak extemporaneously at monthly board meetings, which his

memory deficits would now preclude him from doing. This

example dramatizes the dilemma which therapists face. They

must institute strategies which will result in maximal

independence; however, the treatment decision is not always

clear. Should the therapist confront the patient with more








10
information, arrange planned failures, institute psychotherapy

which focuses on change of self-concept, or plan for

discharge? Because a failure to make changes in self-concept

limits rehabilitation progress. These decisions have to be

made every day in rehabilitation of severe CHI patients with

dramatic consequences for patient outcome.

This dilemma also raises several important theoretical

questions which have significant practical consequences. For

example, how can neurologically mediated deficits in awareness

be differentiated from psychological denial and what is the

role of the self-concept in the development of denial? The

present study hopes to specify the relationship between some

of these variables as a step in addressing issues of

awareness, denial, and self-concept after CHI.

The current investigation provides a theoretical

integration of the virtually non-overlapping literature on

awareness of deficits, self-concept, and psychological

distress. The review of the literature is divided into four

parts. The first section reviews the literature on awareness

of deficit following brain injury, followed by a review of the

self-concept literature. The third section discusses the

interaction between awareness deficits, denial and self

concept, and the final section reviews relevant literature on

psychological distress following brain injury.

A model is presented which places the self-concept at a

strategic locus with respect to the various cognitive and








11
emotional changes that result from CHI. The model considers

the relationship between cognitive deficits (presumed to

underlie awareness deficits), denial, self-knowledge and self-

concept.














REVIEW OF THE LITERATURE

Awareness of Deficits After Brain Iniury

A discussion of awareness of deficits after brain injury

is particularly pertinent to CHI patients because of the

consequences it has for adjustment to rehabilitation and

eventual return to the community. Unawareness of deficits

following brain injury creates difficulty progressing through

programmatic rehabilitation and impairs the patient's ability

to adjust to the dramatic changes in their physical,

cognitive, social and occupational functioning (Crosson,

Barco, Velozo, Bolesta, Cooper, Werts & Brobeck, 1989;

Youngblood & Altman, 1989). As Prigatano (1991) suggested

"severely brain-injured patients do not adequately perceive

significant changes in their higher cerebral functioning" (p.

111), resulting in behavior problems which ultimately lead to

alienation of loved ones and isolation. Prigatano and Fordyce

(1986) suggested that unawareness is associated with poor

psychosocial adjustment and poor motivation for

rehabilitation. Several investigators confirmed that the

level of awareness is the best predictor of successful

treatment (Lam, McMahon, Priddy, & Gehred-Schultz, 1988),

vocational outcome (Ezrachi, Ben-Yishay, Kay, Diller &

Rattock, 1991) and psychosocial outcome (Prigatano, Altman &








13

O'Brien, 1990). Unawareness of cognitive and behavioral

dysfunction represents the greatest single impediment to

functional re-entry into society (Prigatano, 1986a).

Despite its importance, the literature on awareness of

deficits after brain injury is fraught with terminological

confusion due to the lack of a useful taxonomy which

accurately describes empirical phenomenon (McGlynn & Schacter,

1989; Prigatano & Schacter, 1991). Brain injury can often

result in unawareness of deficits that may be subtle ('I know

about "those problems" ') or startlingly obvious ('Why do I

have to go to cognitive therapy, my memory is fine'), either

of which proves to be an obstacle to rehabilitation and post-

rehabilitative adjustment. Impaired awareness of deficits can

vary as a function of the type of deficit (e.g. physical or

cognitive) or modality (e.g. vision). It can manifest itself

in the patient's failure to institute behavioral compensations

and in the patient's direct verbalizations (Weinstein & Kahn,

1955). Impaired awareness has been observed for memory

impairments (Levin, Benton & Grossman, 1982; Sunderland,

Harris & Baddeley, 1983), attention deficits (Allen & Ruff,

1990), personality changes (Fahy, Irving & Millac, 1967),

blindness (Antons syndrome), hemianopia, hemiplegia, aphasia,

and dementia (McGlynn & Schacter, 1989). Given that

unawareness of deficits can vary in severity, modality, and

type of deficit and manifest itself in either overt behavior

(or lack thereof) or verbalization, it is likely to be








14
multiply determined. It is no wonder that there have been

several terms to describe this phenomenon. We shall consider

some of the most common terms and define the use of each term

in our research.

Anosognosia, a term introduced by Babinski (1914),

literally means a lack of knowledge of disease, but has

through the years most often come to refer to a lack of

awareness of hemiplegia (half-body paralysis) and hemianopia

due to stroke. Some investigators refer to anosognosia

broadly as a denial of illness (e.g. Heilman, 1991), but we

shall use this term more selectively to describe unawareness

of hemiplegia and hemianopia (Bisiach & Geminiani, 1991).

The term self-awareness is also commonly used in the

literature and generally refers to the perception of changes

in higher cognitive function (e.g. Bergquist & Jacket, 1993).

Prigatano and Schacter (1991) define self-awareness as "the

capacity to perceive the 'self' in relatively 'objective'

terms while maintaining a sense of subjectivity" (p. 13).

A useful distinction to consider in this context is

between awareness and knowledge. If awareness is taken to

refer to the state or process of reflecting upon some fact of

reality, knowledge can be seen as the stored representation of

that awareness. Therefore, self-awareness is a state of

reflecting upon one's self, and self-knowledge is the stored

representation of that self-awareness.








15
Using a computer metaphor for the functioning of the

nervous system, Johnson-Laird (1988) claims that a fundamental

tenant of human consciousness is the ability to be self-aware,

i.e., we have the ability to be aware of ourselves. In this

scheme, self-awareness refers to awareness of the system that

is cognizant. Johnson-Laird (1988) claims that the operating

system must have a model of itself in order for the process of

recursiveness, which underlies self-awareness, to occur. He

claims that as humans we do not have full access to all of our

self-descriptions; however, we do have access to many of our

higher-level capabilities; the capacity to perceive, remember,

reason, and act. Therefore, self-awareness is the conscious

process of reflecting on one's own operating system or higher

cognitive functions, which implies that we possess the

capacity for some level of objective and subjective self-

knowledge.

Self-awareness and self-knowledge are also differentiated

in the temporal dimension. Awareness may be seen as a

temporally limited process and self-knowledge as the

temporally stable trait. The latter term is preferred because

it implies a stable form of information about the self which

can be assessed by comparison with some standard. Self-

knowledge is usually measured by comparing the patient's

ratings with either objective test performances, family

ratings or staff ratings. Therefore, one of the concepts we

shall use in the model is comparative self-knowledge of








16
deficits. This concept is similar to what (Crosson, Barco,

Velozo, Bolesta, Cooper, Werts & Brobeck, 1989) refer to as

intellectual awareness, which will be discussed later.

Denial has also been used to describe awareness

disturbances, but historically it has been used in two

different ways (McGlynn & Schacter, 1989). The first is

neutral, similar to the broader use of anosognosia and

unawareness. The second form is narrower and denotes the

psychological defense mechanism of denial. This latter term

refers to a patient that is aware of their deficits in some

sense but is not psychologically able to confront them

(whether intentional or not). The distinction is between

patients that are unable to become aware of their deficits due

to CNS dysfunction, as in the former, and reactive forms of

unawareness in which the patient is theoretically able to be

aware of the deficit (McGlynn & Schacter, 1989). From the

previous discussion of awareness and denial, we can infer that

the neurological inability to be aware and the reactive form

of unawareness have a common effect; which is reduced self-

awareness and self-knowledge. Because they have different

etiologies, treatments, and long-term prognoses, Barco,

Crosson, Bolesta, Werts & Stout (1991) make a similar

distinction between impaired self-awareness due to

psychological defense, which they called "denial," and

neurologically mediated "awareness deficits." Consistent with

Barco, et al. (1991), in the remainder of this paper denial










and awareness deficits shall refer to the reactive

(psychological) and incapacity (neurological) mediated causes

of impaired self-knowledge of deficits, respectively.

In sum, anosognosia shall refer specifically to

unawareness of hemiplegia and hemianopia, and awareness of

deficits refers to the ability to consciously reflect upon

one's deficits. Self-awareness refers to the state of

conscious perception of changes in higher cognitive function

and self-knowledge to the stored knowledge which results from

that awareness. Self-awareness and self-knowledge are thought

to be affected by both the neurological inability to be aware

and reactive forms of unawareness and are typically measured

by a comparison to relatives, staff members or performance on

tests. Neurologically mediated unawareness or the inability

to be aware shall be referred to as an awareness deficit and

reactive unawareness as denial.

What follows will be a brief review of the literature on

psychological denial and awareness deficits, and theoretical

models which attempt to account for them.



Psychological Denial

Denial is a reluctance to recognize deficits (either

conscious or unconscious), based on psychological factors

(Barco, et al. 1991). Psychological denial is understood to

be a motivated defense mechanism which describes the

individuals tendency to avoid or severely minimize some aspect








18
of reality which is perceived as threatening. While

considered maladaptive and an obstacle to treatment by most,

Lewis (1991) suggested that rather than being simply an

obstacle to treatment, denial has adaptive value to the

patient with brain injury. She goes on to say that "the

patient is attempting to avoid awareness of some aspect of

reality that would cause more pain than he or she can

currently tolerate" (p. 235).

Denial may be due to reaction to illness, to pre-existing

characterological disorders, or may be overlaid upon a

neurological awareness deficit or may be due to any

combination of the above (Crosson, 1987; Deaton, 1986;

Prigatano, 1986a; Weinstein & Kahn, 1955). However, denial is

not unique to head injury. Levine and Zigler (1975) found

that stroke patients showed greater denial than patients with

cancer or heart disease, which they suggested means that

stroke represents a greater threat to the self. They

concluded that denial was greater for stroke patients because

the cognitive and emotional consequences of stroke are more

devastating to the self than those resulting from cancer and

heart disease. It is noteworthy to point out that they failed

to consider the possibility that the "denial" which they

observed in stroke patients was in fact due to CNS lesions

(i.e. awareness deficits).

In their now famous monograph "Denial of Illness"

Weinstein and Kahn (1955) studied the denial language of brain








19
impaired patients and concluded that the brain lesion does not

cause impaired awareness. They claimed that the brain lesion

...provides a milieu of function in which any incapacity or

defect may be denied..." (p. 96). As shall be discussed

later, this book was very influential in that it shifted

interest to the psychological defense mechanism as cause of

unawareness.

Denial may serve as a coping mechanism to reduce grief,

increase self-esteem, avoid negative affect, and increase hope

(Deaton, 1986). For example, Goldstein (1952) suggested that

patients use denial to avoid an intense disorganizing anxiety

reaction after a performance failure which he called a

"catastrophic reaction."



Awareness Deficits

Following the publication of Weinstein and Kahn's (1955)

book, neurologists were discouraged from investigation of

denial, due to the belief that these deficits were topics of

psychiatric study rather than neuropsychological syndromes.

The effect was to emphasize psychodynamic defense mechanisms

and premorbid personality characteristics. However, today

emphasis has shifted toward understanding both the reactive

and neurological aspects of unawareness of deficits (McGlynn,

& Schacter, 1989).

An awareness deficit refers to the inability to recognize

the deficits caused by impaired brain function (Crosson,








20
Barco, Velozo, Bolesta, Cooper, Werts & Brobeck, 1989). It is

assumed that the cause is multifactorial. In order to be

aware of deficits, the patient must be aware of several

different types of functioning, i.e. they must demonstrate

"self-awareness" for many different aspects of the self. For

example, patients can be aware of their 1. sensory/motor

(physical) functioning, 2. cognitive functioning (such as

memory, attention, abstract reasoning, and language), 3.

interpersonal and social functioning, and 4. emotional

functioning. Unawareness in hemiplegia, visual disturbances,

language disturbances, memory dysfunction, closed head injury,

and premorbid levels of awareness are briefly reviewed.

Unawareness of hemipleaia. Altered awareness of deficits

following brain injury was first observed by neurologists such

as von Monakow, Anton, Pick, and Babinski during the late 19th

century (Prigatano, 1991). Babinski (1914) coined the term

anosognosia (literally, lack of knowledge of disease) to refer

to lack of awareness of hemiplegia (half-body paralysis).

Descriptions of such patients are striking; for example,

patients will refuse to believe that a limb is their own

despite repeated questioning and intact intellectual ability.

Frequently, patients will admit their neurological symptoms

but appear totally unconcerned, which is a related condition

called anosodiaphoria (Heilman, Watson & Valenstein, 1985).

In the case of anosognosia for hemiparesis, Cutting

(1978) observed that if properly questioned patients will








21
allow that they have some problem with the paretic limb but it

was frequently phrased in terms of being "stiff" or "heavy."

The preponderance of clinical evidence suggests that

anosognosia for hemiplegia occurs during the acute stages of

illness and the disturbance can be selective. Patients may

deny weakness in the limb while retaining full awareness of

the other deficits in language or visual functioning. For

example, Wagner and Cushman (1994) interviewed 108 stroke

patients and found that 40% of their sample had some degree of

unawareness. However, unawareness was greatest for cognitive

deficits (49% of sample), memory deficits (44%) and perceptual

deficits (36%), and less common for hemiparesis (18%),

affective/mood changes (16%), and speech deficits (4%).

Starkstein, Fedoroff, Price, Leiguarda, and Robinson

(1993) investigated the neuropsychological deficits which

anosognosic patients demonstrate. They administered a full

neuropsychological battery (tests of frontal executive

functioning, language ability, verbal and non-verbal memory,

and attention) and an "anosognosia questionnaire" to 16 stroke

patients. The anosognosia questionnaire primarily assessed

anosognosia for hemiplegia and hemianopia. They found that

anosognosic patients showed significantly lower scores on the

Mini Mental Status Examination, verbal fluency (FAS), and

Trails A and B compared to non-anosognosic patients. They

concluded that anosognosic patients have significantly more








22

cognitive impairments, mainly on frontal lobe-related tasks,

but not on memory tasks.

The bulk of evidence which has accrued since the late

19th century also suggests that neurologically mediated

unawareness of hemiplegia varies as a function of lesion site

(Cutting, 1978; Heilman, Watson & Valenstein, 1985; Lezak,

1983). McGlynn and Schacter's (1989) review of the literature

on unawareness suggested that unawareness of hemiplegia is

more common following large right posterior parietal and

thalamic lesions. Cutting (1978) studied 100 patients with

hemiplegia and found that 58% of those with right hemisphere

dysfunction denied muscle weakness, compared to 14% of those

with left hemisphere dysfunction. Wagner and Cushman (1994)

found that the factors predictive of greater unawareness were

lesion location and degree of global cognitive impairment.

Those with cortical rather than subcortical lesions had

greater unawareness and those with more global cognitive

impairment had the greatest amount of unawareness. They

failed to find overall right versus left hemisphere

differences; however, they failed to include several left

hemisphere cases because of severe aphasia. Hibbard et al.,

(1992) also found that despite high levels of unawareness of

cognitive deficits, there were no differences between right

and left hemisphere stroke patients. However, Wagner and

Cushman (1994) did find greater unawareness of perceptual

deficits for those with right posterior cortical lesions, and








23
many components of unawareness occurred with greater frequency

when the lesions were anterior versus posterior, implicating

right hemisphere and frontal regions. Starkstein, Fedoroff,

Price, Leiguarda and Robinson (1992) found that patients with

anosognosia for hemiplegia had a greater incidence of right

temporoparietal, thalamic and basal ganglia lesions. Several

other authors (Breier, Adair, Gold, Fennell, Gilmore &

Heilman, 1995) also report greater anosognosia for hemiplegia

following right hemisphere dysfunction (sodium amytol

injection). Anderson and Tranel (1989) report that all of

their stroke patients that had unawareness of hemiplegia had

large right fronto-parietal lesions and dense hemiparesis. In

addition, they report that these subjects also were unaware of

cognitive deficits such as neglect of left hemispace,

dysarthria, memory defects, and impaired nonverbal intellect.

When they looked at the entire group of stroke patients

(N=32), they found that 90% of the right hemisphere patients

were unaware of at least one cognitive deficit, whereas only

41% of the left hemisphere subjects were unaware of at least

one cognitive deficit.

The conclusions to be drawn from these studies suggest

that anosognosia for hemiplegia characteristically develops

following large injury to the nondominant hemisphere and is

associated with cognitive impairments. The cortical component

typically involves the postcentral association areas and the

thalamus is a consistent subcortical correlate.








24
In their discussion of unawareness of hemiplegia, McGlynn

and Schacter (1989) discuss the related phenomenon of neglect.

Neglect is a specific neurological syndrome in which the

patient fails to report, respond, or orient to novel stimuli

in the opposite side of a brain lesion (Heilman, et al.,

1985). Several authors include a discussion of neglect along

with anosognosia for hemiplegia because they are both

construed as forms of unilateral misrepresentation (Bisiach &

Geminini, 1991). Neglect can be considered a form of

unawareness (of the perceptual world) or inattention to the

side of space contralateral to the lesion. Studies show they

are frequently related. Heilman and Valenstein (1972) studied

the relation between auditory neglect and anosognosia for

hemiparesis in ten patients. Nine of the patients with

auditory neglect had lesions in the right inferior parietal

lobule and five of these patients also had anosognosia for

their hemiplegia, demonstrating that similar lesions can lead

to both conditions. Bisiach, Vallar, Perani, Papagano, and

Berti (1986) also conclude that anosognosia is more common

following right inferior posterior parietal lesions, similar

to the site of lesions for neglect. In addition, Heir,

Mondlock, and Caplan (1983) found that anosognosia was

significantly correlated with neglect (r=.42). However,

neglect can be seen independently from anosognosia for

hemiplegia. For example, Bisiach et al. (1986) found that

approximately one-third of their patients with anosognosia for








25
hemiplegia did not have unilateral neglect, demonstrating a

dissociation between neglect and anosognosia for hemiplegia.

Therefore, while neglect is dissociable from anosognosia for

hemiplegia, it can be construed as a form of unawareness and

there is a suggestion that it shares similar, but not

completely overlapping, anatomic localization (Bisiach &

Geminiani, 1991).

Unawareness of visual disturbances. As previously

mentioned, patients may also deny visual disturbances that

range from hemifield defects to bilateral cortical blindness

(referred to as Anton's syndrome). Anton (1899; Cited in

McGlynn & Schacter, 1989) was the first to provide a detailed

description of denial of blindness in a 56-year-old woman who

despite total blindness was unaware of her disability.

Autopsy revealed bilateral lesions of the angular gyrus,

occipital association cortex, and splenium of the corpus

callosum. In several reported studies of Anton's syndrome

there has been the suggestion that the disorder is associated

with concomitant intellectual decline and disorientation

(McGlynn & Schacter, 1989). They cite the Redlich and Dorsey

(1945) study in which they reported that all six patients with

unawareness of blindness had at least a moderate amount of

intellectual decline and were generally disoriented, had

impaired memory, and tended to confabulate. However, the

exact role cognitive deficits have in maintaining the disorder

has yet to be determined. Heilman (1991) proposed several








26
mechanisms to explain anosognosia for blindness. He suggested

that a hypothetical monitor of visual input might be damaged

or there may be false feedback to the monitor. This degraded

input may reach the monitor from subcortical visual pathways.

Another form of unawareness for visual disturbances is

that seen with hemifield defects. Bisiach et al. (1986) find

that within a population of right brain damaged patients

anosognosia for hemianopia is very common (88% of those with

hemianopia denied visual disturbances) and is even more

prevalent than anosognosia for hemiplegia. The exact

mechanisms for this form of unawareness are also not well

understood.

Unawareness of language disturbance. Unawareness of

aphasic disturbances are most frequent following Wernicke's or

jargon aphasia (Rubens & Garrett, 1991). Jargon aphasia is a

form of language disturbance in which there is fluent output

with neologistic or lexical jargon, with impaired

comprehension, repetition, and naming. Because such patients

have severe comprehension deficits and significant expressive

deficits with fluent jargon, their unawareness usually cannot

be detected verbally and has to be detected nonverbally. The

first suggestion that they are unaware of their impaired

speech output is the failure to make corrections in their

speech or written productions. Other types of aphasic

patients and non-aphasic people have been shown to make

ongoing corrections in their speech output. The second reason








27

is that jargon aphasics often appear upset and frustrated with

the "uncomprehending" examiner (Heilman, 1991). Unawareness

of linguistic output is present when the speaker does not

attempt to correct an error and, when confronted with that

error, denies its occurrence (Rubens & Garrett, 1991).

Rubens and Garrett (1991) suggest that the reason that

jargon aphasics are unaware of their errors may reflect either

a general lack of awareness of the aphasia, a specific deficit

in monitoring their speech, limitations in attentional

capacity, or loss of a specific language structure (e.g.

semantic, phonological, syntactic). They go on further to

state that self-monitoring of communication functions

primarily requires (a) attentional focus during production and

(b) comprehension of output to assess whether the ongoing

utterance conveys the intended meaning. This amounts to the

conclusion that some patients fail to notice communication

errors because they cannot speak and listen at the same time.

The anatomic localization of anosognosia for aphasia has

shown the expected lesions to left posterior temporal regions

(Wernicke's area). However, some studies suggest that

bilateral lesions are necessary for full jargon aphasia and

anosognosia for aphasia to develop (Rubens & Garrett, 1991;

Weinstein, Lyerly, Cole & Ozer, 1966; cited in Mcglynn &

Schacter, 1989). Weinstein et al. (1966) found that 14/18

jargon aphasics denied difficulty with speech while all 26

non-jargon aphasics did not have anosognosia for their speech








28

output deficits. In addition, among the jargon aphasics 14/18

had bilateral lesions. However, there are jargon aphasics

with unilateral left hemisphere lesions that do not have

anosognosia for their speech output deficits (Gainotti, 1972;

cited in Rubens & Garrett, 1991). While more studies need to

be conducted, the tentative conclusions to be drawn are that

(a) most unawareness of aphasia is seen in jargon aphasia, (b)

posterior left hemisphere lesions are necessary for jargon

aphasia to develop and involvement of the non-dominant

hemisphere is very common. (c) Unawareness of aphasia is

common with bilateral lesions.

Unawareness of memory dysfunction. Memory disturbances

can develop in a variety of neurological disorders (medial

temporal lobe injury due to anoxia, epilepsy and temporal

lobectomies, anterior communicating artery aneurysm, viral

encephalitis, closed head injury, electroconvulsant therapy,

and neoplasms) some of which can impair awareness of the

memory deficit as well. It is reasonable and often suggested

that, given the problems in recall that amnesics face,

patients would be unaware of their deficits because they

simply would be unable to recall their deficits. However,

there are amnesic patients, particularly many with focal

temporal lesions, that are aware of their deficits (Schacter,

1991) which suggests that the awareness deficit is not simply

the result of failure to remember that one has a deficit. But

while impaired memory may not be a sufficient condition for








29
unawareness, it may certainly contribute to unawareness

(Schacter, 1990).

Korsakoff (1889; cited in Schacter, 1991), in his

original discussion of the syndrome which bears his name,

suggested that his patients were often unaware of their memory

dysfunction. Korsakoff patients frequently have

neuropsychological findings suggestive of frontal lobe

impairment (Schacter, 1991). McGlynn and Schacter (1989)

point out that impaired awareness of memory disorder has been

described in other patients with signs of frontal impairment.

Impaired awareness of memory dysfunction has been shown for

patients with frontal tumors, ruptured anterior communicating

artery aneurysm (ACoAA), and bilateral frontal damage

secondary to head trauma. By contrast, patients with intact

awareness of their memory impairment do not show frontal

signs, such as patients with encephalitis affecting temporal

lobe structures. In addition, Schacter (1991) reports that

famous amnestic patients, with primarily non-frontal injuries,

such as patient N.A. (localized lesion to the dorsomedial

thalamic nucleus) and H.M. (bilateral temporal lobectomy) had

normal awareness of deficits.

Unawareness of memory deficits may be due to poor

monitoring of cognitive performance. This phenomenon is

referred to as metacognition when referring to cognitive

skills and metamemory when referring specifically to memory

performance (Shimamura & Squire, 1986). Metacognition refers








30
to knowledge of ones own cognitive performance and is involved

in problem solving. Metamemory includes both knowledge of

one's memory strengths and weaknesses, and general knowledge

of task and strategy variables that influence recall of

information (Cooley & Stringer, 1991). Metamemory is a

complex function which requires monitoring of memory

performance, drawing inferences from this performance, storage

of this information, and gaining access to this information

when planning future behavior. One form of measurement is

obtaining pre-performance predictions of cognitive performance

(Cooley & Stringer, 1991).

Another method of assessing metamemory is the "feeling-

of-knowing" paradigm. The most common feeling-of-knowing

paradigm requires the subject to make judgements of expected

recognition of previously non-recalled memory items.

Shimamura and Squire (1986) investigated metamemory in amnesia

patients with this method. They included three groups of

patients: 1. Korsakoff patients, 2. ECT patients, and 3. a

group of mixed etiology amnesic patients anoxiaa, ischemia,

patient N.A.). In the first part of the study, they asked

patients general information questions and collected the first

24 items that each patient failed to get correct. Subjects

were then given a chance to rate their chances of recognizing

the correct answer if given choices. They rated how likely

they were to recognize the answer on a 4 point scale (1-

indicating high feeling of knowing, 2-medium feeling of








31
knowing, 3-low feeling of knowing, and 4-pure guess). Normal

subjects typically show greater recognition accuracy for

unrecalled items when they give high feeling-of-knowing

ratings. The results showed that the Korsakoff patients had

impaired feeling-of-knowing accuracy. The correlation between

their predictions and recognition performance was lower than

the corresponding correlation for control subjects and the

other amnesia patients. In addition, the accuracy of the non-

Korsakoff amnesia groups was not significantly different from

the control group. Korsakoff patients demonstrated deficits

in metamemory.

However, it was found that Korsakoff patients performed

poorly on the general information test. Therefore, it may be

that feeling-of-knowing accuracy in amnesic patients is only

normal when recall performance is normal. For this reason,

they examined feeling-of-knowing accuracy for newly learned

information in a second experiment. Subjects were instructed

to study sentences (e.g Mary has a garden full of marigolds.).

Five minutes later amnesics were then given a sentence stem

(Mary has a garden full of ) to cue recall of the

missing word (there was a 5 minute delay for amnesics and a 1-

7 day delay for controls, before recall was attempted). They

were then asked to give feeling-of-knowing ratings for the

non-recalled items prior to the recognition trial. The non-

Korsakoff patients had feeling-of-knowing predictions which

were significantly correlated with recognition performance and










the magnitude of the correlation was similar to that obtained

for the control subjects accuracy. Korsakoff patients

feeling-of-knowing ratings were not correlated with

recognition performance. These results suggest that Korsakoff

patients have severe difficulty monitoring their memory

performance while non-Korsakoff amnesia patients do not. This

suggests that deficits in metamemory are dissociable from

memory impairments in amnesics and indicates that Korsakoff

patients are unaware of their memory deficits.

Schacter, McLachlan, Moscovitch, and Tulving (1986)

studied the metamemory of three groups of memory impaired

patients those with closed head injuries, ruptured ACoAA's,

and early Alzheimer's disease patients. Patients and controls

were instructed to study lists of words. They were then

instructed that they would be required to recall the list and

to make predictions of how many of the 20 items from the list

they would recall. As expected all three patient groups were

significantly more impaired than controls in their free recall

performance. However, the CHI and ACoAA groups were about as

accurate as their control subjects in estimating their

performance. The dementia group was very inaccurate in

estimating their recall performance. This is consistent with

the literature which suggests that Alzheimer's patients are

unaware of their deficits and have extensive frontal lobe

pathology later in the progression of the disorder (McGlynn &

Schacter, 1989). An interesting aspect of this study is that








33
it serves as a counterexample to the observation that frontal

lobe dysfunction leads to unawareness because the ACoAA and

CHI patients, which both typically have some frontal lobe

lesions, were found to be relatively aware of their memory

functioning. However, this study does demonstrate that

Alzheimer dementia patients have impaired metamemory.

Schacter (1991) suggests that head injury patient may

show impaired awareness and metamemory if different methods of

assessment are used. Sunderland, Harris, and Baddeley (1983)

administered a questionnaire concerned with everyday memory

functioning to a group of patients with severe head injury.

They compared the patients reports with their actual memory

functioning and found that their ratings were not associated

with their performance on standard memory tests. In contrast,

the family member ratings of the patients' memory were

correlated with their actual memory performance, demonstrating

that the head injury patients had impaired awareness of their

memory disturbance. This study also suggests that the

patients may have been unaware of their deficits because they

were unable to recall instances of memory failure while

filling out the questionnaire. Cooley and Stringer (1991)

used a methodology similar to that used by Schacter,

McLachlan, Moscovitch, and Tulving (1986) to study unawareness

of memory impairment or metamemory in a sample of 23 mixed

amnesic patients (TBI, dementia, tumor, strokes). Patients

and outside observers predicted memory performance on various








34

standard memory tests. The authors designed the questionnaire

to be isomorphic with standard memory tests (e.g. "how many

items do you think you can recall from a 16 item list?" for

1st trial CVLT performance). Results showed that patient

prediction of their own performance was less accurate than the

outsiders predictions (friend or relative), suggesting

impaired metamemory. However, the patients predictive

accuracy was better than observed in the Sunderland et al

(1983) study (note that the groups were different as well).

This suggests that diagnosis of unawareness of memory

impairment may depend, in part, upon the method of assessment.

Unawareness of memory disturbance may also be specific to

a cognitive domain. Prevey, Delaney, and Mattson (1988) find

that left temporal lobectomy patients tend to be inaccurate in

estimating their verbal memory performance but are more

accurate in estimating their spatial memory performance.

The Prevey et al. (1988) study also suggests that the

memory impairment itself may be necessary for metamemory to be

impaired. This is supported by a study by Stringer, Cooley,

and Kertay (1988) in which they administered the Rivermead

Behavioral Memory Test, a battery of everyday memory tasks, to

27 right hemisphere stroke patients. They also had patients

estimate their performance on this task. The correlations

between predictions and performance were poor. However,

patients with poorer recall were least able to make accurate








35
judgements of their performance. This supports the idea that

impaired memory is related to impaired metamemory.

In summary, clinical and experimental evidence (McGlynn,

& Schacter, 1989; Schacter, 1991) suggests that most amnestic

patients with unawareness of memory deficits have signs of

frontal lobe pathology. For example, the Korsakoff patients

have amnestic disturbances with well documented frontal lobe

signs, a relative unawareness of their deficit, and impaired

metamemory (Schacter, 1991). This suggests that deficits in

awareness following memory disturbance may be due to frontal

lobe dysfunction in many instances. Since the frontal lobes

function to integrate information and monitor responses, it is

not surprising that amnestic patients with frontal damage

demonstrate an inability to be aware of their memory

performance (Schacter, 1991).

Unawareness in closed head injury. There is abundant

evidence that CHI patients are inaccurate in judging their

cognitive and behavioral functioning. Given the varied

neuropathology which can result from a closed head injury,

patients often suffer from a variety of cognitive and

sensory/motor deficits. As a result, CHI patients demonstrate

unawareness for a variety of deficits.

As mentioned previously, regarding unawareness for

memory disorders, Sunderland, Harris, and Baddeley (1983)

found that severe CHI patient ratings of everyday memory

performance was not associated with their performance on








36

standard memory tests, demonstrating impaired awareness of

their memory disturbance. McGlynn and Schacter (1989) report

on a study by Cockburn, Wilson, and Baddeley (1986) in which

they investigated head injury patients' accuracy in estimating

their memory functioning. They divided the patients into

three groups based on their memory performance. The patient

and a close relative rated their ability on a scale of

everyday memory functioning. There was no correlation between

self and relative ratings for the poor memory group,

suggesting that poor memory may be related to unawareness of

memory disorders. There was a low correlation between patient

ratings of memory performance and objective performance in the

moderate and poor memory groups. This provided further

evidence for impaired awareness of memory disorders.

Rimel, Giordini, Barth, Boll, and Jane (1981) studied 429

mild head injury patients 3 months after their injury and

found that 59% of the sample reported a change in their

memory. However, family members indicated that the patient's

memory was far worse than they had reported, which suggests

that unawareness of memory impairment may occur even in cases

of mild head injury. However, Miller and Stern (1965)

commented on the notable lack of complaints that severe head

injury patients have while "post-concussional" patients with

only mild injuries frequently complain of their symptoms.

Providing more objective evidence of the differences

between mild and severe head injury patient awareness of their








37

deficits, Allen and Ruff (1990) compared 28 mild-moderate head

injury patients, 28 severe head injury patients and 31 normal

controls ratings of their cognitive performance with their

actual neuropsychological performance. Subjects were

administered a questionnaire which assesses patients self-

ratings of cognitive functioning in several cognitive domains

sensorimotorr, attention, language, arithmetic, learning,

memory and logical thinking). The severe and mild head

injured groups both rated themselves as having "no problem" in

the cognitive domains mentioned. The normal controls rated

their different cognitive abilities as being "minor

strengths." The results also showed that the

neuropsychological performance of the severe group was

significantly inferior to the mild group and normal controls.

The mild head injury group's performance was not significantly

different from normal controls' neuropsychological performance

except for arithmetic. In order to compare ratings with

performance, all scores were converted to z-scores utilizing

a separate normative sample (N=180) that had also completed

the rating scale and tests. When comparing the ratings with

performance, the severe head injury group consistently

overestimated their sensorimotor and attentional functioning.

In contrast, the mild-moderate head injury group

underestimated their performance. They were particularly

pessimistic about their sensorimotor, language, and reasoning

abilities. The test performance and self-ratings for the








38
normal controls was generally congruent except for

overestimation of learning and logical thinking. These

results demonstrate that severe head injury patients do not

rate their cognitive functions in correspondence with test

performance. While self-ratings did not differentiate the

severe and mild-moderate groups, the severe group performed

more poorly on neuropsychological tests. In addition, normal

controls, while generally more realistic, are not so

uniformly. This study also found that those with more chronic

head injuries (greater than 1 year post trauma) tend to rate

their cognitive performance as more impaired. This may

suggest that awareness of deficits may increase with time

(however, this finding may have limited generalizability to a

group of severe head injury patients because both mild-

moderate and severe head injury groups were combined for this

analysis). In summary, this study states that those with

severe head injuries tend to be unaware of their deficits. In

contrast, the mild-moderate head injury patients tend to be

more pessimistic and even hyper-aware of their deficits. It

would appear that mild-moderate patients lose a relatively

normal, positive bias when evaluating their cognitive

functioning. While the severe group did not report their

cognitive functions to be strengths, they still had an

exaggerated positive bias. However, in order for them to be

more realistic they would need to consider themselves as

having some form of impairment, which they did not.








39
There have been advances in the use of questionnaires and

interview formats to evaluate the level of unawareness in a

head injury population. Anderson and Tranel (1989) conducted

an "awareness interview", which assessed motor and cognitive

functioning, with a group of head injury, stroke, and dementia

patients and compared the responses with neuropsychologists'

and neurologists' evaluations. They found that 68% of the

head injury sample was unaware of cognitive deficits.

Unawareness was most common for intellectual functions,

memory, and speech and language. The neuropsychological

variables which correlated with the level of unawareness were

Verbal IQ and temporal disorientation. The investigators

speculated that the deficits in VIQ and orientation are

suggestive of "metacognitive" deficits which accompany

unawareness of cognitive deficits. Utilizing a questionnaire

format, Prigatano, Altman, and O'Brien (1990) compared family

ratings with 64 head injury (mild, moderate, and severe head

injuries) patients ratings on the Patient Competency Rating

Scale (PCRS; a 30 item scale which asks patients, families or

staff to make judgements about perceived competency to perform

various daily activities; Roueche & Fordyce, 1983). The

investigators chose 10 items from the PCRS for which they

anticipated the most disagreement and 8 items for which they

expected the most agreement between patient and family

members. Their hypotheses were correct. The mean difference

score for each of these sets of items were significantly








40

different. For the first set of items the patient ratings

were consistently greater than the relative ratings. These

items assessed complex cognitive activities, emotional

control, and behavioral flexibility. The areas of competence

in which the patients and relatives agreed, assessed basic

activities of daily living (e.g. doing laundry, dressing

self). In addition, seven neuropsychological measures were

administered and correlated with the patient and the relative

ratings on items of the PCRS. The correlations between

ratings and neuropsychological tests revealed that many items

from the PCRS were not related to any neuropsychological

variables. However, the memory measures were generally

related to either patient or relative ratings of memory

ability and neuropsychological test scores had the greatest

predictive power for relative's judgement of the patients'

capacity to dress and prepare meals. Overall, this study

showed that patients consistently underestimated problems in

emotional control and social interaction, and the

neuropsychological measures chosen for this study are not

related to these particular behaviors. This study also

demonstrated that patients and relatives have similar

agreement concerning activities of daily living and

neuropsychological measures were predictive of these

behaviors. Prigatano (1991) reports on further analyses of

the neuroradiographic and neuropsychological correlates of

unawareness of these same 64 patients. Patients were divided








41
into 3 groups based on patient-relative discrepancies on the

PCRS. Group I overestimated their competence, Group II had

similar ratings to family, and Group III underestimated their

competence. Group I patients showed decreased left hand motor

speed but the other neuropsychological measures were not

predictive of group membership. This suggests greater right

than left hemisphere dysfunction but right hand motor speed

was also below normal, suggesting bilateral injury. This was

indirectly supported by radiographic analysis. Group I

patients suffered significantly more lesions as visualized on

MRI or CT scans. In addition, Group I patients also showed

relatively more frontal and parietal lesions than the other

groups.

Gasquoine (1992) investigated several methods of

assessing awareness of sensory and cognitive changes and its

relationship to emotional distress. Forty-two head injury

patients completed three rating scales which asked questions

about the effects of the injury on sensory and cognitive

changes along with a measure of affective state. Therapists

also rated the patients on their sensory and cognitive

changes. Patients first reported changes in sensory and

cognitive changes in a free report format. Patients provided

a paucity of responses with this format; which could have been

a result of the inability to generate responses. The majority

of patients reported one or no problems. Patients then

completed two rating scales with 10 questions about sensory








42
and cognitive functions (speed of performance, ability to

plan, memory, hearing, ability to initiate, vision, ability to

process information, learning, concentration, and word

finding). They were given two formats, the first described

the function and the second just used the name of the function

(memory). The subjects were asked whether they had a problem

with the function (awareness of change scale) and then asked

whether the function was good, average or poor (awareness of

deficit scale). The lack of a difference between abbreviated

and complete behavioral descriptions demonstrated that there

was no difference in rating between the two questionnaire

methods of assessment but the patients reported significantly

fewer deficits on the free report format than the

questionnaire format. On the awareness of deficit scale,

patients most frequently reported speed of performance and

memory as being affected by the injury. When comparison was

made with the therapists ratings, patients significantly

underestimated the number of cognitive and sensory deficits

and changes. Comparison between therapists and patients on

the awareness of deficit scale revealed the highest agreement

for the functions of concentration (38% agreement) and vision

(36% agreement) and the lowest for initiation (23% agreement)

and planning (141 agreement). On the awareness of change

scale the highest agreement was found for vision (81%

agreement) and hearing (73% agreement) and the lowest for

learning (44% agreement) and ability to process information








43
(43% agreement). This study also found that the patients

understanding of the meanings of cognitive and sensory terms

was significantly correlated with the agreement between

patients and therapists on the questionnaires. Poorly

understood terms were the ones which showed the greatest

discrepancies between patients and staff. This suggests that

knowledge of the meaning of neuropsychological terms may be an

important factor in understanding therapist-patient

discrepancies, and the possible need for patient education.

In addition, patients reported a high incidence of emotional

dysphoria (depression, anxiety, and hostility) on the

affective checklist. While none of the affective scales were

correlated with length of post-traumatic amnesia, all of the

affective scales were correlated with the awareness of change

scores. This suggests that increased awareness of sensory and

cognitive changes is paralleled by increased emotional

dysphoria and decreased positive affect. Thus, the results of

this study demonstrate that patients show the greatest

unawareness for changes in initiation, planning, learning and

the ability to process information, and the more they are

aware of deficits or changes in these functions, the more

likely they are to be emotionally distressed. In addition,

two points are worth noting. This study showed that free

report formats are likely to yield high estimates of

unawareness (the most common method of assessment in the

anosognosia literature), which may indicate that this is a










general problem with generating responses rather than a lack

of intellectual awareness. This study also showed that if

patients have a poor understanding of the meaning of

neuropsychological terms this may lead to greater

discrepancies between patient and staff ratings on

questionnaires.

McKinley and Brooks (1984) compared 55 severe head injury

patients (all had PTA greater than 48 hours) reports of

deficits with reports from relatives. They assessed patients

at 3, 6, and 12 months post-injury. They also investigated

the relationship between cognitive performance and patient-

relative discrepancies. The results showed that there was

considerable agreement between relatives and patients

regarding sensory deficits (loss of hearing 85% agreement,

impaired sight 77% agreement), intermediate agreement for

memory and concentration difficulty (65% and 63% agreement)

and the least agreement for emotional and behavioral changes

such as whether the patient had become bad tempered (60%

agreement) or become more anxious (52% agreement). This

agrees with reports in the literature which suggest that head

injury patients are particularly reluctant to admit

emotional/behavioral changes (Fahy et al., 1967). McKinley

and Brooks (1984) also report that there were no significant

correlations between awareness scores, calculated by taking a

count of the number of problems the family reported which the

patient did not report, and a number of psychometric tests








45
that assess verbal and non-verbal intelligence, verbal and

visual recall, verbal fluency, and comprehension. This

finding suggests that when patients deny a deficit which the

relative states they have, this is not related to overall

cognitive functioning, memory ability, and language ability.

However, the authors question the usefulness of relative

reports to assess awareness. They found that relative

"neuroticism" was related to the amount of behavioral

disturbance they report for the patients. This suggests that

relatives that are more stressed will over-report

difficulties, and the poor relationship between "insight" of

the patients and the cognitive tests may be due to over-

reporting of deficits by the family member. However, the

relative which were more distressed may have been related to

more severe patients. In addition, other studies show that

when comparison is made between patients and staff, rather

than family members, there is a negative correlation with the

degree of neuropsychological impairment (Prigatano & Fordyce,

1986).

Fordyce and Roueche (1986) investigated the relationship

between awareness of behavioral limitations, psychological

distress, and response to treatment in head injury patients.

They studied 28 patients with severe head injury at an average

of 19 months post injury. They evaluated the patients level

of awareness and psychological distress before and after 6

months of rehabilitation treatment. They discovered that








46

discrepancies between staff and patients on the PCRS predicted

the degree of emotional distress as measured by the MMPI.

They classified patients into three groups based on pre- and

post-treatment patient/staff discrepancy scores on the PCRS.

Group 1 initially had scores in line with staff and were

significantly more distressed. However, as treatment

continued distress decreased for this group. Group 2 and 3

patients initially overestimated their competency, and were

significantly less distressed than the first group. Over the

course of treatment group 2 subjects showed a trend for self

ratings to approach staff ratings (i.e. greater awareness),

while group 3 ratings did not change. In addition, group 3

patients tended to experience greater distress over the course

of treatment (an interesting finding given their disagreement

with staff about their behavioral functioning). These results

demonstrate that prior to treatment intact awareness is

related to greater emotional turmoil. Results also showed

that group 3 patients had poorer neuropsychological

functioning and they showed a trend toward poorer vocational

outcome. In addition to staff ratings they obtained ratings

from a patient family member. The results show that ratings

of competence were highest for the patient, followed by the

family and the lowest ratings were from the staff, suggesting

that the level of awareness (or level of comparative self-

knowledge) depends on the comparison standard utilized (i.e.

family-patient vs. staff-patient). Other conclusions to be








47

drawn from this study are (a) awareness varies in a head

injury population, (b) prior to treatment greater awareness is

related to more emotional distress, (c) not all patients

respond to treatment interventions (among those beginning

treatment with impaired awareness and low psychological

distress) (d) unaware treatment non-responders have greater

initial neuropsychological deficits and greater emotional

distress at the end of treatment, and (e) impaired awareness

(comparative self knowledge) has consequences for vocational

outcome.

Ranseen and Bohaska (1987; reported by McGlynn and

Schacter, 1989) extended Fordyce and Roueche (1986) findings

by investigating the relationship between staff and patient

ratings on the PCRS and location of lesions following TBI.

Awareness of behavioral competence was examined in 32 patients

with focal right, focal left, or diffuse damage before and one

month into rehabilitation. Patients were found to

consistently over-rate their competencies at both test

intervals. Focal right sided injured patients showed greater

staff-patient discrepancies than focal left hemisphere injured

patients at both test intervals.

As the previous studies demonstrated there are patients

that continue to have awareness deficits for some time

following the injury. Groswasser, Mendelson, Stern,

Schechter, and Najenson (1977; reported in McGlynn and

Schacter, 1989) report that all patients that exhibited








48
unawareness of behavioral disturbances at 6 months continued

to be unaware at 30 months. Fahy, Irving, and Millac (1967)

conducted a 6 year follow up of 32 severe head injury patients

(6 had died and they report findings for the remaining 26).

They found that the patients rarely spontaneously complained

of any difficulties. However, more thorough interview with

the patient and family revealed that while they are aware of

deficits in intellect, memory, and speech, they seldom

acknowledged temperamental difficulties, which caused much

distress in the family members. They reported that nearly 70%

of their sample had some form of psychiatric symptoms. This

study suggests that many severe head injury patients remain

unaware of behavioral and emotional symptoms several years

following their injuries.

There are several general conclusions to be drawn from

these studies of CHI. (a) Unawareness appears to be common

for severely head injured patients and may continue several

years following the injury. (b) Unawareness is typically

assessed by comparison of the patients perceptions with either

actual performance on tests, relative perceptions, or staff

member perceptions. (c) While severe head injury patients tend

to be unaware of a variety of deficits, unawareness of

emotional, cognitive and social functioning are particularly

common findings. (d) More awareness tends to be correlated to

increased emotional distress. In the studies reported here,

the ability of neuropsychological measures to predict








49

unawareness has been mixed. This is likely due to the choice

of tests, and as Prigatano, Altman, and O'Brien (1990)

suggest, the typical neuropsychological measures used do not

capture the higher order behavioral capacities of individuals

which underlie the unawareness phenomenon.

Premorbid levels of awareness A discussion of awareness

of deficits following brain injury would not be complete

without mention of premorbid levels of awareness. Prior to

the illness certain cognitive functions may vary in the level

of awareness which is displayed for their operation. In their

discussion of the mechanisms responsible for unawareness,

Goldberg and Barr (1991) support the idea of variability in

awareness of certain cognitive functions which is based upon

a basic philosophy of linguistic determinism. They claim that

the greater incidence of unawareness following right

hemisphere injury may in part be due to decreased awareness of

their operations prior to the injury. Linguistic determinism

states that the content of intrapsychic processes typically

gets linked with symbolic systems (language being the best

example). Specifically, the internal experience of the

external world is organized by symbolic components of

language. The left (or dominant) hemisphere predominantly

mediates well developed representational systems and

therefore, mediates consciousness and self-awareness. They

point out that the selectivity in unawareness postmorbidly may

be due to factors which predate the illness. They base this








50
conclusion on the assumption that even in neurologically

intact individuals certain cognitive functions are

characterized by greater awareness than others (we are

typically less aware of many right hemisphere functions

relative to many left hemisphere functions). Stated

differently, normal cognition is characterized by varying

degrees of awareness of the operational content of cognition.

The implication is that the patient may be unaware of a

cognitive function because even premorbidly the internal

representation of the intact cognitive function was "fuzzy"

(Goldberg & Barr, 1991).

In addition to variability in awareness of different

cognitive functions, individuals may also vary in their

premorbid level of awareness of their cognitive functions.

This basic conclusion is supported by Weinstein and Kahn

(1955) in their famous monograph "denial of illness."

Prigatano and Leathem (1993) compared the awareness of

behavioral limitations that TBI of different cultural groups

demonstrate. They found that TBI patients from different

cultural groups, but matched demographically (the Maoris and

Non-Maoris of New Zealand), report different levels of

behavioral competency. This suggests that cultural variables

influence perceptions that TBI patients have of their

behavioral limitations and by implication suggests that

premorbid variables influence post-morbid awareness in TBI.








51
In summary, the ability to consciously reflect on one's

deficits results in self-knowledge of deficits, which is

measured by discrepancies between patients' ratings and staff

ratings, relatives' ratings, or performance. Comparative

self-knowledge may be impaired by motivated processes such as

denial, or neurologically mediated processes such as awareness

deficits. In addition, consideration must be also given to

premorbid levels of awareness. There is abundant evidence to

suggest that impaired self-knowledge of deficits is a

ubiquitous phenomenon following CHI, which has drastic

consequences for patient adjustment to society, and functions

as a protection from psychological distress.

As can be gleaned from this brief review, the phenomenon

of unawareness is diverse. It can occur for a variety of

reasons, and there is reason to believe that premorbid

awareness is selective. A consistent theme in the preceding

review is the distinction between unawareness for higher order

perceptual and cognitive deficits (e.g. aphasia, amnesia,

behavioral limitations, emotional and social functioning) and

unawareness restricted to one hemispace or hemifield

(anosognosia for hemiplegia, hemianopia).



Awareness Deficits Theories

There are several neuropsychological theories which

attempt to account for the inability to reflect upon one's

deficits. Some of the theories attempt to account only for a








52
selective form of unawareness, while others attempt to develop

models which account for all the phenomenon from this diverse

field of investigation. Emphasis shall be given to those

theories which are most relevant to the unawareness typically

observed in CHI patients. Some have claimed that awareness

deficits can be the result of impaired attention/arousal

(Heilman, Watson & Valenstein, 1985; Rubens & Garrett, 1991),

memory (Schacter, 1991), frontal executive self-monitoring

(Lezak, 1983; Stuss & Benson, 1986), or modality specific

monitoring deficits (Prigatano, 1991; Bisiach, Vallar, Perani,

Papagno & Berti, 1986; Bisiach & Geminiani, 1991; Heilman,

1991; Schacter, 1990). In addition, there are theories which

explain how awareness deficits are expressed. Each of these

theories shall be reviewed.

Attention. Studies demonstrate that CHI patients

experience attention/concentration deficits several years

following the trauma (Sohlberg & Mateer, 1989), and these

deficits have dramatic consequences for patient adjustment.

Prigatano and Fordyce (1986) review studies which suggest that

severity of CHI is related to the degree of attention deficit.

The inability to apprehend and hold information in conscious

awareness (i.e. attention deficits) creates one of the

greatest impairments for CHI patients (Gronwall, 1989;

Sohlberg & Mateer, 1989). However, investigation is difficult

because a single unifying theory of attention has








53
not generally received wide acceptance (Sohlberg & Mateer,

1989).

Posner and Rafal (1987) differentiate three forms of

attention which are hierarchically arranged: arousal,

selective attention, and vigilance. The first form of

attention is basic alertness and arousal, which they divide

into tonic and phasic arousal. Tonic alertness refers to

diurnal fluctuation and phasic arousal is the instantaneous

facilitation of performance induced by a warning signal. The

second form of attention requires the selection of specific

environmental or internal stimuli for further conscious

processing. Hemispatial neglect can be seen as one type of

deficit in selective attention. The third form of attention

is sustained concentration or vigilance. Vigilance refers to

the maintenance of conscious mental effort across some period

of time.

Sohlberg and Mateer (1989) reviewed the literature on

attention deficits following head injury and devised a model

which extends the forms of attention posited by Posner and

Rafal (1987). Their model accounts for the classic view of

attention as an information processing capacity as well as

incorporating the working memory component of attention

(Baddeley, 1981). They consider attention to be a

multidimensional capacity which is critical to memory and

other forms of cognition. They present five levels of

attention which are hierarchically arranged; focused,








54

sustained, selective, alternating, and divided attention. It

is presumed that deficits in successively lower elements of

attention will result in failure in higher forms. For

example, a deficit in focused attention will create

difficulties maintaining selective and divided attention.

While impaired recognition of attention deficits has been

reported (Allen & Ruff, 1990), few studies speculate directly

on how attention deficits contribute to unawareness. Some

investigators have suggested that attention serves the general

function of maintaining awareness (Buchtel, 1987). Heilman,

Watson, and Valenstein (1985) suggest that impaired

arousal/attention may be the cause of some unawareness

phenomena (anosognosia for hemiplegia). Allen and Ruff (1990)

consider the ability to attend essential to a definition of

awareness. They define awareness as the ability to attend,

encode, and retrieve information concerning the self. Rubens

and Garrett (1991) suggest that a possible mechanism of

unawareness in language disturbances may be due to impaired

focused attention of their speech output.

McGlynn and Schacter (1989) suggest that among head

injury patients poor attentional abilities may contribute to

unawareness. Evidence that attention is related to

unawareness among head injury patients is supported by a study

by Bergquist and Malec (1993). They administered the Patient

Competency Rating Scale (PCRS); which is comprised of items

related to activities of daily living, emotional functioning,








55

and interpersonal skills, to 40 patients with severe traumatic

brain injury and their staff in order to obtain the

discrepancy which was used as a measure of awareness. When

they divided the patients into three groups based on severity

of unawareness they found poor attentional functioning (as

measured by the Freedom from Distractibility Factor from the

WAIS-R) for the groups that showed the greatest unawareness.

Following CHI, deficits in the higher forms of attention

such as alternating and divided attention, are particularly

impaired, resulting in significant impairment in daily life

(Sohlberg & Mateer, 1989). These studies and reviews suggest

that adequate attentional capacity at all levels, from focused

to divided attention, provides the foundation for memory and

cognitive processing; thus, deficits in attention should

contribute to awareness deficits. Therefore, assessment of

the higher forms of attention, particularly the alternating

and working memory components of attention, would assess both

higher and lower forms of attention deficits.

Memory and metamemorv disturbance. In addition to

problems attending, CHI patients have difficulty recalling

recent events and acquiring new information. Baddeley,

Harris, Sunderland, Watts, and Watson (1987) suggest that the

structure of memory is divided into three parts. The first is

a brief sensory memory which includes iconic (visual) and

echoic (auditory) memory. The second, previously referred to

as short-term memory, is currently referred to as working








56
memory. However, Cowan (1988) conceptualizes working memory

as a subset of short-term memory (a scheme which we will adopt

for the current study). Working memory refers to the

temporary activation, storage, and manipulation of information

necessary for understanding, reasoning and learning. It

assumes a central executive system which coordinates several

other subsidiary systems. The third component is long-term

memory, which implies the long-term storage of information.

Distinctions have been suggested for long-term memory, such as

semantic versus episodic, procedural versus declarative, and

prospective memory (Baddeley et al., 1987).

CHI can result in difficulty recalling preinjury events

or retrograde amnesia, and difficulty acquiring new

information or anterograde amnesia (Baddeley et al., 1987).

Posttraumatic amnesia refers to the early stage of confusion

and disorientation following trauma in which new memories are

not formed and can be considered a subtype of anterograde

amnesia.

Evidence suggests that impaired anterograde memory may

contribute to unawareness, but by itself does not preclude

adequate self-knowledge from developing (Schacter, 1991).

Some have suggested that unawareness of deficits may be due to

poor monitoring of cognitive performance. This phenomenon is

referred to as metacognition when referring to cognitive

skills and metamemory when referring specifically to memory

performance (Shimamura & Squire, 1986). Metacognition refers








57

to knowledge of one's own cognitive performance and is

involved in various aspects of problem solving such as

consideration of the cognitive operations required to solve a

particular problem. Metamemory includes both knowledge of

one's memory strengths and weaknesses, and general knowledge

of task and strategy variables that influence recall of

information (Cooley & Stringer, 1991). Metamemory is a

complex function which requires monitoring of memory

performance, drawing inferences from this performance, storage

of this information, and gaining access to this information

when planning future behavior. In the literature reviewed

previously, metamemory procedures such as the feeling-of-

knowing paradigms are considered to be experimental indices of

unawareness of memory impairments and in some cases have been

used synonymously.

As stated in the previous section on unawareness of

memory impairment, clinical and experimental evidence (McGlynn

& Schacter, 1989; Schacter, 1991) suggests that amnestic

patients with unawareness of memory deficits have signs of

frontal lobe pathology and metamemory disturbances. For

example, the Korsakoff patients have amnestic disturbances

with well documented frontal lobe signs, a relative

unawareness of their deficit (Schacter, 1991), and

disturbances in metamemory (Shimamura & Squire, 1986). These

findings suggest that unawareness of memory disturbance and

impaired metamemory may be due to frontal lobe dysfunction.








58
Schacter (1991) suggests that since the frontal lobes function

to integrate information and monitor responses (Stuss and

Benson, 1986), it is not surprising that amnestics with

frontal damage demonstrate an inability to be aware of their

memory performance. It is this "on-line" monitoring that

frontal patients lack, which leads to unawareness. When this

mechanism is intact it allows awareness which frequently leads

to distress about the deficit (Schacter, 1991). The other

frontal mechanism that may be responsible for unawareness of

memory impairments is the frequent problem frontal lobe

patients have inhibiting strong response tendencies. So when

a frontal patient is asked about their memory impairment the

strongest response tendency may be to report on "premorbid"

memory function (Schacter, 1991).

In summary, studies suggest that impaired monitoring of

memory performance (i.e. metamemory) is a necessary element

for unawareness of memory disturbances and impaired memory

sustains unawareness (Schacter, 1991). Metamemory

disturbances are common for head injury patients and these

deficits are related to frontal executive functioning.

Frontal executive functioning. The frontal lobes are

thought to subserve many of the complex integrative functions

of cognition (Stuss & Benson, 1986). As previously mentioned,

frontal functions are involved in attention and memory

contributions to impaired awareness. Also previously

mentioned, the frontal lobes are frequently damaged following








59
CHI. Descriptions of frontal lobe unconcern and unawareness

of deficits are also well documented (Stuss, 1991).

Stuss and Benson (1986) developed a framework for

understanding the specialized functions of the frontal lobes.

They hypothesized that there are three major areas of frontal

function. They postulated that the brain consists of a number

of organized integrated functional systems; sensory-motor,

emotion, memory, and language (Stuss, 1987; Stuss, & Benson,

1986). Each system has direct and reciprocal connections to

the frontal cortex. Posterior-basal brain areas are thought

to mediate the various functional systems, thus damage to

frontal areas frequently leaves overlearned abilities and

overall intellect intact. This frequent finding correlates

with clinical evidence which suggests that frontal patients

can have intact IQ, but when tasks require the patient to

structure responses, performance deteriorates (e.g. Wisconsin

Card Sorting Test; Stuss, 1987). The first set of functions

combines two anterior functional systems: sequencing and

drive. Sequencing is dependent on intact lateral (dorsal and

orbital) frontal structures, and drive mediated by the medial

frontal structures. Sequencing organizes bits of information

in meaningful sequences, and drive initiates action (pathology

results in either decreased and apathetic or excessive and

impulsive behavior).

The second function of the frontal lobes is their

executive or control abilities. In routine environments the








60
posterior system functions adequately; however, with novelty,

the frontal executive is active. The executive system

extracts information from posterior regions, anticipates,

plans, selects, experiments, and modifies as the demands

require. These functions are thought to be particularly

prefrontal, and often dysfunctional following CHI (Lezak,

1987b). Lezak (1987b) suggests that executive function is

defined by goal-directed behavior, i.e. the ability to

formulate goals, plan and organize behavior relevant to those

goals, monitor performance, and self-correct behavior to bring

it into line with the original goal.

The third, related function of the frontal lobes,

particularly prefrontal regions, is introspection, self-

awareness, and self-consciousness. Lezak (1987b) identifies

this as taking the "abstract" attitude, i.e. taking a

perspective different from one's own. In the case of self-

awareness it means taking one's self as the object of study.

Damaged frontal lobes frequently leave patients with very

shallow interests, and loss of self-concern. The lack of

self-awareness is likened to disturbed metacognition (i.e. the

inability to think about one's thinking). Self-awareness is

necessary for the correction of a present state with a mental

comparison (Stuss & Benson, 1986). Stuss (1991) maintains

that this frontal system unawareness is not a lack of

knowledge; it is instead impaired judgement of the facts in

relation to one's own life. In behavioral terms, self-








61
awareness deficits are revealed in unconcern, impaired self-

monitoring, and deficient self-regulation. Impaired self-

awareness leads to deficits in alteration of behavior and

belief system. Lezak (1987b) identifies the later two

functions of executive control and introspection as essential

requirements of successful vocational re-entry.

In sum, Stuss and Benson (1986) and Lezak (1987b) are

suggesting that the frontal lobes are directly involved in

self-awareness and monitoring of cognition and behavior.

Therefore, awareness deficits resulting from frontal pathology

could be viewed as a self-monitoring and self-awareness

deficit.

Modality specific/Modular models. Bisiach and Geminiani

(1991) propose a modality-specific model to explain unilateral

representational disorders such as anosognosia for hemiplegia

and hemianopia, neglect, and somatoparaphrenia. In their

model, they suggest that consciousness is at least partially

composed of modality specific representations which are

parallel, spatially distributed, and sensory specific.

A more encompassing modality-specific or modular model is

presented by Prigatano (1991) in which the "type" of

unawareness observed varies as a function of the particular

heteromodal cortex which is lesioned. Heteromodal cortex,

previously termed tertiary cortex by Luria, responds to

multiple modalities of stimulus input, and therefore,

subserves the highest functional organization of the various










inputs to that cortical region. Thus, unawareness of body

image may result from inferior parietal lobe damage; impaired

awareness of linguistic output dependent upon intact superior

marginal, angular, and temporal gyri; and higher level

unawareness of social judgment, resulting from damage to

prefrontal regions. This model implies that awareness of a

particular function is served by the same cortical region

which represents that function. He suggests that this may be

why CHI frequently impairs many higher cognitive functions

along with deficits in awareness of those functions.

Schacter (1990) makes the similar claim that site of

lesion determines the particular form of unawareness and

deficit. He attempted to explain unawareness of deficits

following brain injury by postulating a phenomenal awareness

system named the Dissociative Interaction and Conscious

Experience (DICE) model. In his model he suggests that there

are specific knowledge modules, such as lexical, conceptual,

facial, and self, which normally contain specific overlearned

information. These knowledge modules normally have reciprocal

connections with a higher level processing system, or

Conscious Awareness System (CAS). Should one of these

connections dysfunction, deficits in awareness of that

specific module would be impaired, similar to Prigatano's

model. However, if damage occurred to the CAS, awareness

would be impaired across multiple domains. Damage to specific

modules can result in unawareness for that specific function,








63
and it is likely that the function impaired will vary

according to the site of lesion. Schacter (1990) also

suggests that the anatomical correlate to the CAS is a

posterior system involving the inferior parietal lobule. The

inferior parietal region is where visual, somesthetic and

auditory pathways converge.

The DICE model also posits that the CAS has connections

to a frontal "executive system" which initiates, organizes,

and modulates complex ideas and behaviors. This is consistent

with Stuss and Benson's (1986) conceptualization of executive

functioning. Studies show that there are reciprocal afferent

connections between the frontal lobe and the inferior parietal

lobe (McGlynn & Schacter, 1989). The DICE model suggests that

the CAS mediates awareness of relatively simple perceptual and

motor responses, and the executive system is responsible for

awareness of complex functions. Thus, damage to the parietal

lobes should result in classic unawareness of hemiplegia and

hemianopia, etc., while damage to the frontal lobes will

result in unawareness of complex deficits, such as problem

solving, social, behavioral and personality changes. For

example, Anderson and Tranel (1989) provide evidence which

suggests that unawareness of motor impairments is dissociable

from unawareness of cognitive deficits, consistent with

Schacter's (1990) formulations. In addition, the Wagner and

Cushman (1994) study confirms some of the anatomic

localization predictions of the DICE model. They found that








64
unawareness of perceptual deficits were more common following

right posterior cortical lesions and unawareness for complex

deficits (reason for hospitalization, cognitive deficits, and

memory deficits) were more common following anterior lesions.

With the intact brain, our sensations and perceptions

have contact with our thoughts, past experiences, and

feelings. Our brain allows us to evaluate ourselves and the

world around us, decide what is right, and take appropriate

action when necessary. However, self-evaluation and

behavioral initiation may be particularly impaired following

CHI. As Schacter (1990) and Prigatano's (1991) theories

suggested, awareness deficits may exist for relatively lower

order sensory-motor deficits, or higher cognitive-emotional

functions (Anderson & Tranel, 1989; McGlynn & Schacter, 1989).

The latter form of unawareness has come to be termed a deficit

in self-awareness. Stuss and Benson (1986) also suggest that

self-awareness deficits are distinct from simple unawareness

of deficit, such as for hemiplegia or hemianopia. Despite

these endorsements the term is not without confusion, because

deficits in awareness of motor behavior are still related to

the self and constitute impaired "self-awareness." In spite

of this confusion, the distinction between awareness of motor

and higher cognitive dysfunction appears to have functional

and anatomical significance. The importance of these modality

specific and modular models is their ability to encompass many

unawareness phenomena, integrate such phenomena with knowledge








65
of anatomy, and therefore, serve as rich sources of theory

based research.

Levels of awareness model. Another integrated model of

awareness deficits was developed by Crosson, Barco, Velozo,

Bolesta, Cooper, Werts & Brobeck, (1989). They find that head

injury patients demonstrate different types of awareness

deficits which are interdependent and hierarchically arranged.

The model they developed helps to explain why patients may

report deficits while not demonstrating this awareness in

their behavior i.e why awareness deficits may lead to

functional impairments, even when a patient can verbally

report a particular deficit. These forms of awareness help

elucidate how patients become unaware of their deficits while

possibly suggesting mechanisms which underlie these functions.

The first type of awareness is intellectual awareness,

which is defined as the ability to understand that a

particular function is impaired. This type of awareness is

fundamental for more "on-line" forms of awareness. Knowledge

of impairments represent anterograde information, thus

intellectual awareness may be impaired by many of the

mechanisms reviewed such as problems obtaining information

caused by abstract reasoning, memory, or metamemory

disturbances (Shimamura & Squire, 1986).

The second level of awareness is emergent awareness,

which is the ability to recognize a problem while it is

occurring. This requires intellectual awareness. It also








66
requires monitoring the relationship between their actions,

the effect they are having on the environment, and the desired

cognitive or behavioral product. This on-line form of

awareness is described by Goldberg and Barr (1991) as a

process of error monitoring. They posit three mechanisms of

error monitoring which underlie an awareness of deficits. The

first is an internal representation of the desired cognitive

process or behavior, the second is the feedback of the actual

output, and the third is an intact mechanism which compares

the actual output with internal representations of the desired

cognitive and behavioral product. This latter mechanism is

similar to working memory, i.e. the temporary activation,

storage, and manipulation of information necessary for

understanding, reasoning, and learning. Working memory

implies a central executive which coordinates the manipulation

of information. The central executive's function is similar

to that of a CPU in a computer, selecting information to be

stored in RAM while comparing information obtained from memory

storage. The central executive is needed in order to select

information to be retrieved into working memory.

While performing a behavior which is being affected by

their deficits, patients must first receive feedback regarding

their actions, then compare their current behavior and the

desired cognitive or behavioral product. In addition, it

requires that they access the stored knowledge of the deficit

in long term memory and make a decision regarding whether such








67

behavior is related to the deficit, i.e. if it fits some

exemplar of the "deficit" or behavior that would result from

the deficit.

Barco, Crosson, Bolesta, and Stout (1991) present a case

study which illustrates the following form of awareness. The

client was a well educated woman in her 20's who had sustained

a severe closed head injury in a motor vehicle accident. MRI

revealed bilateral contusion to frontal and temporal lobes, as

well as contusion to the left posterior internal capsule.

Five months post-injury she was found to have difficulty with

verbal memory, moderate language problems, and lapses of

attention. Exacerbating her deficits was a lack of awareness

of the existence of these problems, i.e. a deficit in

intellectual awareness. Her attention deficits were assessed

to be one of the greatest impediments to her functional

recovery. For example, during an occupational therapy

assessment which required her to follow a simple route, she

distracted herself with her own conversation to such an extent

that she did not attain her goal. When these errors were

pointed out to her she made "excuses." With constant feedback

during 3-4 weeks of therapy she was able to gain a greater

level of intellectual awareness about her deficits. However,

she was unable to utilize this information during a task.

This represented a lack of emergent awareness. For example,

during a study skills trial, she had great difficulty

attending to the task, and she did not recognize the








68
difficulty as it was occurring. Although she had the

knowledge that she had a problem with attention and being

distracted, she failed to utilize it "on-line" which made the

knowledge of her deficits useless in that particular

situation. In terms of error monitoring as presented by

Goldberg and Barr (1991), the "desired behavior" was that she

attend to her studies. Since previous evaluation suggested

that she developed intellectual awareness, i.e. she knew the

"desired behavior", this suggested that she either lacked

feedback regarding her behavior, or the mechanism which

compares the desired product was dysfunctional. Through

further training she was able to learn to recognize when she

was getting inattentive, thus increasing her emergent

awareness. However, therapy was unsuccessful at improving her

ability to anticipate when and where she might be more

vulnerable to experiencing attention difficulties.

This last form of awareness that the patient lacked is

anticipatory awareness, i.e. the ability to anticipate that a

problem will occur due to the deficit. This is the most

complex form of awareness and is dependent upon the other two

forms of awareness. Anticipatory awareness may be needed even

when completing a rating scale. For example, in order for

patients to rate their competence performing several of the

behaviors listed on the PCRS, patients must have either had

experience with the behavior or been told that their deficits

will cause difficulty performing these behaviors. Otherwise








69

patients are required to use anticipatory awareness to

evaluate their competence. In other words, patients must have

intellectual awareness to complete the PCRS, while feeling-of-

knowing paradigms require anticipatory awareness, specifically

for memory. The ability to anticipate that a problem will

occur as a result of a deficit also requires adequate abstract

reasoning ability.

In summary, intellectual awareness, emergent awareness,

and anticipatory awareness are hierarchically dependent levels

of awareness. Some of the neuropsychological mechanisms

necessary for their functioning may be adequate memory,

metamemory, executive and error monitoring, working memory,

and abstract reasoning.



Summary

Several themes emerge from the above review of awareness

of deficits:

1. Awareness deficits are common, particularly for severe

closed head injury patients.

2. Awareness deficits can occur because a variety of

underlying deficits.

3. Decreased awareness has consequences for rehabilitation,

vocational and occupational adjustment.

4. The review also supports several distinctions: (a) the

literature suggests that unawareness can be due to an

incapacity to be aware (awareness deficit) or the result of a








70

defensive reaction to deficits (denial). (b) Self-awareness

is a state of reflection on one's self while self-knowledge is

the stored representation of this knowledge. (c) The level of

self-awareness and self-knowledge is usually assessed by

comparison with some "objective" standard. (d) A common

distinction is between awareness of relatively simple

functions versus awareness of higher level functions.

5. Awareness deficits vary as a function of lesion site. The

frontal and parietal lobes have been implicated most often,

and the right hemisphere appears to play a special role in

mediating awareness.

6. The more patients become aware of their deficits the more

psychological distress they experience.

7. Patients may have been unaware of certain cognitive

functions premorbidly, which impacts awareness after injury.

8. Theories that have been presented suggest various

neuropsychological mechanisms to explain awareness deficits.

The theories suggest that awareness deficits may be caused by

impairments in attention, memory, metamemory, working memory,

frontal executive self-monitoring, and abstract reasoning.

Frontal functioning figures prominently in many of these

theories and they suggest that one of the functions of the

frontal system is to mediate self-awareness.

9. Denial is thought to be an important cause of unawareness.










Self-Concept After Closed Head Iniurv

While CHI frequently results in impairments of cognition,

physical functioning, social functioning, and self-knowledge,

patients continue to have conceptions about themselves.

Patient evaluation of their status has significant

consequences for their adaptation and emotional well being.

For example, Lewis and Rosenberg (1990) suggest that low self-

esteem and anxiety are the most common themes in psychotherapy

with CHI patients. In addition, recent evidence suggests that

CHI patients' self-reports and self-evaluation of their status

is an important area for study and provides a needed adjunct

to neurobehavioral testing (Allen & Ruff, 1990; Fordyce &

Roueche, 1986; Tyerman & Humphrey, 1984). The purpose of the

current section is to describe the structure and function of

the self-concept in CHI.

Only a handful of investigators have measured self-

concept and self-esteem with CHI patients (Lynch, 1989; Newton

& Johnson, 1985; Thomas, 1990; Tyerman & Humphrey, 1984),

despite the general agreement that self-esteem functions as a

protection against psychological distress (Bednar, Wells, &

Peterson, 1989; Rosenberg, 1989), and despite the negative

relationship between self-esteem and psychological distress in

other populations (Harter, 1983; Homey, 1937; Robson, 1988;

Rogers, 1961; Rosenberg, 1989). Lewis and Rosenberg (1990)

suggest that self-esteem is lower in those with head injury

and .....frequently a patient's low self-esteem and lack of








72

motivation result from the psychological impact of the trauma

and it's sequelae."

Lynch (1989) evaluated the global self-esteem (using the

Rosenberg Self-Esteem Scale), self-consistency, and self-

consciousness of 40 mild head injury patients several months

after their expected neuropsychological recovery. She found

that the patients had moderate to high levels of self-esteem;

however, she did not make statistical comparison to a control

group. In addition, their self-concept was stable, i.e. they

did not demonstrate low scores on a measure of self-

consistency. She also found that patients had mild

neuropsychological deficits on attentional and memory tests

(e.g. the PASAT, and CVLT), and their self-concept was

moderately related to neuropsychological outcome. They found

that decreased cognitive deficits were associated with high

self-esteem, high self-consistency, and low self-

consciousness.

One of the only studies designed to evaluate the self-

concept in a severe head injury population was done by Tyerman

and Humphrey (1984). They had 25 severe CHI patients, seven

months post-injury, rate the following; the semantic

differential (a measure of self-concept), measures

psychological distress, and measures of physical disability.

On the semantic differential subjects made judgements of their

present, past, and future self, as well as for the typical

person and for the typical head injury patient. They found








73
that CHI patients have drastic changes in their self-concept

while expecting to return to premorbid levels in a short time.

Their ratings for present self were significantly below both

the ratings for past self and future self. The ratings for

past self and future self were nearly identical. This

suggests that their self-concept had declined but was expected

to return to normal, premorbid levels. When rating the same

scale for a typical person and typical head injury patient the

results showed that patients believed that there were no

differences between their present self-concept and that of a

typical person. However, they did believe that they were

better off than the typical head injury patient. They

reported themselves to be more interesting, in control,

mindful, active, and cooperative. They also believed that the

typical head injury patient has lower self-concept than the

typical person.

Tyerman and Humphrey (1984) also evaluated the

relationship between physical deficits and the physical self-

concept. They administered the Litman Physical Disability

Self-Conception scale and found that with regard to their

social discomfort, and self-image of their physical

disability, many patients (30-40%) had a reduced sense of

personal worth and were self-conscious about their physical

disabilities. This suggests that CHI patients have a physical

self-concept which is affected following the physical injuries

they receive. In addition, they found that patients








74
experienced high levels of depression and anxiety, and

moderate amounts of unawareness, which was measured by the

relative congruence of pre- and post-injury ratings of self.

However, Deaton (1986) has suggested that this may not be

denial so much as it is an indicator of the slow process of

self-concept change. Thomas's (1990) findings also suggest

that severe CHI patients have low self-esteem, which is

negatively related to depression. Newton and Johnson (1985)

reported on the social and psychological adjustment of 11

severe CHI patients, comparing them to normal controls and

outpatient psychotherapy patients. They found that CHI

patients have significantly lower self-esteem and impaired

social adjustment as compared to normal controls.

These studies demonstrate that self-esteem and self-

concept are lower in CHI patients, suggesting that

investigation of self-concept is warranted.



Self-Concept and Self-Esteem Defined

William James (1890) developed a formula that described

self-esteem as being a function of "successes" divided by

"pretensions" (beliefs about our own potentialities). With

this brief but eloquent formula the modern investigation of

self-esteem began. Fueled by the cognitive revolution, there

has been a resurgence of interest in self-concept theory,

particularly in the field of social psychology (Bednar et al.,

1989; Epstein, 1987; Gecas, 1982).








75
Following a review of the literature on self-esteem

Bednar, Wells, and Peterson (1989) reported that there is

overwhelming agreement that realistically high self-esteem is

a beneficial and desirable personality trait. Some go further

to suggest that high self-esteem is essential for mental

health (Branden, 1969; Rogers, 1959). However, if one

accounts for the importance ascribed to it, self-esteem

remains a poorly understood concept, despite some of the

recent contributions to self-concept theory (Bednar et al.

1989; Markus & Wurf, 1987).

Gecas (1982) defines the self-concept as "the concept the

individual has of himself as a physical, social, and spiritual

and moral being" (p. 3). The self-concept for Rosenberg

(1979) is defined as the "totality of the individual's

thoughts, and feelings with reference to himself as an object"

(p. 7) and is itself only a part of the total personality.

The self-concept is thus the realm of "self ideas." For

Rosenberg (1979) the structure of the self-concept is divided

into three areas. The extant self is the current or existing

self which represents what one sees when looking in the

mirror. In contrast, the desired self is what one aspires to

be. The presented self is the self-concept presented to

others, which is dynamic, changing and therefore situationally

dependent. The content of the self-concept includes social

identity (race, sex, social status, and memberships),

dispositions (traits, attitudes, beliefs and values) and








76

physical attributes (body image), all of which can be

described and evaluated. Thus, the self-concept is a

multidimensional multifaceted construct (Markus & Wurf, 1987;

Shavelson, Hubner & Stanton, 1976).

Self-esteem is thought of as the evaluative component of

the self-concept, i.e. the valence attached to the various

characteristics of the self-concept (Markus & Wurf, 1987;

Rosenberg, 1979). Fleming and Watts (1980) suggest that

studies have been unable to support a statistical distinction

between the evaluative and descriptive aspects of the self-

concept because scales which measure "self-esteem" have often

been interchangeable with scales measuring "self-concept",

suggesting that either better measurements are needed or it

may not be possible to distinguish them. However, we shall

continue to maintain this theoretical distinction, while

reminding the reader that studies often confuse these terms.

Current theories of self-concept portray it as a

multidimensional, multifaceted dynamic structure implicated in

virtually all social information processing (Markus & Wurf,

1987).



The Dynamic Self-Concept

Markus and Wurf (1987) developed a "dynamic self-concept"

model, in which the self-concept is viewed as a collection of

self-representations; with a working self-concept that is a

subset of representations that are active at any one time.








77
Self-representations are particular self-conceptions which can

vary in importance or centrality to the self. The working

self-concept is a continually active, shifting array of

accessible self-knowledge, which is involved in goal setting,

planning, monitoring, judgement, and self-evaluation when

information is relevant to the self (i.e. self-regulatory

functions). It is the working self-concept which regulates

both intrapersonal (information processing, affect regulation,

and motivational processes) and interpersonal (social

perception, social comparison, and shaping interactions with

others) behavior.

The representations that are active in the working self-

concept may invoke what Rosenberg (1979) refers to as self-

concept motives; self-enhancement and self-consistency. To

these Epstein (1987) adds the motive of maintaining reality

contact and assimilating the data of reality. Most often

these three motives work in concert, to influence behavior and

support the self-concept. These motives have been useful for

describing the responses people make in reaction to evaluative

feedback. These theories claim that changes in thought,

affect or behavior are attempts to maintain either self-

consistency, positive self-esteem, and contact with reality.

Self-consistency motivation is the desire to maintain a stable

self-concept in the face of potentially threatening or

contradictory information (Rosenberg, 1979). Because the

self-concept is anchored in a broad network of beliefs,








78
significant changes would destabalize the entire system and

cause extreme anxiety (Epstein, 1987). The self-enhancement

motive is the desire to seek explanations for behavior which

emphasize the positive aspects of the individual. These

motives usually act together, with the result of small upward

changes in self-concept being the most acceptable. While

these motives usually act in concert, there are instances in

which they are opposed to one another, such as following a

perceived failure. For a relatively high self-esteem person

the full acceptance of negative feedback runs counter to self-

enhancement motives, and self-consistency demands that the

current self-concept be maintained. However, the reality

which confronts the individual demands that accommodations be

made in the self-concept.

This interaction of motives may explain why dramatic

changes in self-esteem are so uncommon and so hard to come by

in psychotherapy (Epstein, 1987), and why self-concept is very

slow to change following CHI (Deaton, 1986). When the CHI

patient is confronted with information about deficits, which

is discrepant with premorbid self-conceptions, self-

enhancement and self-consistency motives predict that the

information should be denied, while the motive to accommodate

reality would predict acceptance of the feedback. However, as

Epstein (1987) suggests one of the these motives may be

sacrificed for another, and reality may be sacrificed in order

to maintain self-esteem and stability. In fact, the reason








79
that reality may get "sacrificed" could be due to an awareness

deficit.

In summary, the self-concept is a continually active

entity which describes our attributes and characteristics.

Self-esteem by contrast is the evaluation of those

characteristics. At any one time, there are different

elements of our self-concept active which mediate our

intrapersonal and interpersonal behavior. The evaluative

aspects of self-concept, as just described, would fit into the

realm of frontal functions, as described earlier. Epstein

(1973) summarized the current perspective on self-concept by

claiming that a healthy self-concept organizes the data of

experience and maintains self-esteem and when new evidence

threatens the self-concept, it is either assimilated

(acceptance) or avoided (defenses erected).



Self-Concept. Denial and Awareness Deficits

So far self-concept, denial, and awareness deficits have

each been considered in isolation. There have been very few

studies which have speculated on the relationship between

awareness, denial, and self-concept in CHI. Deaton (1986)

devoted an entire monograph to ".. the type of denial that is

characterized by a failure to change one's self-concept

despite adequate information following an injury, and that

acts as a psychological defense."(p. 232) The denial to which

she was referring includes both psychological denial and








80
neurological awareness deficits. (In this document the phrase

"self-knowledge of deficits" has been used as a supraordinate

construct to encompass both psychological denial and awareness

deficits.) Of awareness deficits she states "..damage to the

brain disrupts self-concept and cognition, resulting in an

unawareness of deficits that is organically mediated." (p. 232)

The relationship between the self-concept, awareness deficits,

and denial is captured in a statement made by Ford (1976)

(cited in McGlynn and Schacter, 1989) who suggested that

following head injury the patient will deny intellectual

impairments and "at first he will identify with his own

premorbid self-image, and only after many destructive failures

comes to see he is not the man he was" (p. 603). This

statement hints at the transformation of the self-concept as

the patient recovers but it assumes that the patient does not

have an awareness deficit which would preclude the self-

concept change from taking place.

Crosson (1987) suggests that in the rehabilitation

environment one of the manifestations of denial may be that

the patient will not begin to apply compensations to their

behavior because the compensation does not fit their self-

concept. There is abundant evidence which suggests that

defensive processes are activated in order to maintain self-

esteem (Harder, 1984). Denial is also thought to be

proportional to the threat posed to one's self-esteem (Levine

& Zigler, 1975) and may allow patients to maintain self-esteem








81
and self-concept stability (Deaton, 1986; Markus & Wurf,

1987). Some studies show that when evaluative feedback is

incongruent with the self-concept it will be distorted,

rejected, and considered less credible (Shrauger & Terbovic

1976). Denial serves a function for CHI patients, just as it

does for the non-head injured person. There are several

studies with normals which suggest that maintaining an overly

optimistic attitude and positive self-evaluation (similar to

the "rosy glow effect") is related to psychological health

(Taylor & Brown, 1988). Bednar, Wells and Peterson (1989)

present a model which suggests that consistent high self-

esteem is maintained by the process of coping with the sources

of negative evaluative feedback, rather than avoiding the

feedback. Deaton (1986) suggests that, following CHI, denial

is activated as a result of stability needs, i.e. the desire

to maintain the old self-concept at the cost of neglecting

facts relevant to the self. Denial is thus activated in order

to protect the self-concept; however, coping with the negative

feedback may be necessary in the long run in order to maintain

self-esteem. In this case, awareness is assumed to be intact

enough to allow comparisons to be made between the pre-morbid

self-concept and currently impaired status (Allen & Ruff,

1990) in order for denial to be activated.

Because self-awareness is necessary for self-conception

(Carver & Scheier, 1982) there are instances in which CHI

patients are unable to become aware of the conflict between








82

their old self-concept and current status; thus, these

patients are rendered unable to form new self-concepts. As

mentioned previously, CHI frequently results in damage to the

frontal lobes causing self-monitoring and self-awareness

deficits. Self-awareness deficits are impairments in judging

the significance of an event for the self. More abstractly,

it involves the inability to integrate and maintain two or

more representations simultaneously, which is partly dependent

upon intact working memory. Impairment of working memory,

then, may be one reason why CHI patients have difficulty

changing self-concept (Goldman-Rakic, 1992). This is

characterized by Prigatano (1991) as the "experience of

normality despite brain damage, coupled with the simultaneous

perception of an altered sense of self" (p. 112). Given that

frontal damage often causes impairments in working memory and

therefore self-awareness, it is intriguing to consider the

similarities between the model of self-concept presented by

Markus and Wurf (1987) and Stuss and Benson's (1986) model of

frontal lobe functioning. For example, the frontal lobe

functions (such as self-monitoring, self-regulation, and self-

awareness) proposed by Stuss and Benson (1986) are nearly

identical to the functions of Markus and Wurf's (1987) working

self-concept. The regulatory functions such as formation,

initiation, enacting, and monitoring of goals are functions

ascribed to both models. The working self-concept is also a

dynamic entity which mediates most behavior, much the same way








83

working memory controls or regulates behavior. Working self-

concept is also of limited capacity. Working self-concept may

in fact be a component of the complete working memory active

at any one time. It is in this regard that awareness

deficits, particularly "self-awareness" deficits, result in

deficits in self-conception. A self-concept deficit is the

acquired inability to alter self-concept due to neurological

impairment.

Considering the relationship between denial, awareness

deficits, and self-concept, the common element is that both

denial and awareness deficits result in decreased self-

knowledge. In the case of denial, threatening information is

avoided in order to protect the premorbid self-concept while

awareness deficits inhibit information from gaining access to

the premorbid self-concept.



Psychological Distress Following Closed Head Injury

Psychological distress is a negative affective reaction

to the underlying psychological or neurological pathological

state of an organism. As mentioned earlier, emotional

distress is common following CHI. Prigatano (1987) suggests

that management of emotional disorders is essential for

successful patient outcome. Depression, anxiety, and

catastrophic reactions may be due to a reactive maladjustment

to illness, neurological insult, or a combination of these

factors (Crosson, 1987). Anderson and Tranel (1989) suggested








84
that emotional expression may actually be disrupted by the

same lesion which causes an awareness deficit, because

patients are unable to be anxious about a deficit about which

they do not know. However, while a severe awareness deficit

would preclude awareness of deficits, patients may be able to

understand that undesirable changes have occurred, though they

cannot make a connection to their own deficits. Therefore,

emotional functioning may be affected by either reactive or

neurological factors, particularly denial and awareness

deficits. Fordyce and Roueche (1986) found a negative

relationship between awareness deficits and psychological

distress (also see, Olson, 1990). Boake, Freeland, Ringholz,

Nance, and Edwards (1987) studied 34 severely head-injured

patients and confirmed the lack of association between self-

rating of memory performance and actual memory performance

found in the Sunderland et al. (1983) study. In addition, the

Boake et al. (1987) study showed a significant relationship

between self-rated memory impairment and emotional distress

(measures of depression and anxiety). They found that those

rating more memory impairment were more distressed, suggesting

that patients that are more unaware are less emotionally

distressed. Emotional distress usually increases as the level

of awareness of injury increases and self-esteem decreases.

Studies of CHI patients frequently demonstrate greater

emotional distress as time since onset of illness increases

(Alfano, Neilson, Paniak & Finlayson, 1992; Fordyce, Roueche








85
& Prigatano, 1983; Levin & Grossman, 1978; Lishman, 1979).

Fordyce et al. (1983) found that chronicity of CHI was

positively associated with depression and anxiety on the MMPI,

despite equivalent severity of dysfunction (length of coma)

and level of neuropsychological functioning. Emotional

distress following CHI also portends later maladjustment

(Levin, Benton & Grossman, 1982). The most common emotional

reactions to CHI are depression and anxiety.

Depression is a common negative emotional reaction

following brain injury (e.g. Code, 1986; Fordyce & Roueche,

1986; Fordyce, Roueche & Prigatano, 1983; Gainotti, 1972;

Lishman, 1978; Prigatano, 1987; Robinson, Kubos, Starr, Rao &

Price, 1984; Schoenhuber & Gentilini, 1988), which may be the

result of failure to live up to one's own ideal self (Higgins,

Klein & Straumann, 1985). Depression is usually in response

to the various cognitive and physical deficits following CHI

(Prigatano, 1986a). Thomas (1990) found that over half of 47

severely head-injured patients questioned had mild to severe

depression. Utilizing the Brief Psychiatric Rating Scale

(BPRS) with CHI patients, Levin, Benton, and Grossman (1982)

found depression to be relatively common at long-term follow-

up. Armstrong (1991) found that patients with cerebral

dysfunction were distinguished by their diminished self-

esteem, and elevated depression and anxiety as measured on the

MMPI. Tyerman and Humphrey (1984) also found CHI patients to

be depressed. Alfano et al. (1992) found that the most








86
commonly elevated scale on the MMPI is the Depression scale

(Scale 2), suggesting that severe CHI patients experience

significant depression.

Lewis and Rosenberg (1990) report that patients with

brain injury suffer from high levels of anxiety, which is one

of the primary reasons for psychotherapeutic treatment.

Anxiety following CHI is frequently the result of a failure to

cope with environmental demands which results in altered

emotional functioning such as a catastrophic reaction

(Goldstein, 1952). In comparison to depression, Higgins et

al. (1985) find that anxiety may be the result of a

discrepancy between the "ought" self (what you should be) and

real self. Working with severe CHI patients, Levin, Benton

and Grossman (1982) found severity of injury to be positively

related to level of anxiety immediately and at long term

follow-up. Newton and Johnson (1985) also found that chronic

severe CHI patients suffer from severe anxiety. Lishman

(1978) reports that chronic anxiety following CHI is a common

reaction. Similar to the relationship with depression, it has

been suggested that as the level of awareness of deficits

increases, anxiety also increases (Lewis & Rosenberg, 1990).













RATIONALE FOR THE STUDY

Statement of the Problem

The combined impact of CHI is devastating. Virtually

every aspect of the patient's life is negatively affected,

including cognitive, physical, and social functioning. Some

of the most common cognitive and emotional sequelae of CHI

involve impaired awareness of deficits, low self-esteem, and

psychological distress. There may be several sources of

unawareness (or decreased self-knowledge). Decreased self-

knowledge of deficits may be due to a process of denial in

reaction to illness, or it may be the result of an incapacity

to be aware due to the neurological injury. Decreased self-

knowledge of deficits may be for motor impairments, or complex

cognitive deficits. The latter have come to be termed self-

awareness deficits, and are thought to be the result, at least

in part, of frontal damage. Frequently, deficits in awareness

and denial occur in combination, and they have proven very

difficult to differentiate.

In addition to problems of awareness, problems of self-

esteem and self-concept are common. It has been reported that

CHI patients have low self-esteem, and it has been suggested

that CHI sequelae represent a threat to the patients self-

concept. All of the drastic changes which occur to patients








88
have consequences for their sense of self. Denial and

awareness deficits can be viewed as the psychological and

neurological mechanisms, respectively, which either diminish

or preclude self-knowledge of current functioning, which in

turn may impact self-concept/self-esteem. As with many other

drastic life changes, it is assumed that following CHI the

self-concept must go slowly through a stage of transition.

Some individuals may make this transition easily; others

experience great difficulty; and a few are unable to make this

transition at all. The reason for this variability in self-

concept change is the result of competition between the

motives of self-enhancement, self-concept consistency, and

accommodations with reality which is itself dependent upon the

capacity of the patients to be aware of changes they have

undergone.

Depression and anxiety are common for CHI patients,

unless protected by denial and unawareness. Studies

demonstrate that distress is higher when awareness is high and

when self-esteem is low.

Though the relationship between these variables is

complex, there has been virtually no theory which relates

them. The impact of gaining a greater understanding of

awareness deficits, denial, self-esteem, and psychological

distress following CHI is significant. The focus of this

study is on the relationship between awareness deficits,

denial, comparative self knowledge, and self-concept.








89
However, since the self-concept is a multidimensional,

multifaceted construct (Markus & Wurf, 1987; Shavelson, Hubner

& Stanton, 1976), separate dimensions of self-concept will be

evaluated (physical, cognitive, and social self-concept).

An experimental model is proposed (see Figure 1) which

attempts to specify the relationships outlined above in the

form of a path model and path diagram. It should be noted

that the direct measurement of awareness deficits is deferred

for the experimental model, primarily because quantitative

measures which isolate this construct do not currently exist.

Barco, et al. (1991) suggest that awareness deficits can be

assessed; however, assessment involves qualitative

observations during extensive treatment. Unfortunately, this

state of affairs discourages measurement for the present

study. Nonetheless, as the literature review attests,

knowledge of awareness deficits is important, which is why we

included it in the full model. We are attempting to measure

awareness deficits indirectly by choosing cognitive measures

which have a probability of being related to the awareness

dimension. This path analysis model concerns the relationship

between cognitive deficits which are thought to underlie

awareness deficits, denial, comparative self-knowledge and

self-concept/self-esteem. As previously mentioned, self-

concept and self-esteem are interdependent constructs. In







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92
addition, current measurement of self-concept is confounded

with measurement of self-esteem. Therefore, for the present

study we have decided to combine these constructs into a

supraordinate construct called self-concept/self-esteem which

encompasses self-descriptions and self-evaluation.

Experimental hypotheses will be made concerning this model and

a second model is presented (see Figure 2) which provides the

wider context for the first model. All variables in the

second model which are highlighted in bold represent the

portion of the model being tested. Based on the literature

review the second model predicts the relationship between

cognitive deficits which are thought to influence awareness

deficits, comparative self-knowledge, current and premorbid

self-concept/self-esteem, and psychological distress. The

wider model states that cognitive deficits which influence

neurologically mediated awareness deficits have an impact upon

comparative self-knowledge. Likewise, psychological denial

has an influence upon comparative self-knowledge. Next,

comparative self-knowledge influences the self-concept/self-

esteem. Awareness deficits and denial have an influence upon

self-concept/self-esteem but indirectly through comparative

self-knowledge. The wider model also posits that self-

concept/self-esteem is influenced by premorbid levels of self-

concept/self-esteem. The final part of the model is the

influence of current levels of self-concept/self-esteem, and

all its' influences, on level of psychological distress.