CORTICAL DEMENTIA VERSUS SUBCORTICAL DEMENTIA:

NEUROPSYCHOLOGIC DIFFERENCES
by
SHERRY D. CROWELL, B.A., M.A.
A DISSERTATION
IN
PSYCHOLOGY
Submitted to the Graduate Faculty
of Texas Tech University in
Partial Fulfillment of
the Requirements for
the Degree of
DOCTOR OF PHILOSOPHY
Approved

Accepted

Dean of the Graduate School

December, 1992
^T 1.

Copyright 1992 Sherry D. Crowell

 ACKNOWLEDGMENTS

I wish to thank my dissertation committee for their

guidance.
I wish to thank Charles and Jo Diegel, my parents, for
their support.
Most of all I wish to thank Charles Michael Crowell, my
son, for his encouragement.

11
 TABLE OF CONTENTS

ACKNOWLEDGEMENTS ii
LIST OF TABLES vii
LIST OF FIGURES ix
CHAPTER
I. DEMENTIA: AN OVERVIEW 1
Definition 1
Neuroanatomic Classification System 3
Types of Dementia. 4
Distinguishing Characteristics of Cortical
and Subcortical Dementias 6
Clinical/Research Studies . 8
Literature Review Organization 11
II. CORTICAL DEMENTIA: DEMENTIA OF THE
ALZHEIMER'S TYPE 13
Overview 13
Clinical Characteristics 16
Neurologic Characteristics 16
Progression 17
Stages of DAT 17
Diagnosis 19
Neuropsychologic Features . 20
Depression 29
III. SUBCORTICAL DEMENTIA: AIDS DEMENTIA
COMPLEX 32
Historical: Wilson's Disease 32
111
Human Immunodeficiency Virus 34
Historical Overview. . 34
Prevalence of HIV Infection 35
Mechanism of HIV 39
Stages of HIV Infection 40
Groups at Risk for HIV Infection.. 43
Secondary Dementias Associated with AIDS.... 44
Definition 44
Prevalence 45
Etiology 46
Primary Dementia Associated with AIDS....... 48
Definition 48
Prevalence 49
Etiology 50
Neurologic Involvement. 51
Mechanism of HIV 54
Course of ADC 56
Clinical Characteristics of ADC 57
Neurologic Characteristics. 57
Neuropsychologic Characteristics 57
Stages of ADC 60
Treatment 63
Neuropsychologic Features 64
Summary of DAT and ADC 72
Statement of Problem 74

IV
 Hypotheses 77
IV. METHODOLOGY 78
Method 78
Subjects 78
Instruments 83
Procedure 87
Age and Educational Level Correction 87
Post-test Analysis of Stage and Severity
of Disease 90
V. RESULTS 98
Power Analysis . 98
Stage of Disease Process: Group
Comparisons 102
Wechsler Memory Scale and Russell Revision.. 106
Trail Making Test Ill
Self-rating Depression Scale 117
Semi-structured Interview 117
Occupation 119
Memory Difficulties 119
Motoric Slowing 120
HIV Infection and Diagnosis 120
Mood and/or Personality Change 121
VI. DISCUSSION 122
REFERENCES 130
APPENDICES
A. RAW DATA, Z SCORES, AND SCALED SCORES 154
B. BIOPSYCHOSOCIAL INFORMATION SHEET 157

VI
 LIST OF TABLES

1. Clinical Characteristics of Cortical and

Subcortical Dementias. . 7
2. Dementia of the Alzheimer's Type 23
3. Botwinick et al. (1986) Longitudinal Study
Comparing CDRO and CDRl 27
4. Botwinick et al. (1988) Cross-Sectional and
Longitudinal Study 28
5. Stages of HIV Infection 41
6. HIV Infection 66
7. HIV Infection: Cross-Sectional Overview 70
8. Dementia of the Alzheimer's Type: Stage of
Disease Process Based on Interview Information
by Estimated Number of Years Diagnosed. . 80
9. AIDS Dementia Complex: Stage of Disease Process
Based on Interview Information by Estimated
Number of Years Diagnosed 82
10. Dementia of the Alzheimer's Type: Stage of
Disease Process Based on Clinical Dementia
Ratings by Estimated Number of Years
Diagnosed 91
11. AIDS Dementia Complex: Stage of Disease Process
Based on Wechsler Memory Scale Logical Memory by
Estimated Number of Years Diagnosed 93
12. Dementia of the Alzheimer's Type: Stage of
Disease Process Based on Test Results by
Estimated Number of Years Diagnosed 95
13. AIDS Dementia Complex: Stage of Disease Process
Based on Test Results by Estimated Number of
Years Diagnosed 97
14. Means and Standard Deviations to Calculate
Power Analysis 99
15. Power Analysis to Determine N 101
vii
16. Stage of Disease Process Based on
Neuropsychologic Test Data by Estimated Years
Diagnosed 103
17 . Neuropsychologic Test Results 10 /
18. Wechsler Memory Scale Logical Memory Percentiles
for Immediate Recall and Short-term Memory........ 109
19. Wechsler Memory Scale Visual Memory Percentiles
for Immediate Recall and Short-term Memory 112
20. Self-rating Depression Scale: Percentiles 118

Vlll
 LIST OF FIGURES

1. Dementia of the Alzheimer's Type: Immediate

Recall for Visual Memory 113
2. Dementia of the Alzheimer's Type: Model Present
for Visual Reproduction 114
3. AIDS Dementia Complex: Immediate Recall and
Short-term Memory for Visual Memory 115

IX
 CHAPTER I
DEMENTIA: AN OVERVIEW

Definition

Dementia, a decline in intellectual functioning with or

without a known cause, is becoming a major public health
concern as the lifespan of the typical American continues to
increase. Half of the United States population lives to at
least age 75, and one-fourth lives to age 85 (Mortimore &
Schuman, 1981). With increasing age, there also is an
increasing risk for developing a dementing illness. Among
people over the age of 65 in the general community, 4
to 5 percent have a moderate to severe dementia (Berg,
Frazen, & Wedding, 1987). Over 50 percent of patients in
nursing homes are diagnosed as having dementia (Lechtenberg,
1982). By age 70, the probability of being diagnosed with
dementia is approximately 12:1000; by age 80, this
probability increases to 55:1000 (Wiederholt, 1982).

Dementia may be defined as a loss of intellectual

functioning "characterized by persistent deficits in at
least three of the following areas of mental activity:
memory, language, visuospatial skills, personality or
emotional state, and cognition (abstraction, mathematics,
judgment)" (Cummings, 1985a, p. 75). The Diagnostic and
statistical Manual of Mental Disorders-III-R (DSM-III-R:
American Psychiatric Association, 1987) states
The essential feature of Dementia is impairment in
short- and long-term memory, associated with
impairment in abstract thinking, impaired
judgment, other disturbances of higher cortical
function, or personality change. The disturbance
is severe enough to interfere significantly with
work or usual social activities or relationships
with others, (p, 103)

DSM-III-R stipulates that an "underlying causative organic

factor is always assumed" (p. 103). Memory impairment may
include inability to remember recent events (e.g.,
forgetting names or conversations) or to remember long-term
information (e.g., names of relatives). Formal testing may
demonstrate memory impairment by asking the patient to learn
new material or to remember facts about common information.
Impairment for abstract thinking may be demonstrated by the
patient's difficulty coping with novel tasks, or finding
similarities or differences between related words. Impaired
judgment may be exhibited by a patient's poor impulse
control, inappropriate behavior, or neglect of personal
appearance. Other disturbances of higher cortical
functioning may be demonstrated by abnormal language, such
as aphasia, or word finding difficulty; constructional
apraxia, in which the patient is unable to copy simple,
geometric figures; agnosia, in which the patient is unable
to recognize common objects; or apraxia, in which the
2
patient is unable to carry out motor activities.
Personality change may include a patient becoming withdrawn
or apathetic, irritable, or an accentuation of preexisting
personality traits.

Dementia is distinguished from other disorders, such as

mental retardation, delirium, aphasia, and amnesia. The
acquired nature of dementia distinguishes it from congenital
mental retardation syndromes, in which the intellect was
never normal. The persistent nature of dementia
differentiates it from acute confusional states or
"delirium," in which the duration typically is short,
lasting hours or days (Cummings, 1985b). Alterations in
intellectual functions in multiple areas distinguishes
dementia, for example, from aphasia or amnesia, in which
only specific cognitive deficits are present.

Neuroanatomic Classification Svstem

Dementia is a symptom of many disorders. That is, it
is not a specific disease entity. The different etiologies
of dementia affect the age of onset, whether the onset is
sudden or insidious, the neurologic and neuropsychologic
signs associated with the disease process, and the response
to therapy (reversible or irreversible). Thus,
classification of dementias is problematic. Currently,
dementias are classified on the basis of their neuroanatomic
localization as their signs and symptoms are dependent on
which area(s) of the brain is (are) affected rather than on
the etiology of the disease process. Joynt and Shoulson
(1985) note several drawbacks to this system of
classification: (1) pathology may be restricted to specific
regions of the brain, but neuronal systems or specific
neurotransmitter systems may blur anatomic distinctions; (2)
behavioral patterns, or other symptoms of dementia, may
relate to the amount of brain damage as well as to the
location of brain damage; (3) specific mental functions may
not be assignable to specific regions of the brain; and (4)
in advanced cases of dementia, classification based on
localization is problematic as more and more of the brain is
involved.

Recognizing these difficulties, classifying dementias

based on neuroanatomic localization still appears to be the
most useful classification at this time because major signs
and symptoms often are dependent on the area of damage
rather than on etiology. Huber and Paulson (1985) stated
that "defining the mental symptoms of dementias as a
function of localization could lead to additional insight
into neuroanatomic structures and their relation to
cognition" (p. 1312).

Types of Dementia. Dementias typically are classified

as either mixed or localized. The mixed dementia category
4
includes conditions such as multi-infarct dementia, while
localized dementias are classified as cortical, subcortical,
or axial. Perhaps the best known of the cortical dementias
is Dementia of the Alzheimer's Type (DAT). Pick's Disease
also is classified as a cortical dementia. Subcortical
dementias include acquired immunodeficiency syndrome (AIDS)
Dementia Complex, Huntington's Disease (HD), Parkinson's
Disease (PD), and Wilson's Disease (WD). Axial dementias
include Wernicke-Korsakoff Syndrome and transient global
amnesia.

DAT has been described as a cortical dementia, based on

neuropsychologic testing and subsequent autopsy findings
revealing neurofibrillary tangles and neuritic placques in
the cortical region of the brain (McMenemey, 1940). A
plethora of neuropsychologic and neurologic research has
confirmed a profile which emphasizes abnormal intellectual
functions and normal motor functions in DAT patients (see
Cummings & Benson [1986] for a review). These data are
consistent with a clinical pattern emphasized by Alois
Alzheimer (1907/1977), when he first reported the disease.
More recently, researchers have turned their attention
to a newly discovered form of dementia, AIDS Dementia
Complex (ADC). Navia and colleagues (Navia, Cho, Petito, &
Price, 1986; Navia, Jordan, & Price, 1986) have suggested
that ADC be classified as a subcortical dementia based on
neurologic and neuropsychologic findings. Histopathologic
findings of ADC indicate abnormalities are most prominent in
the subcortical brain structures, affecting the central
white matter with a relative sparing of the cortex, or gray
matter.

DistinQuishino Characteristics of
Cortical and Subcortical Dementias
Benson and Cummings (1983a) described the
distinguishing characteristics of cortical and subcortical
dementias, which are summarized in Table 1. The primary
clinical characteristics of cortical dementias involve
progressive deterioration of memory (difficulty learning new
material) and higher-order associative functions (aphasia
[impairment of expressive and comprehensive language],
anomia [word finding difficulty], agnosia [perceptual
misinterpretation], and apraxia [deficits in
perceptual-motor activity]). Typically, mood is normal.
The prominent clinical characteristics of subcortical
dementias include slowing of mental processes, progressive
memory impairment (i.e., difficulty in retrieving stored
material), and cognitive dilapidation (deficits in
manipulating or using spontaneously acquired information,
such as abilities necessary for problem solving, or poor
problem solving) (Cummings, 1988; Cummings & Benson, 1983c;
Cummings & Benson, 1984). Higher-order associative

6
Table 1
Clinical Characteristics of Cortical and Subcortical
Dementias

Characteristic Cortical Dementia Subcortical Dementia

Verbal Output
Language Aphasic Normal
Speech Normal Slowed
Mental Status
Memory Amnesic Forgetful
(abnormal storage) (retrieval deficit)
Cognition Acalculia, poor Slowed
judgment, impaired
abstraction
Affect Unconcerned Apathetic, depressed
Motor Speed Normal until late Abnormal
in course (i.e., tremor, rigid,
slowed)

Causes Alzheimer's or AIDS Dementia Complex,

Pick's Disease Huntington's,
Parkinson's, Wilson's

(Adapted from Benson & Cummings, 1986)

functions are spared until end-stage disease; intellectual
impairment is milder; personality and affective changes
appear; and dysfunctions of the motor system, such as speech
difficulties and slowed motor speed, commonly are present in
subcortical dementias (Bridge, 1988). Within the clinical
setting, these characteristics may be used to assist the
neuropsychologist in arriving at a differential diagnosis
based on neuropsychologic testing.

Clinical/Research Studies. Huber and Paulson (1985)

noted that distinguishing the nature of the cognitive
disturbances associated with various forms of dementia
provides "information (which) would be of theoretical
interest and may have practical implications for developing
diagnostic procedures, evaluating therapeutic effectiveness,
and making rehabilitative judgments" (p. 1315). Thus,
research that compares and contrasts the various types of
dementia may add to the overall understanding of dementias.
For example. Smith, Butters, and Granholm (1988) examined
activation of semantic relations of patients with DAT and HD
to assess whether memory disorders of patients with cortical
and subcortical dementias involve different processing
deficits. They found that patients with cortical dementia
had difficulty storing new information, whereas patients
with subcortical dementia had difficulty retrieving material
which had been stored. Moss, Albert, Butters, and Payne
8
(1986) examined the patterns of memory loss among patients
with DAT and HD. Their results suggested that, for patients
with HD, capabilities for storage and recognition of verbal
material were relatively spared, but abilities to retrieve
information from storage were impaired. Patients with DAT
exhibited qualitatively different memory impairments,
demonstrating a rapid decay of stored information.

Cummings et al. (1988) reported that patients with DAT

exhibited significantly greater language disturbances,
including anomia (word finding difficulty) and decreased
information content of spontaneous speech than patients with
PD. Patients with PD demonstrated significantly greater
impairment of speech melody, dysarthria (difficulty in
speech production), and agraphia (loss of previously
possessed writing ability) than patients with DAT. Cummings
et al. (1988) suggested that the dementia of PD (a
subcortical dementia) is distinguishable from DAT as
patients with PD have prominent motor speech abnormalities,
and patients with DAT exhibit profound language alterations.
Further evidence for the distinction between cortical
and subcortical dementias was reported by Huber et al.
(1986) who compared patients with DAT and PD. Patients with
PD exhibited mild deficits for memory and visuospatial
function, significant depression, no impairment of language,
and no evidence of apraxia. Patients with DAT exhibited
deficits for overall mental functioning and memory, more
severely impaired visuospatial skills, disturbance on all
language-related tasks, and evidence of apraxia.

Burns, Folstein, Brandt, and Folstein (1990) assessed

irritability, aggression, and apathy in patients with HD and
DAT. Patients with HD were more aggressive than patients
with DAT. When patients with HD and DAT were matched for
degree of cognitive impairment, patients with HD were found
to be more apathetic than patients with DAT.
Mayeux and colleagues (Mayeux et al., 1983) compared
patients with DAT, HD, and PD, and concluded that "the
clinical aspects of dementia are similar in patients with
DAT, HD, and PD" (p. 282). Their conclusion was contrary to
the vast literature on clinical distinctions between
cortical and subcortical dementia. Other researchers (Huber
et al. , 1986) noted that Mayeux et al. had administered a
lengthened version of the Mini-Mental Status Examination
(Folstein, Folstein, & McHugh, 1975) which was not designed
to detect differences between types of dementia. Huber et
al. (1986) further suggested that a neuropsychologic
procedure "specifically designed to quantitatively evaluate
the proposed clinical differences" (p. 392) between types of
dementia will differentiate the syndromes. Benson (1983)
stated

10
 It is obvious that the clinical features alone
provide a clear distinction between the two types
of dementia (cortical and subcortial) . . . On the
basis of the striking clinical differences,
acceptance of the two distinct types of dementia
would appear mandatory, (pp. 189-190)

To date, no clinical studies have examined the

differences or similarities between patients with DAT and
patients with ADC. In the proposed study, the differences
between DAT (a cortical dementia) and ADC (a subcortical
dementia) will be examined. DAT was selected as it is the
best known and best researched of the cortical dementias.
ADC is a new subcortical dementia; thus, research has
focused on determining its clinical characteristics. A next
step in investigation of ADC is to compare its clinical
characteristics to a cortical dementia. Dickson and Ranseen
(1990) noted a similarity between Alzheimer's Disease and
AIDS Dementia Complex: "other causes carry a prognosis
similar to that of Alzheimer's disease a steady,
irreversible, downhill course. One such illness is the
recently recognized AIDS Dementia Complex (ADC)" (p. 291).

Literature Review Organization

An overview of DAT ia presented first, which includes
clinical characteristics of DAT and recent neuropsychologic
research on DAT. As AIDS is a relatively new and poorly
understood syndrome, a historical overview of AIDS is
offered including a brief review of various neurologic
11
disorders associated with AIDS. Next, an overview of ADC i-
presented, including the clinical characteristics and
neuropsychologic research on ADC. Next, a brief summary of
the clinical characteristics of, and distinctions between,
DAT and ADC is presented. Neuropsychologic assessment
procedures appropriate for evaluating specific clinical
characteristics of DAT and ADC are presented. Finally,
hypotheses are stated.

12
 CHAPTER II
CORTICAL DEMENTIA: DEMENTIA
OF THE ALZHEIMER'S TYPE

Overview

Alzheimer's Disease is the most common cause of serious

cognitive decline in the elderly, accounting for up to 55
percent of patients referred for evaluation of suspected
dementia (Rocca, Amaducci, & Schoenberg, 1986). Other
researchers (Sulkava et al., 1983) found that 82 percent of
the deceased patients in their study, who had been
clinically diagnosed with primary degenerative dementia,
had Alzheimer's Disease. The incidence of onset of
Alzheimer's Disease typically increases with age; the
earliest onset usually occurs after the age of 40. A
controversy exists whether a higher incidence of Alzheimer's
Disease occurs in women (Swihart & Pirozzolo, 1988; Thai,
Grundman, & Klauber, 1988). Thai and colleagues suggested
that since women live longer than men, it is not unexpected
that women have a greater prevalence of age-related disease
such as DAT.

Some researchers (Cook, Bard, & Austin, 1979) have

described Alzheimer's Disease as an inherited autosomal
dominant condition in 20 percent of cases. The remaining 80
percent of DAT cases have an increased incidence among

13
family members for unknown reasons (Feldman, Chandler, Levy,
& Glasser, 1963). Thai et al. (1988) found that patients
with DAT who had a positive family history for developing
DAT at an earlier age than those who have a negative family
history.

The time course of the disease is variable, and the

clinical progression of symptom severity is not uniform.
For example, some patients have been reported to remain at a
mildly demented state for seven years (Botwinick, Storandt,
& Berg, 1986). Most patients with DAT experience a
progressive decline at a relatively constant state (Thai et
al., 1988). A diagnosis of DAT should be viewed skeptically
if the patient's course deviates from this pattern
(Cummings, 1985a).
In the past, Alzheimer's Disease and senile dementia
were distinguished by their age of onset. Patients whose
illness began before the age of 65 were diagnosed as having
Alzheimer's Disease. Thai and associates (1988) found that
patients with DAT, who exhibited an early onset of symptoms,
appeared to have a higher incidence of a positive family
history for DAT. Patients whose illness began after the age
of 65 were diagnosed with senile dementia of the Alzheimer's
type (SDAT). Martin and Guthrie (1988) suggest that most
dementing diseases are manifest after the age of 65.
Filley, Kelly, and Heaton (1986) examined the

14
neuropsychologic features of early- and late-onset
Alzheimer's Disease. Filley et al. (1986) found that
patients with early onset (before age 65) had significantly
more language impairment than patients with late onset
(after age 65); late-onset patients exhibited more
visuoconstructional deficits than early-onset patients; and
all patients demonstrated severe memory deficits. Filley
and associates suggested that a left hemisphere
vulnerability exists for patients with early-onset DAT, and
right hemisphere vulnerability exists for patients with late
onset DAT. Filley and associates suggested "it seems most
parsimonious to consider AD as one disease that has
different manifestations depending on the age of the
affected patients" (p. 576). Distinctions based solely on
age of onset have been abandoned. Currently, all patients
are grouped under the same nosology of DAT.
Persons who have DAT rarely refer themselves for
treatment or evaluation since there is a concomitant loss of
insight, which occurs relatively early in the disease
process (Wade et al., 1987). Wells (1978) noted that "it is
often the appearance of a crisis rather than the appearance
of symptoms which precipitates the call for medical
assis-tance" (p. 4 ) . That is, the patients are insensitive
to their own shortcomings. O'Connor et al. (1990) found
that "although many moderately demented elderly persons
15
admitted to having difficulties on direct questioning, their
replies often lacked conviction and few of them were
distressed when their deficits were exposed" (p. 227). In
fact, DAT patients may be able to function quite well living
alone in familiar surroundings. Changes in living routine
or medication or a mild illness may make their underlying
dementia more obvious, as they become confused. In
contrast, persons who refer themselves for neurologic
evaluation due to concern about possible declines in
performance typically are depressed rather than demented.

Clinical Characteristics
Neurologic Characteristics. Patients with DAT undergo
a steadily progressive intellectual decline. The
progressive nature of DAT is due to neuropathologic
deterioration of the cortical regions of the brain
(Weingartner et al., 1983). Characteristic aspects of
progressive brain deterioration are atrophy of the cortical
nerve cells, argentophile plaques, which have a mixed
granular and fibrillary structure, and nerve cell fibrils,
which form tangles and loops (Sim & Sussman, 1962).
Weingartner et al. (1983) suggested that continued
neuropathologic deterioration is related to "how well these
patients (with progressive dementia) can obtain access to

16
and use their previously acquired knowledge in processing
ongoing events" (p. 380).

Progression. Thai et al. (1988) described a

stereotypic progression of symptoms in DAT patients. The
most common presentation was memory impairment, then
impairment of higher cortical functions followed by
personality change, and finally by behavior change. The
clinical course of DAT typically is divided into three
relatively distinct stages (Berg, Franzen, & Wedding, 1987;
Cummings, 1985a; Cummings & Benson, 1983a; Cummings &
Benson, 1986; Schneck, Reisberg, & Ferris, 1982). Swihart
and Pirozzolo (1988) labeled the three stages as: (1) the
forgetfulness phase, (2) the confusional phase, and (3) the
dementia phase.

Stages of DAT. During the first stage, the

forgetfulness phase, the patient demonstrates subtle
decrements in memory function (exhibited by misplacing
objects) and difficulty remembering names and appointments.
The patient exhibits confusion in response to slight
provocation (i.e., a change in schedule). The patient
exhibits mild visuospatial deficits (clumsy drawings with
minimal distortions) and mild impairment for cognitive
functions (complex abstractions and calculations). The
patient may exhibit affective changes, such as social
withdrawal and decreased spontaneity and initiative.

17
However, major depressive symptoms are absent. Current
research indicates the prevalence of depression in patients
with DAT ranges between 0 percent (Knesevich et al., 1983)
and 19 percent (Reding, Haycox, & Blass, 1983). Other
researchers (Cummings, Miller, Hill, & Neshkes, 1987)
reported that 17 percent of patients with DAT exhibited
symptoms of depression, but that none met the diagnostic
criteria for major depressive episode. Typically patients
in the first stage of DAT are not unhappy (Rubin, Zorumski,
& Burke, 1988). Although patients may be aware of their
declining intellectual abilities, they often feel a sense of
detachment about the disease. Those patients who do worry
about their cognitive decline do not experience feelings of
guilt, suicidal ideation, or vegetative changes. The
patient may exhibit empty speech, or poverty for content of
speech, but articulation and fluency will remain normal.
Berg et al. (1987) noted, "It is rare for the
medical/neurological evaluation of the patient to be
positive in the early phase of the illness; however,
cognitive deficits will typically be apparent on
neurological screening" (p- 15).
During the second stage, the confusional stage, all
intellectual functions continue to decline. Language output
continues to be fluent, and repetition abilities still are
intact, but language comprehension is impaired. Memory

18
functions, for both short- and long-term information, are
impaired and aided only partially by cues. Cognitive
skills, including spatial and temporal orientation,
judgment, and simple calculation and abstraction, are
impaired severely. The "classical signs" of cortical
dementia, such as aphasic symptomatology and apraxia, become
more prominent. Impaired visuospatial skills are
demonstrated by an inability to accurately copy designs,
which are characterized by flattening, distortions, and
omissions. During the second stage, definite declines in
activities of daily living are readily apparent, such as
diminished concern for appearance and personal hygiene. The
patient's mood may be flat or labile.

The third and final stage of DAT, the dementia phase,

is characterized by profound disturbances in orientation and
memory, severe and global decline in intellectual level of
functioning, inability to recognize significant persons in
the patient's life, and psychotic symptomatology. Cognitive
abilities become untestable at this stage due to profound
disturbance. Language output eventually is reduced to
echolalia, the parrot-like repetition of overheard words or
fragments of speech (Stone, 1988), palilalia, the
involuntary repetition of words or sentences, or mutism.

Diagnosis. The diagnosis of DAT usually is made by

exclusion. That is, it is based on the elimination of
19
other, more easily diagnosed causes of dementia. However,

diagnosis based on exclusion renders DAT a nonspecific

diagnosis. In order to increase the homogeneity of DAT
patients, Cummings (1985a) suggested that all patients who
are diagnosed as having DAT should have similar clinical
features and a similar course: "an insidiously progressive
clinical syndrome, including aphasia, amnesia, and
visuospatial abnormalities, and motor, reflex and sensory
function should be normal throughout most of the clinical
course" (p. 76). Kruz, Romero, and Lauter (1990) noted that
the clinical diagnosis of Alzheimer's disease is
composed of three consecutive steps: (1)
Identification of the syndrome of dementia. (2)
Identification of the typical course and clinical
picture. (3) Exclusion of all clinically
demonstrable underlying causes, (p. 55)
In an effort to refine diagnostic criteria, Kruz, Romero,
and Lauter (1990) recommended that, based on informant
interviews and clinical examination, impairments of memory
and another area of cognition (e.g., intelligence, abstract
thinking, judgment, or language) be present in sufficient
severity to interfere with daily living. They noted that
disturbances in both areas are "explicitly stated in ICD-10
(International Classification and Diagnosis), but less
clearly expressed in DSM-III-R" (p. 55).
Neuropsychologic Features. DAT is characterized by
prominent aphasia, amnesia, and cognitive impairment with a

20
relative sparing of motoric functions until the final stages
of the disease process (Alzheimer, 1907/1977; Cummings &
Benson, 1983b). Patients with DAT experience a concurrent
progressive decline in attentional and semantic memory
functions (Berg et al., 1984; Flud, 1984; Ober et al.,
1985). As semantic retrieval declines, so does performance
on other neuropsychologic tests assessing attention,
language, and memory.
Weingartner et al. (1981) reported that patients
exhibited deficits for logical memory, associative learning,
and visual reproduction. Researchers (Wilson et al., 1983)
suggest that patients with DAT fail to encode verbal
information, and this processing deficit may contribute to
impaired recognition memory performance or retrieval
process. Larrabee, Largen, and Levin (1985) found that
memory measures were sensitive in discriminating the DAT and
normal subjects, and that Weschler Adult Intelligence Scale
- Revised (WAIS-R) cognitive subtests were sensitive to the
severity of dementia. However, Berg et al. (1987) reported
the WAIS-R is not especially sensitive to early
dementia . . . The Wechsler Memory Scale is apt to
be more sensitive to the cognitive changes seen in
dementia than is the WAIS-R . . . Part B of the
Trail Making Test [is] likely to indicate clear
cognitive impairment, (p. 16)
Quantitative data of the neuropsychologic data
available for primary degenerative dementia (DAT and Pick's

21
Disease) are summarized in Table 2. On the WAIS-R,
Performance subtests indicate greater overall decline than
Verbal subtests. The most prominent deficits for
Performance subtests are perceptual organization (Block
Design, Picture Arrangement, and Object Assembly), spatial
visualization (Block Design), temporal sequencing and time
concepts (Picture Arrangement), and anticipation of
relationships among parts (Object Assembly). All of the
WAIS-R Performance subtests were affected adversely, and
"even more than would be expected based simply on age of the
patients" (Farr, Greene, & Fisher-White, 1986, p. 227). On
the WAIS-R Verbal subtests, the most prominent deficits are
for calculation abilities (Arithmetic), categorical thinking
and abstraction abilities (Similarities), and immediate
recall (Digit Span). WAIS-R standard scores for Verbal
subtests, Vocabulary (fund of information). Information
(acquired information), and Comprehension (social judgment),
appeared most resistant to the disease process. On the
Trail Making Test (TMT), parts A and B, scores indicate very
severe deficits for sequencing abilities, visuospatial
scanning abilities, and alteration of mental sets. Farr et
al. (1986) noted that "Trails A and B (Trail Making Test:
TMT), respectively, are the most sensitive indexes of this
disease process with the HRB (Halstead-Reitan
Neuropsychologic Test Battery)" (p. 231). On the Wechsler

22
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25
Memory Scale (WMS), the most prominent deficits were for
mental control and verbal learning abilities (Associate
Learning and Verbal Memory), indicating deficits for mental
alertness, verbal expression, and new learning abilities
(abilities to store new information).

In longitudinal and cross-sectional studies (see Tables

3 and 4 ) , researchers (Botwinick et al., 1986; Botwinick,
Storandt, Berg, & Boland, 1988) demonstrated progressive
cognitive decline in patients with DAT. In these studies,
patients with depression or major medical illnesses were
ruled out. Table 3 summarizes quantitative data for
subjects with no dementia (Clinical Dementia Rating-0:
CDRO) and subjects with mild DAT (CDRl) over a six-year
period. The two groups were matched for age, sex, and
education. CDRO subjects demonstrated no neuropsychologic
decline, whereas CDRl subjects demonstrated a progressive
decline on all neuropsychologic tests. Table 4 summarizes
quantitative data for subjects with mild (CDRl), moderate
(CDR2) and severe (CDR3) dementia over a period of six
years. These data (see Table 4) suggest that the
progressive decline seen in longitudinal studies is of the
same type and magnitude seen in cross-sectional studies.
Overall, patients with DAT exhibited a progressive decline
for WAIS-R subtests, including acquired knowledge
(Information), social judgment (Comprehension), freedom of

26
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28
distracti^bility (Digit Symbol), and visuospatial and
constructional abilities (Block Design). Verbal-semantic
memory abilities (WMS: Verbal Memory) showed the greatest
decline over time. WMS scores exhibited progressive decline
for mental alertness (Mental Control), immediate recall for
verbal information (Digit Span Backwards), and new learning
abilities for verbal information (Associate Learning).
Immediate recall for digits forward (WMS Digit Span) showed
the least decline, although it reflected much decline.
Botwinick et al. (1988) noted that "aphasia plays a
particularly important role in decline. . . performances on
the 16 tests were so poor overall, that this fact [aphasia],
more than that of differential decline, was the prominent
feature" (p. 496).
Depression. During the past decade, researchers have
turned their attention to whether patients with DAT
experience depression. Rubin, Zorumski, and Burke (1988)
noted that Alzheimer's Disease and geriatic depression have
several features in common.
Both illnesses involve cognitive changes,
agitation, passivity, psychotic symptoms,
decreased interest, decreased concentration,
decreased energy, and other psychomotor changes.
Both illnesses lead to functional disability in
terms of interactions with family, friends, and
community. Both lead to diminished ability for
se3^f-care, and both are associated with increased
morbidity and mortality. (p. 1078)

29
Lazarus et al. (1987) studied the frequency and presentation
of depressive symptoms in patients with primary degenerative
dementia using the Hamilton Rating Scale and the Sandoz
Clinical Assessment-Geriatric Scale. They found that
patients with primary degenerative dementia had
significantly higher scores than controls on items that
reflect inner feeling states of depression and despair
(e.g., depressed mood, anxiety, and feelings of
helplessness). Patients with primary degenerative dementia
did not score significantly higher than controls on items
assessing vegetative symptoms, such as sleep disturbance,
weight loss, and insomnia. A review (Wragg & Jeste, 1989)
of 30 studies to determine the prevalence of affective
symptoms in patients with DAT found reports of depression
ranging from 0 percent to 86 percent. Hart, Kwentus, Wade,
and Hamer (1987) proposed using the WAIS-R Digit Symbol test
and a measure for incidental memory to differentiate between
patients with mild DAT and patients with depression.
Patients with mild DAT and patients with depression both
performed poorly on the Digit Symbol test due to psychomotor
slowing. Immediately after the Digit Symbol test was
administered, their patients were given a sheet with nine
Digit Symbol test boxes, minus the symbols, and were asked
to recall the symbols. They found that patients with
depression recalled more digit-symbol pairs and total
30
symbols than patients with DAT. However, in another study,
Lopez et al. (1990) found no significant difference in the
pattern of neuropsychologic deficits between patients with
DAT who were depressed and patients with DAT who were not
depressed, Wragg and Jeste (1989) stated "the considerable
literature on 'depressive pseudodementia' highlights the
difficulty of initially distinguishing between depression
and dementia" (p. 583). They concluded that it was unclear
whether patients with DAT experienced concomitant
depression, or whether affective symptoms in patients with
DAT were due to cognitive impairment itself.

31
 CHAPTER III
SUBCORTICAL DEMENTIA:
AIDS DEMENTIA COMPLEX

Historical; Wilson's Disease

The category of subcortical dementia was alluded to
first in 1912 by Wilson (Wilson, 1912), who was studying a
disorder that now bears his name, Wilson's Disease
(hepatolenticular degeneration). On autopsy, Wilson found
physiopathologic changes in basal ganglia, particularly in
the global thalamus. Patients with WD exhibited two
different types of personality and behavior changes. One
group exhibited profound apathy, lack of spontaneity, and
childish behavior. The second group exhibited psychotic
features, characterized generally by manic symptoms,
although some resembled schizophreniform psychoses. Medalia
and Scheinberg (1989) found that patients with WD exhibited
more clinically significant psychopathology on the MMPI than
neurologically asymptomatic patients.

Wilson also identified cognitive changes, motoric

slowing, slowness of speech, and problems of concentration
in patients with WD- These patients did not demonstrate
naming problems and apraxic difficulties that patients with
senile dementia (DAT) exhibited. Medalia, Isaacs-Glaberman,
and Scheinberg (1988) reported that patients with WD

32
exhibited impairment for timed visuomotor tasks (Trail
Making Test). They concluded that the impairment was due to
motoric slowing rather than to visuoperceptual problems or
inability to shift cognitive sets and plan correctly; their
conclusion was based on the observation that patients did
not make errors, indicating that they did not have deficits
for visuoperceptual and planning abilities. The patients
also demonstrated mild memory impairment for verbal but not
visual material (Wechsler Memory Scale). Memory quotients
and Verbal IQs (Wechsler Adult Intelligence Scale) were
within normal limits, although their patients reported
noticeable memory difficulties in daily living activities.
The patients' Performance IQs (WAIS) were impaired due to
poor motoric performance on timed tests (Block Design and
Digit Symbol).

The subcortical region of the brain described by Wilson

is the same area implicated in ADC (Navia et al., 1986a;
Navia et al., 1986b), and the clinical characteristics of WD
are similar to those exhibited by patients with ADC (Price
et al., 1988c; Price et al., 1988d). Before reviewing the
literature on neurologic and neuropsychologic findings for
ADC, a historical overview of AIDS and human
immunodeficiency virus (HIV) is presented.

33
Human Immunodeficiency Virus

Historical Overview. From October 1980 to May 1981, 5

previously healthy, young, gay men were diagnosed with
Pneumocystis carinii pneumonia (PCP) in Los Angeles
(Gottlieb et al., 1981). In July 1981, researchers (Centers
for Disease Control, 1981a; Centers for Disease Control,
1981b) reported that Kaposi's sarcoma (KS), an uncommon
malignancy, had been diagnosed in 26 young, gay men living
in New York City. The sudden occurrence of PCP and KS was
unusual. Previously PCP had been seen primarily in severely
immunosuppressed patients, and KS, a rare, malignant
neoplasm, had been diagnosed in elderly men and was rarely
fatal. The clustering of PCP and KS in gay men suggested a
common underlying factor. Initially, researchers
hypothesized that gay men, who had a large number of sexual
partners, experienced an auto-immune response to their
sexual partners' sperm; this hypothesis was discarded in
favor of immune suppression by a yet unidentified cause
(Centers for Disease Control, 1981a; Centers for Disease
Control, 1981b).
In 1982, the Centers for Disease Control (CDC) named
this new disease process acquired immunodeficiency syndrome
(AIDS) and defined it "as a disease, at least moderately
predictive of a defect in cell-mediated immunity, occurring
in a person with no known cause for diminished resistance to
34
that disease" (p. 508). Such diseases include KS, PCP, and
serious Other Opportunistic Infections (001). "Diagnoses
are considered to fit the case definition only if based on
sufficiently reliable methods (generally histology or
culture)" (Centers for Disease Control, 1982, p. 514).
Between June 1, 1981 and September 15, 1982, CDC
received reports of 593 cases of acquired immune deficiency
syndrome (AIDS), with death occurring in 41 percent of the
cases (Task Force on Acquired Immune Deficiency Syndrome,
CDC, 1982). By late 1981, AIDS was reported in heterosexual
intravenous drug abusers. In mid-1982, the first cases of
AIDS among hemophiliacs and transmission from male
intravenous drug abusers to female sexual partners were
reported (CDC, 1982). These cases led to the hypothesis
that AIDS was blood-borne and transmissible. In late-1983,
French and American researchers discovered a retrovirus
found in AIDS patients. The French team (Barre'-Sinoussi et
al., 1983) named the virus lymphadenopathy associated virus
(LAV), the American team (Gallo et al., 1984) human T-cell
lymphotropic virus type III (HTLV-III). This virus now is
designated as human immunodeficiency virus (HIV) (Coffin et.

al, 1986).
Prevalence of HIV Infection. As of June 1992, the CDC

(1992) reported 230,179 cases of AIDS in the United States.

The doubling time for new AIDS cases was eleven months by
35
1986 (State and Territorial Epidemiologists, AIDS Program,
CDC, 1986). New cases are being reported at a rate of 2,500
to 3,000 per month. In January 1990, new cases were being
reported at a rate of 1,200 to 2,000 per month.

It has been estimated that at least 1.5 million

Americans are infected with HIV (World Health Organization,
1988). Epidemiologic research (Public Health Service, 1986)
suggested that by 1991 nearly 300,000 people in the United
States would have AIDS, and 15 million Americans would have
HIV infection. Although HIV infection rates remain highest
for gay males, there is evidence of increasing HIV infection
among intravenous drug abusers (IVDAs). Infection rates
among IVDAs is estimated at 25 percent for gay and
heterosexual drug abusers. The number and percentage of
AIDS cases in this risk group is expected to increase
rapidly in future years (Chaisson et al., 1987; Friedland et
al., 1985; Marmor et al., 1987), with the number doubling
every 14 to 16 months (Schuster, 1988). Surveys have been
conducted of hemophiliacs who received clotting factor
concentrates before 1984 or 1985, when HIV screening of
plasma and treatment of clotting factor concentrates began
(Curran et al., 1988). HIV infection rates range from 15
percent to over 90 percent, varying with the type and
severity of hemophilia. Lower rates of infection are

36
associated with hemophilia B and mild to moderate hemophilia

A; higher rates are associated with severe hemophilia A.

Lentivirinae are a subfamily of viruses (Retroviridae)
that includes the slow viruses of sheep (e.g., Visna virus)
and human T-cell lymphotropic viruses. This subfamily of
viruses resemble the C-type RNA tumor viruses in many ways,
including production of reverse transcriptase.
"Characteristic of lentiviruses is their tendency to have
protracted delays between acquisition and expression of
disease and to produce latent or persistent disease"
(Lechtenberg & Hollenberg, 1988; p. 5 ) . The time from HIV
infection to onset of symptoms is known as the incubation
period, or latent period. Researchers generally agree that
the latent period for developing symptoms of AIDS is longer
than the initial estimates of approximately 2 years. It may
be as long as 7 to 10 years (Adams & Victor, 1989) or longer
(CDC, 1986b). Researchers (Bacchetti & Moss, 1989; Lifson
et al., 1989) found that 39 percent of HIV-infected gay men
in San Francisco are diagnosed with AIDS after 8 years of
HIV infection. Persons who were infected by contaminated
blood products showed a relation between age at time of
seroconversion (i.e., when HIV antibodies were detected) and
a diagnosis of AIDS. When infection occurred after age 34,
44 percent were diagnosed with AIDS within 8 years of
infection; between ages 18 and 34, 27 percent were diagnosed
37
with AIDS within 8 years of infection; and between ages 1
and 17, 13 percent were diagnosed with AIDS within 8 years
of infection (Goedert et al., 1989). The mortality rate for
persons with AIDS approaches 75 percent 2 years after
receiving a diagnosis of AIDS, and 100 percent at 5 years
(Fernandez, Holmes, Levy, & Ruiz, 1989).

That people do not die from AIDS should be emphasized;

rather they die from the various opportunistic diseases
associated with AIDS. In addition to PCP and KS, other
opportunistic diseases caused by protozoa, fungi, bacteria,
and viruses are common infections in AIDS cases. Neurologic
involvement associated with the human immunodeficiency virus
(HIV) and opportunistic diseases has been reported and is
discussed in another section of this report. Researchers
now propose that, without a cure for HIV infection,
eventually all persons who have HIV infection will progress
to AIDS and die of opportunistic diseases or lymphomas.
AIDS is the eleventh most common cause of premature
death in the United States (Abrams, 1988). By 1989, AIDS
was the leading cause of death in men aged 25 to 44 in San
Francisco and women aged 25 to 44 in New York City,
surpassing the cumulative impact of accident, homicide,
suicide, and cancer (American Academy of Neurology AIDS Task
Force, 1989). By 1992, AIDS is projected to be the third or
fourth leading cause of death before age 65. In addition to

38
the effect of AIDS on the health care system, there is
significant societal impact in that AIDS primarily affects
people in their most productive years (Piot et al., 1988).

Mechanism of HIV. According to Boccellari (1987), when

a foreign substance enters the body, an elegant combat
system is activated. Macrophages, the body's first line of
defense, send out a signal to the T-4 cells (helper cells or
natural killer cells). The T-4 cells secrete lymphokins,
which enable the B cells to produce specific antibodies to
the foreign antigens. Boccellari (1987) noted that when the
body is invaded by the HIV, the normal immune response does
not occur. The macrophages signal the T-4 cells, and it is
at this point that the immune system response changes. The
T-4 cell antigen itself acts as a receptor for a specific
HIV protein. Once inside the T-4 cell, the HIV copies its
RNA into DNA through the enzyme reverse transcriptase. The
viral DNA then integrates itself into the genome of the host
cell, where it may remain dormant until the host T cell is
stimulated to divide by interlukin-2. Once the T cell is
stimulated by interlukin-2 (i.e., whenever the immune system
is activated), the new virus, HIV, begins to replicate, thus
destroying the host T cell. The virus is released from the
dead cell and invades other T cells. The depletion of T
cells results in the clinical manifestation of an impaired
immune response as the T-4 cells are no longer able to

39
activate the B cell response (Selwyn, 1986). The normal
T-4:T-8 ratio is about 2:1. For persons with impaired
immune systems, the ratio is reversed, 1:2. Additionally,
HIV antibodies that are produced become ineffective over
time in combating the HIV. The reason for this is not
known.

Stages of HIV Infection. In 1987, the CDC issued a

revised classification system (CDC, 1987) for identifying
stages of HIV infection (see Table 5). Group I consists of
those individuals who have symptomatology associated with
initial HIV infection. These symptoms are described as
"flu-like" or may present as an acute asymptomatic
meningitis. "Most patients recover from the acute
illnesses; the relationship to AIDS may pass unrecognized,
since these illnesses are quite nonspecific clinically and
may precede seroconversion" (Adams & Victor, 1989, p. 612).
Seroconversion usually follows this initial, acute stage.
Group II is designated for those individuals who have
progressed through the first stage of infection, usually
within 4 to 12 weeks, and now are asymptomatic, that is,
persons who have HIV infection but are not exhibiting any
symptoms of illness. Group II patients are in the
incubation or latent period. Groups I and II patients
formerly were classified as having only HIV infection, and
were designated as asymptomatic carriers. Persons in Groups

40
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41
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(Adapted fr Centers Disease Control, 19 187)
I and II are considered to be infectious, and may transmit
the virus to others. For example, infants born to
asymptomatic mothers, who have HIV infection, have developed
AIDS shortly after birth.
Group III is designated for persons who are exhibiting
symptoms of persistent generalized lymphadenopathy
(enlarged, prominent lymph nodes). This group category
formerly was known as AIDS Related Complex (ARC). For ease
of discussion. Group III will be referred to ARC.
Typically, persons with ARC also exhibit one or more of the
prodromal symptoms of AIDS: night sweats or fevers, chronic
diarrhea, profound fatigue, easy bruisability or unexplained
bleeding, or thrush or oral candidiasis (thick, persistent,
whitish coating on the tongue or in the throat). Persons
with ARC typically have inverted T-4:T-B ratios.
Group IV now includes neurologic disease, such as ADC,
and chronic wasting, a debilitating condition characterized
by severe weight loss, in addition to criteria specified in
1982. Therefore, persons with AIDS, or Group IV
designation, may have one or more of the prodromal symptoms
experienced by persons with ARC, and have at least one
opportunistic infection or neoplasm, or ADC, or chronic
wasting. The opportunistic infections are (1) protozoal
infections (PCP and toxoplasma gondii), (2) fungal
infections (Candida albicans)t (3) bacterial infections
42
(Mvcrobacterium tuberculosis and Mvcrobacterium avium
intracellulare). and (4) viral infections (cytomegalovirus
and Herpes simplex). The neoplasms are Kaposi's sarcoma,
primary central nervous system (CNS) lymphoma, and systemic
lymphoma with CNS involvement. As the popular term, "AIDS,"
still is used in the literature, "AIDS" rather than "Group
IV" will be used in this paper.

On November 15, 1991, the CDC, issued a draft proposing

a revised classification for HIV infection and expanded AIDS
surveillance case definition for adolescents and adults
(CDC, 1991). The purpose for revising the current
classification system was to emphasize the clinical
importance of T-4 lymphocyte count in the categorization of
HIV-related clinical conditions. The CDC received several
thousand comments during the public comment period on the
proposed expansion of the AIDS case definition.
Implementation of any proposed change in definition has been
postponed until further notice (Texas Department of Health,

1992) .
Groups at Risk for HIV Infection. When AIDS first came
to the attention of epidemiologists, it was believed that
only gay men who had an enormous number of sexual partners
were at risk for HIV infection. Since that time researchers
have found that no pattern of sexual behavior distinguishes
those who have HIV infection from those who do not (Mayer et
43
al., 1986). Cases of AIDS, ARC, and HIV seropositivity have
been reported among sexual partners of bisexual men,
intravenous drug abusers, hemophiliacs, and people who
received HIV infected blood transfusions. Pediatric cases
(i.e., children born to mothers with HIV infection) also
have been reported. Kennedy (1987) reported that 25 percent
of all known cases of persons who are seropositive for HIV
in Scotland were female, and that "we can expect to acquire
considerably more experience in this" (p. 107). It is
possible that sexual behavior, such as the number of sexual
partners or type of sexual activity, may increase the
probability for HIV infection. For example, the probability
of HIV infection increases with the number of different
sexual partners or the practice of high-risk sexual
activities, including anal intercourse and unprotected
vaginal intercourse. It also follows that once one has been
infected, the probability of contracting AIDS increases with
the number of infected sexual partners, because each new
infection will activate the HIV, thus stimulating viral
replication.

Secondary Dementias Associated with AIDS

Definition. AIDS Dementia Complex, or primary

dementia, is caused by HIV infection of the brain. Other

opportunistic infections and neoplasms found in AIDS

44
patients may produce aseptic meningitis, peripheral
neuropathies, or intracranial space-occupying lesions,
causing changes in mental status (delirium), or secondary
dementia associated with AIDS (Rosenblum, Levy, & Bredesen,
1988). Secondary dementia associated with AIDS is caused by
infection of the brain (encephalitis) or the lining of the
brain (meningitis) by an opportunistic infection, or by
primary brain tumors (Snider et al., 1983b). Perry and
Markowitz (1986) suggested two broad categories for
secondary dementias associated with AIDS:
[1] an insidious depression characterized by
apathy, withdrawal, fatigue, hypersomnia, weight
loss, anorexia, psychomotor retardation and subtle
cognitive deficits, [2] and an acute psychotic
presentation with delusions, halucinations,
psychomotor agitation, mania, and grandiosity, and
more profound cognitive impairment, (p. 1004)
Secondary dementias associated with AIDS generally are
responsive to early, aggressive treatment.
Prevalence. It has been estimated that 35 percent to
75 percent of patients with HIV infection exhibit neurologic
complications and neuropsychologic symptoms prior to death
(Elder & Sever, 1988; Fauci, 1988; Gapen, 1982; Horoupian et
al., 1984; Kelly & Brant-Zawadzki, 1983; Marx, 1985;
McArthur & Johnson, 1988; Namir, 1985; Shaw et al., 1985).
A review of 52 charts of patients with AIDS indicated that
mood disturbance and cognitive dysfunction were pervasive
clinical features of AIDS (Perry & Tross, 1984). It is
45
estimated that neuropsychologic symptoms are the first
manifestation of AIDS in at least 20 percent of AIDS cases
and may mimic psychopathology (Berger, 1987; Hoffman, 1984).
Nath, Jankovic, and Pettigrew (1987) reported that 21.3
percent of 253 patients with AIDS had neurologic
complications, and 11 percent had movement disorders.
One-third of their AIDS patients had neurologic findings.

Despite the high incidence of neuropsychologic

disorders reported by researchers. Perry and Tross (1984)
noted that psychiatric consultations were requested for only
19 percent of patients with AIDS. Neuropsychologic symptoms
also may be ignored or not evaluated because of the
"overwhelming nature of the patient's problems" (Gapen,
1982, p. 2941). As AIDS has a frustrating and unpredictable
medical course (people may feel well one day and poorly the
next), assessing mood and cognitive disturbances presents a
challenge (Mandel, Moulton, Temshok, & Woods, 1985).
Secondary dementias associated with AIDS can take various
and complex forms (e.g., paranoia, emotional symptoms, and
delirium), which may cause researchers and
neuropsychologists (Fenton, 1987; Rundell, Wise, & Ursano,
1986) to overlook organic causes.
Etiology. The two more common neurologic syndromes
affecting persons with AIDS are encephalitis and meningitis
(Gapen, 1982; Namir, 1985). Encephalitis is believed to be
46
caused by opportunistic viral infection, presenting as a
progressive dementia, manifest by withdrawal and psychomotor
retardation (Armstrong, 1984). Herpes viruses that infect
the central nervous system include herpes simplex (types I
and II), cytomegalovirus (CMV), and herpes varicella-zoster
(Reichert, Kelly, & Macher, 1985). Papovavirus, a central
nervous system demyelinating disorder, causes progressive
multifocal leukoencephalopathy (PML). PML progresses
rapidly. Focal deficits are dependent on the location of
the lesions (Bedri, Weinstein, DeGregorio, & Verity, 1983).

Meningitis, which may be preceded by days or weeks of

headache, is caused by nonviral infections (bacterial,
protozoal, or fungal infections) (Gottlieb, 1984).
Cryptococcal meningitis is caused by Crvptococcus neoforms,
an encapsulated budding yeast (Loewenstein & Sharfstein,
1984; Mildvan, 1984; Reichert et al., 1985). Toxoplasma
meningoencephalitis is caused by protozoa. Toxoplasma
gondii, which rapidly multiply within the cytoplasm of host
cells. The host cells degenerate, producing intracerebral
lesions (Whelan et al., 1983). Toxoplasmosis may produce
focal lesions as well as meningitis (Anderson, Atlas, Ahern,
& Weisbrot, 1983; Danziger & Leibman, 1983; Handler, Ho,
Whelan, & Budzilovich, 1983; Levy, Pons, & Rosenblum, 1983;
Wong et al., 1984) .

47
 Primary brain tumors due to Kaposi's Sarcoma or primary
central nervous system (CNS) lymphomas (Pitchenik, Fischl, &
Walls, 1983; Snider, Simpson, Aronyk & Nielsen, 1983; Welch
et al., 1984) and vascular episodes have been described
(Penington et al., 1984). Headaches, personality or
cognitive changes, dementia, alteration of levels of
consciousness, convulsions, or focal sensory or motor
disorders may result from lesions in the meninges, cortex,
brainstem, or spinal cord.

Primary Dementia Associated with AIDS

Definition. AIDS Dementia Complex (ADC), caused by HIV
itself, is referred to as a primary dementia. ADC has been
referred to variously as subacute encephalitis, AIDS
encephalopathy, and HIV dementia. Researchers (Navia,
Jordan, & Price, 1986; Price, Sidtis, & Rosenblum, 1988)
distinguish ADC from secondary dementias associated with
AIDS in the following ways: (1) ADC is chronically
progressive, whereas secondary dementias typically are
subacute in evolution; (2) brain inflammation is virtually
absent in ADC, where as brain inflammation is prominent in
secondary dementias; and (3) ADC infects and affects the
subcortical region of the brain, whereas secondary dementias
affect the menges, cortical regions, and subcortical regions
of the brain.

48
 Prevalence. Estimates of the proportion of persons
with AIDS having ADC at the time of death range from 70
percent to 90 percent (Levy, Bredesen, & Rosenblum, 1985;
Navia et al., 1986a; Wolcott, Fawzy, & Pasnau, 1985).
Estimates of persons with ARC exhibiting some form of
neuropsychologic dysfunction range from 41 percent to 54
percent (Grant et al., 1987; Petito et al., 1985; Schmitt et
al., 1988). As many as 10 percent of persons who develop
AIDS and ARC develop a neurologic syndrome as the first
manifestation of their illness as much as 12 months before
receiving a formal diagnosis of AIDS or ARC (Levy, Bredesen,
& Rosenblum, 1985). Perry (1990) outlined "six reasons to
suspect that organic mental changes could at least
occasionally occur before physical signs or symptoms" (p.
697): (1) Some persons with HIV infection report a
subjective sense of mental slowing, forgetfulness, apathy,
lethargy, social withdrawal, avoidance of complex tasks, and
personality change before receiving a diagnosis of AIDS.
Other persons with HIV infection initially present with
acute psychosis, delirium, amnesia, depression, or
manic-like episodes. (2) Research indicates that HIV enters
the nervous system shortly following infection. (3)
Children with HIV infection manifest a delay in reaching
motoric or intellectual milestones for reasons not directly
related to physical illness. (4) Patients with AIDS and ARC,
49
who did not have opportunistic infections or tumors in the

CNS, exhibited brain abnormalities on computerized

topography, magnetic resonance imaging (MRI), and
electroencephalogram (EEG). (5) Neuropathologic studies
revealed predominant subcortical involvement which was
consistent with vague psychologic symptomatology and absence
of intellectual impairment. (6) Neuropsychologic studies
with patients who had AIDS but were "currently free of
illness" and patients with ARC found neuropsychologic
impairment. The CDC (1987), recognizing the growing
incidence of neurologic and neuropsychologic complications
due to HIV infection, broadened its original criteria for
AIDS diagnosis to include ADC.
Navia and Price (1986) concluded:
It is now clear that [AIDS] dementia is one of the
most common and most important complications of
AIDS in both adults and children. Its morbidity
is high, and for many patients it becomes the
dominant aspect of their illness. Dementia can be
the presenting manifestation of AIDS or complicate
the course following the development of various
systemic manifestations. The clinical profile of
the disease is that of a 'subcortical dementia'...
Accumulating evidence favors the hypothesis that
the disorder results from direct brain infection
by [HIV], although further studies are necessary
both to establish this with certainty and to
understand the pathogenetic processes involved,
(pp. 165-166)
Etiology. "One of the many puzzling aspects of AIDS

has been the high frequency of degenerative brain changes,

which cause dementia and other neurological problems and do
50
not appear to be the result of the patients' opportunistic
infections" (Marx, 1985, p. 156). Since AIDS was first
described in 1981, there has been an increasing recognition
of a wide range of neuropsychologic problems associated with
the syndrome (e.g., Thomas & Szabadi, 1987). Perry and
Jacobsen (1986) concluded that the unusual psychiatric
manifestations of AIDS and ARC "may arise not only as
functional reactions to the stress of contracting this fatal
disease, but also from direct organic effects on the central
nervous system of malignancies, opportunistic infections,
and, most likely, the HTLV-III (HIV) itself" (p. 136).
Price and Brew (1988a) defined ADC as:
a distinct, relatively stereotyped, neurologic
disorder complicating HIV infection and is
characterized by a constellation of cognitive,
motor, and behavioral symptomatology. Each of the
three components of the term "AIDS Dementia
Complex" has a supporting rationale. "Dementia"
is a central component because cognitive
dysfunction (slowing) is most often the
predominant factor determining the presentation
and morbidity of the syndrome. "AIDS" is included
in the title in order to draw attention to the
relation of this nervous system syndrome to the
underlying systemic condition and to underscore
its high morbidity. The third component,
"complex," is also important because the syndrome
prominently affects motor function and, at times
behavior, (p- 1079)
Neurologic Involvement. Although the prevalence and
natural history of this condition is not known completely,
researchers have begun to track primary HIV infection of the
CNS, which involves the brain, meninges, spinal cord,
51
peripheral nerves, and cerebral vessels (Dal Canto, 1989;
Levy, 1988b; Petito, 1988). Approximately 25 percent to 30
precent of HIV infected persons develop an acute aseptic
meningitis during the first few weeks of HIV infection
(Stage at Group I level of HIV infection), which presents as
a febrile illness (Levy et al., 1985b; McArthur, 1987; Price
et al., 1988c; Price et al., 1988d). The various lines of
evidence, including the detection of HIV RNA and DNA in
cerebrospinal fluid, and the frequent isolation of HIV in
cerebrospinal fluid of patients with neuropsychologic
symptoms, suggest that HIV plays a primary role with respect
to ADC (Levy, 1988a). Collier (1987) noted that 5 of 10 ARC
patients and 8 of 24 AIDS patients were positive for HIV in
cerebral spinal fluid. Collier noted, however, that not all
of these patients reported neurologic or neuropsychologic
symptoms.
A variety of procedures has revealed HIV infection of
the brain itself: autopsy (Nielsen, Petito, Urmacher, &
Posner, 1984); Southern blot analysis (i.e., a procedure
to separate and identify DNA sequences) (Shaw et al., 1985);
in situ hybridization (Koenig et al., 1986; Shaw et al.,
1985; Stoler et al., 1986); immunohistochemistry (Gabuzda et
al., 1986; Pumarola-Sune, Navia, & Cordon-Cardo, 1987);
electron microscopy (Gyorkey, Melnick & Gyorkey, 1987); and
virus isolation (Ho et al., 1985; Levy, Shimabukuro, Mills,

52
& Kaminsky, 1985). De la Monte and colleagues (De la Monte
et al., 1987) reported lesions of the white matter of the
brain in 90 percent of HIV infected patients. Researchers
(Saaf et al., 1988; Sonnerberg et al., 1988) using magnetic
resonating imaging (MRI) technique, reported demyelination
white matter in patients with HIV infection. Sonnerberg and
colleagues (1988) noted that the degree of white matter
demyelination was related to the duration of HIV infection.
Lenhardt and Wiley (1989) reported that histopathologic
findings in 80 percent of patients with AIDS showed
significant HIV infectious process. Researchers (Lantos et
al. , 1989) found on autopsy 88 percent of the patients with
AIDS had cerebral abnormalities with "the deep grey matter
more severely involved than the cortex" (p. 310).
Researchers (Navia, Jordan, & Price, 1986) using MRI
reported marked demyelination of the white matter of the
brain. Rottenberg et al. (1987) reported alterations in
regional metabolic rate for glucose (rCMRGlc) associated
with the presence or progression of ADC. Using positron
emission tomography (PET), Rottenberg et al. (1987) found
that alterations in metabolism were highly correlated with
gray matter variation and disease severity assessed by
neuropsychologic testing. Rottenberg et al. (1987)
suggested "early relative subcortical hypermetabolism,
perhaps reflecting HIV infection, and progressive cortical

53
and subcortical h^Eometabolism constitute the metabolic
signature of ADC" (pp. 702-701). Markham et al. (1985)
isolated the HIV from biopsy of brain tissue in two-thirds
of their 100 patients. Shaw et al. (1985) studied the
brains of 15 individuals with AIDS and encephalopathy to
determine the presence of HIV infection. Clinical findings
were documented before death by the patients' physicians.
Five patients (33 percent) showed detectable HIV in the
brain. Shaw et al. (1985) noted that brain specimen
sampling was limited, and viral infection may have been
overlooked. Notable from these studies was the finding that
histologic abnormalities were not consistently correlated
with the reported presence or degree of dementia. However,
Brew, Cooper, and Predices (1987) reported that neurologic
signs, such as snout response (i.e., pursing of the lips
induced by light tapping of closed lips near the midline)
and leg weakness, correlate with the degree of dementia seen
in patients with ADC, and that frequency of neurologic signs
in patients without ADC may reflect "subclinical" disease.
Mechanism of HIV. HIV has been found to structurally
resemble the visna virus, which causes a slow, progressive,
degenerative brain disease in sheep (Gonda et al., 1985).
"HIV has since been included in this group of virusesthe
lenti- or 'slow' viruseswhich, after a lengthy period of
infection, cause neurologic disease in a variety of animal
54
hosts including primates, goats, horses, and mice" (Dilley &
Boccellari, 1988, p. 1 ) .

The presence of HIV in brain tissue and cerebral spinal

fluid has been established. At this time, the mechanisms of
viral entry into the central nervous system and the
mechanisms responsible for degeneration of white matter are
unknown. Drawing from research on lentiviruses (Peluso et
al., 1985), Price et al. (1988d) also suggest a "Trojan
horse" type mechanism of entry for HIV, hypothesizing that
either HIV is carried passively into the central nervous
system via infected lympocytes and monocytes, or HIV
infected endothelial cells cross the blood-brain barrier
allowing HIV to infect monocytes and lympocytes in the
brain. Once the brain has been infected by HIV, severe
lesions in the white matter are produced and consist of
extensive areas of demyelination with less severe axonal
destruction. Examination of the brain in patients with AIDS
reveals lesions in at least 80 percent of the cases (Koenig
et al. , 1986; Navia et al., 1986a). It is unknown whether
HIV itself destroys myelin or whether myelin destruction is
a "bystander effect," in which damage occurs as a result of
the host immune response to HIV (Lenhardt & Wiley, 1989). A
major obstacle facing researchers is that HIV infected
central nervous system cells may harbor the virus, thus
acting as a reservoir for persistent infection by the virus.

55
There is no effective long-term treatment of HIV infection
in the CNS; prevention is the only positive alternative.

Course of ADC. ADC is a progressive condition. In a

majority of the patients, symptoms worsen, resulting in
moderate to severe global impairment over a relatively short
period of time (Navia & Price, 1987). Price and Brew
(19B8a) reported that severe progressive forms of ADC
develop "almost exclusively in patients with advanced
immunosuppression" (p. 1080). There also are a number of
cases which seem to progress at a slower rate (Perry &
Jacobsen, 1986).
Currently, there are few longitudinal studies
investigating the course of ADC. In a review of this
literature. Perry (1990) noted that 50 percent of patients
with AIDS developed clinically significant ADC within one
year and that neuropsychologic impairment generally
increases with disease progression. Symptomatic remission
among patients with ADC is rare (Levy et al., 1985b). The
progression of neuropsychologic dysfunction over the full
range of HIV disease has not been studied (Sidtis & Price,
1990). It will be difficult to do so due to the concurrent
development of systemic opportunistic infections and CNS
lymphomas.

56
Clinical Characteristics of ADC

Neurologic Characteristics. Neurologic evidence shows

that HIV infects and affects the subcortical regions of the
brain, producing degeneration and atrophy with a relative
sparing of the grey matter of the brain. In a review of the
literature. Price, Sidtis, and Rosenblum (1988) noted that
the "highest density and greatest frequency of demonstrably
infected cells (are) located in the deep gray structures,
including particularly the basal ganglia and thalamus, and
in the white matter" (p. S28). Neurologic findings are
consistent with those found in other subcortical dementias
(see McArthur [1987] for review).
Neuropsychologic Characteristics. Britton (1984) was
among the first AIDS researchers to describe
neuropsychologic difficulties experienced by persons with
HIV infection. He described a young man who originally was
diagnosed as having acute schizophrenia. The patient had
experienced a personality change, lost his job, became
socially isolated, and experienced paranoid delusions.
After being hospitalized for six weeks, the patient was
diagnosed with an immune deficiency (AIDS). During the
early 1980s, researchers were unaware that manifestations of
HIV infection included neuropsychologic symptomatology.
Britton noted that neuropsychologic syndromes due to HIV
infection often were misdiagnosed, untreated, or treated
57
inappropriately. Kermani, Drob, and Alpert (1984) reported
a "unique constellation of psychiatric symptoms which are
possibly indicative of brain involvement" (p. 294) and part
of the natural history of AIDS for some patients,
characterized by mood disturbance, thought disorder with
grandiose delusions, and severe memory deficits. Recently,
Brody, Serby, Etienne, and Kalkstein (1991) reported
impaired olfaction (impaired odor identification) in
patients with HIV infection and significantly impaired
olfaction in patients with ADC. Brody et al. (1991)
suggested "impaired olfaction might serve as a marker of
early CNS HIV involvement" (p. 250). Navia and Price (1987)
stated that "the AIDS dementia complex may be the earliest,
and, at times, the only evidence of human immunodeficiency
infection" (p. 65). ADC is the most common cause of
neurologic dysfunction affecting patients with AIDS
(Dalakas, Wichman, & Sever, 1989; Gabuzda & Hirsch, 1987;
Levy et al., 1985b).
Although much work needs to be done in terms of
clarifying the nature and course of the neuropsychologic
manifestations of ADC, preliminary studies already have
begun to characterize this syndrome. Navia, Jordan, and
Price (1986) described ADC as a triad of cognitive, motor,
and behavioral symptoms. ADC typically has an insidious
onset, although in a small percentage of the patients the

58
symptoms may appear more abruptly (Morgan, Clark, & Hartman,

1988) or as a psychosis (Beckett et al., 1987; Thomas &

Szabad, 1987). Complaints such as forgetfulness, difficulty
in attention and concentration, and loss of interest in
everyday activities may be misdiagnosed and misinterpreted
as a depression secondary to having HIV infection (Fernandez
et al., 1989). Holland and Tross (1985) reported that the
early stage of DAT "resembles depression and is often
indistinguishable without neuropsychologic testing" (p.
762). Depression is one of the "cardinal features" of
subcortical dementia (Cummings, 1986) and is designated as a
secondary depression as it is produced by identifiable
neurologic, toxic, or metabolic conditions. Cummings (1986)
noted that a wide variety of systemic disorders, including
HIV infection, produce depression.
Price, Sidtis, and Rosenblum (1988) summarized:
Emerging studies of altered brain function
accompanying ADC support the idea that the
syndrome is a subcortical dementia. As in other
disorders tentatively described as subcortical
dementias, clinical and neuropsychological
evaluation of patients with AIDS reveals
psychomotor slowing, impaired problem-solving
abilities, reduced spontaneity, and poor fine
motor control as the early and most prominent
features; frank aphasia, amnesias, or parietal
lobe syndromes are not observed until late in the
disease. The concept of subcortical involvement
is also in keeping with the pathological and
virological findings, (p. S30)

59
 Stages of ADC. Recently Price and Brew (1988a) defined
the stages of ADC by utilizing functional disabilities
rather than specific neurologic and neuropsychologic signs,
producing a hierarchy ranging from 0 (normal) to 4 (end-
stage). Price and Brew's (1988a) stages of functional
disability will be merged with conceptualizations of ADC
stages based on neurologic and neuropsychologic findings
(Elder & Sever, 1988; Kieran, 1987; Navia, Jordan, & Price,
1986; Navia & Price, 1986; Ochitill & Dilley, 1988; Price &
Brew, 1988b).

In Stage One (mild) Early Stage, patients may complain

of being forgetful or having memory problems. They may
demonstrate difficulty concentrating or sustaining
intellectual effort, forgetfulness, cognitive slowing (e.g.,
difficulties for rapid mental processing and performance),
and psychomotor retardation. Cognitive symptoms usually are
apparent before motoric slowing. Neuropsychologic testing
indicates mild impairment. The patient may be described by
others as "different" or "changed." Patients are able to
perform all but the most demanding aspects of work or
activities of daily living and walk without assistance.
Patients may appear apathetic or lethargic, become socially
withdrawn, and appear less spontaneous. This presentation
of symptoms may lead to a diagnosis of depression.
Secondary depression is a cardinal feature of subcortical

60
dementias such as ADC. In this sense, deficits which may be
associated with secondary depression become part of the
sequelae of ADC. Some of the behavioral and personality
changes of ADC may include agitation and periods of
confusion. The onset of a personality change may be seen.
Some early stage ADC patients may present with what appears
to be a bipolar manic episode. Patients may complain of leg
weakness, and may develop hand tremors and complain that
they are less coordinated than usual. Performance on motor
tasks may be slowed due to neuronal degeneration of the
peripheral nervous system. Computerized topography (CT)
scans usually are normal. If the CT scan is abnormal, it
will show diffuse atrophy. Various studies now are
demonstrating the usefulness of MRI which seem to identify
ADC earlier than the CT scan.
In Stage Two (moderate), patients exhibit a continued
decline in cognitive functions, characterized by deficits
for delayed memory, mental flexibility, and overall speed of
mental operations. Neuropsychologic testing indicates
moderate impairment. Although patients are able to perform
basic activities of self-care, they cannot work or maintain
the more demanding aspects of daily life. Patients remain
ambulatory, but may require assistance or a prop.
During Stage Three (severe), patients exhibit severe
intellectual incapacity, which is demonstrated by inability
61
to follow news events or sustain complex conversations, and
by considerable slowing of all output. Patients will
exhibit moderate to severe deficits on neuropsychologic
tests. Motor disability is demonstrated by inability to
walk unassisted and by slowness and clumsiness of the arms.
In Stage Four (end-stage), the most outstanding feature
of the late stage of ADC is the presence of severe global
cognitive impairment. Development of confusion and
psychomotor slowing often is evident. Patients appear
vegetative (i.e., coma-like state) and exhibit a rudimentary
level of intellectual and social comprehension on
neuropsychologic tests. Neuropsychologic deficits may
include problems with concentration, auditory
hallucinations, changes in taste and smell, grandiose
delusions, severe memory deficits, generalized weakness,
repetitive speech, disorientation, inability to abstract,
and confusion. Patients generally are unable to care for
themselves, and may not be able to perform even overlearned
tasks, such as dressing or feeding themselves. Patients may
exhibit signs of muteness. Some patients may become
agitated and require the use of restraints. Obvious motor
abnormalities at this stage include ataxia, spastic leg
weakness, hyperreflexia in the legs, and occasional
myoclonic jerking of the upper extremities. Generalized
seizures may develop at this stage. Patients may become
62
paraplegic with urinary and fecal incontinence. CT scans
and MRIs will indicate cerebral atrophy, with the MRI
showing evidence of a demylinating disorder.

Treatment. Zidovudine, also known as Azidothymidine

(AZT) or Retrovir, is a derivative of thymidine, a component
of DNA needed by the host cell (T-4) and the virus (HIV) to
produce the chemicals necessary for replication. Zidovudine
enters the host cell, flooding it with false DNA so that the
HIV cannot replicate itself. Viral replication (and
infection) is halted. Uninfected T-4 cells are protected
and are able to replicate. However, Zidovudine does not
destroy current HIV infection. The drug, then, may halt
viral replication, thereby increasing longevity without
improving neurologic and neuropsychologic functioning
(Lechtenberg & Sher, 1988). As Zidovudine does cross the
blood-brain barrier, it may provide a crucial link in
preventing ADC in persons with HIV infection, thus
preventing irreversible brain damage (Britton, Miller, &

Jubelt, 1989).
Recent studies have indicated that Zidovudine may be
effective in ameliorating ADC. Researchers (Schmitt et al.,
1988; Thompson et al., Riccio, 1988; Yarchoan et al., 1987;
Yarchoan et al., 1988) reported improvement in
neuropsychologic test performance (retrieval abilities,
sustained attention, alteration of mental sets, and
63
psychomotor speed) in patients with ADC who are taking
Zidovudine. Over time, however, the effectiveness of
Zidovudine declines.

Neuropsychologic Features. Among patients with AIDS

who were average to above average for intellectual
functioning, researchers consistently have reported severe
cognitive dysfunction, characterized by concentration and
attention deficits, memory deficits, and cognitive slowing
(Beckett et al., 1987; Boccellari, 1987; Boccellari, 1988;
Boccellari, Dilley, Baer, & Ochitill, 1990; Boccellari,
Dilley, & Shore, 1988; Dalakas, Wichman, & Sever, 1989;
Dilley, Baer, Boccellari, & Ochitill, 1990; Fernandez et
al., 1989; Jassen, 1987; Kermani, Drob, & Alpert, 1984;
McArthur, 1987; Navia, Jordan, & Price, 1986; Navia & Price,
1986; Ochitill & Dilley, 1988; Price et al., 1988c; Price et
al., 1988d; Rubinow, Joffe et al., 1988; Tross & Hirsch,
1988); impairment for motoric speed (Dalakas, Wichman, &
Sever, 1989; Dilley & Boccellari, 1988; Navia, Jordan, &
Price, 1986; Navia & Price, 1986; Nurnberg, Prudic, Fieri, &
Freedman, 1984; Price et al., 1988c; Price et al., 1988d;
Price, Sidtis, & Rosenblum, 1988e; Sidtis, 1987; Tross &
Hirsch, 1988); and apathy (Beckett et al., 1987; Boccellari,
1987; Boccellari, Dilley, & Shore, 1988; Dilley &
Boccellari, 1988; McArthur, 1987; Navia, Jordan, & Price,
1986; Navia & Price, 1986; Ochitill & Dilley, 1988). Levy,

64
Fernandez, and Pirozzolo (1988) reported that tests which
tax memory span or speed of cognitive information processing
are significantly impaired, and tests for visuomotor and
contructional abilities, and visuospatial abstract reasoning
were intact in patients with HIV related dementia.
Descriptive data indicate the triad of symptoms associated
with ADC: cognitive deficits, slowing of motoric speed, and
behavioral changes, including depression.

Table 6 summarizes quantitative data for four groups:

patients with ARC or lymphadenopathy syndrome (LAS);
patients with abnormal LAS (Schmitt et al. [1988] designated
patients with LAS and neurologic deficts as abnormal LAS);
patients with AIDS; and patients with ADC. The level of
education reported for the four groups indicated that all
patients had at least two years of college. In general, all
groups exhibited relatively well-preserved intellectual
functioning, including abilities for abstract reasoning,
acquired knowledge, immediate recall, and visuospatial and
visuoconstruction abilities. Abilities for sequencing,
visuospatial scanning, and alteration of mental sets or
mental flexibility were within normal limits. Scores
indicate attention and concentration abilities, new learning
abilities, and immediate recall and short-term memory for
verbal-semantic material and visuospatial material generally

were preserved.
65
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68
 The composition of these groups provides a
cross-sectional view of the progressive decline in cognitive
functioning for patients with HIV infection (see Table 7 ) .
Patients with ARC, AIDS, and ADC exhibited well-preserved
intellectual functioning. Persons with ADC exhibited a mild
decline on the tests involving motoric speed and visuomotor
coordination. For sequencing, visuospatial scanning, and
alteration of mental sets/mental flexibility, patients with
ARC performed within normal limits; patients with AIDS
exhibited mild deficits for alteration of mental sets; and
patients with ADC exhibited deficits for all abilities,
indicating cognitive and motoric slowing. All groups
exhibited within normal limits for immediate recall.
Persons with ARC exhibited within normal limits abilities
for immediate recall and short-term memory for
verbal-semantic and visuospatial material; persons with AIDS
and ADC exhibited mild to moderate deficits for immediate
recall and short-term memory for verbal-semantic material.
Only persons with ADC exhibited impairment for visual
memory. These data suggest that as HIV infection
progresses, attention/concentration abilities, sequencing
ability, visuospatial scanning speed, alteration of
sets/mental flexibility, motoric speed, and verbal memory
decline. That is, patients who have HIV infection
experience progressive cognitive and motoric slowing, and

69
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71
inability to retrieve stored material. Intellectual ability

and visuospatial memory are preserved until end-stage ADC.

Researchers (Abrams, Newell, & Friedrich, 1987; Ayers,
Abrams, Newell, & Friedrich, 1987; Saykin et al., 1988)
using the Luria-Nebraska Neuropsychological Test Battery
have reported a similiar pattern of deficits for attention
and slowed visual and auditory information processing with a
preservation of higher conceptual skills.
Although patients with ADC often experience depression
secondary to the disease process, it does not appear to
account for reported cognitive deficits (Price et al.,
1988c). Kovner et al. (1989) administered a test battery of
cognitive, personality, and attention tests to patients with
HIV infection, ARC, and AIDS. They reported that "affective
and attentional factors do not play a significant role in
accounting for the cognitive impairment of HIV-infected
ambulatory subjects" (p. 277).

Summary of DAT and ADC

Histopathologic reports of patients with DAT are
different from patients with ADC. For patients with DAT,
histopathologic reports indicate characteristic fibulary
plaques and tangles found in the cerebral cortex. For
patients with ADC, abnormalities were predominantly in the
white matter in the subcortical structures of the brain,

72
particularly in the basal ganglia and thalamus, with a
relative sparing of the cortex. DAT seems to be located in
the cortical structures of the brain, and ADC in subcortical
structures.

DAT is characterized by deficits involving the cerebral

cortex: aphasic symptoms such as word finding difficulties
and impaired concentration, memory disturbances including
deficits for new learning and remote memory for verbal and
visual material, impaired cognitive abilities, and a general
decline in intellectual functioning. Visuospatial and
constructional deficits are prominent. Calculation
abilities are disrupted. Judgment is poor. Motoric
functioning is normal until advanced stage DAT. Depression
and psychosis generally are absent.

Cummings and Benson (1983a) note that the clinical

characteristics of subcortical dementias "contrast sharply"
with those of cortical dementias. In subcortical dementias,
such as ADC, the cardinal features include a slowing and
dilapidation of cognition, forgetfulness, and alterations in
effect. McHugh and Folstein (1975) described dilapidation
as the ability to perform individual steps of a complex
problem, but failure to synthesize the elements properly to
achieve a correct answer, such as the ability to manipulate
the necessary sequential steps.

73
 Memory disturbances, such as forgetfulness, are
characterized by difficulty in spontaneously retrieving old
information, and retrieval is improved with cues.
Intellectual functioning, such as judgment and calculation
abilities, and visuospatial and visuoconstructional
abilities are generally preserved until end-stage disease.
As suggested in studies of other subcortical dementias,
abilities for sequencing, visuospatial scanning, and mental
flexibility are due to slowed cognitive processing rather
than to cognitive deficits per se. Fine motoric speed is
slowed. Depression is common and secondary to the disease
process.
Statement of Problem. The purpose of this study is to
compare specific cognitive deficits characteristic of DAT, a
cortical dementia, and ADC, a subcortical dementia. To
date, no research has compared these two dementias. This
research will add to the current body of literature on
dementias and increase understanding of the two disease
processes by verifying through comparison of the two groups
the observations reported in the literature about each
group. The proposed test instruments were selected based on
three criteria: (1) reliability, (2) validity, and (3)
compatibility with the current body of research literature,
including normative data. That is, the proposed test
instruments accurately measure specific cognitive functions

74
and are widely used by other researchers so that these test
results may be compared to other test results. Although age
effects are anticipated between patients with DAT and ADC,
the tests selected have a body of literature which provides
standardized scores for normal populations and/or tables for
age correction when computing scores. Although
idiosyncratic tests may be of interest to

neuropsychologists, they do not provide comparative data,

and thus may not contribute substantially to the current
body of literature.
Research shows that patients with DAT exhibit
impairment for higher cortical functions such as deficits
for comprehension, constructional abilities, and
visuospatial, visuotracking, and visuoperceptual abilities
(Botwinick, Storandt, & Berg, 1986; Botwinick, Storandt,
Berg, & Boland, 1988; Cummings, 1985; Cummings & Benson,
1983b; Cummings & Benson, 1986; Schneck, Reisberg, & Ferris,
1982). These deficits are due to neuropathologic
deterioration of the cortical regions of the brain.
Research shows that patients with ADC exhibit cognitive
dysfunction for sequencing abilities, attention/
concentration, and visuospatial scanning speed (Boccellari,
1988; Boccellari, Dilley, Baer, & Ochitill, 1990; Gold &
Armstrong, 1984; Janssen et al., 1988; Navia & Price, 1987;
Nurnberg, Prudic, Fieri, & Freedman, 1984; Rubinow et al.,
75
1987). For patients with ADC, impairment for higher
cortical functions is due to slowed cognitive processing
rather than to cognitive deficits per se.

Research shows that patients with DAT exhibit deficits

for verbal-semantic and figural-spatial memory functions
(Berg et al., 1984; Flud, 1984; Huber & Paulson, 1986; Moss
et al., 1986; Ober et al., 1985; Smith, Butters, & Granholm,
1988) due to progressive cortical deterioration interfering
with the encoding, storing, and retrieval processes.
Research shows that patients with ADC exhibit moderate to
severe deficits for verbal-semantic memory, and only persons
with end-stage ADC exhibit deficits for figural-spatial
memory (Boccellari, 1988; Boccellari, Dilley, Baer, &
Ochitill, 1990; Boccellari, Dilley, & Shore, 1988; Gold &
Armstrong, 1984; Janssen et al., 1988; Kermani, Drob, &
Alpert, 1984; Navia & Price, 1987; Nurnberg et al., 1984;
Rubinow et al., 1987; Tross & Hirsch, 1988).
Patients with cortical dementia present with normal
mood (Benson & Cummings, 1986). Some research shows that
the prevalence of depression in patients with DAT is minimal
(Cummings et al., 1987; Knesevich et al., 1983; Reding,
Haycox, & Blass, 1983). However, depression is one of the
"cardinal features" of subcortical dementia in general
(Cummings, 1985a) and of ADC in particular (Fernandez et
al., 1989; Kovner et al., 1989; Navia & Price, 1986).

76
Hypotheses

The following research hypotheses will be evaluated in

the present investigation.

1. Patients with DAT, a cortical dementia, will

receive a lower memory quotient on the Wechsler Memory
Scale, a test of higher cortical functions, than patients
with ADC, a subcortical dementia.
2. Patients with DAT, a cortical dementia, will
receive a higher score (greater number of minutes to
complete task) on the Trail Making Test Part A and B, tests
of visuospatial, sequencing, and mental flexibility
abilities, than patients with ADC, a subcortical dementia.

3. Patients with DAT, a cortical dementia, will

receive a lower score for depression on the Self-rating
Depression Scale than patients with ADC, a subcortical
dementia.

77
 CHAPTER IV

METHODOLOGY

Method

Subjects. Participants were 30 men: 15 who have DAT

and 15 who have ADC. Participants were limited to men in
order to rule out possible variance in test results due to
sex differences.

Patients (M age = 79.6, S.D. = 9.2, range 59 - 89)

assigned to the DAT group had a preliminary diagnosis of DAT
because of cognitive difficulties not due to other
neurologic disorders, such as multi-infarct, normal pressure
hydrocephalus, or Huntington's Chorea. DAT participants
were recruited from Abilene, Texas, retirement centers. To
insure confidentiality of DAT participants prior to entry
into the study, the Directors of Nursing at the retirement
centers contacted family members, who gave permission to
test the retirees and gave informed consent for them. No
family members for DAT patients requested that a written
report be prepared for the DAT patient's physician.
Of the potential DAT participants (N = 33) interviewed,
18 men were ruled out. Information from the semi-structured
interview and information from other informants (e.g.,
family members and health care staff) was used to determine
the potential participants' stage of disease process

78
described in Chapter II. The stage of disease by estimated
number of years diagnosed for DAT participants is shown in
Table 8. DAT participants (N = 6) who were assigned to
stage one disease process (mild) had a history of difficulty
remembering names and appointments, exhibited social
withdrawal, exhibited decreased spontaneity and initiative,
and exhibited speech production difficulties characterized
by poverty of content or empty speech, but exhibited
articulate and/or fluent speech. DAT participants (N = 9)
who were assigned to stage two disease process (moderate)
exhibited fluent speech production characterized by
repetitions, decreased language comprehension abilities,
impaired abilities for long- and short-term memory,
diminished concern for appearance and/or hygiene, and flat
or labile mood. Potential participants (N = 16) who were
assigned to stage three disease process (severe/end-stage)
and eliminated from the study exhibited severe deficits for
language production characterized by echolalia, palilalia,
or mutism, exhibited severe impairment for long-term memory
characterized by inability to recognize significant others,
and exhibited severe deficits for language comprehension
indicating that their cognitive abilities were untestable.
One potential participant was eliminated from this study due
to a history of stroke, and one due to a history of
alcoholism.

79
Table 8
Dementia of the Alzheimer's Type: Stage of Disease Process
Based on Interview Information by Estimated Number of Years
Diagnosed

Year Diagnosed Stage One Stage Two Stage Three

2 1
3 1
4 1 1
5 2 1
6 2
7 1 3

8 1
9
10
11 1

80
 Men (M age = 32.4, S.D. = 5.3, range 24 - 43) assigned
to the ADC group were limited to self-identified gay men who
experienced cognitive difficulties and/or motoric slowing,
and did not have any known neurologic disorders, such as
cryptococcal meningitis or toxoplasma meningoencephalitis.
ADC participants were referred by the physician at the
Abilene AIDS Clinic. ADC patients were given a "Consent for
Research Participation" form and an optional "Physician
Release" form which they read and signed. All ADC patients
requested that a written report of their test results be
provided to their physician at the AIDS Clinic.
Of the potential ADC participants (N = 22) interviewed,
7 men were ruled out. Referrals for potential ADC
participants were based on health care staff's observations
of memory difficulties or "being somehow different."
Information from the semi-structured interview and
information from other informants (e.g., companions and
health care staff) was used to determine the potential
participants' stage of disease process described in Chapter
III. The stage of disease by number of estimated years for
HIV infection for ADC participants is shown in Table 9. ADC
participants (N = 4) who were assigned to stage one disease
process (mild) had a history of forgetfulness and difficulty
concentrating, cognitive slowing, motoric slowing, and poor
coordination abilities. ADC participants (N = 8) who were

81
Table 9
AIDS Dementia Complex: Stage of Disease Process Based on
Interview Information by Estimated Number of Years Diagnosed

Year Stage One Stage Two Stage Three Stage Four

Diagnosed

2 1
3 1
4 1 1
5 1
6 1 1
7 1 1 1
8 2 1 1
9 1

82
assigned to stage two disease process (moderate) had a
history of decreased short-term memory abilities, decreased
mental flexibility, and were no longer able to work due to
cognitive or motoric difficulties. ADC participants (N = 3)
who were assigned to stage three disease process (severe)
had a history of inability to follow news events, movies,
and television programs, exhibited difficulty sustaining
complex conversation, and increased cognitive and/or motoric
slowing. No potential participants exhibited symptoms
associated with stage four disease process (end-stage),
which is characterized by vegetative (coma-like) symptoms
and complete lack of self-care abilities. Potential
participants (N = 7) who were eliminated from the study did
not subjectively report two symptoms associated with ADC,
cognitive difficulties and/or motoric slowing. The
potential participants who were eliminated from the study
were referred because they seemed "somehow different."
Later clinical work not associated with this study indicated
that these men's difficulties were due to characterologic
traits and/or reactions to environmental stressors.

Instruments. The neuropsychologic battery consisted of

a semi-structured interview and 4 tests.
The semi-structured interview included probes for
motoric slowing, memory difficulties, and mood or
personality changes. "Yes" responses to these three areas

83
elicited further probes, such as when they noticed the
difficulty, if others had noticed the difficulty, how they
compensated for the difficulty, and what changes, if any,
had the difficulty made in their lives. Patients with ADC
were asked the date they suspected that they were HIV
positive and the date they were diagnosed HIV positive.
Information disclosed during the semi-structured interviews
is discussed in the Results chapter.

The Wechsler Memory Scale (WMS: Wechsler, 1945)

measures immediate recall abilities for verbal and
visuospatial material, immediate recall for digits forward
and backward, orientation, knowledge of current information,
and mental control. Verbal memory for immediate recall,
designated Logical Memory 1 (LMl), measures immediate recall
for verbal material. It is assessed by reading two short
stories to the patient- Immediately after reading each
story the patient is asked to tell what he remembers about
the story. Visuospatial memory for immediate recall,
designated Visual Memory 1 (VMl), measures immediate recall
for visual material. It is assessed by presenting a series
of three cards depicting simple geometric figures. After
each card has been presented, it is removed from view. The
patient is asked to draw what he remembers. Patients who
are unable to produce drawings from recall are asked to copy
the figure(s). The points earned for each subtest are

84
totaled. The total raw score is transformed into a Memory
Quotient, indicating overall memory abilities. Computation
of Memory Quotient includes a correction for age. Normative
data for correction for age and educational level are
available for LMl and VMl data and will be discussed later.
The Wechsler Memory Scale-Revised (WMS-R) will not be used
in this study because of the following. (1) The WMS-R
includes extensive and complex visuospatial tests. Patients
with DAT have difficulty replicating even simple geometric
figures. Thus, utilization of the WMS-R may not provide a
sufficiently low baseline. (2) The WMS-R provides norms
which are based on an N = 50, and may not be reliable or
valid for this study's populations. (3) Comparative data
for the Russell-Revision is available for the WMS, but not
for the WMS-R. (4) Utilization of WMS-R data would not be
compatible with the current body of research literature.
The Russell-Revision of the WMS measures short-term
memory (30-minute recall) for Logical Memory, designated
LM2, and Visual Memory, designated VM2. For this procedure,
30 minutes after materials for LMl and VMl are presented,
the patient is asked to tell the stories which were read
earlier and to draw the simple geometric figures which were
presented earlier. Normative data for corrections for age
and educational level are available and will be discussed
later.

85
 Trail Making Test A and B (TMT: Reitan, 1958) measures
visuoscanning abilities, sequencing, and attention and
concentration abilities. Part B also measures mental
flexibility. The TMT is similar to a "connect the dots"
game. For TMT Part A the patient is asked to draw a line
connecting in correct sequence numbers 1 - 2 5 which are
scattered in a random pattern on the page. For TMT Part B
the patient is asked to draw a line connecting a correct
alternating sequence of numbers (1 - 13) and letters (A - L)
which are placed in a random pattern on the page. For
example, the patient draws a line from 1 to A to 2 to B and
so on. The score is the amount of time in seconds needed to
complete the task. The TMT is an excellent screening devise
for detecting dementia, as it indicates organic brain
damage. Normative data are available for correction for age
and educational level and will be discussed later.
The Self-rating Depression Scale (SDS: Zung, 1974) is a
self-rating depression scale for the quantitative
measurement of depression, operationally defined as a
syndrome comprised of signs and symptoms in four areas:
somatic, psychologic, psychomotoric, and mood. The SDS is
comprised of 20 statements, each relating to a specific
characteristic of depression. Each statement is rated "None
or a little of the time," "Some of the time," "Good part of
the time," or "Most of the time." The raw score is

86
converted to an index based on 100, yielding a percentage
score. Clinical interpretations for SDS categories (within
normal limits, presence of mild depression, presence of
moderate depression, and presence of severe depression) are
based on data comparing depressed versus non-depressed
patients, and depressed versus normal participants in the
20- to 60-year-old range (Zung, 1965; Zung, 1968; Zung,
1969; Zung, 1970; Zung, 1972; Zung, 1973).

Procedure. Testing was conducted in one session,

allowing breaks as needed or requested by participants. The
neuropsychologic testing sequence was (1) Semi-structured
Interview, (2) Wechsler Memory Scale, (3) Trail Making Test
A and B, (4) Self-rating Depression Scale, and (5)
Russell-Revision of the Wechsler Memory Scale. Test and
subtest administration for the WMS, TMT, SDS, and
Russell-Revision of the WMS followed the sequence as outline
in the test manuals.
Aoe and Educational Level Correction. It was
anticipated that men with DAT would be much older than men
with ADC. Test results also are affected by educational
level. To correct for variance due to age and educational
level, the following procedures were performed.
Research indicated that TMT scores are affected by age
and educational level (Alekoumbides, Charter, Adkins, &
Seacat, 1987; Heaton, Grant, & Matthews, 1986; Warner et
87
al., 1987). Age and educational effects were controlled by
converting individual TMT scores to ^-scores based on age
and educational level corrections, means, and standard
devisions described by Alekoumbides et al. (1987). For
example, Participant 16 was 36-years-old, had a high school
education (grade level 12), and a TMT Part A score of 42; to
correct his score for age and educational level, 7 was added
to his raw score, producing an age and educational level
corrected score of 49. This score was compared with the
mean and standard deviation (X = 48.60, S. D. = 23.79)
obtained in Alekoumbides et al.'s (1987) sample from which a
^-score of 0.02 was derived:
(0.02 = 49 - 48.60/23.79).
An additional comparison was made for TMT Scores when
determining stage of disease process. The patient's time in
seconds on Parts A and B was compared with percentiles for
normal control subjects at different age levels (Spreen &
Strauss, 1991). The rankings were assigned as follows: (1)
Above average abilities for the 90th percentile; (2) average
abilities for the 75th percentile; (3) borderline deficits
for the 50th percentile; (4) moderate deficits for the 25th
percentile; and (5) severe deficits for the 10th percentile.
Computation of the WMS Memory Quotient included
correction for age based on normal participants. Research
indicated that WMS LMl and LM2 (Abikoff et al., 1987; Power

88
et al., 1979) and WMS VMl and VM2 (Russell, 1988) are
affected by age and educational level. Analysis for WMS LMl
and LM2 provided corrections for age and educational level
based on criteria described by Abikoff et al. (1987). For
these corrections, an expected score was computed based on
the individual's age and educational level; the expected
score was compared with the actual score from which a
^-score was derived. For example. Participant 16 was
36-years-old, had an educational level of 12, and received a
raw score of 9. For immediate recall, Abikoff et al. (1989)
described the expected score as:
6.72 + .20(age) + .93(education) - .0026(age^).
Participant 16 received an expected score of 21.71:
[21.71 = 6.72 + .20(36) + .93(12) - .0026(36^)].
The standard deviation was specified as 6.01. The expected
score 21.71 was compared with the actual score 9, yielding a
^-score of -2.23:
(-2.23 = 9 - 21.71/6.01).
Analysis for WMS VMl and VM2 provided corrections for
age and educational level effects based on criteria
described by Russell (1988). The raw score was corrected
for age and educational level. The corrected score was
assigned to a corresponding scaled score. Russell (1988)
provided levels of severity of impairment for the scaled
scores. For example. Participant 16 was 36-years-old, had

89
12 years of education, and received a score of 10. To
correct for age and education, 1 was subtracted from 10 (raw
score). The corrected score, 9, corresponded to a scaled
score of 1.5, which was within normal limits.

Post-test Analysis of Stage and Severity of Disease.

Entry into this study was based on interview information and
limited to patients who were not at end-stage disease. DAT
participants were limited to those assigned to stage one
(mild) and stage two (moderate) disease processes. ADC
participants were limited to those assigned to stage one
(mild), stage two (moderate), and stage three (severe). As
diagnostic criteria and neuropsychologic symptomatology for
DAT and ADC are different, it was important to determine
each participant's stage of disease process.
The first post-test analysis for stage of disease
process was performed on WMS LMl raw data. DAT
participants' raw test scores for WMS LMl were compared with
the Clinical Dementia Rating (CDR) scale criteria: no
dementia (CDRO), mild (CDRl), moderate (CDR2), and severe
(CDR3) (see Botwinick et al. [1986] Table 2 ) . Botwinick et
al. (1986) reported that CDRl participants received scores
of 1.7 - 1.2; CDR2, 0.6 - 0.4; and CDR3, 0.1 - 0.0. DAT
stages of disease process assigned were CDRO (N = 2 ) , CDRl
(N = 6 ) , CDR2 (N = 0 ) , and CDR3 (N = 7). Table 10 shows CDR
rating by estimated years diagnosed with DAT.
90
Table 10

Dementia of the Alzheimer's Type: Stage of Disease Process

Based on Clinical Dementia Ratings by Estimated Number of
Years Diagnosed

Year Diagnosed CDRO CDRl CDR2 CDR3

2 1
3 1
4 1 1
5 1 1 1
6 1 1
7 2 2
8 1
9
10
11 1

CDRO, Clinical Dementia Rating 0; CDRl, Clinical Dementia

Rating 1 (mild); CDR2, Clinical Dementia Rating 2
(moderate); CDR3, Clinical Dementia Rating 3 (severe).

91
 ADC participants' raw test scores for WMS LMl were
assigned severity ratings based on scales developed by
Russell (1975). Russell (1975) reported scores greater than
or equal to 27 were above average, 24 - 26 average, 1 8 - 2 3
mildly impaired, 14 - 17 moderately impaired, 9-13
severely impaired, and 0 - 8 very severely impaired. ADC
stages of disease process assigned were above average (N =
1 ) , average (N = 1 ) , mild (N = 4 ) , moderate (N = 4 ) , severe
(N = 5 ) , and very severe (N = 0 ) . Table 11 shows the
severity ratings by estimated number of years HIV infected.

The second post-test analysis compared criteria for

stage of disease process and WMS LMl and LM2, WMS VMl and
VM2, and TMT age and educational level corrected scores.
DAT patients (N = 6 ) , who were assigned to stage one (mild),
exhibited average abilities to severe deficits for verbal
memory, and exhibited some abilities for visuospatial,
sequencing, and mental flexibility. Weight was given to the
patient's ability to complete the TMT as memory deficits are
a common sign for all stages of DAT disease process. DAT
patients (N = 3 ) , who were assigned to stage two (moderate),
exhibited mild deficits for verbal memory, and very severe
deficits for visual memory, visuotracking abilities, and
mental flexibility. Patients assigned to stage three
exhibited mild deficits for immediate recall for WMS LM but
were unable to complete the TMT. Weight was given to the

92
Table 11

AIDS Dementia Complex: Stage of Disease Process Based on

Wechsler Memory Scale Logical Memory by Estimated Number of
Years Diagnosed

Year Above
Diagnosed Average Average Mild Moderate Severe

2 1
3 1
4 1 1
5 1 1
6 1
7 1 1 1
8 1 1 2

9 1

93
patient's inability to complete the TMT. DAT patients (N =
6 ) , who were assigned to stage three (severe/end-stage),
exhibited severe impairment for visual and verbal memory,
and for visuotracking abilities and mental flexibility.
Stage three patients exhibited inability to complete the TMT
and VMl. Patients assigned to stage three did not exhibit
severe impairment for language production (i.e., echolalia,
palilalia, or mutism) described as characteristic of
end-stage disease process. Table 12 shows the stage of
disease process by estimated number of years diagnosed.

ADC patients (N = 6 ) , who were assigned to stage one

(mild), exhibited mild deficits only for verbal memory. One
ADC patient, who reported memory difficulties, which was
confirmed by other informants, did not exhibit deficits for
any of the tests administered. This may be due to
sufficient lack of sensitivity of these tests. He was
assigned to stage one (mild) based on self report and other
informants' reports. ADC patients (N = 3), who were
assigned to stage two (moderate), exhibited severe deficits
for verbal memory, and mild deficits for visuotracking
abilities and mental flexibility. ADC patients (N = 6 ) , who
were assigned to stage three (severe), exhibited moderate to
severe deficits for logical memory, visuotracking abilities,
and mental flexibility. Three stage three participants also
exhibited mild to moderate deficits for visual memory. No

94
Table 12

Dementia of the Alzheimer's Type: Stage of Disease Process

Based on Test Results by Estimated Number of Years Diagnosed

Year Diagnosed Mild Moderate Severe

2 1
3 1

4 1 1
5 2 1
6 2
7 2 2
8 1
9
10
11 1

95
ADC participants were assigned to stage four (end-stage).
Table 13 shows the stage of disease process by estimated
number of years with HIV infection.

Since this data were collected for ADC patients, two

more participants started receiving disability benefits.
These men exhibited deficits associated with stage one
disease process when tested. Within seven months, they were
unable to continue working. Since this data were collected,
one ADC participant died. He had exhibited deficits
associated with stage three disease process. Within five
months, he died of unknown complications which caused
extensive and fatal internal bleeding.

96
Table 13
AIDS Dementia Complex: Stage of Disease Process Based on
Test Results by Estimated Number of Years Diagnosed

Year Diagnosed Mild Moderate Severe

2 1
3 1
4 1 1
5 2
6 1
7 1 2
8 1 2 1

9 1

97
 CHAPTER V

RESULTS

Power Analysis

The following procedure was used to determine estimated

sample size. Data to compute the power analysis were taken
from previous research (see Table 14). Power (D) was
computed by comparing the DAT group and the ADC group, and
the DAT group and the HIV+ group:
(D = mean. - mean^ / pooled variance).
Estimated sample size (N) was calculated with power
specified as .80 and alpha as .05:
[N = (2.49 / D)^3.
Computations for the estimated sample size (N) required to
achieve statistical significance were performed for TMT Part
A and B, and WMS subtests Mental Control, Digit Span,
Associate Learning, and Logical Memory (see Table 15). A
much smaller sample size (N = 25) was necessary to achieve
statistical significance for the TMT Part B than for the TMT
Part A (N = 620). The TMT Part B is more difficult to
complete as it requires intact abilities for higher cortical
functions (i.e., mental flexibility). A range of estimated
sample sizes (range 0.5 - 69) for the WMS subtests were
indicated to achieve statistical significance between the
groups. No data were available to calculate the estimated

98
 C M CT> C M rs. i n i n ^- CO . - 4 CO i n i n e 91
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101
sample size for the SDS. Due to the generally small
estimated sample sizes indicated by the power analysis, N =
30 was specified as sufficient to achieve significancea

Stage of Disease Process; Group Comparisons

Severity of neuropsychologic deficits were greater for
DAT patients than for ADC patients. This is a function of
the disease process. Neuropsychologic deficits associated
with DAT are more severe than those associated with ADC.
Patients with DAT exhibit deficits consistent with a loss of
higher cortical functioning. Patients with ADC exhibit
deficits associated with subcortical decline, characterized
by slowed cognitive functions.
The groups were compared for stage of disease process
by estimated number of years diagnosed with DAT or HIV
infection. Each patient was assigned to a stage of disease
process based on quantitative data (test results corrected
for age and educational level). The groups were comparable
for stage of disease process (see Table 16). There also
appeared to be a correlation between the estimated number of
years diagnosed and the stage of disease process. As
estimated number of years diagnosed increased, the stage of
disease process was more advanced.

When DAT stage of disease process was determined by

interview information (see Table 8) as compared with age and

102
Table 16

Stage of Disease Process Based on Neuropsychologic Test Data

by Estimated Years Diagnosed

^^^T Number of Subjects .

Diagnosed Average Mild Moderate Severe
DAT ADC DAT ADC DAT ADC DAT ADC

2 1 1
3 1 1
4 1 1 1 1
5 2 2 1
6 2 1
7 2 1 2 2
8 1 2 1 1
9 1
10
11 1

DAT, Dementia of the Alzheimer's Type; ADC, AIDS Dementia

Complex; Average, no dementia present; Mild, Stage 1;
Moderate, Stage 2; Severe, Stage 3.

103
educational level corrected data (see Table 16), stage one
was the most accurate pre-test prediction and stage three
was the least accurate pre-test prediction. DAT stage of
disease process determined by CDR scales (see Table 10), as
compared with corrected data, was most accurate for
predicting stage one and stage three and least accurate for
predicting stage two. ADC stage of disease process
determined by interview information (see Table 9) and WMS
LMl data (see Table 11) appeared more consistent with stage
of disease process determined by corrected data (see Table
16). Closer inspection of the estimated number of years
diagnosed HIV infected for these data indicated that
interview information and WMS LMl data did not identify the
same patients as did the corrected data. In summary,
researchers and clinicians may establish a working diagnosis
for stage of disease process based on interview information
and raw data. A formal diagnosis for stage of disease
process is most accurate when determined by age and
educational level corrected data.

Comparisons for group comparability indicated possible

shortcomings in the current criteria for DAT stages. Stages
for DAT include 3 levels (mild, moderate, and severe/end-
stage). (Stages for ADC include 4 levels [mild, moderate,
severe, and end-stage].) During the screening interview,
patients with DAT were assigned to stages one, two, or

104
three. Potential participants who exhibited the most severe
deficits described for stage three/end-stage (i.e.,
inability to recognize significant others, echolalia,
palilalia, and mutism) were eliminated from the study. DAT
patients (N = 6) were assigned to stage three based on
interview information. It is suggested that
conceptualization of DAT stages would be more meaningful if
the stages were expanded to include stage four (end-stage).
This strategy would parallel the stages for ADC. DAT
patients who received a stage three designation were
different from DAT patients who were eliminated from this
study. For example, one DAT patient was assigned to stage
two based on interview information and to stage three based
on corrected test data. When he returned to his room after
testing, his wife was waiting for him. He put his arms
around her and said, "This is the best wife in the whole
world." He demonstrated the ability to recognize
significant others and language production abilities. This
patient was significantly different from patients who were
eliminated from the study due to echolalia, palilalia, or
mutism. It is suggested that the DAT stages of disease
process be expanded as follows. Stage three (severe) would
include severe disturbances in cognitive functions but
retention of recognition of significant others and some
language production skills. Stage four (end-stage) would

105
include inability to recognize significant others and severe

language output deficits (echolalia, palilalia, or mutism).

The estimated number of years diagnosed was
operationally defined as (1) the number of years DAT self or
other informants noticed cognitive difficulties and (2) the
number of years ADC participants thought that they were
infected. Among DAT patients, some participants (N = 4)
estimated the number of years that they had noticed memory
difficulties; for the remaining participants (N = 11),
family members provided estimates. Family members'
responses may under-estimate the length of time the patient
experienced difficulties. The first signs of deficits may
be subtle and easily concealed from others. Among ADC
patients, all provided estimates for when they first thought
they might be seropositive. Some of their estimates may be
inaccurate. Some ADC patients were unaware that they were
HIV positive prior to HIV antibody testing.

Wechsler Memory Scale and Russell Revision

Memory quotients for DAT and ADC patients were
corrected for age. As predicted, patients with DAT received
a significantly lower memory quotient on the WMS than did
patients with ADC (see Table 17).
DAT participants numbers 4, 6, and 8 exhibited a higher
memory quotient than did the other DAT participants. These

106
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107
patients estimated the length of time they had been
experiencing memory difficulties, and they produced an
acceptable number of phrases for LMl. It is hypothezied
that these patients were at the beginning phase of stage 1
disease process, rather than at the end phase of stage 1.

Logical Memory and Visual Memory scores for immediate

recall and short-term memory were corrected for age and
educational level. These computations yielded scores for
all participants, including those who received a score of
zero on subtests. Logical Memory scores for immediate
recall and short-term memory were calculated by comparing
the actual score with an expected score, yielding z. scores
for all participants (Abikoff et al., 1989). Visual Memory
scores were calculated by assigning a corresponding scaled
score (Russell, 1988).
Patients with DAT received significantly lower z scores
for immediate recall and short-term memory for Logical
Memory than did patients with ADC (see Table 17). Although
both groups exhibited deficits for Logical Memory, DAT
patients exhibited greater severity of deficits than did
patients with ADC (see Table 18).
Patients with DAT demonstrated a different deficit
pattern for Logical Memory than did patients with ADC.
Patients with DAT exhibited gross impairment for immediate
recall and short-term memory. DAT patients tended to
108
Table 18

Wechsler Memory Scale Logical Memory Percentiles for

Immediate Recall and Short-term Memory

Immediate Recall Short-term Memory

DAT ADC DAT ADC

Above Average 0.0 6.7 0.0 13.3

Average 0.0 6.7 0.0 0.0
Mild Deficits 0.0 26.7 0.0 40.0
Moderate Deficits 6.7 26.7 6.7 33.3
Severe Deficits 6.7 33.3 6.7 13.3
Very Severe Deficits 86.7 0.0 86.7 0.0

DAT, Dementia of the Alzheimer's Type; ADC, AIDS Dementia

Complex.

109
produce two types of stories. (1) The story production
demonstrated impoverished content: "She hadn't eaten in 4
days. The police gave her something to eat to satify her
physical taste." (2) The story demonstrated increased
verbage to compensate for lack of content: "I can remember
the story about the ship running into a block of ice and
sinking, and all of the people were saved. There were a lot
of them. The rescue rate was exceptional. I can remember
hearing about it on the news." Some patients with DAT, who
produced a few memories for immediate recall, denied ever
having heard the material 30 minutes later. Only two DAT
participants were able to produce responses for short-term
memory.

Abilities for immediate recall and short-term memory

for Logical Memory were more intact for patients with ADC
than for patients with DAT. All ADC patients produced some
memories for immediate recall and short-term memory.
Productions followed the story line in a meaningful sequence
and did not contain distortions.
Patients with DAT received significantly lower scaled
scores for immediate recall and short-term memory for Visual
Memory than did patients with ADC (see Table 17). The
differences between the groups for immediate recall and
short-term memory was marked. Group percentiles for
immediate recall and short-term memory (Russell, 1988) are

110
shown in Table 19. Among ADC patients, 86 percent
demonstrated above average to average abilities for
immediate recall and 80 percent demonstrated above average
to average abilities short-term memory for Visual Memory.
Among DAT patients, 80 percent exhibited profound deficits
for immediate recall and 86 percent exhibited very severe
deficits for short-term memory for Visual Memory.

Patients with DAT exhibited two types of deficits for

Visual Memory. (1) Reproductions were characterized by
omissions, rotations, distortions, and perseverations (see
Figure 1 ) . (2) Patients were unable to reproduce any
figures. Patients who were unable to reproduce figures from
immediate recall were asked to copy a figure (see Figure 2 ) .
Attempts to replicate simple, geometric figures were
characterized by gross distortions.
A majority of ADC patients demonstrated average to
above average abilities for immediate recall and short-term
memory for visuospatial material as illustrated in Figure 3.

Trail Making Test

A one-tailed t-test approached significance for TMT
Parts A and B (see Table 17). Calculation of z scores for
TMT Parts A and B (Alekoumbides, 1987) did not provide data
for patients who were unable to complete the tasks. It is
hypothesized that significant differences between the groups

111
Table 19

Wechsler Memory Scale Visual Memory Percentiles for

Immediate Recall and Short-term Memory

Immediate Recall Short-term Memory

DAT ADC DAT ADC

Above Average 0.0 20.0 0.0 73.3

Average 6.7 60.0 6.7 6.7
Borderline Deficits 6.7 13.3 0.0 0.0
Mild - Moderate Deficits 0.0 0.0 0.0 13.3
Moderate Deficits 0.0 6.7 0.0 6.7
Moderate - Severe Deficits 6.7 0.0 6.7 0.0
Very Severe Deficits 0.0 0.0 86.7 0.0
Profound Deficits 80.0 0.0 0.0 0.0

DAT, Dementia of the Alzheimer's Type; ADC, AIDS Dementia

Complex.

112
 I I

stimulus

ac3

Figure 1
Immediate Recall for
Dementia of the Alzheimer's Type:
Visual Memory

113
 Stimulus

Figure 2
Dementia of the Alzheimer's Type: Model Present for
Visual Reproduction

114
 71
Stimulus

Immediate Recall

^J\2r
Short-term Memory

Figure 3
AIDS Dementia Complex: Immediate Recall and Short-term
Memory for Visual Memory

115
 Immediate Recall

1.

Short-term Memory

Figure 3
Continued

116
were not found as many DAT patients were unable to perform
these tasks; thus they did not produce quantifiable data.
Some DAT patients appeared to recognize the task, but were
unable to perform it. For example, when presented with the
TMT Part A, one patient said, "It looks like what you want
is, well that is, this is sequencing, from one to the other,
but what I see is the 6-9-2. It's easier for me to do it
the other way; 6-9-2, that's the sequence."

Self-rating Depression Scale

The SDS score for one participant with DAT was
discarded as he gave the same answer for all items. For
example, the patient responded "good part of the time" to
"I feel hopeful about the future" and "I feel that others
would be better off if I were dead." It appeared that his
responses to items were perseverative and inconsistent.
There were no significant differences between the groups for
the SDS (see Table 17). As is shown in Table 20,
percentiles were similar for each group for no depression
present, mild depression, and moderate depression.

Semi-structured Interview
The following section presents qualitative data
gathered from participants during a semi-structured
interview. Participants with DAT were unable to produce as
many answers to probes as did participants with ADC.

117
Table 20
Self-rating Depression Scale: Percentiles

DAT ADC

Not Present 50.0 40

Mild Depression 49.2 40
Moderate Depression 7.1 20

DAT, Dementia of the Alzheimer's Type; ADC, AIDS Dementia

Complex.

118
 Occupation. All of the DAT patients were retired.
Former occupations included ranching, farming, government
service (military and postal workers), law, accounting,
medicine, and university teaching. Of the ADC patients
seven were receiving disability; the remainder were employed
in various occupations, such as a horse trainer, restaurant
manager, accountant, medical technician, and hairdresser.

Memory Difficulties. Patients were asked if they

thought they had memory difficulties. Patients with DAT
gave responses indicating some degree of memory difficulties
which they typically attributed to the aging process: "My
goodness, yes, to some degree." "When I have time to go
back, dig back, you can see now that I can remember those
dates." "I can't give you thatthat's part of mythat's
becomeI'm afraid II just can't give it to you." For
patients with DAT, estimates of the length of time memory
difficulties had been present varied from two years to 11
years.
Patients with ADC gave varied responses. For example,
one patient who denied having memory difficulties, exhibited
mild to moderate difficulties for WMS Logical Memory. Two
patients who reported having memory difficulties for the
past 1-1/2 year, demonstrated average to above average
abilities for WMS Logical Memory. All remaining ADC
patients accurately reported having memory difficulties.

119
Patients with ADC estimated having memory difficulties for a
period of time ranging from a few months to four years. The
most common memory complaints reported were concentration
difficulties, forgetting appointments, slowed memory ("not
as lucid"), and retrieval difficulties. Regarding whether
others had noticed their memory difficulties, ADC patients
were equally split; 50 percent said "yes," and 50 percent
said "no." Typical strategies utilized by ADC patients to
compensate for memory difficulties included taking notes,
asking others for information, "avoiding situations," and
looking for cues or prompts from others or the environment.

Motoric Slowing. When asked if they had noticed

motoric slowing, patients with DAT tended to respond, "Yes,
but only because I am getting older." One-half of the
patients with ADC noticed motoric slowing and reported
having "coordination" difficulties.
HIV Infection and Diagnosis. Patients with ADC were
asked when they first thought that they might be infected
with HIV and when they were diagnosed seropositive. Five
patients denied knowing or suspecting that they were
positive before they tested HIV positive. Of this subgroup,
patients discovered they were HIV positive when donating
blood, accepting overseas military assignments (the military
routinely tests all personnel who are to be transferred
overseas), and when first hospitalized with an AIDS-related

120
illness. Two patients submitted for testing as soon as they
thought they were HIV positive, and they were. One patient
began HIV antibody testing every six months starting in
1985, and seroconverted in 1987. The remaining seven ADC
patients thought they might be positive for less than one
year to over three years before being tested for HIV.

Mood and/or Personality Change. Patients were asked if

they noticed mood and/or personality change since being
diagnosed. When asked to subjectively report mood state,
the patients with DAT denied any changes in mood or
personality. This is not consistent with their objective
data indicating mild depression. Among ADC patients, 80
percent reported a subjective experience of depression.
However, on objective measures, sixty percent reported very
mild depression.

121
 CHAPTER VI

DISCUSSION

Patients with cortical dementias exhibit deficits for

cognitive tasks. Patients with subcortial dementias exhibit
cognitive and motoric slowing which interferes with their
cognitive abilities. In this study, participants with DAT,
a cortical dementia, exhibited greater severity of deficits
for cognitive tasks than did participants with ADC, a
subcortical dementia.
Patients with DAT received a significantly lower memory
quotient on the WMS than did patients with ADC. The memory
quotient included subtest scores for immediate recall and
short-term memory for Logical and Visual Memory. Patients
with DAT exhibited greater deficits for immediate recall and
short-term memory for Logical Memory than did patients with
ADC. DAT patients demonstrated two patterns for deficits
for immediate recall for logical memory: (1) verbalizations
indicated impoverished story content, and (2) verbalizations
demonstrated increased verbage to compensate for lack of
story content. Before recall may occur, material first must
be encoded and stored. Patients with DAT generally have
aphasia, or loss of language comprehension or production,
and are unable to encode or store verbal material.

122
 Abilities for immediate recall and short-term memory
for Logical Memory were relatively intact for patients with
ADC. Verbalizations followed the story line in a meaningful
sequence and did not contain distortions. The deficits for
Logical Memory were due to slowed cognitive functioning.
Patients with ADC processed verbal material at a slowed rate
which interfered with their abilities to encode and store
all of the verbally presented material. Verbal material
that was encoded and stored was retrieved 30 minutes later.
Significant differences for abilities for Visual Memory
were exhibited between the groups. Patients with DAT
exhibited greater deficits for immediate recall and
short-term memory for Visual Material than did patients with
ADC. DAT patients, who exhibited constuctional apraxia,
were unable to produce or copy simple geometric figures.
Patients with ADC generally exhibited average to above
average abilities for visual material. ADC patients
exhibited fewer deficits for visual material than for verbal
material. Visual stimuli may provide effective cues for
patients with ADC.
Differences between the groups for TMT Parts A and B
approached significance. Greater differences between the
groups were not found as many DAT patients were unable to
complete the task and receive a score. It is interesting to
note that differences between the groups were not
123
significant for patients who were able to complete the
tasks. DAT patients in the early phase of stage 1 may
appear similar on this task to ADC patients in stages 1 , 2 ,
and 3. These findings also highlight the importance of
subjecting raw data to corrections for age and educational
level.

It could be argued that the differences found on the

WMS and TMT between the groups were the result of age
differences. The WMS provides an age correction for the
memory quotient. Scores for the WMS Logical Memory and
Visual Memory, and TMT were corrected statistically for age
and educational level.
It also could be argued that differences found on the
neuropsychologic tests were due to differences for severity
of stage of disease process. Patients with DAT experience
severe deficits for higher cognitive functions because DAT
primarily affects the cortical region of the brain.
Patients with ADC experience deficits characterized by
cognitive slowing, rather than cognitive deficits per se as
the primary area of the brain infected and affected by HIV,
is the subcortical region. The first measure to increase
the probability that the groups would have comparable stages
of disease process was conducted prior to entry into the
study. Potential participants were assigned to a stage of
disease process based on interview information. Potential

124
DAT participants who exhibited end-stage disease process and
potential ADC participants who did not have a history of
memory difficulties or motoric slowing were eliminated from
the study. After data was collected, patients were assigned
to stage of disease process based neuropsychologic deficits
exhibited. The two groups were comparable for stage of
disease process based on age and educational level corrected
test data.

Comparisons were made for stage of disease process,

which was determined by corrected test data, by estimated
number of years diagnosed with DAT or HIV infection. This
comparison indicated that for both groups the severity of
disease process increased with estimated number of years
diagnosed.
Shortcomings were found with the current criteria for
DAT stages of disease process. Criteria for DAT stage of
disease process indicate three stages (stage one [mild],
stage two [moderate], and stage three [severe and end-
stage]). Criteria for ADC stage of disease process indicate
four stages (i.e., stage one [mild], stage two [moderate],
stage three [severe], and stage four [end-stage]). DAT
patients who were assigned to stage three (severe/end-stage)
based on test data did not exhibit symptoms associated with
end-stage disease processs. These patients retained
abilities which were not present in potential DAT

125
participants who were eliminated from the study. It is
recommended that future research explore the validity and
utility of changing DAT stages so that stage three is
divided into two stages (stage three, severe; and stage
four, end-stage). Further refinement of DAT stages may
provide a more accurate conceptualization of disease process
for patients with DAT.

Both groups reported mild depression on the SDS.

Subjective reports differed between groups for depressive
symptomatology elicited during the semi-structured interview
of the test protocol. During the semi-structured
interviews, patients with DAT did not report experiencing
depression or other mood changes. This may reflect DAT
patients' inability to verbalize inner experiences. A
majority of ADC patients reported experiencing mood changes,
notably depression and mood swings. However, their
subjective experiences of depression were not congruent with
objective test measures. It is unclear why patients with
ADC did not score higher on the objective measure of
depression.
Future research may include the following. (1) The
question regarding whether patients with DAT suffer from
depression or not is not resolved. If DAT patients are
depressed, does this indicate that they have greater insight
into their dementing process than has been recognized to

126
date? If so, for how long? (2) Researchers and clinicians
may examine the utility of expanding DAT stages of disease
process from three stages to four. (3) Longitudinal studies
regarding time and course of ADC would provide greater
understanding of this new dementia. (4) Although one
antiviral has been shown to slow, or even reverse, the
dementing process associated with HIV, it is not known for
how long beneficial effects may be expected. Recent reports
suggest that zidovudine (e.g., retrovir or AZT) does not
extend the patient's life span as first suspected, but
delays onset of end-stage disease process. Once end-stage
disease process been reached, acceleration of the final
stage preceding death is swift. (5) Age and educational
level corrected normative data for ranking level of severity
of deficits for TMT Part A and B are not available. For
greater accuracy in research and clinical diagnostic
settings, these data are critical.
In summary, the present data are consistent with the
literature comparing cortical and subcortical dementias.
Global impairment for immediate recall and short-term memory
for Logical and Visual Memory, and moderate to very severe
deficits for visuoscanning, sequencing, and attention and
concentration abilities characterized patients with DAT, a
cortical dementia. Abilities for immediate recall and
short-term memory for Visual Memory, visuoscanning, and

127
sequencing were relatively intact for patients with ADC, a
subcortical dementia. ADC patients exhibited mild deficits
for immediate recall and short-term memory for verbal
material and for mental flexibility, which is consistent
with slowed cognitive functions. The present study does not
resolve the current debate regarding whether or not patients
with DAT experience depression. This study's findings for
depression in patients with ADC is consistent with the
literature, although the magnitude of reported depression
was relatively weak.

Past studies comparing differences between cortical and

subcortical dementias were based on elderly patient
populations (i.e., DAT compared with Huntington's Disease,
Parkinson's Disease, and Wilson's Disease). The current
study's age groups differed by over 200 percent. DAT
patients were elderly, and ADC patients generally had not
reached middle age. The study implemented several methods
to control extraneous variance. Only men were included in
the study to control for variance due to sex differences.
Potential DAT participants, who had a history of additional
illness (e.g., stroke and alcholism), were eliminated from
the study. Potential ADC participants, who did not have a
history of cognitive or motoric difficulties, were
eliminated from the study. A pre-test screening for stage
of disease process increased the probability of

128
comparability between groups by eliminating patients who
exhibited end-stage disease process. Data were corrected
for age and educational level to control for variance due to
these extraneous variables. Stage of disease process was
compared with estimated number of years diagnosed. There
appeared to be a correlation between the estimated number of
years diagnosed and the stage of disease process. As
estimated number of years diagnosed increased, the stage of
disease process was more advanced. A final analysis for
stage of disease process based on corrected test data
confirmed that the groups were comparable. The current
study showed that, although symptom severity and age are
greater among patients with DAT, than among patients with
ADC, a relatively young population, quantitative and
qualitative differences exist between cortical dementias and
subcortical dementias.

129
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153
 APPENDIX A

RAW DATA, Z SCORES, AND SCALED SCORES

Subjects Age Education Wechsler Memory Scale

MQ LMl LM2 VMl VM2

Dementia of the Alzlheimer's Type

1 72 12 54 0 0 0 0
2 87 20 59 2 0 0 0
3 87 12 63 4 0 0 0
4 79 12 83 4 0 6 0
5 72 7 62 3 0 0 0
6 72 12 103 14 9 5 5
7 89 18 49 0 0 0 0
8 66 16 100 13 7 1 1
9 86 12 48 0 0 0 0
10 89 13 48 0 0 0 0
11 83 10 51 0 0 0 0
12 85 7 48 0 0 0 0
13 59 12 48 0 0 0 0
14 86 7 49 2 0 0 0
15 82 7 55 2 0 0 0

AIDS Dementia Complex

16 36 12 96 9 6 10 11
17 29 16 105 19 15 14 13
18 31 15 108 17 15 14 14
19 24 14 129 25 27 13 13
20 30 12 90 13 12 12 11
21 32 14 132 21 19 14 13
22 31 12 106 12 10 10 5
23 43 13 110 20 15 10 11
24 36 13 93 17 13 9 5
25 28 13 97 19 13 6 6
26 28 13 95 13 9 10 10
27 26 12 97 12 10 11 11
28 40 13 112 17 16 11 11
29 36 12 129 28 23 12 11
30 36 12 103 17 16 11 12

MQ, Memory Quotient; LMl, Logical Memory Immediate recall;

LM2, Logical Memory Short-term; VMl, Visual Memory Immediate
Recall; VM2, Visual Memory Short-term.
154
Appendix A

Continued

Subject ^ Wechsler Memory Scale

Logical Memory z Scores Visual Memory Scaled Scores
Immediate Short-term Immediate Short-term
Recall Memory Recall Memory

Dementia of the Alzheimer's Type

1 -3.13 -2.33 6.0 5.0

2 -3.50 -2.79 6.0 5.0
3 -1.93 -1.74 6.0 5.0
4 -2.24 -2.06 1.5 5.0
5 -1.86 -1.65 6.0 5.0
6 -0.80 -0.96 2.0 1.5
7 -3,44 -2,41 6.0 5.0
8 -1.74 -2.01 4.5 4.0
9 -2.64 -0.02 6.0 5.0
10 -2.66 -1.72 6.0 5.0
11 -2.45 -1.61 6.0 5.0
12 -1.82 -1.10 6.0 5.0
13 -3,43 -2.70 6.0 5.0
14 -1.53 -1.10 6.0 5.0
15 -1.69 -1.24 6.0 5.0

AIDS Dementia Complex

16 -2.12 -2,01 1.5 0.5

17 -1.39 -1,14 0.5 0.0
18 -1.23 -1,02 0.5 0.0
19 0.33 1.02 1.0 0.0
20 -1.42 -1.06 1.0 0.5
21 -0.39 -0.28 0.5 0.0
22 -1.60 -1.37 1.5 3.0
23 -0.43 -0.76 1.5 0.5
24 -0,94 -1.08 2.0 3.5
25 -0,56 -1.02 3.5 3.0
26 -1,56 -1,63 2.0 1.5
27 -1,55 -1.32 1.0 0.5
28 -0.94 -0.62 1.0 0.5
29 1,05 0.59 1.0 0.5
30 -0.78 -0.48 1,0 0.0

155
Appendix A

Continued

Subject Trail MakiLnq Test SDS

Part A Part B
Raw Score z. Score Raw Score z. Score

Dementia of the Alzheimer's Type

1 65
2 58
3 227 6.99 51
4 48 -0.53 198 0.51 48
5 96 1.03 167 -0.39 40
6 117 2.58 192 0.63 48
7 a_ 41
8 169 5.40 213 1.19 45
9 ^^ 48
10 58
36
11
^ 55
12
"
13
59
14
0.02 54
15 77
AIDS Dementia Complex

16 42 0.02 75 -0.30 54
17 24 -0.28 55 -0.07 49
18 28 -0.11 69 -0.48 49
19 23 -0,61 38 -0.58 56
20 21 -0.70 134 0.64 65
21 17 -0.87 44 -0.50 64
22 27 -0.45 56 -0.35 31
23 26 -0.66 41 -0.73 64
24 31 -0.45 243 1.83 55
35 -0,11 91 OalO 41
25
26 42 0,19 107 0.30 56
27 21 -0,70 63 -0.26 51
28 30 -0.49 66 -0.41 49
29 44 0.10 137 0.49 59
30 20 -0.91 46 -0.67 40

SDS, Self-rating Depression Scale.

156
 APPENDIX B

BIOPSYCHOSOCIAL INFORMATION SHEET

Patient Name: Date of Birth:

Date: Age:
Education Level:
Date DAT/HIV+ Dx:
Date suspected DAT/HIV+:
DAT/HIV+ Sx:
Current Sx:

Motoric Slowing
When pt noticed:
When others noticed:
How pt compensates:
Changes this has made in pt's life:
Memory Difficulties/Slowing
When pt noticed:
When others noticed:
How pt compensates:
Changes this has made in pt's life:
Mood/Behavioral/Personalitv Changes
When pt noticed:
When others noticed:
How pt compensates:
Changes this has made in pt's life:

Medications:

Other tx (e.g., support group):

Comments:

157