l']:I ?II I ‘ l
I. '-‘E‘:’2.)1‘III":Y7'I(“IJf
‘I’. > .IIIIIII IIIJIIII I IIIIUIII

 

 

 

H. ' I I , II" 'I‘ II” IQ: I
I .-".III II.I IIIII" 'IIIIIIIII III'I'T? TI'IIIIII FI I IIII' I'IIIII ‘ I I I'II
.4 I II n IIIIIII IIJI‘III

. IIII‘IIII IIII 1:1,‘I‘IHI HIII'IIIMI'IJIIW‘IhLIiIII1:332PM
IIIII‘ II‘II I 'II ‘I . 3L: IIIII- "IIII"IIII,,III ItIIIIII III ”1’1 ’I‘I"I:IIIII
| ~' ' IIII II II” IIIIIIFI Li;
I LIII ITI‘III II‘I
I‘IiiIIIII III I Y"; I . I;
:II' , 'III III I III III-II III'I'. IIIIII IIIIIIHII VIII NI III III II III} I“
IIIIII" I"'I ‘ III M; ’I‘”

.IIIIIJCIIH II

I . I I l
WIIIIII IIIIzIII‘I «I III III IIIIIIIIIIII I'
. “If” I I

IIIIIIII

HI
‘IiIIIIjI IIfiI/III 'I‘I‘IIIIIIIII III
III I”: IIIIIIII II’ 'IIIIII

   
  
   
  

   
 

  
   
 
  
   

--

     
  
 
 
 

HIII I I I

n’. , —
*“ W .— A -
‘1‘ -- {2‘ _ _J,, A
. , r. -.
m T.-- (FT-"3‘34;
w" 2:”?
r

n - .
_ !
YnnA
-u
_—-‘.
w

M m:
‘3.
; 1.
“I h... 125—:
“ ‘5"fix";
A ”2%?

I ”1"”?

   

[Iii-i" III‘IIIHI'II I

IIIII RIIII; IIII'II l
IIII'I’ I’qI IIIHI
III III:

“III” ‘I III
III

    
     
   

    
 
 

  

TIII‘I II

    

III .II'“ III

        
  
 
 

 

IiIII IIIIr " I ‘
:IEIII‘II’7'I.I:“ I I I ' I
fififlflv 'I“'II %
I

 
 
 

‘ I
9"-” .
~ on -
w. -
01-Hw -

n .. I . a ‘

'. - . .

" I

I.

   

.
”ma-w
u.

     
  
 

w“.
a
a

  

O

  

 

.
~__ ...
1722.1. - ~ .c:

  
 

   

r“;
M
..
. _
M—

u—q
f-IN

 

    
     

   
 
  
 
  
 

.—
V yvv.~".~n

r ‘0. -~..—o.
.,

         
  
 
  
 
 

 

o.
oo-
.
.9

   
  

”_ n. so.
4‘04 7"
.- .4.
- .
.

m
u ..
. . .73....

:Jfig' . .21“fi7.~“~"~'

III [I In}
I' I?

II“ IIII' I {III—'1 Q‘IIIIIII LII”

    
  
   

4 p p-..-
(M...
«u
”—un.
.a-or

,1
D
‘2

I
.....
o « 7‘.-
, . ,
:Ta ----

M:-
"
w.
.o

““5

n I
- o .‘M
o. u
t

3,‘

u
-
a a
. I‘WC.‘
. n

:8 ~ ”Lyn-I“. 1:.
w <¢m%
5313.33.
Imgwmwi
I 12:!9I! hi

 

. I:
if“?! {Aggfbiifi IIEEI
3.1! 213?. ”‘31-
.-. i;:‘31ft?i§ :

I .«1- q . .;I‘I,..’.| . I .
‘Iig‘SEIIFE .Ififi‘:;;. 5;} “3,5“
I I“? _;o ‘I'I 1..” III
1;? II

IA:

  
 
   

 

‘MII'J‘
n.
no -
.._.,

  
 
    
  

  

n 0'.
. .wfl'w
_ I. . IIIIIIIIIII'IIIISII .IIIII
- 25:5 “g;:I-:I:~.=:Iz§?

     
 

  

3 I

   
 
  

  
  

.‘u .-.-
5-».
- o
.

1.173.213.
- - «‘
— 't.~

:If .- hu'dF-L‘i:
—' Vacs; -' 7.3 a ’
#:JI . I . e..'.'p {we
w. .. N. g .

.77.? LC ‘.'.71.‘.’_é

   
  

-_h.——~y....~

-.
1—-“ .4
’31; v "9-

  
   

IIwI
’x'éIIIEi I :_‘.

\
7::3r;
Mu. :3.
3,... V‘...- 1.
K;:.:‘ 5"“. ‘a

 
 
  

 

W"

.'9 t‘ztslf;;HII:L
II IIII .93;
I' IIIIIIITE

. ’ .- ' ' I;
I . ' II :;.I 'IE“ I n . .. I». . I I
‘ I‘? “1%.. :3: I‘ ,.‘:§§::S'I;i;;::1§.,: .- ‘ ‘1 ' I
' ‘ .:om 1. l, u .1 . ‘ . I‘llu, Q . A
. IIIVII 1‘,€<3I"II'. ‘III I. ”In-5“? I
III‘I “MIR: . a.“ II ’I
.1 A ' 1a.! ‘ a I . U

  
    
  

 
     
    
     
     
 

   
  

   
 
  

.-I
I, .3?

_ “I” ‘ ‘SI'IIIK
IIIu-‘IIIIII‘I’IMMII ,

 
 

I'I yIaI - IIIIII ‘I III “I I ..
.45???” III I 1} IIIIIIH
. I IIIIIWIIHIII ngI‘; IIII‘IIII IIIIIIIIIIEI ”jig. IIIIIIMMI

 

LIBRARY
Michigan State
University

 

 

 

This is to certify that the

dissertation entitled

Memory, Metamanory and Depression
in
Parkinson ' 3 Disease

presented by

Lila Coulter

has been accepted towards fulfillment
of the requirements for

 

 

Ph. D. degree in Clinical Psychology

Major professor

4/469” ((44;
Date July 23, 1282

MSU is an Affirmative Action/Equal Opportunity Institution 0-12771

 

 

 

 

 

rv1531_1 RETURNING MATERIALS:
Place in book drop to

LJBRARJES remove this checkout from

—r:——- your record. FINES will

 

 

 

be charged if book is
returned after the date
stamped below.

 

 

 

MEMORY, METAMEMORY AND DEPRESSION IN PARKINSON'S DISEASE

BY

Lila Coulter

A DISSERTATION

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

DOCTOR OF PHILOSOPHY

Department of Psychology

1987

ABSTRACT
MEMORY, METAMEMORY AND DEPRESSION IN PARKINSON'S DISEASE

BY

Lila Coulter

The present study examined the relationships among
depression, memory and two aspects of metamemory in
Parkinson's disease. Both memory dysfunction and depression
are reported to occur in persons with Parkinson's disease.
It has been unclear, however, what the relationship is
between the symptoms. In non-Parkinsonian depressed
persons, complaints of impaired memory are reported to be
greater than actual impairment, suggesting an impairment of
metamemorial processes. The Feeling-of—Knowing aspect of
metamemory has not been evaluated in either Parkinsonism or
depression. 12 depressed and 16 non-depressed Parkinsonian
outpatients were compared with 20 normal controls matched
for age, education and intelligence. Both depressed and
non-depressed Parkinson's subjects were impaired in
consistent retrieval and total score on a list-learning task
relative to controls, but not in encoding, immediate or
remote memory. Feeling-of-Knowing accuracy was equivalent
across all groups. Both Parkinsonian groups complained of
greater memory deficit than controls, but self-assessment of

memory functioning was unrelated to objective memory

performance in any group. Depressed Parkinsonian subjects
endorsed more of each physical symptom of depression, but
not of each affective symptom. Duration of disease was
differentially related to memory performance, self-
assessment and level of depression in depressed and non-
depressed Parkinsonian subjects. In both Parkinsonian
groups, self-assessment was less related to memory
performance in those patients who had had the disease longer
than in those patients who had a shorter history of the
disease, but this was expressed in different ways in the
depressed and non-depressed groups. Non-depressed subjects
with longer disease duration exhibited a significant deficit
in list-learning abilities relative to non-depressed
subjects with shorter disease duration, but this was not
accompanied by increase in memory complaint or depression.
Depressed subjects with longer disease duration demonstrated
no difference in memory performance relative to those with
shorter disease duration, but endorsed more depressive
symptoms and complained of greater memory deficit. These
results suggest that memory and affective changes are both
primary“ but independent symptoms in Parkinson's disease.

It was hypothesized that the pattern of presentation between
memory, self-assessment and depression is dependent on an
interaction between the Parkinsonian subjects' premorbid

personality style and pathophysiological changes.

ACKNOWLEDGEMENTS

A number of people have contributed to the success of
this study, and I am glad to have this opportunity to thank
each of them.

Dr. Albert Aniskiewicz was the chairperson of my
doctoral committee, but he is also much more. Over the past
years he has been consistently supportive of my efforts, and
has allowed me to find my own way. He encouraged my
attempts to integrate information from a variety of sources,
and always asked the right questions to help me sort out
ideas. Insightful, intelligent and caring, he has gracefully
provided an example of what a fine psychologist can be, and
I am grateful for the opportunity to have worked with him.

Dr. Rose Zacks was an active member of my committee.
She regularly routed relevant journal articles to me, and
was always available for discussion of points on which I was
unclear. She challenged me and some of my assumptions, and
I have grown in my critical thinking abilities from knowing
her.

Dr. Dozier Thornton consistently provided thoughtful
input into this work. Each meeting with him resulted in my
deeper understanding of the material, and gave me new ways
to View it.

Dr. Antonio Nunez helped me to evaluate and integrate

theories of biological functioning as they were relevent to
iv

Ar

 

 

 

.3
FL-

 

..«
Br-

 

P»

this work. I thank him for his straightforward input and
easy, relaxed manner.

Two men without whom this study would literally been
impossible are Jack Penny, Jr" M.D., Co-director of the
movement disorders clinic at University of Michigan, and
George Ristow, D.O., Head of the Division of Neurology in
the College of Osteopathic Medicine at M.S.U. Both of them
graciously provided access to their Parkinson's disease
patients, and paved the way for their patients to respond to
my invitation to participate.

My special thanks and admiration go to those
Parkinsonian patients who agreed to take part in this study.
They welcomed me into their homes and bravely shared their
experiences with this devastating disease with me. I
learned from them beyond what can be shown in this document,
and will remember them always. I also am appreciative of
the time and effort spent by those people who took part as
members of the control group. Although most were retired,
they were busy people who took part because of their
continuing interest and excitement with life.

I thank Marge Curtis and Suzy Pavick of the department
of Psychology support staff for their help. Marge will be
retiring this year, and that will be a loss for this
department. Suzy Pavick guided me through the bureaucratac
maze that could make a person crazy, and remained cool and
collected in the process.

My parents, two special people, deserve special

thanks. Respectful and loving, they have been both
v

emotionally and, at times, financially supportive throughout
my graduate career. I know they are proud of me, but no
more than I am of them.

Finally, I give my most heartfelt thanks and love to
my husband and friend, Leonard Paauwe. Having lived through
the process with me each step of the way, he knows better
than any the meaning of this work. While it has been in
process, he has delayed his own career goals, and has done
so with few complaints. I cherish his support and

sacrifice.

TABLE OF CONTENTS

Page

List of Tables.........................................ix

List of Figures........................................ x
Chapter

I INTRODUCTION..................................... 1

Background.................................. 1

Depression in Parkinson's Disease........... 8

Memory Deficits in Parkinson's Disease......18

The Relationship between Memory and
Depression in Parkinson's Disease...........24

The Relationship between Memory and
Depression in Non-Parkinsonian Subjects.....28

MetamemorYo I O O O O O O O O O O O O O I O O O O O O I O O O O C C O O O I O 29
self-Assessment. O I C O O O O O O O O O O O O O O O O O O O O O O 30
Feeling Of KnOWing. O O O O O O O O O O O O O O O O O C O O O I 32

SummarYOCOOOOOOOOOOOOOOOOOOOOOOOOOOO00......34

Proposed StUdYOO0.0....00.0.000000000000000035
HypotheseSOOOOO0......0.00.00.00.0000000035

II METHODOOOOOOOOO0..0......0....0.00.00.00.0000000037
SUbjeCtSOOOOOOOOOO0....0.0.0.00000000000000037

Instruments
Aphasia Examination.......................4O
WAIS Vocabulary Subtest...................40
WAIS Digit Span Subtest...................41
Structured Interview......................41
Beck Depression Inventory.................41
Geriatric Depression Scale................42
Memory Self-Rating Scale..................42
Buschke Selective Reminding Procedure.....42
Feeling of Knowing Test...................44

vii

TABLE OF CONTENTS (Continued)
Chapter Page

II ProcedureOOOOO0.0.0....OOOOCOOOOOOOOOOOOO.45

III RESULTS.........................................48
Subject Matching............................48
Results of Hypotheses.......................50
Depression Scales...........................56
Feeling of Knowing..........................59

Effect of Duration of Parkinson's Disease...59

IV DISCUSSIONOOOOOO000......OOOOOOOOOOOOOOOOO0.0.0.62
Qualiinng Statement. 0 I O O O O C O O O O O O O O O O O O O O O O 62
summary Of Findings. 0 O O O O O O O O O O O O O O O O O O O O O O O 63

Interpretation
overVieWIOOOOOOOO0.0...0.0.0.00000000000065

DepreSSion. O O I O O O O O O O O O O O O O O O I O O O O O O O O O O .66
Memory...O...O...0.0.00.00.000.000000000069
Metamemory. O O O O O O O O C O C O O O O O O O C O O O O O O O O O O O 72

The Relationship between Memory,
Metamemory and Depression................74

Parkinson's Disease as a Subcortical
Dementia....0...0.00000COOOOOOOOOOOOO0.0.78

Implications for Future Research.........81

Appendices
A Recruitment and Consent Forms...................84
1B Structured Interview Outline....................91

(2 Data Collection Instruments.....................111

List Of ReferenceSOOOCOO0....OOOOOOOOOOOOOOOOOOOOO0.0.0129

viii

 

LIST OF TABLES

Page
Table

1 Results of Mailed Invitations to

PartiCipateOOOOI0.00.00.00.00.0.00.00.00.00038
2 SUbjeCt CharacteristiCSOOOOOOCOO0..000......49
3 Comparison of Groups on Memory and

Memory Complaint Variables..................51
4 Intercorrelations Between Memory

Complaint and Memory Variables..............55
5 Intercorrelations Between BDI Score

and Memory Variables........................58
6 Intercorrelations Between GDS Score

and Memory Variables........................58
7 Intercorrelations Between Age and

Memory Variables............................6l
8 Partial Correlations Between Disease

Duration and Memory Variables (Effects
Of Age Removed)OOOCOOOOOOOOOOOOOOOOOOO0.0.0.61

LIST OF FIGURES

Page
Figure
1 Self Rating Scale of Memory Function,
Patterns of Response........................53
2 Beck Depression Inventory,
Patterns of Response........................57
3 Proposed Relationships among Depression,

Memory Performance and Disease Duration.....7l

INTRODUCTION

"SHAKING PALSY. (Paralysis Agitans.)
Involuntary tremulous motion, with
lessened muscular power, in parts
not in action and even when supported:
with a propensity to bend the trunk
forward, and to pass from a walking
to a running pace: the senses and
intellect being uninjured"

(Parkinson, 1817).

Parkinson's disease occurs in approximately 1% of the
jpopulation over 50 years of age, worldwide (Duvoisin, 1984).
It is a progressive neurological disorder that involves
<degeneration of the structures of the nigrostriatal tract
eand resultant deficiencies in the dopaminergic system.
Iklthough Parkinson's original description included clear
iaffect and sensorium, there has been ongoing debate over the
loresence or extent of cognitive and affective changes
auccompanying the motoric symptoms. To date, there have been
rub reports on the status of metamemorial processes in
Parkinson ' 5 disease .

This review will examine the current state of knowledge

nuith regard to depression and memory in Parkinson's disease

.aIud relate it and issues of metamemory to current views of

ruauropathology of the disease.

Background
Parkinson's disease is a degenerative neurological

Chisease that affects approximately 1 in 100,000 people in
1

the United States, with 20 new cases per 100,000 appearing
annually. It is a disease that affects primarily adults
over 50 years of age, with mean age of onset at 55.3 years
(Hoehn and Yahr, 1967) although it can occur in younger
adults as well. It shows no sex or racial preference.
Although first defined as a distinct syndrome by Parkinson,
the disease symptoms had been described succinctly in
antiquity by Galen (Parkinson, 1817).

The disease is characterized by the cardinal
neurological deficits of tremor, muscular rigidity and
hypokinesis. The tremor of Parkinson's disease is generally
classified as "resting tremor", and most commonly affects
the extremities. However, it is usually absent during
sleep, and many patients complain of a tremorous feeling in
the abdomen as well. Initiation of an action generally
inakes the tremor disappear, but it will reappear during
ccnnpletion of the action, making daily tasks difficult.
Aruciety or concentration seem to exacerbate this symptom.

Muscular rigidity is seen in resistance to passive
nmrvement of the joints. Often this takes the form of
"(nogwheel rigidity" in which the resistance appears as a
jerfltiness of movement. Rigidity also contributes to
Postnaral changes, due to shortening of the muscles,
Parfxicularly of the back and neck. This contributes to back
and Ileck pain as well as difficulty with walking and
increased falling.

ITypokinesis refers to both slowness and poverty of

movement. Voluntary movements are few, and associated
movement becomes increasingly rare. Facial musculature is
also affected, leading to a "mask-like" face. Many patients
are plagued with a festinating gait consisting of short,
shuffling steps which cannot seem to "keep up" with the
upper body which is characteristically pitched forward.

This may result in what looks like a headlong forward rush
ending in a fall. Typically, the voice becomes slow, low in
volume and monotonous.

In addition to the three cardinal signs, other symptoms
may be present such as constipation, decreased libido,
excessive sweating, edema, seborrhea and others. Symptom
patterns are idiosyncratic to each person, and may vary
within the same person. One might have a "good" day with
few symptoms followed by several in which one or all are
worse than previously. Nevertheless, the disease is
irrevocably progressive in nature. Hoehn and Yahr (1967)
studied the history of 802 patients with Parkinson's disease
and found that by 14 years post-onset, three quarters were
classified as end-stage or had died.

Onset of the disease is insidious. Often a patient
will be unaware of early signs, such a favoring one leg,
softness of speech, or holding an arm in a Characteristic
Parkinsonian stance with the arm bent at the elbow and held
close to the body. The on-off pattern of the symptoms also
makes it easier to ignore or misread early signs. Diagnosis

of the disease is typically made by a neurologist. Aside

from postmortem anatomical study, there are few specific
diagnostic tests for Parkinson's disease as a separate
entity. Homovanillic acid, the end product of dopamine
metabolism has low concentration in the cerebrospinal fluid
of untreated Parkinson's disease patients, and this
information may help in differential diagnosis. Like many
degenerative neurological diseases, however, Parkinson's
disease is a diagnosis generally made by ruling out other
possibilities. At the least, the three cardinal signs must
be present, and the pattern must appear to be progressive.
The latter fact is determined by interview of the patient
and/or significant other, and frequently by several return
visits to the physician to document changes.

The symptoms of Parkinson's disease are caused by
neuronal degeneration of the basal ganglia. Mild cortical
atrophy has also been reported, most marked in the frontal
lobes. This appears to be in response to the subcortical
degeneration which compromises the integrity of projections
connecting subcortical with cortical structures.

Axons of the substantia nigra synapse with neurons
in the globus pallidus, caudate and putamen. Dopamine, the
neurotransmitter produced in the substantia nigra is
reduced in the nigrostriatal tract of the Parkinson patient,
at times to 10% of normal, due to the neuronal degeneration.
Marked decreases in dopamine have also been reported in the
ventral tegmental and limbic areas (engavoy-Agid and Agid,

1980).

Parkinsonism has been divided into several types, named
largely for their supposed antecedents. Post-encephalitic
Parkinson's disease is generally found in younger patients.
It was a common finding in the aftermath of the encephalitis
lethargica epidemic that occured during the second decade of
this century. Since then, it has become a rare phenomenon.

Drug-induced Parkinsonism is caused by either reducing
the amount of dopamine available for binding or by blocking
the dopamine receptor. It is generally reversible with
withdrawal of the offending drug, typically a neuroleptic
such as a phenthiazine or butyrophemone.

Arteriosclerotic Parkinson's disease was a common
diagnostic type prior to 1964 when Eadie and Sutherland
demonstrated an equal amount of arterial disease in age-
matched controls. Since then, the diagnosis has fallen into
disrepute (Lishman, 1978).

Carbon monoxide poisoning at some point prior to onset
of the symptoms may cause Parkinsonism. Again, this is a
more common etiology in younger patients who are not prey to
idiopathic Parkinson's disease.

The largest diagnostic category by far is that of
idiopathic Parkinson's disease. The specific causal agent
is unknown, but specific degeneration of the pigmented cells
of the brain stem is the hypothesized origin. There is no
indication that it is hereditary, as shown in a study of
monozygotic twins in which there was found a zero

concordance rate for Parkinson's disease (Duvoisin,

Eldridge, Williams, Nutt & Calne, 1981). Snyder and D'Amato
(1986) have proposed that N-methyl-4-phenyl-1,2,3,6-
tetrahydropyridine (MPTP) may be an environmentally occuring
substance that may be an etiological agent of idiopathic
parkinsonism. It is a neurotoxin that selectively destroys
nigrostriatal dOpamine neurons and creates clinical symptoms
of parkinsonism.

The current pharmacologic explanation for
parkinsonism rests on two main ideas (Klawans, 1968).
First, dopamine and acetylcholine are antagonistic to one
another in the striatum, and effects of these two
transmitters must be balanced for normal functioning.
Second, a decrease of dopamine availability shifts the
balance to an overabundance of acetylcholine which produces
the parkinsonian symptoms.

Chemical treatment may include anticholinergic agents
to reduce the level of acetylcholine and restore the balance
between the two neurotransmitters. However, the most common
contemporary treatment is levodopa, the medicinal form of L-
Dopa, dopamine's immediate precursor. This amino acid
crosses the blood-brain barrier and is then converted to
dopamine for use by the striatum. This treatment provides
considerable symptom relief, but does not cure one of the
disease. Patients receiving this treatment require
increasingly large doses, as it seems to lose its
effectiveness with continued use.

To reduce the amount of levodopa prescribed, and to

hopefully inhibit habituation and negative side effects,
patients are often prescribed a combination drug comprised
of carbidopa and levodopa (Sinemet). Carbidopa, a DOPA
decarboxylase inhibitor, allows a greater percentage of the
levodopa dosage to reach the brain by inhibiting the
conversion of levodopa to dOpamine in the rest of the body.

Less effective, but longer lasting is bromocriptine
mesylate (Parlodel), which is a dopamine receptor agonist.
Rather than adding to dopamine supplies, the result of this
drug is to make the most of the dOpamine that is already
available in the system by activating striatal dopamine
receptors.

A recent addition to the pharmacologic treatment
armamentarium is Amantadine hydrochloride (Symmetrel),
although its precise mechanism of action is as yet unclear.
It does not reduce cholinergic activity, and does cause an
increase in dopamine release in animal brains.

A stereotaxic surgical approach that destroyed a
portion of the thalamus was used during the 1950's and
1960's. The thalamus plays a role in motor regulation, and
it was thought that lesioning the structure would correct
the movememt disorder seen with parkinsonism. Due to the
number of possible complications, the transience of
improvement, and more importantly the advent of levodopa as
a treatment, the intervention has essentially been dropped
as a viable treatment (Duvoisin, 1984). Recently,

transplantation of dOpamine—producing tissue of the adrenal

gland to the striatum has produced encouraging results in
younger patients with parkinsonism (Backlund et al., 1985;
Madrazo et al., 1987), but has yet to be tested in older

patients.

Depression in Parkinson's disease

 

 

Although Parkinson declared that the "senses...(are)
uninjured", he described the observed subject patients as
"unhappy", "melancholic" and "dejected" regarding their
difficulties. The descriptive passages in his landmark
essay poignantly suggest that, "harassed by this tormenting
round" of symptoms, the affected patient welcomes the
"wished-for release" of death at the end.

The earliest writers on this phenomenon of depressive
symptomotology accompanying Parkinson's disease believed
that both the affective and physical manifestations were, at
least in some cases, due to intrapsychic conflict (eg:
Patrick & Levy, 1922). In an alternate view, the affective
changes were seen as understandable reactions to the
devasting motoric symptoms and the requirement for changes
in self-concept and interpersonal roles (eg: Machover,
1957). When the biochemical basis for the disease was
discovered, the former view lost favor. The latter view has
for the most part been set aside, as researchers are putting
their efforts into relating the physical and emotional
symptoms to the same biochemical process, (see Dakof &
Mendelsohn, 1986).

Prevalence estimates of depression have varied widely

from study to study, ranging from 12 percent (Rondot, de
Recondo, Coignet & Ziegler, 1984) to 90 percent (Mindham,
1970). A variety of criteria and tools for measurement of
depression have been employed, perhaps contributing to the
wide range of prevalence estimation. Measurement tools have
included structured interview (Celesia and Wanamaker, 1972,

Warburton, 1967), criteria from the Diagnostic and

 

Statistical Manual, third editon (Mayeux, Williams, Stern

 

and Cote, 1984; Santamaria, Tolosa and Valles, 1986),
"clinical ratings" from retrospective chart study (Mindham,
1970), investigator's judgement (Strang, 1965), MMPI d.30
scale (Horn, 1974), Beck Depression Inventory (BDI) (Mayeux,
Stern, Rosen and Leventhal, 1981; Santamaria, et al., 1986;
Taylor, Saint-Cyr, Lang, and Kenny, 1986), and the Hamilton
Depression Scale (Brown and Wilson, 1972; Mayeux, Williams
et al., 1984; Robins, 1976).

Clinical diagnosis of depression in Parkinson's disease
is difficult, as it is with the elderly population in
general (Mintz, Steuer & Jarvik, 1981; Yesavage et al,
1983), regardless of health status. Many of the physical
manifestations of the disease mimic those found in
depression. Psychomotor retardation, restlessness,
monotonic voice, masked facies and poverty of affect are all
strong indicators of each disorder independently. In
addition, many Parkinson's disease patients report a
decrease in libido as well as sleep disorders due to

physical discomforts which awaken them at night. These two

10

changes are also considered to be vegetative signs of
depression.

It may be that utilization of depression scales which
rely on vegetative and behavioral signs inadvertantly
inflate the actual rate and degree of depression found in
Parkinson's disease. Brown, Marsden, Quinn and Wyke (1984),
as well as Rodriguez and Levin (1987) attempted to correct
for this source of error by deleting those items that could
be measuring the physical rather than the emotional
manifestations of Parkinson's disease. In the latter study,
a lower incidence of depression was reported with removal of
somatic items. Taylor et a1. (1986) noted that responses by
Parkinson's disease patients to the BDI fell into two
general categories: those responses one might find in a
random sample of normal subjects, and those that could be
attributed to a movement disorder.

Often, operational definitions of depression are
lacking, particularly in those studies relying on
investigator's judgement or clinical ratings. A
particularly problematic study is Mindham's (1970) which
reports 90% prevalence based on 89 parkinsonian patients who
were culled from Parkinson's disease patients admitted to a
psychiatric facility. In addition, diagnosis was made by
chart study and "clinical ratings" made by unidentified
persons, reducing the probability of objectivity of report.

Despite such methodological problems, there is

consensus that depression accompanies parkinsonism in a

11

significant number of patients. Regardless of type of
measurement or Parkinson's disease subject pool, in all
reviewed studies in which a control group was utilized, the
rate of depression was higher in the Parkinson's disease
population, suggesting a link between the symptom and the
syndrome. Control groups utilized have included healthy
probands (Horn, 1974; Levin Rodriguez, Llabre & Weiner,
1985; Mayeux et al., 1981; Taylor et al., 1986), and
patients with other diseases or medical problems selected to
share as many qualities as possible with Parkinson's disease
(Warburton, 1967; Horn, 1974; Robins, 1976).

Greater depression in ill versus healthy others is not
surprising, regardless of type of disease. What is more
interesting is the finding that Parkinson's disease patients
demonstrate higher rates of depression than those with a
variety of other disabilities. Warburton (1967) compared
Parkinson's disease to a mixed group of medical, surgical
and gynecological patients and found a higher incidence and
greater severity of depression in the Parkinson's disease
group. Horn (1974) utilized paraplegic patients without CNS
dysfunction as a comparison group, and reported the
Parkinson's disease group to be more depressed, but only
when severity and duration of disability were controlled
for. Robins (1976) used a mixed comparison group of
patients suffering from spinal cord disease, orthopedic
conditions, amputation consequent to extensive peripheral

vascular disease, or cerebrovascular disorder with

12

hemiplegia. Although the comparison group was more
disabled, Parkinson's disease patients were more depressed,
regardless of level of disability.

Dakof and Mendelsohn (1986) have criticized the
limitations of the comparison groups in these three studies
on four counts. First, they claim the onset of disability
in the comparison groups is traumatic, versus the insidious
onset of Parkinson's disease. Second, the progression does
not share the degenerative and uncertain quality of
Parkinson's disease. Third, the major disability is
physical in these contrast groups versus the combined
physical and cognitive changes reported with Parkinson's
disease. Last, rehabilitation holds out some hope for the
comparison patients, in contrast to the current
irreversibility of Parkinson's disease. They conclude that
"at best, then, these studies provide only circumstantial
evidence for the hypothesis that depression is a primary
symptom of Parkinson's disease" (p. 379).

While their critique may be accurate for the first two
studies reviewed, Robins' choice of patients addresses each
of the concerns presented by Dakof and Mendelsohn. Each of
the diagnoses in their contrast group may show slow onset,
and progression is often uncertain. Cognitive changes
secondary to cerebrovascular disorder are well documented.
Rehabilitation, while helpful for some of the named
disorders, is not likely to cure the major disabilities

presented. The argument against depression as a primary

l3

symptom of Parkinson's disease, and possibly biochemically
based, remains an open one.

Other possible correlates of depression within
Parkinson's disease have been explored with generally
negative results. Neither duration of disease (Celesia &
Wanamaker, 1972; Mayeux, Williams, et al, 1984; Warburton,
1967), age at onset (Warburton, 1967), nor age at time of
study (Celesia & Wanamaker, 1972; Mayeux, Williams, et al.,
1984; Warburton, 1967) appear to be correlated to severity
of depression. There is no consistent finding regarding a
link between severity of physical impairment and depression
(Celesia & Wanamaker, 1972; Hoehn, Crowley & Rutledge, 1976;
Mayeux, Williams, et a1. 1984; Mayeux et al., 1981; Mindham,
Marsden & Parkes, 1976; Warburton, 1967).

A history of psychiatric symptoms appears to be related
to diagnosis of Parkinson's disease (Damasio, Lobo-Antunes &
Macedo, 1971, Mayeux et al., 1981; Rodriguez & Levin, 1987;
Rondot et al., 1984; Santamaria et al., 1986). However,
in each of these studies, the reports are retrospective in
nature, which presents a methodological problem. Given the
difficulty of accurately dating the onset of Parkinson's
disease, it is virtually impossible to tease out whether the
reported psychiatric symptoms predate the disease, or are
only the first symptoms of the disease process.

Levodopa has been reported to increase (Damasio et al.,
1971; Mindham et al., 1976), decrease (Celesia & Barr,

1970), and have no effect on (Hoehn et al., 1976; Mayeux et

14

al., 1981; Marsh & Markham, 1973) depressive symptomatology
in persons with Parkinson's disease. The effect on mood
appears to be idiosyncratic, and may be based on
interpretation by each patient of the physical changes
effected by the drug. This unreliable effect regarding
depression remains to be explicated by research.

Treatment with some antidepressants has been found to
be useful for depressed Parkinson's disease patients. Strang
(1965), in a double-blind placebo study reported improvement
of depression with imipramine. Nortriptyline improved the
mood of Parkinson's disease patients in a study by Andersen,
Aabro, Gulmann, Hjelmstead & Pederson (1980).

Electroconvulsive therapy (ECT) has also been reported
to have a beneficial effect in individual cases (Asnis,
1977; Lebensohn & Jenkins, 1975; Yudofsky, 1979), although
these reports have not been validated with controlled
studies.

There are three positions taken in the literature
regarding the etiology of depression accompanying
Parkinson's disease: it is organically based (due to either
biochemical imbalance or anatomical lesion), psychoreactive,
or a combination of these two.

If the affective changes were reactive in nature, one
would not expect depression to be an early, or in some
cases, prodromal symptom, but to appear only after the
physical deficits were established. However, a history of

affective disturbance prior to onset of physical symptoms

 

 

15

has been established as not uncommon in Parkinson's disease
patients.

With improvement in physical functioning due to adequate
pharmacologic regimen, a positive affective change would be
expected if the depression were reactive to the physical
deficits. However, studies with L-Dopa have established
that there is no predictable affective change despite
physical improvement with the drug. In the same vein,
depressive symptomology may improve with antidepressant
drugs regardless of physical symptoms. The counter
argument, supporting the case for reactive depression,
states that if affective and physical symptoms were tied to
the same neurological substrate, improvement in one would
presage concurrent improvement in the other, which is not
the case.

Level of disability is not reliably related to
depression in Parkinson's disease, contrary to an intuitive
sense that as dependence increases, so will depression.
This appears to implicate an organic versus a reactive
depression. However, it should be remembered that the
course of Parkinsonism is inexorable. The patient may be
responding to what will be, not necessarily that which is.
Knowing s/he will be, but is not yet, disabled may well
create an ambiguity of role to which some react with
depression. Zahn (1973) found that applicants for
disability benefits who were found "not fit to work"

(therefore more disabled) had better relationships with

16

significant others than did those whose status was more
ambiguous. As their status became more clear-cut (eg: they
were so disabled as to be "unfit to work"), relationships,
and presumably affective states, also improved.

There is no clear confirmatory argument regarding the
etiology of depression in Parkinson's disease. Recently,
some researchers have begun discussing the possiblity of
subtypes of Parkinson's disease to explain the otherwise
confusing findings. A biochemical subtype is proposed by
Mayeux, Stern, Cote and Williams (1984), who note that
serotonin is reduced with Parkinson's disease, although it
has not been previously related to physical manifestations
of the disorder. They found that depressed Parkinson's
disease patients had less of the major metabolite of
serotonin 5-hydroxyindoleacetic acid (5-HIAA), in their
erebrospinal fluid than did non-depressed Parkinson's
disease patients. This reflects Schildkraut's (1973)
finding of a correlation between behavioral indices of
depression and decreased serotonin metabolites in CSF in
non-parkinsonian patients. Mayeux et al. suggest that those
Parkinson's disease patients with disordered serotonin
metabolism are prone to depression, while those with normal
serotonin metabolism are not. They suggests that
Parkinson's disease may be a multi-level process, not the
unitary one as previously thought. Santamaria et a1. (1986)
found that those drug—free recent-onset Parkinson's disease
patients with depression were younger, less impaired and

were more likely to have a family history of Parkinson's

 

 

17

disease. They postulate a subgroup based on these clinical
characteristics, and following Mayeux et al., hypothesize
that chronically low 5-HIAA CSF levels may be found to
predate physical manifestations.

This is an appealing line of thought, but research on
the effects of serotonin depletion on both animal and human
behavior refute this theory. Mayeux et a1. (1984) report
that in their own research, some non-depressed Parkinsonian
patients had CSF 5-HIAA as low as their depressed
counterparts. This alone invalidates the notion that
decreased serotonin explains depression in Parkinson's
disease. An excellent review and commentary on the role of
serotonin in behavior (Soubrie, 1986) demonstrates that,
while the role of serotonin in behavior is not fully clear,
decreased levels are more likely associated with impulsivity
and aggression than depression. Thus, the evidence
supporting reduced S-HIAA in Parkinson's disease as either a
cause or result of depression is minimal at best.

Fibiger (1984) postulated that the high rate of
depression in Parkinson's disease is secondary to
degeneration of the mesocorticolimbic dopamine pathway.
This bundle arises from the ventromedial tegmental area of
the midbrain and projects to the cingulate, entorhinal and
frontal cortex. It is hypothesized to be involved in the
frontal lobe functions of monitoring and mediating mood and
behavior (Javoy-Agid & Agid, 1980). Taylor et al. (1986),

in support of Fibiger's hypothesis, report that depressed

 

r.
!

 

18

Parkinson's subjects did not endorse items on the BDI
characteristic of negative moods or self-attributes in
contrast to persons with endogenous depression. Rather,
they endorsed items consistent with symptoms of a movement
disorder as well as random items commonly endorsed by non-
depressed normals. Regardless of BDI score, however, the
majority of their Parkinson's disease subjects showed
outward signs of depressive affect such as tears and
distressed agitation when asked about their difficulties.
They relate this situational and labile expression of affect
to Fibiger's hypothesized disordered regulation of mood
state secondary to disruption of the mesocorticolimbic
pathways. This disruption due to dopamine depletion makes
the patient vulnerable to depression which is "easily
provoked by realistic frustrations and/or direct probing of
emotional state". Thus, they propose an organically
exacerbated reactive depression in some Parkinson's disease

patients.

Memory Deficits in Parkinson's Disease

 

 

A variety of cognitive changes have been reported to
co-occur with Parkinson's disease. There are number of
studies that present prevalence rates of the "dementia" that
accompanies the disease, but the rates vary widely depending
largely on criterion of diagnosis and investigation tools.
Some investigators accept loosely or undefined "mental
changes" as evidence of dementia (eg: Hakim & Mathieson,

1979). Others accept mild levels of impairment or few

19

errors on a mental status exam (Martin et al., 1973, Sweet,
McDowell, Feigenson, Loranger & Goodell, 1976) and still
others are precise and restrictive in their categorization
(Danielczyk, 1983; Matison, Mayeux, Rosen & Fahn, 1982).
Despite this confusion, specific deficits have been
identified by several investigators. These include
impairment in visuospatial performance (Garron, Klawans &
Narin, 1972; Mortimer, Pirozzolo, Hansch, & Webster, 1982)
speed of scanning in visual recognition tasks (Wilson
Kazniak, Klawans & Garron, 1980), conceptual flexibility
(Albert, 1978; Bowen, 1976, Lees & Smith, 1983), as well as
bradyphrenia, a slowing down of the thinking process
(Wilson, et al., 1980).

In contrast, Parkinson's disease patients appear to
retain premorbid "crystallized intelligence" abilities as
measured by tests such as the Vocabulary and Information
subtests of the WAIS (Bowen, 1976; Lees & Smith, 1983;
Loranger, Goodell, McDowell, Lee & Sweet, 1972; Mortimer et
al., 1982; Riklan, Whelihan, Cullinan, 1976).

In examining the status of memory abilities in
Parkinson's disease patients, a number of tests and
paradigms have been used. The Weschler Memory Scale, a tool
used both with clinical and experimental groups has been
used in a number of studies. Mortimer, Kuskowski,
Pirozzolo & Webster (1986) report that 23% of their
Parkinson's disease patients scored in the impaired range on

the Logical Passages subtest, and that this group was

20

significantly younger than the non-impaired Parkinson's
disease population. Bowen (1976) and Riklan et al. (1976)
reported a deficit in Logical Passages as well as in Paired
Associates and Visual Reproduction. These researchers
concluded that Parkinson's disease patients are deficient in
short term memory processes, regardless of modality, and
that this deficit is unrelated to age or IQ. Bowen reported
that Parkinson's disease patients appear to adequately
register the to-be-remembered data on the Wechsler Memory
Scale, but are unable to retrieve it on command.

Taylor et a1. (1986), in contrast, reported that
Parkinson's disease patients scored the same as controls on
these three Wechsler Memory Scale subtests, but that
Parkinson's disease patients evidenced more difficulty with
material that required effortful manipulation while in short
term memory (Arithmetic and Digit Span subtests of the
Weschler Adult Intelligence Scale) than did control
subjects. This is similar to the finding by Weingartner,
Burns, Diebel and Lewitt (1984) that Parkinson's disease
patients were selectively impaired in effort-demanding
learning and memory, but showed no decrement in superficial
information processing.

Delis, Levin and Kramer (1987) contrasted Parkinson's
disease patients with normal controls and patients with
Alzheimer's disease (AD). They found that Parkinson's disease
patients fell between these two groups in recall and

recognition memory performance using the California Verbal

21

Learning Test. However, the strategy of learning was the
same in the two patient groups compared to the control
group, suggesting deficient problem-solving abilities in
both patient groups. This seems to reflect another aspect
of deficiency in effortful processing and cognitive
flexibility among Parkinson's disease patients. In choosing
Alzheimer's patients as a contrast group, Delis et al. were
attempting to elucidate the deficits in common between a
primarily cortical (AD) versus primarily subcortical
(Parkinson's disease) degenerative disease process. In their
qualitative analysis, they demonstrated that although the
Parkinson's disease patients performed quantitatively
better, the two groups shared an inadequacy in mental
planning. This aspect of mentation has been linked with
frontal lobe function, and supports Fibiger's hypothesis as
to the effect of disruptions of the mesocorticolimbic
pathways in Parkinson's disease.

Another study using comparison groups was done by
Gainotti, Caltagirone, Masullo and Miceli (1980). Using
Rey's 15 Words Memory Test (a list-learning paradigm with
immediate and delayed recall), they report Parkinson's
disease patients to be superior to all comparisons groups,
including patients with normal pressure hydrocephalus,.
multi-infarct dementia, Huntington's disease, Alzheimer's
disease and depression. It is difficult to reconcile this
finding with those reported above, but a possible

explanation may be found in the strict inclusion criteria

22

used for the contrast groups by Gainotti et al. (1980).
With the exception of Huntington's and Parkinson's diseases,
a clearly documented dementia was required in order to be
included in the contrast groups. Onset of Huntington's
disease is frequently marked by personality and cognitive
changes prior to onset of the movement disorder. Thus, the
only two diagnostic groups in this study that are only
secondarily noted for cognitive deficit are the Parkinson's
disease and depressed groups. Therefore it is unremarkable
that Parkinson's disease patients performed better than did
the demented groups.

Tweedy, Langer and McDowell (1982) tested free recall,
cued recall and recognition of previously presented lists
with Parkinson's disease patients, patients with right
hemisphere cerebrovascular accidents, and normal controls.
Parkinson's disease subjects were impaired in all three
aspects compared to both contrast groups. Choice of
comparison group for memory function should be based on the
nature of the hypothesized underlying deficit. Tweedy et
al's choice is open to the criticisms levelled by Dakof and
Mendelsohn (1986) regarding choice of contrast group in
studying depression. In addition, it is unsurprising that

right hemisphere CVA patients would do relatively well in
tests of verbal memory, as verbal functions, including

verbal memory are largely mediated by the left hemisphere.
What their study does do is to reflect the basic impairment

in memory accompanying Parkinson's disease relative to one

23

healthy and one otherwise impaired population.

Most investigators report that memory for old or well-
learned information remains stable in Parkinson's disease
(eg: Lees & Smith, 1983; Riklan et al., 1976; Taylor et al.,
1986). Warburton (1967), however reported that long term
memory was impaired in Parkinson's disease relative to
patients diagnosed with a variety of medical, surgical and
gynecological disorders. He used a personal information
questionaire, but in addition to accurate responses,
answers were credited as correct if they were non-
verifiable by the researchers (eg: name of a wedding
guest). Most of the answers would not be available to the
investigator, so it is likely that in order for there to be
a significant difference between the two groups, the
Parkinson's disease group had a larger "don't know" response
rate. This may in itself be significant, but does not
necessarily inform us regarding the status of long term
memory processes. It may reflect a social uncertainty,
depression, or other factor that demonstrates another aspect
of the social/psychological consequences of Parkinson's
disease.

Although severity of "cognitive deficits" are reported
to be correlated with severity of physical symptoms (Brown
Marsden, Quinn & Wyke, 1984; Garron, Klawans, Narin, 1972;
Matthews & Haaland, 1979; Mayeux, Stern et al., 1984), few
studies have examined specifically the relation between

memory and physical symptoms. Mortimer et al. (1986) found

24

no relationship between the performance on the Logical and
Paired Associates subtests of the Wechsler Memory Scale and
motor symptoms, but did report that deficits on the Spatial
Orientation Memory Test were related to bradykinesia and
resting tremor.

A short term cognitive "awakening" effect of levodopa
(Jenkins & Groh, 1970) has been noted. For the long term,
it is generally reported to have either no apparent effect
on cognitive functioning (Bowen, 1976; Riklan et al., 1976;
Sweet, et al., 1976) or to have an ameliorative effect,
especially for memory functions (Marsh, Markham, & Ansel,
1971; Newman, Weingartner, Smallberg & Calne, 1984).
However, Riklan et al. (1976) report a slight decrement in
performance on the Paired Associates subtest of the Wechsler
Memory Scale in patients who had been taking levodopa for 5
years compared to Parkinson's disease controls who have not
been on the drug. Continued long term studies will further
inform regarding the longer term effects.

Relationship Between Memory and Depression in Parkinson's
Disease

 

 

Few authors address the possible relationship between
depression and memory impairment in Parkinson's disease,
although both are independently reported as occurring at a
more than chance level. Mayeux, Williiams et al. (1984) do
report that scores on the BDI are related to performance on
repeating digits backward, and to immediate word recall in a
mental status exam, even when factors such as age, education

and severity of physical symptoms are controlled. The more

25

depressed patients performed less well on these measures of
attention (word repetition) and effortful manipulation of
items in short term memory (digits backward). Swanda and
Kazniak (1985) reported changes in secondary memory as well
as depression in Parkinson's disease patients relative to
controls, but found that depression did not explain the
changes in memory. Taylor et al. (1986), however, reported
that Parkinson disease patients scoring in the depressed
range of the BDI performed equal to nondepressed
parkinsonian patients and normal control subjects in
measures of short term memory, and that these three groups
performed significantly better than did endogenously
depressed non-parkinsonian subjects. Short term memory was
defined by test performance on the Logical Passages, Visual
Reproduction and Paired Associate subtests of the WMS and
the Digit Span and Arithmetic subtests of the WAIS-R.

Brown et al. (1984) examined the relationship between
cognitive changes, affect and physical symptoms in
Parkinson's disease in an effort to integrate these diverse
findings. They started with the assumption that "changes in
arousal, alertness and mood need to be measured, and their
contribution to the pattern of cognitive impairment
assessed, before conclusions can be drawn as to the nature
of any underlying cognitive deficit in Parkinson's disease."
(p.455) They report that during the "off" phase of
fluctuation in motor functioning that is typical of the "on-

off" pattern of physical symptoms, Parkinson's disease

26

patients show disturbance in affect-arousal state, and
somewhat decreased cognitive performances. Affect-arousal
was measured by 16 bi-polar adjective scales, and cognitive
performance was examined with the Modified Alice Heim Test.
The latter is a multiple choice test of general reasoning
ability for verbal, numerical and spatial concepts. They
conclude that the mild decrease in cognition during the
"off" phase is mediated by affect-arousal mechanisms. This
conclusion matches nicely with Fibiger's (1984) hypothesized
disruption of mesocorticolimbic pathways accompanying the
dopamine depletion of Parkinson's disease. It will be
recalled that these pathways connecting cortical with
subcortical structures assist in monitoring mood and
behavior. In addition to monitoring affect-arousal, an
intact mesocorticolimbic system is essential for unimpaired
memory functioning. Therefore, attack on the integrity of
this system would result in both mood and memory changes.
Mayeux et al. (1981), in support of autopsy data
presented by Hakim and Mathieson (1979) have hypothesized
that up to 30% of Parkinson's disease patients with severe
cognitive impairment suffer from a dual disease process,
with coexistence of Alzheimer's and Parkinson's diseases.
Mayeux et al. also estimate that another 50% of Parkinson's
disease patients suffer from a mood disorder and milder
cognitive deficits secondary to Parkinson's disease itself.
However, Ball (1984) presents evidence that most Parkinson's

disease patients with dementia do not have concomitant

27

Alzheimer's disease, and states that other pathologic
mechanisms must be found to account for cognitive decline in
Parkinson's disease. He reviewed the data presented by
Hakim and Mathieson (1979) and reported that there were no
more neurofibrillary tangles in their Parkinsonian patients
with dementia than in those without. He also criticizes
Hakim and Mathieson for failing to report information on
inter-observer agreement regarding the pathological
findings.

More purely psychological etiologies may be considered
in understanding both mood and memory changes accompanying
Parkinson's disease. Many Parkinson's disease patients
experience acute embarassment regarding their physical
symptoms, particularly their slowness (Duvoisin, 1984).
Problems with initiation of speech makes simple conversation
excruciatingly difficult for some Parkinson's disease
patients. Without a great deal of effort and self-
confidence, this may lead to withdrawal from one's social
circle, which in turn allows significantly less
environmental stimulation. Without the daily give and take
of ordinary life, quality of mental performance inevitably
declines. At the same time, the affected patient has less
opportunity to receive positive input from others, and may
retreat into apathy and depression (Dakof & Mendelsohn,
1986). These psychological ramifications may be postulated
to be present with or without primary dysfunction of memory

and mood due to biochemical and structural changes.

28

Relationship Between Memory and Depression i3
non-Parkinsonian Subjects

Depression in persons without Parkinson's disease
has been linked with impairment in short term memory
(Sternberg & Jarvik, 1976), particularly with the
learning of new material (Cronholm & Ottoson, 1961;
Taylor et al., 1986). Tests used to measure short term
memory have included figure recognition and
reproduction, digit span, learning word pair lists, and
repeating paragraphs. Elderly depressed persons
sometimes present clinically with intellectual deficits,
particularly complaints of memory dysfunction. Some
authors report that memory in these "pseudodemented"
patients is in fact impaired on objective testing (Nott
and Fleminger, 1975; McHugh and Folstein, 1979).
Depressed persons are reported to be deficient in their
ability to perform "effort-demanding" memory tasks such as
recalling trigrams after an activity-filled delay (Cohen,
Weingartner, Smallberg, Pickar & Murphy, 1982), which may
well explain the deficits in short term memory. Weingartner
(1985): in his work On effortful processing in dementia and
depression, suggests that deficits in effortful cognition,
such as are reported with Parkinson's disease, are likely to
be accompanied by an impaired noradrenergic-dopaminergic
neurochemical system.

In contrast to the above studies, however, other

authors report that depression is not consistently

linked with objective deficits in memory. Gass and

29

Russell (1986) found the impact of depression (as
measured by the MMPI) on long and short term memory to
be nonsignificant, while organicity was related to
memory performance. Memory abilities were measured with
the WMS-R and the Digit Span subtest of the WAIS. They
hypothesized that the belief that depression is linked
with deficient memory performance may be based on the
exaggerated complaints of depressed patients. There is
a body of literature that supports this statement. A
growing number of researchers who have examined the
relationship between depression and memory have found no
consistent link between depression and memory
impairment, but do report significant associations
between depression and self-reports of impaired memory.
This is an area of continuing controversy, and more work
remains to be done in clarifying the relationships among

memory, memory complaint and depression.

Metamemory

 

Metamemory is a constellation of memory control
processes, and includes the assessment of whether
specific information is available in memory, how
accessible it is, and how certain one is of its
accuracy. Metamemory processes theoretically direct
efforts to retrieve information stored in memory, and
likely influence one's willingness to act on retrieved
information, depending on assessment of its accuracy

(Lachman & Lachman, 1980).

30

Metamemory processes may be examined in several
ways. One approach has been to examine the relationship
between self-assessment of general memory abilities and
objective memory performance. A second approach
examines accuracy of metamemory regarding the presence
or absence of specific information in one's own memory
through the "Feeling of Knowing" paradigm. These two

areas will be discussed separately.

Self-Assessment

 

As suggested by Gass and Russell (1986), a number
of researchers have reported that depressed subjects have
more complaints of memory deficits than non-depressed
subjects, although performance on objective memory tests is
similar between the groups.

Elderly depressed psychiatric outpatients were
reported by Kahn, Zarit, Hilbert and Niederehe (1975) to
complain more about memory deficits, independent of
presence or absence of such deficits compared to
nondepressed controls. Niederehe (1986) examined the
episodic, semantic and constructive memory functions of
young and old depressed women. He found no consistent
evidence that depression is linked with memory
impairment in either age group. However, more depressed
subjects perceived greater memory problems and had more
concerns about their memory. This finding was
replicated by Popkin, Gallagher, Thompson and Moore

(1982), Gilewski and Zelinski (1983), Larabee (1985), as

31

well as Ohara, Hinrichs, Kohout, Wallace and Lemke (1986).
Using a variety of measures, their elderly depressed
populations reported more problems with memory than did
controls, but there was no significant difference between
depressed and non-depressed groups on objective memory
tests. O'Hara et a1. (1986) noted, however, that self-
reported symptoms of depression correlated with memory
complaints, but that clinical diagnosis did not. They
present the continuity hypothesis to explain this finding.
This hypothesis states that symptom severity is more
predictive of impairment (in this case impairment of
accurate self-perception) than is a diagnosis.

Popkin (1985) gave a memory questionaire to
community dwelling elderly and found that those subjects
who complained of memory problems scored higher on
depression measures (although not in the clinical
range). The number of complaints was not related to age
or objective memory performance. These studies support
the position that affective state is not necessarily
related to performance on objective memory tests.

Rather, one's affective state is associated with self-
rating of general memory abilities. More depressed
persons complain about memory deficits that are not
supported by objective test findings.

Beck (1967) suggests that the discrepency between
self—evaluation and actual performance reflects the very

nature of depression. Persons who are depressed are

dominated by negative thoughts about themselves, the world,

32

and the future. These thoughts form the structure for a
negative self-schema, and prevent accurate perceptions about
themselves.

It would appear that depression in the elderly
is associated with an increase in complaints of memory
loss, but not associated with actual memory impairment
as measured by objective tests. The inaccurate self—
perceptions of memory ability that accompany depression
in the elderly seem to reflect impairment of metamemory

processes.

Feeling pf Knowing

The "Feeling of Knowing" (FOK) paradigm was
developed by Hart (1965). He found that college
students have accurate information regarding the
contents of their memories. If they cannot recall an
answer to a question, their FOK allows them to predict
whether they will recognize the answer from a group of
alternatives. This appears to be an ability that
remains stable over the life-span (Lachman, Lachman &
Thronesbury, 1979, Larabee, 1985), and may in fact
become more accurate with age (Lachman, & Lachman,
1980).

The FOK paradigm has been used to examine
metamemory processes in subjects with known or suspected
memory deficit to determine the extent to which memory

impairment is due to disruption of control processes.

33

Patients with temporal lobe epilepsy were found to have
impaired recall, and impaired accuracy in their FOK
ratings (Prevey, Delaney, & Mattson, 1985). Korsakoff
patients had significant impairment in ability to make
accurate FOK judgements, but other patients, amnestic
secondary to ECT, hypoxia, open head injury and
hypotension during surgery, were unimpaired in
metamemorial abilities (Shimamura, & Squire, 1985).
This suggests that amnesia may occur independent of
metamemory impairment, but not vice-versa. Brandt and
Mower (1985) compared FOK in Huntington's disease
patients, patients with senile dementia of the
Alzheimer's type (SDAT), and controls. Patient groups
were equally impaired in recall of general information,
but metamemory accuracy was impaired only in the SDAT
group.

There have been no studies reported that examine
the FOK accuracy in persons with depression or
Parkinson's disease. Brandt and Mower (1985) did not
report affective state of their subjects, which is
unfortunate as Huntington's disease is almost always
accompanied by affective changes. If their subject
sample was representative, it may be hypothesized that
there was affective disruption, and that metamemory

accuracy was unaffected by that state.

34

Summary

There is no question in the literature that depression
co-occurs with Parkinson's disease in at least a subgroup of
the population. It is also generally reported that memory
is impaired relative to controls, especially for material
that requires effortful recall. Despite the logical notion
that the two symptoms may be related to the same
neurological dysfunction and therefore tied, there are
competing findings regarding the relationship between
depression and memory in Parkinson's disease. In the few
studies done, some researchers report a strong association,
while others indicate no or minimal relationship between the
two variables.

There are reports that in non-Parkinsonian subjects,
depression is related to an increase in memory complaints on
self-assessment questionaires, but not necessarily to
decreased performance on objective tests of memory. This
suggests that depression is accompanied by impairment in at
least one aspect of metamemory. This relationship between
depression, memory and metamemory has not yet been examined
in Parkinsonian groups.

Another aspect of metamemory, the Feeling of Knowing,
appears robust in normal aging and in some groups with
neurological dysfunction, but is impaired in other clinical
groups. The relationship between this measure of metamemory
and either Parkinson's disease or depression has not yet

been explored.

35

Proposed Study

 

Three subject groups will be recruited. Depressed and
non-depressed Parkinsonian patients will be matched with
non-Parkinsonian subjects on sex, age, education and general
intelligence as measured by the WAIS vocabulary subtest.
Each subject will be administered a battery of depression,

memory and metamemory measures as described in Chapter II.

Hypotheses

 

Hypothesis I: FOK accuracy will be unrelated to group
membership.

 

Studies of elderly non-depressed persons suggest that
metamemory, as measured by FOK accuracy, is stable through
adulthood, and is robust in the face of other cognitive
impairments. However, it is impaired in persons with
diffuse cognitive deficits. Given the type of cognitive
impairment reported to accompany Parkinson's disease, and
assuming that assessment of specific contents of memory
(FOK) is not an overly emotional task, this ability should
remain unimpaired in Parkinson's disease.

Hypothesis 1;: Level of memory complaint, as measured by the
Memory Self Rating Scale will predict group membership. The

PDD group will report more complaints than PD or control
groups.

 

Memory complaint and FOK are measures of two separate
aspects of metamemory, the former being more affectively
tinged, and the latter a more factual, rational, yes/no
assessment of the contents of memory. If, secondary to

disturbance in the affect-arousal system, some PD patients

36

are vulnerable to depressive thoughts when presented with
potentially emotional material (questions regarding loss of
memory capacity), they should demonstrate this with more
negative self evaluation of daily memory functions.

Hypothesis III: Level of memory complaint will be unrelated
to level of performance on objective tests of memory.

 

In elderly non-parkinsonian pOpulations, high and low
complainers have been found to score approximately the same
on objective memory assessment. As level of complaint is
not expected to vary by diagnosis of parkinsonism versus
non-parkinsonism, level of complaint is not expected to
predict performance in this sample.

Hypothesis 1!: On objective tests of more effortful memory
(eg: Digit Span Backward, long term and consistent long term

retrieval in a list-learning paradigm) PD and PDD patients
will show deficient performance relative to controls.

 

It has been suggested that effortful memory processes
are mediated by the dopaminergic system. Since compromise
of this system is the hallmark of Parkinson's disease,
deficit of effortful memory is expected to accompany the
disease.

Hypothesis y: On objective tests of memory that require less
effort (Digit Span Forward, short term retrieval in a list

learning-paradigm), there will be no significant difference
in performance by parkinsonian and non-parkinsonian subjects.

 

These processes have not been consistently reported as
impaired in parkinsonism, and are not thought to be

implicated in function of the dOpaminergic system.

METHOD
Subjects
All patients of a University-based movement disorder

clinic (N=258) and of a University-based neurology clinic
(5:47) diagnosed with Parkinson's disease were invited by
mail to participate in this study. Of the former group, 108
(42%) patients responded to the invitation, and 22 (47%) of
the latter group replied. Table 1 defines the nature of the
responses and the final disposition regarding participation
in the study.

Exclusion criteria for all subjects included history
of: cerebrovascular accident, head injury with a period of
unconsciousness lasting more than 5 minutes, epilepsy, drug
or alcohol abuse. Current use of psychotropic medication,
psychotic symptoms discovered during interview, or signs of
focal cortical deficit as determined by the Aphasia
Examination also excluded potential subjects. All of these
factors have been linked to cognitive dysfunction. Although
there are indications that a variety of systemic illnesses
affect intellectual functioning, to screen for all such
illnesses would be to create an unrepresentative sample of
persons over 60 years old, as systemic disease is quite
prevalent in this group (Albert, 1981). Parkinsonian
patients with a non-idiopathic etiology were excluded, as

were potential subjects who lived more than 150 miles from

37

38

Table 1

Results of Mailed Invitations to Participate

 

 

Response Number % of total
NO RESPONSE 175 57 57
REFUSALS
*Deceased 14 5
*In nursing home or untestable 10 3 10
Patient denied having PD 4 2
PATIENT INTERESTED, BUT EXCLUDED
Out of town during study 7 2
More than 150 miles away 9 3
Release of information unfilled 10 3 24
Excluded by record review 4O 13
Excluded during interview or testing 8 3
TOOK PART IN STUDY:
PD 16 5
PDD 12 4 9
TOTAL 305 100

 

*Relative responded

39
Michigan State University.

Two groups of Parkinsonian subjects were defined: Those
with idiopathic Parkinson's disease without depression (PD,
2:16), and those with idiopathic Parkinson's disease with
depression (PDD, 2:12). To insure accurate judgment
regarding presence or absence of depression, three measures
were used. In addition to a diagnosis of PD, subjects in the
PDD group achieved a score of 11 or more on the BDI,
indicating at least a mild level of depression (Beck, 1971).
This inventory has been widely used in studies of
Parkinson's disease, but may be an invalid instrument with
this population due to the overlap between depressive and
parkinsonian symptomatology. Subjects in the PDD group also
achieved a score of 11 or more on the Geriatric Depression
Scale (GDS), indicating at least a mild level of depression
on this instrument (Yesavage, Brink, Rose, Lum, Huang, Adey
& Leirer, 1983). This instrument attempts to correct for
the overlap in symptoms by deleting physical symptoms which
often accompany normal aging. Finally, based on responses
to a structured interview PDD subjects met criteria for
diagnosis of Probable Major (p=3), Major (p=8) or Minor
(3:1) Depressive Disorder, using the Research and Diagnostic
Criteria (RDC) (Spitzer, Endicott & Robins, 1978). It was
hoped that by using these three instruments, an accurate
judgment regarding depression would be made.

Subjects for the control group were recruited from

senior citizen groups, and from a group of older people who

40

had been recruited for previous, unrelated research studies.
Two younger control subjects (under 60 years old) were
recruited by referral from persons unrelated to the study.

There were 20 subjects in the final control group.

Instruments

 

Aphasia Examination (Russell, Neuringer, & Goldstein, 1970)

 

This test, a revision of the Halstead-Wepman Aphasia
Screening Test (Halstead & Wepman, 1959), reveals impairment
in naming, spelling, writing, calculating, word
pronunciation, visuospatial reception, praxic abilities, and
discriminating right from left. It discriminates between
patients with left and right hemisphere lesions and those
without cortical dysfunction (Lezak, 1983). An error-
counting scoring system, which converts to a six-point
rating scale, indicates absence or presence and severity of
disorder.

Weschler Adult Intelligence Scale, Vocabulary Subtest
IWeschler, 1955)

 

This standardized test has been described as the best
single estimator of general intelligence (Lezak, 1983), and
as one which "holds" as an indicator of mental ability into
old age (Botwinick, 1977). Subjects are asked to define a
standard list of words, and are scored with 0, 1 or 2 points
for the quality of their answer. The points are added and

the raw score is converted to an age corrected scaled score.

41

Weschler Adult Intelligence Scale, Digit Span Subtest
(Weschler, 1955)

 

This standardized two-part test measures both simple
passive auditory attention (digits forward), and more
complex, effortful memory processes (digits backward). The
scores obtained on the two subtests are added together to
obtain a total subtest score which is then translated to an

age-corrected scaled score.

Structured Interview

 

A structured interview, adapted from the Schedule for
Affective Disorders and Schizophrenia (SADS) (Endicott &
Spitzer, 1978) was used to obtain information regarding
current symptoms of depression, psychosis, alcohol and drug
abuse. The SADS, in conjunction with the Research and
Diagnostic Criteria (Spitzer, Endicott & Robins, 1978) has
been found to reliably classify a group of elderly
depressives, and to distinguish them from a non-depressed
elderly community sample (Dessonville, Gallagher, Thompson &
Finnell, 1980).

Beck Depression Inventory (Beck, Ward, Mendelson, Mock, &
Erbaugh, 1961)

 

The BDI is a standardized 21-item self-report
instrument that measures the presence and severity of
depression. Subjects respond to each item on a scale form
zero to three. A higher overall score indicates more severe

depression.

42

Geriatric Depression Scale (Yesavage, Brink, Rose, Lum,
Huang, Adey & Leirer, 1983)

 

The GDS was developed as a screening instrument for use
with the elderly. The authors developed and validated the
GDS on physically healthy and ill depressed and
non-depressed elderly samples, and found that it
differentiated depressed from non-depressed regardless of
health status. The 30 questions are presented in a yes/no
format, with 20 questions indicating depression when
answered positively, and 10 questions indicating depression

when answered negatively.

Memopy Self-Rating Scale

 

A self-rating scale of memory complaints has been
adapted from Squire, Wetzel & Slater (1979) and Zelinski,
Gilewski & Thompson (1980). The 20 item scale requires
subjects to rate their memory on a variety of factors, using
a 9 point scale ranging from -4 (worse than ever before) to
+4 (better than ever before). The items derived from the
Squire, Wetzel and Slater questionnaire are sensitive to
perceived differences in self assessment of memory,
differentiating between normal and depressed persons, and
differentiating memory complaints before and after

electroconvulsive therapy (ECT) for depressed patients.

Buschke Selective Reminding Procedure (Buschke, 1973)
Buschke (1973) described a procedure to evaluate verbal
learning and memory that has been used to measure memory

abilities in a variety of clinical populations. It has been

43

used most widely in research protocols testing the effects
of pharmocological interventions on memory functioning in
clinical populations (eg: Peters & Levin, 1979; Thal & Fuld,
1983). A list of words is read to the subject, and the

subject is then asked to recall as many of the words as

possible. The subject is reminded of words not recalled on

the previous trial, and the sequence is repeated for p

trials. As the subject is only reminded of words not

previously recalled, the assumption is that when words are
recalled without reminding, they are being recalled from
long term memory. As this is a procedure, not a test, the
word lists used vary from study to study, making comparisons
difficult. However, support for the construct validity of
the procedure was demonstrated by Trahan and Larrabee (1985).
The procedure has demonstrated sensitivity to changes in
verbal memory due to a variety of etiologies, including but
limited to normal aging, closed head injury, and

Alzheimer's disease (Larrabee, Trahan & Levin, 1986), as

well as Huntington's dementia (Caine, Ebert & Weingartner,
1977). In this study, subjects were presented a 12 word list
(words are 50% high imagery, 50% low imagery and of
equivalent common usage) over 6 trials.

Following the standard scoring system (Buschke, 1973),
scores are obtained for each trial. The SUM is the total
number of words recalled in the trial. Words recalled on
two consecutive trials (that is, remembered immediately

after presentation, plus at least once without examiner

44

presentation) are scored as being in long term storage (LTS)

 

regardless of whether they are again recalled. Once a word
has entered LTS, it is counted in all subsequent trials
regardless of recall. Any word recalled that is already in

LTS is scored as long term retrieval (LTR). Consistent long

 

 

term retrieval is scored on the first and each subsequent

 

 

trial of an unbroken string of successful recall. Non-

standard scoring was used to acquire a short term recall

 

(STR) score in order to break the normal tie between LTR and
STR. For this study, all words recalled on the first trial
were considered to be a measure of STR.

Scores are summed across trials to obtain summary

scores .

Feeling pf Knowing (Nelson & Narens, 1980)

Nelson and Narens (1980) assembled an original pool of
300 general information questions (eg: what is the name of
the thick layer of fat on a whale?), and provided normative
data on the responses of 270 college students. From this
pool, a subset of 240 questions was used to develop the
FACTRETRIEVAL program which provides a multiple-choice
recognition phase (Shimamura, Landwehr & Nelson, 1981). In
preparation for the present study, 100 FACTRETRIEVAL
questions were chosen with a recall probability range of .99
to .00 in the college sample and administered to a sample of
20 community-dwelling elderly persons (mean age = 71.6, mean
education = 13.75, 30% male, 70% female). This provided

information on recall probability in an elderly sample. The

45

test consists of three phases: the recall phase in which the
subject is asked to answer general information questions
until there are 24 accumulated incorrect answers; the
Feeling of Knowing (FOK) phase in which the subject ranks
the incorrectly answered questions in terms of how likely
they feel they are to recognize the correct answer when
given some choices; the recognition phase in which the
subject is re-administered the general information questions
in a multiple-choice format. FOK accuracy is determined by
comparing the subject's prediction of recognition with
actual recognition performance. In the present study, the
first 3 questions to be presented have a recall probability
in the elderly sample of .100, and the last 30 questions
have a recall probability of .25 to .00. The questions are
printed in large type on separate 5 inch by 8 inch index
cards. The recognition cards also have the question printed

in large type, along with 7 choices.

Procedure

 

All outpatients with Parkinson's disease who had been
evaluated in the past 5 years by the Movement Disorders
Clinic of the University of Michigan Hospital or by the
Neurology Department of the Michigan State University
Clinical Center were invited to participate in the study. A
letter from the co-director or director of the clinic,
respectively, was mailed from the clinic with an enclosed
explanation of the study from the primary investigator and a

release of information form (Appendix A). Those patients who

 

 

46

were interested in participating signed and returned the
release of information form to the primary investigator.
She then requested and examined the medical records of the
potential subjects to ascertain whether exclusion criteria
were met.

If the potential subject appeared apprOpriate for the
study, the investigator called him/her on the telephone to
discuss the study, answer any questions, and arrange an
appointment in the subject's home.

In recruiting control subjects, the primary
investigator spoke to a senior citizens' group, briefly
explained the study, answered questions, and asked for
volunteers. When recruiting from former research
participants, she contacted them by telephone, briefly
explained the study and invited their participation.
Medical records of the control group subjects were not
examined.

Data collection procedures were identical for all
subject groups. Testing took place in a quiet room in the
subjects' homes. Upon arriving at the subject's home, the
investigator again explained the study to the subject,
answered questions regarding the study, provided a written
explanation, and obtaind the subject's written consent to
participate. The structured interview was then conducted,
followed by the Aphasia Examination. Subjects completed the
BDI, GDS and Memory Complaint Questionnaire in counter-

balanced order. The WAIS Vocabulary and Digit Span

 

 
 

!.
..

.A

47

subtests, Buschke Selective Reminding Procedure and the FOK
Test were then administered in that order.

If the battery was not completed within two hours, a
second appointment was made to complete the testing.
Occasional breaks were included during testing as needed to
minimize subject fatigue. After completion of the tests,
participants were invited to ask questions regarding their
performance or other aspects of the study. Subjects

received no compensation for participation in the study.

RESULTS

Subject Matching
Table 2 details descriptive characteristics of the

groups. One-way analyses of variance indicated no
significant differences among the three groups in age, F (2,
45) = .29, p < .752, education, F (2, 45) = .52, p < .599,
or scores on the Vocabulary subtest of the Weschler Adult
Intelligence Scale, 3 (2, 45) = .55,p < .580. Chi-square
analysis showed no difference in sex distribution by group,
(2, N = 46) = 1.22, p > .10.

75% of PD and PDD patients were married, compared to
65% of controls. Occupational status was roughly equal
across groups, with a plurality in each falling into the
professional/technical group. 80% of the control group was
semi-retired or retired, compared to 69% in the PD and 83%
in the PDD group. No differences in scores on the BDI or
GDS were found between subjects in the PD and control
groups, and these two groups were different from the PDD
group (BDI: F (2, 45) = 63.71, p < .0000, GDS: E (2, 45)
= 60.54, p < .0000). There were no differences between the
PD and PDD groups in age of onset, E (1, 26) = .27, p <
.611, duration of the disease, F (1, 26) = .24 p (.626, or
pharmocologic regimen for treatment of PD.

One control (5%), 4 PD (25%) and 8 PDD (66%) subjects

required two meetings to complete the testing. One control

48

49

Table 2

Subject Characteristics

 

 

Descriptor PDD PD Control
N 12 16 20
Age 68.25 66.06 68.5
range 48-85 44-81 46-89
standard deviation (9.98) (8.9) (11.1)
Education 15.38 14.17 14.6
range (years) 8-20 12-20 10-20
standard deviation (3.0) (4.0) (3.0)
Sex: Male 5 10 11
Female 7 6 9
Mean Vocabulary Scale Score 13.25 14.12 13.55
standard deviation (3.25) (1.5) (2.09)
Mean BDI Score *15.58 3.06 3.15
range 11-28 0-7 0-8
standard deviation (5.31) (1.65) (2.73)
Mean GDS Score *16.08 4.18 3.45
range 11-27 0-7 0-10
standard deviation (4.69) (2.36) (3.10)
Mean years since first symptom 8.58 8.25 -----
range 2-20 2-15
standard deviation (5.31) (4.68)
Mean years since diagnosis 7.41 6.56 -----
range 3-15 2-15
standard deviation (4.52) (4.54)
Mean age at diagnosis 59.66 57.81 -----
range 43-79 42-71
standard deviation (10.94) (8.13)
Parkinsonian medication:
Carbidopa/Levodopa 10 14 -----
(Sinemet) (83%) (88%)
Amantadine hydrochloride 4 4 -----
(Symmetral) (33%) (25%)
Bromocriptine mesylate 3 3 -----
(Parlodel) (25%) (19%)

*2 < .0000

 

 

 

50

subject discontinued testing on the Buschke Selective
Reminding Procedure (BSRP) due to frustration. In any

analysis using this test, this subject has been dropped.

Results pf Hypotheses

 

Hypothesis I predicted that FOK accuracy would be
unrelated to group membership. In order to attain an
index of FOK accuracy, the measure of association called
gamma ("G") was used, as recommended by Nelson (1984). "G"
is attained by the following formula:

# concordances - # discordances

 

# concordances + # discordances
"G" was calculated for each subject, with concordance being
defined as a correct prediction of ability or inability to
recall an item from memory. Discordance was defined as an
inaccurate prediction. The "G" score may range from -1
(perfect discordance) to +1 (perfect concordance). The mean
"G" scores were: PDD, .457; PD, .499; Control, .447.
Analysis of variance revealed no difference in FOK accuracy
by group, F (2, 45) = .18, p < .837, verifying the
hypothesis.

Hypothesis 11 predicted that level of memory complaint
would differ by group, with the PDD subjects complaining of
more memory problems than the PD and control subjects.
Table 3 offers descriptive information regarding means and
standard deviations by group.As predicted, the level of

complaint did vary by group, with the PDD group having the

51

 

woo. v were

 

 

 

 

 

.mo. v was
.No. v Mk
.uchHmEoo Hmumwum mmumowccw mnoom HmBOAm
H.m m.~H v.m «.ma o.m m.mH mnoom mamom
m.H H.m ~.H H.m m.H m.v pnm3xomm
H.m o.n m.H v.0 o.H m.m pum3uom
comm phase
a.ma em.mm m.va o.>H h.m m.mH mBAU
m.vH m.om m.mH m.vm m.~H 0.0m man
m.¢a >.mm o.mH ¢.~N m.HH o.mH mag
m.H n.m m.a v.m v.H m.m mew
m.m seem.m¢ h.oa H.mm h.oa m.mm 55m Bmmm
H.Hm o.mm H.0H ¢.>> m.m m.mh mucflmamaoo vamaoomm
m.m 44¢.em a.m m.om ~.s m.m~ mueamfiasoo Hmumemo
v.m~ av.o~a H.ma n.5oa m.mH m.wm mcofluocsm K50am:
mo wamom weflummnmfimm
mm .m .mm .m mm a
onsmmoz
Homecou on com

 

moanmaum> “camamEoo >HOEoZ can >HOEo2 co mmsouw mo somwummfioo

m manna

52

greatest complaint level. However, analysis of variance
with least-significant difference contrast showed that the
PD and PDD groups were not significantly different from each
other, and that both had significantly greater complaints
than controls, E (2, 45) = 4.55, p < .016.

As the Self Rating Scale of Memory Function was derived
from two sources, separate analyses were run to determine if
different results would be obtained for Hypothesis II
depending on type of question asked. The questions taken
from Zelinski et al. (1980) are more general in nature (eg:
"How would you rate your memory in terms of the kinds of
problems you have with it?"), while those from Squire et al.
(1979) address a variety of specific possible problem areas
("My ability to remember the names and faces of people I
meet 15..."). Analysis of variance with least-significant
difference contrast revealed that the more general questions
(items 1 and 2a-f) differentiated the sample in the manner
postulated in Hypothesis II, with the PDD group having more
complaints than the PD and control groups, 5 (2, 45) = 6.31,
p (.004. The group of questions addressing more specific
areas of complaint were not significantly different across
groups, F (2, 45) = 2.91, p < .10. Figure 1 shows the
breakdown by item.

Hypothesis III predicted that level of memory complaint
would be unrelated to level of memory performance. As
predicted, Pearson product-moment correlation coefficients

revealed no significant association between level of

 

 

1 L
K L.
ofie sainugw ma; 2 pauaddeu
191-1“ "838.1 '9 11:0wa fiw ,. L
U! 11399 HUBBJ 01 fillllqe __
L
L.
j L.
‘ L
L.
/ L
am 0; alqeuexxe iou

inq _an6uo} fiw 1° :11}. uo \\p* *-
aq 0} Woman: 3 JD} finuapua} I / __
p8UJBB] 8A.] sfiugu} ,,, K L
fiJouJauJ u! plug 0} fiiglgqe / L
‘ L
3| 58M 4» __
I uauM o; paJeduJoa MDU : L.

068 sf: DZ 0; paledmoo mou 4.-
ofie SJfi 0| 0} paJedwoo MDU * L-
068 SJfi g o; paledwoo MDU at / b
l.
ofie pm 2 o; PBJBUUJD‘J mow / -

lfi7fil'1j7j77171717

UJCDNLDLDVCUN—D
L.

E? “E’ m“;
05> Sm (1101
_,_,w on '-
35 mm 3w
1: :5 :5

4.;

1011121314151817181820

ZaZchZdZer 3 4 5 B 7 B 8

1

Hem number

[D
um:
QC!
vv
ma:
‘-
*4-
c
.9
+0
0
c
:1
“a
3':
03
Em
a:
9.’ “a...
a ”0
... m
u. —m
m
05
mm
3
on
to“:
+0
m
[E
:0:
m
an
L0
C3.
V
:11
1
'5
L
.0.)
r: :3 :3
c :1 c:
L.) EL :1.
o 4 I

54

complaint and any objective memory test, either across or
within groups. The correlation matrix is displayed in Table
4. As a different pattern was seen in Hypothesis II when
only general self-assessment was requested, the association
between general self-assessment questions and memory
performance was also examined. As with the complete
questionaire, the association between memory complaint and
memory performance was non-significant.

Hypothesis IV predicted that PD and PDD subjects
would perform more poorly than controls on effortful
memory tasks. This was confirmed with analysis of
variance and least significant difference contrast in
two measures:

BSRP SUM, 44)

g (2, 2.46, p < .05,
BSRP CLTR, g (2, 44)

2.17, p < .05.

On three other measures of effortful memory, there was

no significant difference found among the groups:

BSRP LTR, 3 (2, 44) = 1.81, p < .175,
BSRP LTS, g (2, 44) = 2.05, p < .140,
Digit Span Backward, F (2, 45) = .28, p (.756.

Hypothesis V predicted that there would be no
difference among groups in performance on less effortful
memory tasks. This hypothesis was confirmed by analysis of
variance:

BSRP STR, F (2, 44) .134 p < .875,

Digit Span-Forward, E (2, 45) = .582, p < .563,
Digit Span, g (2, 45) = .082 E < .922.

 

 

55

Table 4
a
Intercorrelations Between Memory Complaint
and Memory Variables

 

 

 

 

Measure PDD PD Control

BSRP Sum -.30 -.10 .08
LTR -019 -017 016
STR -.08 .19 -.25
LTS -.26 -.22 .14
CLTR -.002 -.16 .22

Digit Span

Forward -.10 -.12 -.30

Backward -.16 -.06 .24

Scale Score -.22 -.15 .30

a

Self Rating Scale of Memory Functioning:
Lower score indicates greater complaint

 

56

Depression Scales

 

Every person tested for this study was rated as
depressed or not depressed in each of the three measures
used. There was no subject or potential (but excluded)
subject rated as depressed by one measure, but not by the
other two, indicating that the three instruments are
measuring the same phenomenon.

The Pearson product-moment correlation between the EDI
and GDS across groups showed a high degree of relatedness, p
= .901, p < .001.

Item analysis of the BDI showed that the PDD group was
significantly different (more depressed) on all but 5 of the
items. Four of these five items seem to be related to
feelings of guilt. Figure 2 illustrates the pattern of BDI
item scores across groups.

In order to examine further the relationship between
depression and memory performance, within-group Pearson
product-moment correlations were performed. Table 5
illustrates the finding that there is no direct relationship
between level of depression as measured by the BDI and the
various memory variables for the PD and PDD groups.

However, there is a significant positive relationship
between level of depression and performance on the BSRP in
the control group.

The patterns are different when evaluating the
relationship between memory performance and scores on the

GDS. While no relationship was found in the PD group, there

xas u! isalaiug
'squd Iengsfiqdzu UJaauozi
550] 11-1513“
amadde

anfige}

deals

)‘JDM 0} page
aaueJeadde

fiupgew uogspap
ISBJBIUI i0 ssol
firmer-Us

Fun

sppgns

swap—“as

“as u; pawgpddeslp
pausgund

filllnfi

ungoeisges

8.111118} 8 188}

57

‘/

 

.A“"

/
\

/\
Afi’

 

pafieJnoosgp
pes

1 ‘ 7 1 1
v m N

More
Depressed

Less
Depressed

flu—i

D

**¥¥*¥-¥***¥
B 7 8 E1 101112131415181718182DZI

S

+<r

< .009

.D3
< .05

<

CLICLICLIQI

{-

Hem number

' Control

-*-
*

1 +

Figure 2

APD

Beck Depression Inventorg,
Patterns of Response

I PUD - p < .0008

Intercorrelations Between BDI Score

58

Table 5

and Memory Variables

 

 

 

Measure PDD PD Control
BSRP Sum .003 .12 -.55*
LTR -.01 .08 -.46**
STR -001 -001 .18
LTS .02 .10 -.38***
CLTR -.24 .01 -.46**
Digit Span
Forward -.08 .21 .34
Backward -.10 .35 -.26
Scale Score -.001 .09 -.09
* p < .008
** p < .02
*** p < .05
Table 6

Intercorrelations Between GDS Score

and Memory Variables

 

 

 

Measure PDD PD Control
BSRP Sum -.35 .11 -.31
LTR -.22 .06 -.28
STR -.26 .11 .07
LTS -.17 .06 -.13
CLTR -.55* -.04 -.38**
Digit Span
Forward -.52*** .17 .45****
Backward -.41 -.28 -.25
Scale Score -.38 -.04 -.24
* p < .03 *** .04
** p < .05 **** p < .02

 

59

was a significant negative correlation between performance
on the CLTR and GDS score in the PDD and control groups.
Digit Span Forward was negatively correlated with the GDS in
the PDD group, and positively correlated in the control

group. Table 6 displays the correlations.

Feeling pf Knowing

FOK accuracy was not correlated with any variable in
this study, including age (p = .15, p < .14), education (E =
.17, p (.12), disease duration (3 = -.05, p < .37), level of
depression (BDI: p = .04, p <39; GDS: p = -.09, p < .28),
digit span (p = .15, p (.15), memory complaint (p = .15, p <
.15), or any of the Buschke variables (Sum: p = .13, p <
.19; LTR: E = .01, p < .48; STR: E = .14, p < .17; LTS: £ =
-.01, p (.48; CLTR 5 = .17, p < .13).

The mean number of items correctly identified during
the first phase (free recall of information) of the FOK test
was: PDD, 25.83; PD, 26.87; Control, 23.10. There was no
statistical difference among the groups on this variable, F

(2, 45) = .342, p < .713, demonstrating intact remote memory

in the PD and PDD groups relative to controls.

Effect pf Duration 9: Parkinson's disease

 

In order to explore possible sources of difference
between the PD and PDD groups in memory performance and
complaint, post-hoc analyses were done examining the effects
of duration of disease. Age was related to disease duration

in the PD group (5 = .46, p (.04), and memory scores in both

 

60

groups (see table 7). Therefore partial correlations were
computed to examine the relationship between duration of
disease and memory performance with the effects of age
removed. The overall result indicates that time since
diagnosis was negatively correlated with memory performance
in the PD group; however, time since diagnosis and memory
variables were not significantly correlated in the PDD
group. The detail for this analysis is shown on Table 8.
Conversely, Pearson product-moment correlations showed
significant positive relationships between disease duration
and level of depression as measured by the BDI (5 = .66, p <
.01), as well as between disease duration and memory
complaint (5 = .49, p (.05) in the PDD group. There was not
a significant correlation between disease duration and
depression as measured by the GDS in the PDD group (p =

.34). No significant relationships were found in the PD

group between disease duration and depression (BDI, E

.17; GDS, 5 = -.17) or memory complaint (p = .16).

 

61

Table 7

Intercorrelations Between Age and Memory Variables

 

 

 

Measure PDD PD Control
BSRP Sum -.35 -.69* -.40****
LTR -.30 -.74* -.30
STR .19 .23 .09
LTS -028 -074* —.17
CLTR -.56*** -.72* -.36
Digit Span
Forward -.08 -.56** .05
Backward .04 -.55** .21
Scale Score .17 -.41**** .47**
* p < .007 *** p < .03
** p < .01 **** p < .05
Table 8

Partial Correlations Between Disease Duration
and Memory Variables
(Effects of Age Partialed Out)

 

 

 

Measure PDD PD
LTR .37 -.78*
STR -.04 .22
LTS .36 -.76*
CLTR .28 -.68**
Digit Span
Forward .06 -.24
Backward .30 -.32
Scale Score .23 -.29
* p < .001
** p < .003

I; ALI-lily 7?. is

DISCUSSION

Qualifyipg Statement

 

This study excluded subjects with a history of
neurological insult, those who demonstrated visuomotor
impairment and those who showed signs of cortical
deficit such as aphasic symptoms and acalculia. This
insured that those patients who may have had a dual
disease process (eg: Alzheimer's disease superimposed on
Parkinson's disease) were not compared to those with
only Parkinsonism. Given the rather stringent inclusion
criteria and the self-selection inherent in recruitment,
caution must be exercised in generalizing to the larger
Parkinsonian population.

On the other hand, the care in sampling may allow
a more precise look at patterns of functioning in
Parkinsonism itself, unconfounded by other variables.
Every interested Parkinsonian subject who met inclusion
criteria was included in the sample. 43% of these
subjects were depressed, which is in the middle range of
prevalence estimates derived from previous studies.
This adds credence to the possiblility that the findings
of this study are not idiosyncratic to this small
sample, and suggests that they may be fruitfully

considered in extending the results to other
62

63

Parkinsonian patients.
Summary pf Findings

Accuracy of FOK ratings was equivalent across all
three groups.

PD and PDD groups had significantly greater
complaint of memory deficit than did the control
subjects. However, when only general self-assessment
questions were included in the analysis, PDD subjects
had significantly more complaints than than PD or
control subjects.

Level of memory complaint did not correlate with
actual test performance in any group, even when the
subset of general self-assessment questions were
specifically analysed.

PD and PDD patients were deficient relative to
controls in some memory processes. Although not every
presumed measure of "effortful" memory processing
differentiated between groups, PD and PDD subjects were
impaired relative to controls on a measure of overall
ability in list-learning and on a measure of consistent
retrieval of newly learned material. There was no
statistical difference in performance on any test of memory
between PD and PDD subjects.

PD and PDD subjects scored equivalent to controls
on presumed measures of less effortful (immediate)
memory tasks.

Remote memory performance was not impaired in

 

64

PD or PDD subjects relative to controls.

Post hoc analyses revealed that level of depression
measured by the BDI was not related to performance on
any memory test in the PD or PDD groups unless disease
duration was considered, but there was a consistent
negative correlation between level of depression as
measured by the BDI and memory performance on the BSRP
in the control group. The relationship of GDS scores to
memory performance on the BSRP was similar in the
control and PDD group in that there was a negative
correlation between the GDS and CLTR. In the PD group,
there was no significant correlation between BSRP subtests
and the GDS.

Duration of disease was differentially related to
memory performance, self-assessment of memory abilities
and level of depression in PD and PDD patients.
Controlling for effects of age, PD subjects
demonstrated a significant decline in list-learning
abilities (both encoding and recall) corresponding to
disease duration. This was not associated with an
increase in memory complaint or depression scores. The
opposite pattern was seen in the PDD group: there was no
change in memory performance corresponding to disease
duration, but these patients endorsed more items on the
BDI and complained of increased memory deficit as the
disease progressed.

Comparison of the three measures of depression

65

showed a high degree of relatedness among them. Every
person tested who scored as depressed by one measure
also scored in the depressed range on each of the other
two instruments. Nevertheless, the pattern of
relationship between disease duration and BDI and
disease duration and GDS was different. In the PDD
group, there was a significant correlation between
disease duration and response to the BDI, but not
between disease duration and response to the GDS. In the
PD group, neither depression scale was correlated with

disease duration.

Interpretation

 

Overview

 

The results of this study demonstrate that an
understanding of affective and memory functioning in
Parkinson's disease must acknowledge the
interrelatedness of a number of factors. With few
exceptions, prior studies have been limited in that they
examine one or two aspects of Parkinson's disease
without considering moderating variables. Those which
do attempt to address additional factors have not
typically allowed for differential effects based on type
of symptomotology. (An excellent exception is seen in
the work by Brown et al., 1984). For instance, Mayeux et
al. (1981) reported that in their sample of Parkinsonian
patients, disease duration did not correlate with level of

depression, but they did not examine the effect of disease

66

duration in depressed versus nondepressed patients. This
simple approach has led to discrepant findings regarding the
effects of the disease, and the impact of factors such as
duration, on depression and memory.

The results of this study demonstrate that only
when a multi-level, integrated approach is taken can the
patterns of deficit in parkinsonism be discerned. The
present study suggests that the interactions among
memory, metamemory and depression are moderated by
length of disease. When this factor was not considered,
the differences between PD and PDD groups did not
emerge. But a clear, heuristically useful pattern was
brought into sharp relief once disease duration was
included in the analyses. An understanding of the
pattern can best be reached through incorporation and
integration of neuropsychological, cognitive and

intrapsychic approaches.

Depression

 

It has been hypothesized that instruments which
rely on physical or vegetative manifestations of
depression will over-report depression in aged or
physically disabled persons. This does not appear to be
true of this sample. No subject who scored in the
depressed range on the BDI (which is heavily loaded with
vegetative signs) failed to score in the depressed range
on the GDS which was purposely designed to minimize

somatic complaints that are associated with normal

 

67

aging. The modified SADS also reliably differentiated
between the PDD and other groups. Although this
instrument relies in part on vegetative signs that may
mimic Parkinson's disease symptoms, depressed mood is
the most rigid criterion for inclusion in a diagnosis of
depression. Thus, two of the three instruments utilized
to measure depression do not rely on vegetative signs,
but were associated with an instrument that does. At
first blush, the high degree of relatedness among the
measures of depression, one of which (the GDS) provides
no opportunity for somatic complaint, suggests that the
somatic difficulties reported by the PDD group on the
BDI are more related to the effects of depression than
to symptoms secondary to the Parkinson's disease
process.

The pattern of endorsement on the BDI for this
sample showed that PDD subjects scored significantly
higher than PD and control subjects on every measure of
vegetative complaint, but not on every affective one.
In particular, those items which appear to reflect
feelings of guilt and self-blame did not differentiate
among groups. This echoes the Taylor et al. (1986)
finding that depressed Parkinson's subjects did not
endorse items characteristic of negative affect as did
persons with endogenous depression. It may be argued
that the PDD subjects are merely reporting an objective

change in physical functioning due to the disease

68

process that is unrelated to the presence of depression.
PDD patients endorsed more BDI symptoms as the disease
progressed, while the PD subjects did not. A hallmark

of Parkinson's disease is its progressive nature, and

one would expect to find more disability in those
patients who had had the disease longer. Perhaps the

PDD subjects did not become increasingly depressed as

the disease progressed, but did become more physically
disabled relative to the PD group. If this were the case,
the BDI would be an inaccurate measure of depression for
this subject group, as the increase in item endorsements
by PDD patients would be merely reflecting changes in
physical functioning that are primary to the disease
process. This would also imply that the PD group was not
experiencing or reporting such an increase in physical
disability. The greater BDI scores in those PDD subjects
who had the disease longer, compared with no difference in
the GDS (which does not have items to measure somatic
complaints) supports this interpretation.

A criticism of the present study is that there was
no direct or objective measure of the physical symptoms
of Parkinsonism. Had such a measure been included, the
relationship between BDI complaints and physical
functioning would be easily clarified. Previous studies
have reported no consistent relationship between
depression and severity of physical symptoms, so there

is not strong support for the liklihood that the PDD

69

group had more objective physical symptoms than the PD

group.

Memory
Two subtests of the BSRP differentiated PD and PDD

subjects from controls. It is useful to consider these
results of objective memory testing in terms of encoding
versus retrieval abilities. That subtest (CLTR) which is
hypothesized to be most sensitive to retrieval deficits
demonstrated deficient memory in the PD and PDD groups, as i
did SUM, which is considered a general measure of learning
ability. Those subtests which theoretically measure
immediate memory (STR and Digit Span Forward), encoding
(LTS), and remote memory (recall of general information on
the FOK test) did not distinguish among groups. LTR, a less
stringent measure of retrieval than CLTR did not illustrate
the retrieval deficit. It appears that these Parkinsonian
patients exhibit a specific deficit of retrieval that
affects their ability to reliably access newly learned
material. This supports Bowen's (1976) report of adequate
registration but impaired retrieval of information on the
Weschler Memory Scale. (However, one criticism of the BSRP
is that while LTR and CLTR theoretically measure
"retrieval", deficits in these subtests may actually be due
to the material being stored in a degraded or incomplete
manner {Loring & Papanicalaou, 1987]).

The results of objective memory testing do not provide

support for the concept of specific impairment in

70

"effortful" manipulation of material in memory, as there was
no difference among groups in Digit Span Backward, the test
most likely to deteriorate with deficit of "effortful"
memory abilities. PD and PDD patients were able to hold and
manipulate sequential information in memory to the same
degree as controls.

Although both PD and PDD subjects were equally
impaired in objective memory testing, the relationship of
memory to disease duration was dramatically different
between the two groups. PDD subjects demonstrated impaired
memory performance whether they were tested early or later
in the disease process. However, PD subjects who had the
disease for a shorter time performed better than those PD
subjects who were tested later in the disease process. This
supports Swanda and Kazniak's (1985) findings that both
depression and memory deficit are found in Parkinsonism, but
that level of depression does not "explain" the memory
changes.

Figure 3 offers a schematic representation of how
memory deficits might progress differently in depressed
versus non-depressed Parkinsonian patients. This schema
suggests that there are two subtypes of Parkinsonism:

The first is defined by presence of depression and
accompanying memory deficit that remains stable over the
duration of the disease. The second subtype experiences
no depression, and a progressive memory decline.

These patterns may be contrasted with those seen

 

71

 

szmtna mmmmmE .w mucmEcptmm mCUEmE
.cpfimmfima mcoEm mufmcozflmm pmmpucta

m mtDmE

szmcjo mmmmmfi

 

Dam

 

an.

 

mmLDZ

mucmEcptmm 35:62

5:3

 

72

in other dementing illnesses. Alzheimer's patients
reliably demonstrate a progressive memory decline, and
only rarely show affective changes. When depression is
reported, it tends to disappear as the dementia
progresses. Huntington's disease, a syndrome

associated with degeneration of striatal cells and other
subcortical structures, is also accompanied by
progressive memory loss, but is also strongly associated
with affective changes. The pattern seen in the PD
group seems to mimic (although at a much milder level)
that seen in Alzheimer's disease. That seen in the PDD

group is distinctive.

Metamemory

 

PD and PDD subjects were equivalent to control
subjects in their accuracy of FOK, and FOK was unrelated
to disease duration. This finding supports and extends
previous findings that impairment in retrieval of
information may occur independent of deficit in FOK
abilities. Particularly, it adds to the work by
Brandt and Mower (1985) which demonstrated intact FOK
with impaired retrieval from remote memory in
Huntington's disease. They also demonstrated impaired
FOK and impaired retrieval from remote memory in
Alzheimer's disese, a cortical degenerative disease.
This sample of Parkinsonian patients exhibited
unimpaired retrieval from remote memory, impaired

retrieval of newly learned information, but unimpaired

 

 

73

FOK accuracy, demonstrating a neuropsychological profile
different from either Alzheimer's or Huntington's
disease patients. The subcortical structures compromised
in Parkinson's and Huntington's disease do not appear to
play an important role in monitoring the contents of
one's own memory, but accuracy of FOK would appear to
require intact cortical structures. Neither does
depression adversely affect performance on the FOK
tasks, a previously unreported finding.

In evaluating accuracy of self-assessment, it is
important to recall that performance on memory measures
is impaired in both PD and PDD groups. Both groups
complained of more memory deficit than did the control
group, and in no group was level of complaint related to
objective memory performance. Without considering the
effects of disease duration, it appears that the self-
assessment aspect of metamemory in Parkinson's disease is
equal to controls'.

However, as disease duration increased, the
integrity of self-assessment abilities seemed to
deteriorate in both PD and PDD subjects, but in opposite
ways. PDD subjects demonstrated stable objective
memory performance over time, but they expressed more
complaints about memory as the disease progressed. In PD
subjects, objective memory performance declined, but
complaint level remained stable. The Parkinsonian patients

appear to become increasingly unable to accurately reflect

 

74

and report on their own level of functioning as time since
onset increases. The implications of this pattern will be
discussed in the next section.

The self-assessment questionaire used was derived
from two sources, and required essentially two types of
assessment. When subjects were asked to compare
their current general memory functioning to some specific
time in the past, PDD subjects exhibited significantly
greater complaints. When the time was not specified, there
was no difference between PD and PDD groups. Apparently,
being required to focus on the previously "healthy" self
promoted a more negative current evaluation in the PDD than
PD patients.

It appears that "metamemory", is not a unitary
concept. Even though the two measures employed in this
study required self-assessment, only one differentiated
among three groups. It appears that the measure requiring a
more global self-assessment of memory functioning is more
sensitive to impairment in self-view than is the measure

requiring evaluation of specific contents of memory.

The Relationship Between Memory, Metamemory and Depression
The various data from this study form a coherent
pattern. It appears that as their disease progresses, PDD
subjects complain more about memory difficulties than do PD
subjects, even though their performance does not decline

over time, and performance on memory measures is not

significantly different between the two groups. The

‘3

.513.“ _—~'_-TLr

.t "La

 

75

increase in physical complaints with disease duration that
is reflected in the BDI may also be a manifestation of
general negative self-evaluation unrelated to actual
decrement compared to other PD patients. Seen in this
light, the correlation between the BDI score and disease
duration as well as the correlation between memory complaint
and disease duration reflect an increasing preoccupation
with both bodily and mental integrity by depressed patients

that exceeds that found in non-depressed patients.

F‘

The manner in which progressively impaired self-
assessment is expressed likely reflects patients'
psychological "styles". Depressed patients, responding
to feelings of helplessness and low self-worth,
exaggerate their negative attributes. Those questions
which focused most on comparing current to younger self
accentuated this tendency. Non-depressed patients, on
the other hand, rather than admitting the extent of their
real difficulties, perhaps engage in healthy denial to help
them cope with the cognitive (and possibly with the
physical) consequences of the disease process. Cohen and
Lazarus (1973) present data suggesting that some medical
patients who are "avoidant" of information regarding their
medical status may have better recovery from surgery than
those who are "vigilent". This coping style may be
effective in patients with long-term disability, such as
Parkinson's disease as well.

Kobasa, Maddi and Courington (1981) discuss the

76

concept of "hardiness" as contributing to a style of coping
with stress. Those people who are psychologically "hardy"
are characterized by glad acceptance of change, ability to
commit themselves completely (to an idea, project, person),
and feelings of being in control. Less hardy persons feel
powerless to affect their environment and view any change as
overwhelming and stressful. Perhaps those "hardy" pe0ple
who develop Parkinson's disease are less vulnerable to
affective changes associated with the disease process.
Those persons who have historically lacked the "hardiness"
factor in coping with stress may be more vulnerable to the
depressive symptoms. They may be more likely to respond
with feelings of helplessness and negative evaluations of
themselves (Beck, 1967).

The inherent ambiguity of this disease, especially its
idiosyncratic course and "on-off" nature would seem to
accentuate a characteristic "hardy" or "unhardy" style.

The current data do not allow for conclusions
regarding causal relationships between depression and memory
deficits in Parkinsonism. Although clear conclusions cannot
be drawn, there are at least three possibilities: memory
deficit is a symptom of depression (pseudodementia), the two
are separate symptoms of Parkinsonism, or depression is a
reaction to memory decline.

In this sample, the PDD subjects showed impairment in
memory, but it did not worsen with duration of illness.

Therefore one possibility is that the subgroup of

77

Parkinsonian patients who show primary affective changes due
to subcortical degeneration experience a decline in memory
ability earlier in the disease due (at least in part) to a
pseudodementing process.

Another possibility is that while both symptoms are
directly due to Parkinson's disease, they are independent of
each other. Contrary to the report by Brown et al. (1984)
which noted a tie between affect-arousal and cognition, the
present findings suggest that memory functioning and
affective state are independent. There is evidence that
those Parkinson's disease patients who exhibit rigidity
primarily on the right side of the body show greater
depression (Mortimer, Warrior, Jun, Kuskowski & Webster,
1987) than those who show left-side symptoms. This is
consistent with depressive symptoms being associated with
left-hemisphere lesions. Therefore, the expectation would
be that those persons who initially show greater left-
hemisphere involvement would be those who were depressed.
The present study did not differentiate between left versus
right side symptom focus, so the validity of this hypothesis
cannot be examined here.

As memory deficit was seen equally in both the PD and
PDD groups, one might suppose that this symptom is primary
to the Parkinsonian process. It is possible that a subgroup
of patients experience an immediate onset of memory deficit
with the Parkinsonian process which triggers a reactive

depression. Given the robustness of findings regarding

 

78

prevalence of depression in Parkinsonism, it is possible
that the disease creates a predisposition to depression
which interacts with an individual's own psychological
"style" as discussed above.

Fibiger's (1984) hypothesis of mesocorticolimbic
involvement is also a useful concept in understanding the
pattern of results. Perhaps those patients who experience
greater degeneration of these pathways are more susceptible
to affective symptoms. The PDD patients may have
compromised mesocorticolimbic projections gag have less
"hardy" coping styles, both of which promote depression. In
this view, both pathophysiologic and psychological deficits

create the depressed behaviors.

Parkinson's Disease gg g Subcortical Dementia

 

 

Several writers (Albert, Feldman & Willis, 1974;
Cummings & Benson, 1984; McHugh & Folstein, 1975) have
discussed the concept of subcortical dementia to describe
the intellectual motor and affective deficits found in
Parkinson's disease and other disorders known to affect
subcortical structures. Proponents of this concept report
that subcortical dementia is distinguishable from the so-
called "cortical dementias" such as Alzheimer's disease.
Speech is soft, poorly modulated and dysarthric in contrast
to the aphasic syndromes seen in the cortical dementias.
Memory is marked by deficits in retrieval (with relatively
intact encoding and storage abilities) rather than anmesia

in which learning new material becomes virtually impossible.

 

79

Cognitive functions tend to be slow but intact (with the
exception of visual-spatial skills) in subcortical dementia,
while cortical dementias are noted for strikingly disordered
mental abilities such as judgment, abstraction, and
calculations. Motor and postural symptoms are primary in
subcortical dementias, but essentially absent in cortical
dementia. If there are any affective changes in cortical
dementias, they tend to be marked by unconcern contrasted

with the depression or euphoria reported in subcortical

I? -o - 3::

disorders.

The concept is not universally accepted. Mayeaux,
Stern, Rosen and Benson (1983) found no significant
difference in test patterns on a modified Mini-Mental State
Exam among patients with Alzheimer's, Parkinson's and
Huntington's diseases, and concluded that the subcortical—
cortical breakdown was not validated. Use of a screening
instrument is not likely to adequately measure the range or
be sensitive to subtleties of difference among groups.
Albert (1984) critiques this study on the basis of skewed
patient selection, and notes that despite the methodological
problems, the published data in fact revealed neuropsycholo-
gical differences between the Alzheimer's group compared to
the Huntington's and Parkinson's groups.

Another argument against the presence of a distinct
subcortical dementia syndrome is the presence of cortical
changes in some demented Parkinson's patients like those

seen in Alzheimer's disease (eg: Boller, Mizutani,

80

Roessmann, and Gambetti, 1980). While these changes have
clearly been documented, they do not rule out subcortical
damage as a separate contributing factor in dementia.
Albert (1984) suggests two subtypes: those with subcortical
dementia and those with co-occuring cortical dementia.
Those with subcortical changes would present with the
described distinctive pattern, while those with a dual-
disease process would exhibit both more severe and more
diffuse impairment.

In the present sample of Parkinsonian patients,
memory deficit marked by difficulties in retrieval of
recently learned material were evident. Immediate and
remote memory and ability to learn were unimpaired.
Approximately 43% of the Parkinsonian patients were
depressed. Both PD and PDD groups required two sessions to
complete testing (25% and 66% respectively) compared to only
5% of controls, suggesting a general slowness, whether of
thinking or movement, particularly in the PDD subjects.
(Data collection procedures did not include recording the
"reason" for two sessions, so the fact of multiple sessions
should be carefully interpreted. It should be noted that at
least some of the time, it was due to a wish by the patient
or spouse to talk over their difficulties with a perceived
"expert". Other subjects felt socially isolated and simply
wished to prolong contact. To the extent possible, these
conversations were deferred until testing was complete.

Despite the caveat, it is the investigator's impression that

 

 

81

most of those subjects who required more than one session
did so due to fatigue or slowness of thought and/or
movement.)

The pattern of impairment found in this subject sample
(impaired retrieval, depression, slowness) reflects that
reported to occur in subcortical dementia, and supports the
view that cognitive impairment can and does occur in
Parkinsonian patients independent of cortical degeneration.

Recall that those patients who exhibited "cortical signs"

 

were excluded from this study, reducing support for the
position that cognitive deficits in Parkinsonism are best
explained by co-occurring cortical pathology.

However, there is not a one-to-one relationship
between diagnosis of Parkinsonism and depression. It
appears likely that presence of this disease makes one
vulnerable to depression, but this vulnerability may be

overcome if one has available a "hardy" coping style.

Implications for Future Research

 

 

One interesting result of the present study is that
despite the known symptom variability across and within
Parkinson patients, a definite pattern emerged. The
link between disease duration, affective state, pattern
of self-assessment and memory performance has not been
previously reported. Future work might fruitfully
include longitudinal studies to test the viability of
the schema presented in Figure 3. The between and

within-subject variability that occurs with this disease

82

would best be controlled through such an approach. It
would be especially interesting to incorporate Brown et
a1.'s (1984) approach of testing the same subjects in "on"
and "off" conditions in such a longitudinal approach. This
would increase the richness of data by examining how
physical symptoms interact with cognitive and affective
ones.

The prOposed interaction between pathophysiological
changes and pre-existing psychological style of coping
should be pursued as well. Use of Kobasa, Maddi and
Courington's (1981) theoretical construct and measurement
tools would extend the literature on the etiology of
affective symptoms in Parkinsonism.

Regarding neurOpathological localization and the
pattern present in this study, future studies would record
whether physical symptoms were primarily left or right-
sided. An additional approach might include repeated brain
images or positron emmission tomography to document
degeneration of specific sites. This would help clarify the
hypothesized roles of mesocorticolimbic projections.

The present work demonstrated that FOK accuracy is not
impaired either by presence of Parkinsonism or depression,
while accuracy of self-assessment appears to be compromised
with disease duration. However, this conclusion may be
faulty, as it was not demonstrated that responses to the
Self-Rating Scale of Memory Function, which relates to

complaints of everyday functioning should correspond to

 

83

performance on a list-learning task. In the present
study, subjects were not asked to predict their ability to
perform on a list-learning task, which would be a more
pointed measure of self-assessment accuracy. The
relationship of complaints about everyday memory to
laboratory test performance has not been resolved. Loring
and Papanicolaou (1987), reviewing this problem, present
evidence that at least some objective memory measures do
relate to everyday memory problems or strengths. Future
studies will need to consider these issues as well as the
result that the type of assessment requested (eg: general
comparison of present and past self versus assessment of
specific functions) affected the differentiation possible.
Further instrument evaluation is needed to determine the
items that would best differentiate in the Parkinsonian
and/or depressed pOpulations. Other areas to explore in
self-assessment of memory in Parkinson's patients might be
frequency of forgetting, effort to remember, and the
perceived seriousness of memory failures (Gilewski and

Zelinski, 1986).

 

APPENDI X A

j“: :2m‘1

Appendix A

Recruitment and Consent Forms

NEUROSCIENCE LABORATORY BUILDING 1103 EAST HURON
ANN ARBOR. MICHIGAN 48104-1687

 

September 6, 1985

Dear Parkinson's disease patient,

I have been contacted by Lila Coulter. a graduate student in
psychology at Michigan State University. She is doing research on
mood and memory in Parkinson's disease. To complete her research she
needs to interview a large number of patients with Parkinson's disease.

I feel that her research is worthwhile and I would like University
of Michigan patients to have an opportunity to participate in it. I
also feel that nobody should have access to information about U of H
patients without the patient's consent. Therefore, I am sending you
the enclosed information but I am not telling Lila Coulter to whom it
has been sent. If you are interested in participating in the research,
please contact her at:

Lila Coulter

Department of Psychology
Snyder Hall

East Lansing, MI 48824
(517) 351-9256

Sincerely yours,

John B. Penney. Jr., M.D.
Associate Professor of Neurology
Co-Director Movement Disorders
Clinic
JBP:jp

Encl:

84

 

"1

u. .1'
9‘

85

MICHIGAN STATE UNIVERSITY

 

COLLEGE OF OSTEOPAMC MEDICINE 0 FE HALL EAST LANSING 0 MICHIGAN 0 48824-1316

DEPARTMENT OF INTERNAL MEDICINE
April 18. was

 

Dear Parkinson's Disease Patient:

I have been contacted by Lila Coulter. a graduate student in psychology at Michigan
State University. She is doing research on mood and memory in Parkinson's Disease.
To complete her research. she needs to interview a large number of patients with
Parkinson's Disease.

I feel that her research is extremely worthwhile and would like Michigan State University
patients to have an opportunity to participate in it. I also feel that no one should have
access to information about Michigan State University patients without the patient's
consent therefore I am sending you the enclosed information but I am not telling Lila
Coulter to whom it has been sent. If you are interested in participating in the research.
please contact her at:

Lila Coulter

Department of Psychology
Snyder Hall. MSU

East Lansing. MI 1188211
[517] 351-9256

Sincerely yours.

George E. Ristow. D.D.
Professor and Chairman
Department of Internal Medicine
Head. Division of Neurology

GER/mh

MSU it an Ill/inactive Action/Equal Opportunity Institution

86

MICHIGAN STATE UNIVERSITY

 

DEPARTMENT OF PSYCHOLOGY EAST LANSING - MICHIGAN - “IN-Ill‘
PSYCHOLOGY RESEARCH BUILDING

Dear Parkinson disease patient:

This is an invitation for you to be a part of a research project
on memory and mood in people with Parkinson's disease. Your
experiences with this syndrome would be a valuable part of this
study. The results will add to our understanding of Parkinson's,
and may be helpful in treating peOple who deveIOp it in the
future.

Should you agree to participate, I will meet with you in your
home on two occasions, for about two hours each time. During
these meetings, I will ask you about your current and past mood,
and ask you to complete some tests measuring mood, memory and
other cognitive abilities. The results of these tests will
remain confidential between you and me. Although_there may be no
direct benefit to you, I think that you personally will find the
various tests interesting, and will learn more about how your own
mind works in the process.

If you think that you would like to take part in this research,

please complete and sign the enclosed release of information form

and return it to me in the envelope provided. This form gives
permission for limited access to your medical records. and tells
me I may contact you by telephone. After I receive the form, I
will call you to answer questions you may have about the study
and to make an appointment with you. If you have questions
before you sign the form, plese call me at (517) 351-9256.

I hepe you will take part in this study, and look forward to
hearing from you.

Sincerely,

M/d/ (2212/7579

Lila Coulter, M.A.

 

"'1'.

23:“ ”ms—-

 

87

RELEASE OF INFORMATION

To: University of Michigan Medical Center
Medical Information
Ann Arbor, Mi. 48104

Please release the following information:
All dictated hospital summaries and clinic notes from 9/83 to
the present.

Send this information to:
Lila Coulter, M.A.
Department of Psychology
Snyder Hall
Michigan State University
East Lansing, Mi. 48824

This information will be used for research purposes.

 

 

 

 

 

Thank-you.

name (please print) signature
street address date

city

 

phone

 

88

RELEASE OF INFORHATION

TO: HSU Clinical Center
Medical Records
138 Service Road
East Lansing, HI 46824

Please release the following information:
A copy of all dictated hospital summaries and clinic notes

from 9/83 to the present.

Send this information to:
Lila Coulter, M.A.
Department of Psychology
129 Psychology Research Building
Michigan State University
East Lansing, HI 48824-1117

 

This information will be used exclusively for research purposes,
and will be destroyed upon completion of the research project.

Thank you.

 

 

 

 

 

 

Name (please print) Signature
Street Address Date

City

I 1

Phone

I l

 

Clinic Number (if known)

89

INFORMATION FOR PARTICIPANTS

We are asking your help in understanding memory and mood in
people with Parkinson's disease.

Should you agree to participate, a researcher will meet with you
in your home on two occasions for about two hours each time.
During these meetings, you will be interviewed regarding your
current and past mood, and asked to complete a variety of tests
measuring mood, memory and other cognitive abilities.

There is no treatment implied in this study. Nevertheless, it is
my belief that you will find it interesting. Further, the re-
sults of the study will contribute to our understanding of how
mood and memory interact in people with and without Parkinson‘s
disease.

Your identity will be strictly protected, and your name will not
be mentioned in any reports that may come from this work. Should
you decide to participate, you will, of course, be free to with-
draw at any time without affecting current or future services to
which you may be otherwise entitled.

A copy of the results of the study will be available to you on
your request.

Thank you for your interest.

Lila Coulter, M.A.

" ' 2);...ij

‘5

9O

MOOD AND MEMORY
Consent Form

Primary Investigator: Lila Coulter, M.A.

I have read the attached "Information for Participants”, received
a copy of it and this consent form, and understand both.

I understand that there will be no guarantee of direct benefit to
me as a result of this project, but that new knowledge may be
gained, and this knowledge may be of value to me or to others.

I was given the Opportunity to ask any questions about the proce-
dures and all were answered to my satisfaction. I also know that
Lila Coulter ([517] 351-9256) will answer any further questions I
may have about this study at any time during or after my partici-
pation. For answers to questions regarding research, my rights,
or injury I believe is related to this research, I may contact
Dr. Henry Bredeck, Chairperson of the Institutional Review Board
at Michigan State University ([517] 355-2186).

I know that I am free to withdraw this consent without penalty or
loss of benefits to which I may be otherwise entitled.

I understand that approximately 45 subjects will be involved in
this study. I have been assured that my personal identity will
not be revealed and will remain confidential in reports and
releases of the results of this project.

At my request, a summary of the results will be given to me.

Of my own free will, I consent to participate in the procedure.

 

 

Date Participant

 

Interviewer-Witness

 

 

APPEND I X B

 

Date of birth:

 

Education:

 

Occupation:

 

History of: Head injury
No

Appendix B

INTERV IEN OU'I'L INE

8#

Group
Date

Sex:

 

Marital status:

 

Retired: yes

Yes (give date. medical sequalae)

CVA
No

 

Yes {give date. medical sequalae)

Epilepsy
No
Yes

——

All current medical dx:

Current medications:

(PD only): Date of diagnosis:

Time since diagnosis:

Earliest sx:

91

no

LR? .Afl‘mnj

r

 

92

(Rest of interview to all as)

1.

I would like to hear about any problems or difficulties you are
having in your life now.

How different has this trouble been from the way you were before
or usually are?

When did you last feel like your usual self for a couple of months?

When would you say you first noticed that something was wrong?
What was happening in your life at that time?

Was there any big change in your life. like your health. finances.
job. family? (rate stress)

Current episode associated with:
Pregnancy

Menopause within 3 years
Drugs/medications just before
Physical illness (other than PD)
Onset of PD

Death of someone close

Do You think that this is related to your becoming depressed:

Stress:

N

NHOP

5

6

Not applicable. e.g.. CNS injury. drug reaction

No information

No apparent stressful event or circumstances

Minimal. e.g.. vacation. minor violations of the law. small bank
loan

Mild. e.g.. began or ended school. argument with neighbor or boss.
change in work hours

Moderate. e.g.. change to different line of work. death of close
friend. pregnancy. child leaves home

Severe. e.g.. severe illness in self or family. bankruptcy.
marital separation. marriage. birth of child

Extreme. e.g.. death of close relative. divorce. jail term

Subject stress rating:

0

L‘UJN

No information or too confused or deluded to evaluate real life
events

Aware of no stressful event or believes it had nothing to do with
development of episode

Possibly related

Most likely related

Almost certainly related

 

93

Classification:

0 No information. not ill

1 The current episode of illness has lasted less than 5 years and
developed in a person who was relatively free of psychiatric
symptoms for at least the 2 months preceding the episode. There
may have been previous episodes of illness but with little resid-
ual psychopathology. Examples: Recurrent depressions; second
episode of acute psychosis.

2 The current episode of illness has lasted less than 5 years and
is a new syndrome that is superimposed on preexisting psychopath—
ology of any other disorder. Examples: Chronic alcoholic devel-
ops a depression. Someone mildly depressed for years develops a
manic or depressive episode.

3 The current episode of illness has lasted less than 5 years and
is apparently an exacerbation of an ongoing chronic condition.
Examples: Acute exacerbation of schizophrenia or alcoholism.
Chronically depressed man develops an episode of severe
depression.

4 Chronic condition with numerous exacerbations or cycling so that
it is practically impossible to determine when this episode began
or has an episode that lasted over 5 years.

5 Ill with essentially the same condition for more than 5 years and
only entering a treatment facility or being evaluated now for
some reason unrelated to a change in psychopathology.

Duration:

0 No information

1 Less than 2 days

2 2 days to less than 1 week

3 1 week to less than 2 weeks

4 2 weeks to less than 1 month

5 1 month to less than 2 months

6 2 months to less than 3 months

7 3 months to less than 1 year

8 1 year to less than 2 years

9 2 years or more

 

94

B. Dysphoric mood
I. How have you been feeling? Describe your mood.
(Have you felt depressed [sad. blue. moody. down. empty. as if

you didn't care]? Have you cried or been tearful? How often?
How long does it last?)

Rating:

0 No information at all

1 Not at 811 '

2 Slight (only occasionally feels sad or down)

3 ‘Mild (often feels somewhat depressed. blue) Fan
4 Moderate (most of the time feels depressed)

5 Severe (most of the time feels wretched)

6 Extreme (most of the time feels extreme depression which

"I can't stand") .“w
Very extreme (constant unrelieved extremely painful
feelings of depression)

”s1

(How bad is the feeling? Can you stand it?)
How long have you been feeling this way?

1 1 week
2 1-2 weeks
3 over 2 weeks

2. Is it worse at any particular time of day? (morning.
evening?)

3. Is this feeling different from the usual feelings that you
would get after someone close has died (or from a sad movie or
story)?

(How is the feeling different? [Describe])

No information or unable to understand question
No difference or just more severe

Questionable or minimal difference

Definitely different. but only mildly so

Very different

bUJNl—‘O

Describe:

 

4.

95

When you feel this way do you always know what you are
(depressed) about or do you sometimes just feel bad and not

know why?

0 No information or unable to understand question

1 Nearly always. e.g.. "It's all because of my business
failing."

2 Most of the time

3 Usually not

4 Practically never. e.g.. "There is absolutely no reason
for me to feel this way."

5 When something good or nice happens. do you feel better.

or happy for a while? If someone tried to cheer you up.
could they?

Yes

m

No

 

 

96

Sought or was referred for help during the dysphoric period.
took medication. or had impairment in functioning with family. at
home. work or socially.

Have you seen any professional person for these problems? Has
anyone suggested to you that you should see a professional person
for these difficulties?

Referred: Yes No
Took referral: Yes No

 

(What did the doctor do? Were you given medication? Hospital-
ized? ECT?)

Current treatment(s) received:

ECT

Lithium

Antidepressants

Minor tranquilizers (e.g.. Miltown. Valium)
Major tranquilizers (e.g.. Thorazine)

Other or unknown medication

Psychotherapy or counseling

Other (describe)

 

Have you sought help for these problems before? (What did the
doctor do then? Medications? Hospitalized? ECT?)

ECT

Lithium

Antidepressants

Minor tranquilizers (e.g.. Miltown. Valium)
Major tranquilizers (e.g.. Thorazine)
Other or unknown medication

Psychotherapy or counseling

Have your family or friends seemed concerned about how you are
feeling or acting?

Not at all
Somewhat

Quite a bit

Are very worried

WNI—‘O

 

 

 

97

C. Additional symptoms

1.

Guilt. self-reproach

Do you blame yourself for anything you.have done or not done?
What about feeling guilty?

Do you feel you have done anything wrong?

Do you deserve punishment?

(Do you feel you have brought this on yourself?)

0

1
2
3

No inf omation

Not at all

Slight. e.g.. occasional feelings of mild self-blame

Mild. e.g.. often feels somewhat guilty about past
actions. the significance of which he exaggerates. such as
consequences of his illness

Moderate. e.g.. often feels quite guilty about past
actions or feelings of guilt which he cannot explain
Severe. e.g.. pervasive feelings of intense guilt. or
generalizes feelings of self-blame to most situations
Extreme. e.g.. delusions of guilt. hallucinations in.which
he is accused of having done something terrible. or agon-
izing constant feelings of guilt

Discouragement. pessimism and hopelessness

Have you been discouraged (pessimistic. felt hopeless)?
What kind of future do you see for yourself?

(How do you think things will work out?)

(Can you see yourself or your situation getting any better?)

NHO

amps)

No information

Not at all discouraged about the future

Slight. e.g.. occasional feelings of mild discouragement
about future

Mild. e.g.. often somewhat discouraged

Moderate. e.g.. often feels quite pessimistic about future
Severe. e.g.. pervasive feelings of intense pessimism
Extreme. e.g.. delusions or hallucinations that he is
doomed. or that the world is coming to an end

 

 

3.

98

Suicidal thoughts

When a person gets upset. depressed. or feels hopeless. s/he
may think about dying or even killing him/herself. Have you?
(thought about how. told anyone about. done anything?)

0
l
2

No information

Not at all

Slight. e.g.. occasional thoughts of his death (without
suicidal thoughts). "I would be better off dead" or "I
wish I were dead."

Mild. e.g.. frequent thoughts that he would be better off
dead or occasional thoughts of suicide but has not thought
of a specific method

Moderate. e.g.. often thinks of suicide or has thought of
a specific method

Severe. e.g.. often thinks of suicide and has thought of.
or mentally rehearsed a specific plan or has made a sui-
cidal gesture of a communicative rather than a potentially
medically harmful type

Extreme. e.g.. has made preparations for a potentially
serious suicidal attempt

Very extreme. e.g.. suicidal attempt with definite intent
to die or potentially medically harmful

Sleep disturbance

Have you had trouble sleeping?

(What about falling asleep. waking up in the middle of the
night. early in the morning?)

(How bad does it get?)

@U‘J-‘UJNHO

No information

Not at all. or feels no need for any sleep

Slight. e.g.. occasional difficulty

Mild. e.g.. often has some significant difficulty
Moderate. e.g.. usually has considerable difficulty
Severe. e.g.. almost always has great difficulty
Extreme. e.g.. claims he almost never sleeps and feels
exhausted next day

Note type(s)

Initial insomnia: Difficulty falling asleep

Middle insomnia: Difficulty staying asleep or returning
to sleep. preceded and followed by sleep

Terminal insomnia: Difficulty staying asleep the usual
amount of time (beyond 5 hours). or final awakening after
less than 5 hours of sleep

 

5.

99

(Are you sleeping longer or more than usual--how much more.
how often? Do you take long naps during the day?)

No information

Not at all. or needs less sleep than usual
Occasionally sleeps more than usual

Frequently sleeps at least 1 hour more than usual
Frequently sleeps at least 2 hours more than usual
Frequently sleeps at least 3 hours more than usual
Frequently sleeps at least 4 hours more than usual

OsUlthl—‘O

Lack of energy or fatigue
[Do not confuse with lack of interest]

Have you had less energy than usual to do things--or have you
been getting tired more easily?

0 No information

1 Not at all or more energy than usual

2 Possibly less energy than usual

3 At times definitely more tired or less energy than usual

4 Often feels tired or without energy

5 Almost all the time feels very tired or without energy or
spends a great deal of time resting

6 Constant feeling of extreme fatigue or lack of energy or

spends most of the time resting
Appetite compared to usual

What about your appetite for food compared to the way it
usually is.

(Do you have to force yourself to eat. eating less than usual?
How much less?)

Poor appetite:

No information

Not at all--normal or increased

Slight decrease of questionable clinical significance
Mild decrease

Moderate decrease

No appetite. but forces self to eat

No appetite. and has to be fed

O‘Ulkle-‘O

 

100

Have you lost any weight since ?

No information

No weight loss

Doubtful or up to 5 lbs.
5-10 lbs.

10-15 lbs.

15-25 lbs.

Over 25 lbs.

O‘Lnwat-IO

Have you had an increase in appetite? How much have you been
eating?

Increased appetite:

 

O No information

1 Not at all--normal or decreased

2 Slight increase of questionable clinical significance
3 Mild increase

4 Moderate increase

5 Hungry all the time. but restrains self

6 Hungry all the time and eats without restraint
Have you gained any weight since -?
O No information

1 No weight gain or only regained lost weight

2 Doubtful or up to 5 lbs.

3 5-10 lbs.

4 10-15 lbs.

5 15-25 lbs.

6 Over 25 lbs.

Indecisiveness. trouble concentrating or thinking

Have you had any difficulty making everyday decisions?

Has it taken longer to make decisions than when you were
feeling good. like what to wear. what to cook. where to go.
what to buy?

Are there things that you don't get done because you can't
decide what to do?

0 No information

1 Not at all

2 Slight and of doubtful clinical significance

3 Subjective feeling that it is harder to make decisions and
may take longer. but decisions are made

4 Unable to make some decisions. or decision-making process

is so prolonged as to cause difficulties

5 Important activities are delayed or not done because of
difficulty deciding

6 Paralyzed in many important activities by inability to
decide between alternative actions

8.

101

Loss of interest. social withdrawal

Do you find that you have lost interest in or get less
pleasure from things that you used to enjoy--like your job.
friends. family. sex. hobbies. watching TV. eating?

(What things have you lost interest in?)
(Which things do you still enjoy?)

Loss of interest:

No information

All activities as interesting or pleasurable. or more so
1 or 2 activities less interesting or pleasurable
Several activities less interesting or pleasurable

Most activities less interesting or pleasurable

Almost all activities less interesting or pleasurable
All activities less interesting or pleasurable

O‘U'bU-JNHO

(Have you had less to do with people than usual?)

(What about being less active in (church. club. bowling.
cards. etc.]?)

(Have you preferred to be by yourself?)

(Have you turned down or avoided situations where you knew you
would be with people?)

(Have you stopped calling your friends or answering the
phone?)

Social withdrawal:

0 No information

1 Not at all. no change from usual or increased contact

2 Less contact or slight avoidance. but of doubtful clinical
significance

3 Mild. e.g.. is somewhat less involved (e.g.. has less to
say to co-workers) or sometimes avoids social contact
that he ordinarily participates in

4 Moderate. e.g.. is definitely less involved when with
people or often avoids social contact that he ordinarily
participates in

5 Severe. e.g.. goes out of his way to avoid many social
situations that he ordinarily participates in

6 Extreme. e.g.. actively avoids all social contact that he
ordinarily participates in

 

102

Psychomotor agitation/retardation

Are you having trouble sitting still. do you always have to be
moving or pacing up and down?

Agitation:

O No information

1 Not at all. retarded. or associated with manic syndrome
2 Slight. e.g.. increase which is of doubtful significance
3 Mild. e.g.. unable to sit quietly in a chair

4 Moderate. e.g.. paces about a great deal

5 Marked. e.g.. almost constantly moving and pacing about
6 Extreme. e.g.. almost constantly moving and pacing about

in a frantic manner

”“7

_ ' ‘1'

Note manifestations:

Unable to sit still

Pacing

Hand-wringing

Pulling or rubbing on hair. skin. clothing. etc.
Outbursts of complaining or shouting

Talks on and on or can‘t seem to stop talking

 

(How long has this lasted?)

Less than 4 days
More than 4 days

Are you slowed down? Speech?
(Is it hard to start talking? Do you talk a lot less than
usual? Do you feel like you are moving in slow motion?)

Retardation:

O No information (Go to item 348)

1 Not at all (Go to item 348)

2 Slight. and of doubtful clinical significance (Go to item
348)

3 Mild. e.g.. conversation is noticeably retarded but not

strained

Moderate. e.g.. conversation is strained. moves very slowly

Marked. e.g.. conversation is difficult to maintain.

hardly moves at all

6 Extreme. e.g.. conversation is almost impossible. sits in
one position for hours

LII-b

Manifestations included:

Slowed speech

Increased pauses before answering

Low or monotonous speech

Mute or markedly decreased amount of speech
Slowed body movements

D.

103

(How long has this lasted?)

Less than one week
More than one week

R/O Manic states

I know you have been feeling (depressed). However. many people
have other feelings mixed in or at different times. so it is
important that I ask you about those feelings also.

1. Elevated/expansive mood

Have there been times recently when you felt very good. or too
cheerful--not just your normal self (when you felt on top of
the world. or as if there was nothing you couldn't do)?

(If people saw you. would they think youLwere just in a good
mood or something more than that?)

What about during the past 2 weeks?

0 No information

1 Not at all. normal. or depressed

2 Slight. e.g.. good spirits. more cheerful than most people
in his circumstances. but of only possible clinical
significance

3 Mild. e.g.. definitely elevated or expansive mood and
overly optimistic which is somewhat out of proportion to
his circumstances

4 Moderate. e.g.. mood and outlook are clearly out of

proportion to circumstances

Severe. e.g.. quality of euphoric mood

Extreme. e.g.. clearly elated. exalted expression and says

"Everything is beautiful. I feel so good."

O‘U‘I

2. Less need for sleep to feel rested
Have you needed less sleep than usual to feel rested?

No information

No change or more sleep needed
Up to 1 hour less than usual

to 2 hours less than usual
Up to 3 hours less than usual
Up to 4 hours less than usual

4 or more hours less than usual

O‘U'I-bWNP-‘O
C
'U

4."

3.

104

Unusually energetic. more active than usual without expected
fatigue

Have you had more energy than usual to do things--too much
energy?

No information

No different than usual or less energetic

Slightly more energetic but of questionable significance
Little change in activity level but less fatigued than
usual

Somewhat more active than usual with little or no fatigue
Much more active than usual with little or no fatigue
Unusually active all day long with little or no fatigue

WNHO

O‘Ulb

Increase in goal-directed activity
Are you more active or involved in things compared to usual?

(What about your work. housekeeping. family. friends. sex.
hobbies. new projects or interests?)

(How much of your day has been spent in this?)

0 No information

1 No change or decrease

2 Slightly more interest or activity but of questionable
significance

3 Mild but definite increase in general activity level in
one or a few areas. e.g.. cleans house several times a
day. more productive at work

4 Moderate generalized increase in activity level involving
several areas

5 Marked increase and almost constantly involved in numerous
activities in many areas

6 Extreme. e.g.. constantly active in a variety of activi-
ties from awakening till he goes to sleep

wr—

D.

R/O

105

Grandiosity

Have you felt more self-confident than usual? As if you are a
particularly important person or that you had special talents
or abilities? What about special plans?

0 No information

1 Not at all or decreased self-esteem

2 Slight. e.g.. is more confident about himself than most
people in his circumstances but of only possible clinical
significance

3 Mild. e.g.. definitely inflated self-esteem or exaggerates
his talents somewhat out of proportion to circumstances

4 Moderate. e.g.. inflated self-esteem clearly out of

proportion to circumstances

Severe. e.g.. clear grandiose delusion

Extreme. e.g.. preoccupied with. or acts on the basis of.

grandiose delusions

GUI

Schizophrenic sx

Delusions No Yes

 

Has your imagination been playing tricks on you in any way?
Have you had any ideas that other people might not understand?

If yes. type:

Being controlled
Thought broadcasting
Thought insertion
Thought withdrawal
Persecutory

Jealousy

Guilt/Sin

Grandiose

Somatic

Hallucinations No Yes

 

Has there been anything unusual about the way things looked.
or sounded. or smelled?

Have you heard voices or other things that weren't there or
that other people couldn't hear. or seen things that were not
there?

If yes. type:
auditory
visual
olfactory
somatic

3.

106

Thought disorder. Rate each:
Impaired understandability of speech due to psychopathology

This may be due to any combination of the following: lack of
logical or meaningful connections between words. phrases. or
sentences; excessive use of incomplete sentences which is not
seen as a part of psychomotor retardation: excessive irrele-
vancies or abrupt changes in subject matter: distorted grammar
or syntax: idiosyncratic word usage: use of empty. repeti-
tious. stereotyped. or obscure phrases.

Example: "I don't quite gather. I know one right and one
left use both hands. but I can't follow the system that's
working. The idea is meant in a kind way. but it's not the
way I understand life."

0 No information

1 No impairment at all. or impairment is due to a nonpsycho-
pathological reason. e.g.. lack of education

2 Occasional instances that are of doubtful clinical sig-
nificance

3 A few definite instances of impairment but they are never
gross

4 Marked impairment in understandability due to frequent
instances when subject cannot be understood

5 Severe impairment in understandability because most of the
time it is difficult or impossible to understand what the
subject is talking about

6 Extreme impairment in understandability because almost all
of the time it is impossible to understand what the sub-
ject is talking about

 

 

107

Loosening of associations (derailment)

Repeatedly saying things in juxtaposition which lack a readily
understandable relationship or shifting idiosyncratically

from one frame of reference to another. Example: "I'm tired.
All people have eyes."

0 No information

1 Not at all--may be difficult to understand due to unneces-
sary details. little education. rambling. or other non-
pathological impediments to clear communication. or
simple flight of ideas which is completely understandable

2 Occasional instances which are of doubtful clinical
significance

3 Occasional instances of distorted or idiosyncratic speech
but little impairment in understandability

4 Frequent instances with some impairment in understandabil-
ity

5 Very frequent instances with some impairment in under-
standability

6 Most of speech is distorted so that it is almost impos-
sible to understand

Illogical thinking

Thinking in which facts are obscured. distorted or excluded

or thinking which contains clear internal contradictions or in
which one premise does not follow from another. Examples:
Patient refuses to sit on the chair because it is yellow.
Patient explains that she gave her family IBM cards she
punched in an effort to overcome communication difficulties
with them.

0 No information

1 Not at all or impairment due to alcohol. depression. etc.

2 Occasional instances which are of doubtful clinical
significance

3 Thinking is odd and somewhat illogical but not grossly

deviant

Definite defect in logical thinking

Marked defect in logical thinking

Much of his thinking is completely illogical

O‘U'lb

 

I; "

108

Poverty of speech content

Speech is adequate in amount but conveys little information
because of vagueness. talking past the point. empty repeti-
tions or use of stereotyped or obscure phrases. Example:
When asked how the patient liked the hospital. the patient
answered: "Well. er . . . not quite the same as. er . . .
don't quite know how to say it. It isn't the same being in
the hospital as. er . . . working. er . . . the job isn't
quite the same. er . . . very much the same but. of course.
it isn't exactly the same."

0 No information

1 Not at all or some other form of disturbance of thought or

speech

2 Slight. e.g.. occasional instances which are of doubtful
clinical significance

3 Mild. e.g.. definite instances

4 Moderate. e.g.. frequent instances

5 Severe. e.g.. most of remarks

6 Extreme. e.g.. typical of almost all remarks

Neologisms

Distortion of words. new words invented by the subject. or
standard words to which the subject has given new meaning.
They may he invented to designate an experience which is
outside of normal experience. e.g.: "I was accused of
midigation" (meaning that she was accused of breaking the
law).

No information
Absent

Suspected or likely
Present

WNHO

 

 

 

109

R/O Alcohol use/abuse

If two or more of the following are affirmative. question further:
What have your drinking habits been like?

Was there ever a period in your life when you drank too much?

Has anyone in your family--or anyone else--ever objected to your
drinking?

Was there ever a time when you often couldn't stop drinking when
you wanted to?

Currently has problem with alcohol:
No

Yes

Describe:

 

How much are you currently drinking? Amount:

 

Formerly had problem with alcohol:
No

Yes

Describe:

When you were drinking. how much did you drink? Amount:

F.

110

R/O Drug abuse

(Degree to which the use of some nonalcoholic substance is
excessive or compulsive. causes physical symptoms or an alteration
in mood or behavior. or interferes with performance of expected
daily routines or duties. Medically prescribed drugs are excluded
as long as the drug is medically indicated and the intake is
proportionate to the medical need.)

Have you ever taken anything on your own for sleeping. or your
mood. or to get high--like Dexedrine. Seconal. or some other
barbiturate?

Have you ever used marijuana. narcotics. LSD. or things like
that?

(Have you used anything else to get high. lose weight. or stay
awake?)

(Have you ever wanted to stop taking drugs. but couldn't?)

0
l
2

No information or unclear if present

Not at all

Clinically insignificant. e.g.. occasional use of marijuana. or
amphetamines to stay awake

Some minor interference with normal functioning or cannot
feel good without use of drug

Drug use results in important modifications in his life. or
often takes an addicting drug. or has withdrawal symptoms
Drug use results in major changes in his life or frequently
takes an addicting drug (e.g.. hospitalized because of drug
use)

Drug use results in major disruption in his life (e.g.. major
activities revolve around getting drugs)

Note type(s) of drug(s)

I I

I I

Narcotics (e.g.. Heroin. Morphine. Demerol. Codeine. and other
synthetic narcotics)

Amphetamine-like substances (e.g.. Dexedrine. Preludin. Speed.
Methamphetamine)

Cocaine

Sedatives. Hypnotics. Tranquilizers (e.g.. Seconal. Quaalude.
Valium. Equanil)

Cannabis derivatives (e.g.. Marijuana. Hashish. Hashish Oil.
THC)

Hallucinogens (e.g.. LSD. mescaline. psilocybin)

Solvents (e.g.. glue)

 

 

 

APPENDIX C

Appendix C

Data Collection Instruments

REITAN-INDIANA APHASIA SCREENING TEST
Form for Adult: and Older Children

Name: Age: Date: _.____ Examiner:

 

 

 

 

 

Copy SQUARE

Repeat TRIANGLE

 

Name SQUARE

Repeat MASSACHUSETTS

 

 

 

 

Spell SQUARE Repeat METHODIST EPISCOPAL
Copy CROSS Write SQUARE

Name CROSS Read SEVEN

Spell CROSS Repeat SEVEN

 

Copy TRIANGLE

Repeat/Explain HE SHOUTED THE WARNING.

 

Name TRIANGLE

Write HE SHOUTED THE WARNING.

 

SpeII TRIANGLE

Compute 85 - 27 =

 

 

 

 

 

 

 

 

Name BABY Compute 17 x 3 -

Write CLOCK Name KEY

Name FORK Demonstrate use oI KEY

Read 7 SIX 2 Draw KEY

Read MGW Read PLACE LEFT HAND TO RIGHT EAR.
Reading I Place LEFT HAND TO RIGHT EAR
Reading II Place LEFT HAND TO LEFT ELBOW

 

 

111

 

 

 

112

 

Date

 

BECK INVENTORY

Instructions: This questionaire contains groups of
statements. Please read each group of statements carefully.
Then pick out the one statement in each group which best
describes the way you have been feeling during the past
week, including today. Circle the number beside the
statement you have chosen.

 

Be sure to read all the statements in each group ,
before making your choice. '

 

 

 

1. O I do not feel sad.
1 I feel sad.
2 I am sad all the time and I can't snap out of it.
3 I am so sad or unhappy that I can't stand it.

2. O I am not particularly discouraged about the future.
1 I feel discouraged about the future.
2 I feel I have nothing to look forward to.
3 I feel the future is hopeless and that things

cannot improve.

3. O I do not feel like a failure
1 I feel I have failed more than the average person.
2 As I look back on my life, all I can see is a lot
3 I feel I am a complete failure as a person.

 

4. O I get as much satisfaction out of things as I used
to.
1 I don't enjoy things the way I used to.
2 I don't get real satisfaction out of anything
anymore.
I am dissatisfied or bored with everything.

 

 

5. O I don't feel particularly guilty.
1 I feel guilty a good part of the time.
2 I feel quite guilty most of the time.
3 I feel guilty all of the time

6. don't feel I am being punished.

feel I may be punished.
expect to be punished.
feel I am being punished.

“NI-‘0
HHHH

WMHO

 

113

don't feel disappointed in myself.
am disappointed in myself.

am disgusted with myself.

hate myself.

HHHH

 

UN HO

I don't feel I am any worse than anyone else.

I am critical of myself for my weaknesses or
faults.

I blame myself all the time for my faults.

I blame myself for everything had that happens.

 

HO

(AN

 

I don't have thoughts of killing myself.

I have thoughts of killing myself, but I would not
carry them out.

I would like to kill myself.

I would kill myself if I had the chance.

 

10.

UNI-‘0

I don't cry any more than usual.
I cry more than I used to.

I cry all the time now.
I used to be able to cry, but now I can't cry even
though I want to.

 

11.

HO

MN

I am no more irritated now than I ever am.

I get annoyed or irritated more easily than I used
to.

I feel irritated all the time now.

I don't get irritated at all by the things that
used to irritate me.

 

12.

HO

(AN

1 have not lost interest in other people.

I am less interested in other people than I used to
be.

I have lost most of my interest in other people.

I have lost all of my interest in other people.

 

13.

w NHO

I make decisions about as well as I ever could.

I put off making decisions more than I used to.

I have greater difficulty in making decisions than
before.

I can't make decisions at all anymore.

 

14.

U NHO

I don't feel I look worse than I used to.

I am worried that I am looking old or unattractive.
I feel that there are permanent changes in my
apperance that make me look unattractive.

I believe that I look ugly

15.

UN H0

114

I can work about as well as I used to.

It takes an extra effort to get started at doing
something.

I have to push myself very hard to do anything.
I can't do any work at all.

 

16.

U NHO

I can sleep as well as usual.

I don't sleep as well as I used to.

I wake up 1-2 hours earlier than usual and find it
hard to get back to sleep.

I wake up several hours earlier than I used to and
cannot get back to sleep.

 

17.

WMHO

I don't get more tired than usual.

I get tired more easily than I used to.
I get tired from doing almost nothing.
I am too tired to do anything.

 

18.

UNI-‘0

My appetite is no worse than usual.

My appetite is not as good as it used to be.
My appetite is much worse now.

I have no appetite at all anymore.

 

l9.

WHO-‘0

haven't lost much weight, if any, lately.
have lost more than 5 pounds.

have lost more than 10 pounds.

have lost more than 15 pounds.

HHHH

 

20.

HO

(AM

I am no more worried about my health than usual.

I am worried about physical problems such as aches
and pain or upset stomach or constipation.

I am very much worried about my physical problems

and it's hard to think of much else.

I am so worried about my physical problems that I

cannot think about anything else.

 

21.

“NH O

I have noticed any recent change in my interest in
sex.

I am much less interested in sex than I used to be.
I am much interested in sex now.

I have lost interest in sex completely.

 

22.

I am purposely trying to lose weight by eating less:

YES l'lO

 

115

 

Date

GOD'S.

 

(:hoose the best answer for how you felt over the past week.

1.
2.

:3.
43.
£5-
(5

1.23 -
1.4; -

1.55
1-(3
1.17

1~E3
1.S3

22(3‘.

Are you basically satisfied with your life?

Have you dropped many of your activities and
interests

Do you feel that your life is empty?
Do you often get bored?
Are you hOpeful about the future

Are you bothered by thoughts you can't get out
of your head?

Are you in good spirits most of the time?

Are you afraid that something bad is going to
happen to you?

Do you feel happy most of the time?
Do you often feel helpless?
Do you often get restless and fidgety?

Do you prefer to stay at home, rather than
going out and doing new things?

Do you frequently worry about the future?

Do you feel you have more problems with memory
than most?

Do you think it is wonderful to be alive now?
Do you often feel downhearted and blue?

Do you feel pretty worthless the way you are
now?

Do you worry a lot about the past?
Do you find life very exciting?

Is it hard for you to get started on new
projects?

yes/no

yes/no

yes/no
yes/no

yes/no

yes/no

yes/no

yes/no
yes/no
yes/no

yes/no

yes/no

yes/no

yes/no
yes/no

yes/no

yes/no
yes/no

yes/no

yes/no

 

.21.
122.
I23.

24.
25.
26.
27.
28.
29.
30.

Do
Do

Do

116

you feel full of energy?
you feel that your situation is hopeless?

you think that most people are better off

than you are?

Do
Do
Do
Do
Do
Is

18

you frequently get upset over little things?
you frequently feel like crying?

you have trouble concentrating?

you enjoy getting up in the morning?

you prefer to avoid social gatherings?

it easy for you to make decisions?

your mind as clear as it used to be?

yes/no

yes/no

yes/no
yes/no
yes/no
yes/no
yes/no
yes/no
yes/no

yes/no

 

1.

3.

4.

117

#

 

 

DATE

 

SELF RATING SCALE 0F I‘IEI’IORY FUNCTION

HOW WOULD YOU RATE YOUR MEMORY 1N TERMS OF THE KINDS OF PROBLEMS
YOU HAVE HITH IT: (CIRCLE ONE)
-4 -3 -2 -1 0 +1 +2 +3 +4
major problems some minor problems no problems
How Is YOUR MEMORY COMPARED TO THE HAY IT HAS: (CIRCLE ONE)
A. 1 MONTH AGO
-4 -3 -2 -1 0 +1 +2 +3 +4
much worse same much better
B. 1 YEAR AGO
-4 -3 -2 -1 0 +1 +2 +3 +4
much worse same much better
C. 5 YEARS AGO
-4 -3 -2 -1 0 +1 +2 +3 +4
much worse same much better
I). 10 YEARS A60
-4 -3 -2 -1 0 +1 +2 +3 +4
much worse same much better
E. 20 YEARS A60
-4 -3 -2 -1 0 +1 +2 +3 +4
much worse same much better
F3. HHEN YOU HERE 18
-4 -3 -2 -1 0 +1 +2 +3 +4
much worse same much better
F1Nf ABILITY TO SEARCH THROUGH MY MIND AND RECALL NAMES OR MEMORIES

I KNOW ARE THERE Is:(CIRCLE ONE)

-4 -3 -2 -1 0 +1 +2 *3 *‘
worse than about the same better than
ever before ever before

g THINK MY RELATIVES AND ACOUAINTANCES How JUDGE MY MEMORY TO BE:
c l RCLE ONE)

-4 -3 -2 -1 0 +1 +2 +3 +4
worse than about the same better than
ever before ever before

 

118

sel f Rating Scale of Memory Function Page 2

5 . MY ABILITY TO RECALL THINGS HHEN I REALLY TRY IS: (CIRCLE ONE)

-4 -3 -2 -1 0 +1 +2 +3 +4
worse than about the same better than
ever before ever before

6 . MY ABILITY TO HOLD IN MY MEMORY THINGS THAT I HAVE LEARNED IS:
(CIRCLE ONE)

-4 -3 -2 -1 0 +1 +2 +3 +4
worse than about the same better than
ever before ’ ever before

 

7 0 IF I WERE ASKED ABOUT T A MONTH FROM NON; MY ABI ITY TO REM MBER
FACTS ABOUT THIS FORM AM FILLING OUT WOULD BE: CIRCLE ONE

-4 -3 -2 -1 0 +1 +2 +3 +4
worse than about the same better than
ever before ever before

8 . THE TENDENCY FOR A PAST MEMORY TO BE "ON THE TIP OF MY TONGUE" BUT
NOT AVAILABLE TO ME 15: (CIRCLE ONE)

-4 -3 -2 -1 0 +1 +2 +3 +4

worse than about the same better than

ever before ever before

9. MY ABILITY TO RECALL THINGS THAT HAPPENED A LONG TIME AGO IS:
(CIRCLE ONE)

-4 -3 -2 -1 0 +1 +2 +3 +4

worse than about the same better than

ever before ever before

II). Q?\r ABILITY To REMEMBER THE NAMES AND FACES OF PEOPLE I MEET IS:

(:IRCLE ONE

-4 -3 -2 -1 0 +1 +2 +3 +4

worse than about the same better than

ever before ever before

11. MY ABILITY TO REMEMBER HHAT I HAS DOING AFTER I HAVE TAKEN MY MIND
OFF IT FOR A FEW MINUTES IS: (CIRCLE ONE)

-4 -3 -2 -I 0 +1 +2 +3 +4
worse than about the same better than
ever before ever before

 

119

Se! f Rating ScaIe of Memory Function Page 3

a "Y WAPSLIIYT TO REMEMDER THINGS THAT HAVE HAPPENED MORE THAN A YEAR
CIR ONE

CLE
-4 -3 -2 -1 0 +1 +2 +3 +4
worse than about the same better than
ever before ever before

13 . MY ABILITY NON TO REMEMBER HHAT I READ AND HHAT I HATCH ON TELE~
- VISION IS: (CIRCLE ONE)

-4 -3 -2 -1 ‘0 +1 +2 +3 +4
worse than about the same better than
ever before ever before

ll} . MY ABILITY To RECALL THINGS THAT HAPPENED DURING MY CHILDHOOD Is:
(CIRCLE ONE)

-4 -3 -2 -l 0 +1 +2 +3 +4
worse than about the same better than
ever before ever before

1'5 . MY ABILITY To KNOH HHEN THE THINGS I AM PAYING ATTENTION TO ARE
GOING TO STICK IN MY MEMORY Is: (CIRCLE ONE)

-4 -3 -2 -I 0 +1 +2 +3 +4
worse than about the same better than
ever before ever before

16 . MY ABILITY TO MAKE SENSE OUT OF HHAT PEOPLE EXPLAIN TO ME IS:
(CIRCLE ONE)

-4 -3 -2 -1 0 +1 +2 +3 '+4
worse than about the same better than
ever before ever before

170 MY ABILITY TO REACH ACK IN MY SIEMORY AND RECALL WHAT HAPPENED A
FEW MINUTES A60 18: CIRCLE ONE

-4 -3 -2 -1 0 +1 +2 +3 +4
worse than about the same better than
ever before ever before

18 - (MY ABILITY TO PAY ATTENTION TO HHAT GOES ON AROUND ME Is: (CIRCLE

NE)
-4 -3 -2 -1 0 . +1 +2 +3 +4
worse than about the same better than
ever before ever before

 

120

SeTf Rating Scale of Memory Function Page 4

19. MY GENERAL ALERTNESS TO THINGS HAPPENING AROUND ME IS: (CIRCLE ONE)

-4 -3 -2 -I 0 +1 +2 +3 +4
worse than about the same better than
ever before ever before

20. MY ABILITY TO POLLOH HHAT PEOPLE ARE SAYING IS: (CIRCLE ONE)

-4 -3 -2 -1 0 +1 +2 +3 +4
worse than about the same better than
ever before , ever before

-8

eofloreyvr

i

. Winter

. Breakfast
. Fabric

. SIBce

. Assemble
. Conceai
. Enormous
. Hasten

. Sentence

. Commence

. Ponder

. Cavern

. Domestic

. Consume

. Terminate
. Obstruci

. Remorse

. Matchless
. Reluctant

. Fortitude
. T
. Edifice

121

‘- VOCAIULARY

 

Date

 

I’

 

Circle

 

 

 

 

 

SCORE

"

 

 

 

 

 

 

 

 

DI GIT SPAN

6-4-3-9
7.2-8-6

 

 

 

 

[Digits Forward

5-8-2
6-9-4

I

DigIts Outward
5+3-9-4-I-U
7.2.4.8 0506

 

 

 

 

Date:

 

 

 

122

 

 

 

BUSCHKE SELECTIVE REMINDING PROCEDURE

 

 

 

 

 

 

 

 

CUP
JOIN
LARK
NEEDLE
VEST
MINNOW
FAULT

 

KETTLE

 

 

 

 

 

 

 

DOOR
SAID
RUMOR
BEFORE
GROWN
PAGE
THUNDER

NLY

 

 

 

 

 

um

 

123

FEELING OE KNOWING
GENERAL INFORMATION QUESTIONS

1. What is the name of the horse-like animal with black and
white stripes? (Zebra)

2. What is the name of the crime in which a building or
property is purposely set on fire? (Arson)

3. What is the name for a medical doctor who specializes in
cutting the body? (Surgeon)

 

4. What is the last name of the man who was the voice of Mr.
Magoo? (Backus)

5. What was the name of Tarzan's girlfriend? (Jane)

6. What is the last name of the first person to set foot on
the moon? (Armstrong)

7. What is the name of the largest desert on Earth? (Sahara)
8. What is the name of Batman's butler? (Alfred)

9. What is the substance derived from a whale that is used
to make perfume? (Ambergris)

10. Who is known as the “Father of Geometry"? (Euclid)

11. What is the last name of the author who wrote “Oliver
Twist”? (Dickens)

12. What kind of a metal is associated with a 50th wedding
anniversary? (Gold)

13. Which game uses a doubling cube? (Backgammon)
14. What is the capitol of Canada? (Ottowa)

15. What is the last name of the doctor who first developed
a vaccine against polio? (Salk)

16. What is the name of deer meat? (Venison)

17. What is the last name of the criminal who was known as
“Scarface”? (Capone)

18. What is the unit of sound intensity? (Decibel)

19. What is the palace built in France by King Louis XIV?
(Versailles)

20. What is the last name of the man who rode horseback in
1775 to warn that the British were coming (Revere)

21.

22.

23.

24.

25.

26.

27.

'28.

29.

30.
31.

32.

33.

34.
35.

36.
37.

38.

39.

124

Over which river is the George Washington Bridge?
(Hudson)

What is the name of the unit of measure that refers to a
six-foot depth of water? (Fathom)

What is name of the zeppelin that exploded in Lakehurst,
N.J. in 1937? (Hindenberg)

What is the name of an airplane without an engine?
(Glider)

What is the last name of the boxer who was known as the
'Manassa Mauler”? (Dempsey) '

What is the last name of the first person to climb Mount
Everest? (Hillary)

What is the last name of the judge who was known as the
”Law West of the Pecos"? (Bean)

What is the name of the desert people who wander instead
of living in one place? (Nomads)

What is the name of Germany's largest battleship that
was sunk in World War II? (Bismark)

Who was the leader of the Argonauts? (Jason)

What is the last name of the first person to complete a
solo flight across the Atlantic Ocean? (Lindbergh)

In which game are the standard pieces of Staunton
design? (Chess)

What is the name for a cyclone that occurs over land?
(Tornado)

What was the last name of Buffalo Bill? (Cody)

What is the last name of the woman who founded the
American Red Cross? (Barton)

What was Frank Lloyd Wright's profession? (Architect)

What is the last name of the singer who recorded
"Heartbreak Hotel" and "All Shook Up"? (Presley)

What is the last name of the pilot of the U-22 spy plane
shot down over Russia in 1960? (Powers)

What is the name of the mountain range in which Mount
Everest is located? (Himalayas)

 

_L.a_.__e n-

 

40.

41.

42.

43.

44.
45.

46.

47.
48.

49.

SO.

51.
52.

53.

54.

55.

56.

57.

58.

125

What is the name of the chapel whose ceiling was painted
by Michelangelo? (Sistine)

What is the last name of the man who is regarded as the
national poet of Scotland? (Burns)

In addition to the Kentucky Derby and the Belmont
Stakes, what horse race is included in the Triple Crown?
(Preakness)

In what ancient city were the “hanging gardens“ located?
(Babylon)

What are people who make maps called? (Cartographers)

What island is the largest in the world, excluding
Australia? (Greenland)

What is the last name of the actor who played Rhett
Butler in ”Gone with the Wind? (Gable)

What is the name of the collar bone? (Clavicle)

What is the last name of the first woman to swim across
the English Channel? (Ederle)

What is the name of the rubber roller on a typewriter?
(Platen)

Which game uses a rubber ball and little metal pieces?
(Jacks)

Who was the most famous Greek doctor (Hippocrates)

What was the name of the clown on the “Howdy Doody'
television show? (Clarabell)

What is the proper name for a badminton bird?
(Shuttlecock)

What was the last name of the character portrayed by
Robert Stack on the television show “The Untouchables“?
(Ness)

What is the longest river in South America? (Amazon)

What is the last name of the most popular pin-up girl of
World War II? (Grable)

What is the name of the constellation that looks like a
flying horse? (Pegasus)

What breed of cat has blue eyes? (Siamese)

 

59.
60.

61.

62.
63.

64.

65.

66.

67.
68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

126

What is the capitol of Denmark? (Copenhagen)

What is the name of the extinct reptiles known as
”terrible lizards"? (Dinosaurs)

What is the last name of the author who wrote I'Brave New
World?” (Huxley)

What is the name of a dried grape? (Raisin)

What is the last name of the man who wrote the 'Star
Spangled Banner?” (Key)

What is the last name of the mythical giant lumberjack?
(Bunyon)

What is the last name of the author who wrote "The Old
Man and the Sea"? (Hemmingway)

What is the name of the hillbilly family that had a
famous feud with the McCoy family? (Hatfield)

What is the name of a young sheep? (Lamb)

Of which country is Buenos Aires the capitol?
(Argentina)

What was the last name of the actor in the role of Perry
Mason on television? (Burr)

What is the name of the furry animal that attacks cobra
snakes? (Mongoose)

What is the name of the island on which Napoleon was
born? (Corsica)

What is the name of the man who removed the thorn from
the lion's paw in the story from Aesop's fables?
(Androcles)

What is the name of the navigation instrument used at
sea to plot position by the stars? (Sextant

What is the last name of the Cuban leader that Castro
overthrew? (Batista)

What was the name of the largest Confederate military
prison during the Civil War? (Andersonville)

What is the last name of the boxer who won the boxing
title from John Sullivan? (Corbett)

What is the longest river in Asia? (Yangtze)

78.

79.
80.

81.

82.
83.

84.

85.

86.

87.

88.

89.

90.

91.
92.

93.

94.

95.

 

127

What is the last name of the first man to run the mile
in under four minutes? (Bannister)

What is the capitol of Australia? (Canberra)

What is the last name of the poet who wrote the line
'Into each life a little rain must fall"? (Longfellow)

What is the last name of the first flier to fly solo
round the world? (Post)

Which planet was the last to be discovered? (Pluto)

 

What is the last name of the movie actor who portrayed
Spartacus? (Douglas)

What was the name of the Appolo lunar module that landed
the first man on the Moon? (Eagle)

What is the name of the baseball player with the highest
lifetime batting average in the major leagues? (Cobb)

What is the last name of the author of “The Agony and
the Ecstasy"? (Stone)

What is the last name of the man who was most
responsible for photographing the 0.5. Civil War?
(Brody)

What is the last name of the man who supposedly killed
Jesse James? (Ford)

What is the last name of the composer of the "Maple Leaf
Rag"? (Joplin)

What is the last name of the European author who wrote
"The Trial"? (Kafka)

In which country is Angel Falls located? (Venezuela)

What is the last name of the man who wrote the song “How
Deep is the Ocean”? (Berlin)

What is the last name of the man who wrote the poem 'It
Couldn't be Done”? (Guest)

Who was the Racehorse of the Year for many successive
years in the 1960's? (Kelso)

What was the last name of the astronomer who published
in 1543 his theory that the Earth revolves around the
Sun? (Copernicus)

128

96. What is the name of the avenue that immediately follows
Atlantic Avenue in the game of Monopoly? (Ventnor)

97. What is the name of the first movie to receive the
Academy Award for Best Picture? (Wings)

98. What is the last name of the boy in the book 'Treasure
Island?'(Hawkins)

99. The deepest part of the ocean is located at which
trench? (Mariana)

100. What is the name of a number two wood in golf?
(Brassie)

ffifiwii

T ...'-
I

LIST OF REFERENCES

Albert, M.L. (1978). Subcortical dementia. In R. Katzman,
R.D. Terry, & K.L. Bick (Eds.), Alzheimer's Disease: Senile
Dementia and Related Disorders. New York: Raven Press.

 

Albert, M.L. (1984). The Controversy of Subcortical
Dementia. Neurology and Neurosurgery, Update Series, 5. New
Jersey: Continuing Professional Education Center, Inc.

Albert, M.L., Feldman, R.G., & Willis, A.L. (1974). The
"subcortical dementia of progressive supranuclear palsy.
Journal of Neurology, Neurosurgery g Psychiatry,37, 121-130.

 

 

Albert, M.S. (1981). Geriatric neuropsychology. Journal of
Consulting and Clinical Psychology, 42, 835-850.

Anderson, J. Aabro, E., Gulmann, N., Hjelmstead, A. &
Pederson, H.E. (1980). Anti-depressant treatment in
Parkinson's disease: A controlled trial of the effect of
nortriptyline in patients with Parkinson's disease treated
with L-DOPA. Acta Neurologica Scandinavica, 63, 210-219.

 

Asnis, G. (1977). Parkinson's disease, depression and ECT: A
review and case study. American Journal 9: Psychiatry, 134,

 

 

Backlund, E.O., Graanberg, P.O., Hamberger, B., Knutsson,
E., Martensson, A., Sedvall, G., Seiger, A. & Olsen, L.
(1985). Transplantatiion of adrenal medullary tissue to
striatum in parkinsonism - First clinical trials. Journal of
Neurosurgery, 62, 169-173.

 

Ball, M.J. (1984). The morphological basis of dementia in
Parkinson's disease. The Canadian Journal of Neurological
Sciences, 11, 180-184.

 

 

 

Beck, A.T., Ward, C.H., Mendelson, M., Mock, J.E., &
Erbaugh, J. (1961). An inventory for measuring depression.
Archives 9: General Psychiatry, 4, 561-571.

 

Beck, A.T. (1967). Depression. New York: Harper & Rowe.

 

Beck, A.T. (1971). Depression: Clinical, Experimental and
Theoretical Aspects. New York: Paul B. Hoeber.

 

 

 

Boller, F., Mizutani, T. Roessman, R., & Gambetti, P.
(1980). Parkinson disease, dementia and Alzheimer disease:
Clinicopathological correlations. Annals of Neurology, 1,
329-335. 129

 

I

130

Botwinick, J. (1977). Intellectual abilities. In J.E.
Birren & K.W. Schaie (Eds.), Handbook 9: the Psychology gf
Aging. New York: Van Nostrand.

 

 

Bowen, F.P. (1976). Behavioral alterations in patients
with basal ganglia lesions. In M.D. Yahr (Ed.), The Basal
Ganglia. New York: Raven Press.

 

Brandt, J., Mower, P. (February, 1985). Searching for old
memories 1g Alzheimer's and Huntington's dementia. Paper
presented at the International Neuropsychological Society
meeting, San Diego, Ca.

 

 

Brown, G.L., & Wilson, W. P. (1972). Parkinsonism and
depression. Southern Medical Journal, gg, 540-545.

 

Brown, R.G., Marsden, C.D., Quinn, N, & Wyke, M.A. (1984).
Alterations in cognitive performance and affect-arousal
state during fluctuations in motor function in Parkinson's
disease. Journal 2: Neurology, Neurosurgery, and Psychiatry,
31, 454-465.

- ____f__
_ . .~. In. .u. ._.' .._
t

Buschke, H. (1973). Selective reminding of memory and
learning. Journal gf Verbal Learning and Verbal Behavior,
13, 543-550.

Caine, E.D. (1981). Pseudodementia: Current concepts and
future directions. Archives 2: General Psychiatry, 38,
1359-1364.

 

Caine, E.D., Ebert, M.H. & Weingartner, H. (1977). An
outline for the analysis of dementia: The memory disorder of
Huntington's disease. Neurology, 31, 1087-1092.

 

Celesia, G.G., & Barr, A.N. (1970). Psychosis and other
psychiatric manifestatiions of levodopa therapy. Archives 9f
Neurology, 23, 193-200.

 

Celesia, G.G., & Wanamaker, W.M. (1972) Psychiatric
disturbances in Parkinson's disease. Diseases 2: the
Nervous System, 33, 577-583.

 

Cohen, R., & Lazarus, R.C. (1973). Active coping processes,
coping disposition and recovery from surgery. Psychosomatic
Medicine, 35, 375-389.

 

 

Cohen, R.M., Weingartner, H., Smallberg, S.A. Pickar, D.,
Murphy, D.L. (1982). Effort and cognition in depression.
Archives 9: General Psychiatry, 32, 593.

Cronholm, B., & Ottoson, J.O. (1961). Memory functions in
endogenous depression. Archives 9: General Psychiatry, 5,
193.

 

131

Cummings, J.L., & Benson, D. (1984). Subcortical dementia:
Review of an emerging concept. Archives g: Neurology, 51,
874-879.

Dakof, G.A. & Mendelsohn, G.A. (1986). Parkinson's disease:
The psychological aspects of a chronic illness.
Psychological Bulletin, 22, 375-387.

Damasio, A.R., Lobo-Antunes, J., & Macedo, C. (1970). L-
DOPA, parkinsonism and depression. Lancet, 2, 611-612.

Danielczyk, W. (1983). Various mental behavioral disorders
in Parkinson's disease, primary degenerative senile
dementia, and multiple infarction dementia. Journal gf
Neural Transmission, gg, 161-176.

Delis, D.C., Levin, B.E., & Kramer, J.H. (February, 1987).
Verbal learning and memory deficits in Parkinson disease.

Paper presented at the meeting of the International .
Neuropsychological Society, Washington, D.C. !

 

Dessonville, C., Gallagher, D., Thompson, L., & Finnel, K.
(August, 1980). Depressive symptomatology ig normal and
depressed elderly. Paper presented at the American
Psychological Association meeting, Montreal, Canada.

 

 

 

Duvoisin, R.C. (1984). Parkinson's disease: A guide for
patient and family (2nd ed.). New York: Raven Press.

 

 

 

Duvoisin, R.C.m Eldridge, R., Williams, A., Nutt, J., &
Calne, D. (1981). Twin study of Parkinson disease.
Neurology, 31,77-80.

 

Eadie, M.J. & Sutherland, J.M. (1964). Arteriosclerosis in
parkinsonism. Journal 9: Neurology, Neurosurgery 3
Psychiatry, 21, 237-240.

 

 

Endicott, J., & Spitzer, R.L. (1978). A diagnostic
interview: The schedule for affective disorders and
schiZOphrenia. Archives 9: General Psychiatry, 35, 837-844.

 

Fibiger, H.C. (1984). The neurobiological substrates of
depression in Parkinson's disease: A hypothesis. The
Canadian Journal gf Neurological Sciences, 11, 105-107.

 

 

Gainotti, G., Caltagirone, C., Masullo, C., & Miceli, G.
(1980). Patterns of neuropsychologic impairment in various
diagnostic groups of dementia. In L. Amaducci, A.N. Davison
& P. Antuono (Eds.), Aging 9: the Brain and Dementia. New
York: Raven Press.

Garron, D.C. Klawans, H. L., & Narin, F. (1972). Intellec-
tual functioning of persons with idiopathic parkinsonism.
Journal g: Nervous 3 Mental Disease, 154, 445-452.

 

132

Gass, C.S., & Russell, E.W. (1986). Differential impact of
brain damage and depression on memory test performance.
Journal 9: Consulting and Clinicl Psychology, 53, 261-263.

Gilewski, M.J., & Zelinski, E.M. (1983). Memory complaint
and mood in the elderly: A new wrinkle. Unpublished
manuscript.

Gilewski, M.J. & Zelinski, E.M. (1986) Questionnaire
assessment of memory complaints. In L.W. Poon (Ed.),
Handbook for Clinical Memory Assessment 95 Older Adults,
(pp.93-107). Hyattsville, Md: American Psychological
Association.

 

Hakim. A.M. & Mathieson, G. (1979). Dementia in Parkinson's
disese: A neuropathologic study. Neurology, 35, 1209-1214.

 

Halstead, W.C., & Wepman, J.M. (1959). The Halstead-Wepman
aphasia screening test. Journal 95 Speech and Heaaring

‘E‘“"*“‘~"“‘.i‘]

 

 

Hart, J.T. (1965). Memory and the feeling-of-knowing
experience. Journal 95 Educational Psychology, 55, 208-216.

 

Hoehn, M.M., Crowley, T.J., & Rutledge, C.O. (1976).
Dopamine correlates of neurological and psychological status
in untreated parkinsonism. Journal pf Neurology,
Neurosurgery 5 Psychiatry, 55, 941-951.

 

 

 

Hoehn, M.M., Yahr, M.D. (1967). Parkinsonism: Onset,
progression and mortality. Neurology, 51, 427-442.

 

Horn, 8. (1974). Some psychological factors in parkinsonism.
Journal 9; Neurology Neurosurgery 5 Psychiatry, 51, 27-31.

 

 

Javoy-Agid, F. & Agid, Y. (1980). Is the mesocortical
dopaminergic system involved in Parkinson's disease?
Neurology, 59, 1326-1330.

 

Jenkins, R.B., & Groh, R.H. (1970) Mental symptoms in
parkinsonian patients treated with L-Dopa. Lancet, g, 177-
180.

Kahn, R.L., Zarit, S.H., Hilbert, N.M., & Niederehe, G.
(1975). Memory complaint and impairment in the aged.
Archives pf General Psychiatry, 5;, 1569-1573.

 

Klawans, H.L. (1968). The pharmacology of parkinsonism.
Diseases 95 the Nervous System, 35, 805-816.

Kobasa, S.C., Maddi, S.R., Courington, S. (1981).
Personality and constitution as mediators in the stress-
illness relationship. Journal 95 Health and Social Behavior,
33, 368-378.

 

 

133

Lachman, J.L., & Lachman, R. (1980) Age and the
actualization of world knowledge. In L.W., Poon, J.L.
Fozard, L.S. Cermak, D. Arenberg, L.W. Thompson (Eds.), 999
Directions 59 Memory and Agipg: Proceedings 9: the George 59
Talland Memorial Conference. Hillsdale, NJ: Lawrence Erlbaum
Associates.

 

Lachman,J.L., Lachman, R., & Thronesbery, C. (1979).
Metamemory through the adult life span. Developmental
Psychologyy 55, 5443-551.

 

Larrabee, G.J. (February, 1985). Memory Self-ratings and
Objective Test Performance 59 9 Normal Elderly Sample.
Paper presented at the International NeurOpsychological
Meeting, San Diego, Ca.

Larrabee, G.J., Trahan, D.E., & Levin, H.S. (1986) Normative
Data for the Verbal Selective Reminding Test. Paper
presented at the International NeurOpsychological Meeting,
Denver, Co.

Lebensohn, Z.M., & Jenkins, R.B. (1975). Improvement of
parkinsonism in depressed patients treated with ECT.
American Journal 99 Psychiatry, 132, 283-285.

 

 

Lees, A.J., & Smith. E. (1983). Cognitive deficits in the
early stages of Parkinson's disese. Brain, 106, 257-270.

 

Levin, B.E., Rodriguez, M.L., Llabre, M., & Weiner, W.J
(February, 1985). Cognitive and affective changes in early
Parkinson's disease. Paper presented at the meeting of the
International Neuropsychological Society, Denver, Co.

Lezak, M.D. (1983). Neuropsychological Assessment (2nd ed.).
New York: Oxford University Press

 

Lishman, W.A. (1978). Organic Psychiatry: The Psychological

 

 

Consequences 99 Cerebral Disorder. Oxford, England:
Blackwell Scientific Publications.

 

 

Loranger, A., Goodell, H. McDowell, F.H., Lee, J.E., &
Sweet, R.D. (1972). Intellectual impairment in Parkinson's
syndrome. Brain, 95, 405-412.

Loring, D.W., & Papanicolaou, A.C. (1987). Memory assessment
in neuropsychology: Theoretical considerations and practical
utility. Journal 9: Clinical and Experimental
Neuropsychology, 5, 340-358.

 

 

Machover, S. (1957) Rorschach study on the nature and origin
of common factors in the personalities of parkinsonians.
Psychosomatic Medicine, 59, 332-338.

 

134

Madrazo, I, Drucker-Colin, R., Diaz, V., Martinez-Mata, J.,
Torres, C., Becerril, J.J. (1987). Open microsurgical
autograft of adrenal medulla to the right caudate nucleus in
two patients with intractaable Parkinson's disease. 599
England Journal 99 Medicine, 99, 83-834.

 

 

Marsh, G.G., Markham, C.M., & Ansel, R. (1971). Levodopa's
awakening effect on patients with parkinsonism. Journal 99
Neurology, Neurosurgery 9 Psychiatry, 59, 209-218.

 

 

Martin, W.E., Loewenson, R.B., Resch, J.A., Baker, A.B.
(1973). Parkinson's disease: A clinical analysis of 100
patients. Neurology, 23, 783-790.

 

Matison, R., Mayeux, R., Rosen, J., & Fahn, S. (1982). "Tip
of the tongue" phenomenon in Parkinson disease. Neurology”,

 

3;, 567-570.

Matthews, G.G., & Haaland, K.Y. (1979). The effects of
symptom duration on cognitive and motor performance in
parkinsonism. Neurology, 55, 951-956.

 

Mayeux, R., Stern, Y., Rosen, J., & Benson, F. (1983). Is
"subcortical dementia" a recognizable clinical entity?
Annals 99 Neurology, 99, 278-283.

 

Mayeux, R., Stern, Y., Rosen, J., & Leventhal, J. (1981).
Depression, intellectual impairment and Parkinson disease.
Neurology, 59, 645-650.

 

Mayeux, R., Williams, J.B.W., Stern, Y., & Cote, L. (1984).
Depression and Parkinson's disease. Advances 99 Neurology,
95, 241-251.

 

Mayeux, R., Stern, Y, Cote, L., & Williams, J.E. (1984).
Altered serotonin metabolism in depressed patients with
Parkinson's disease. Neurology, 59, 642-646.

 

McHugh, P.R., & Folstein, M.F. (1979). Psychopathology of
dementia: Implications for neuropathology. In R. Katzman
(Ed.), Congeniatl and Acquired Cognitive Defects. New York:
Raven Press.

 

Mindham, H.S. (1970) Psychiatric aspects of Parkinson
disease. Journal 99 Neurology, Neurosurgery and Psychiatry,

 

39, 188-191.

Mindham, R.H.S., Marsden, C.D., & Parkes, J.D. (1976).
Psychiatric symptoms during L-DOPA therapy for Parkinson's
disease and their relationship to physical disability.
Psychological Medicine, 5, 23-33.

 

Mintz, J., Steuer, J. & Jarvik, L. (1981). Psychotherapy
with depressed elderly patients: Research considerations.
Journal 99 Consulting and Clinical Psychology, 95, 542-548.

135

Mortimer, J.A., Kuskowski, M.A., Pirozzolo, F.J., & Webster,
D.D. (1986). Prevalence and age distribution of intellectual
deficits in Parkinson's disease. Paper presented at the
meeting of the International Neuropsychological Society,
Denver, Co.

Mortimer, J.A., Pirozzolo, F.J., Hansch, E.C., & Webster,
D.D. (1982). Relationship of motor symptoms to intellectual
deficits in Parkinson disease. Neurology, 55, 133-137.

Mortimer, J.A., Warrior, A.S., Jun, S.P., Kuskowski, M.A., &
Webster, D.D. (July, 1987) Depression in Parkinson's
disease: Relationship to motor signs, neurOpsychological
performance and demographic factors. Paper presented at the
meeting of the International NeurOpsychological Society,
Barcelona, Spain.

Nelson, T.O., & Narens, L. (1980). Norms of 300 general-
information questions: Accuracy of recall, latency of recall
and feeling-of-knowing ratings. Journal 99 Verbal Learning
and Verbal Behavior, 95, 338-368.

firms-

 

Newman, R.P., Weingartner, H., Smallberg, S.A., Calne, D.B.
(1984). Effortful and automatic memory: effects of dopamine.
Neurology, 59, 805-807.

 

Niederehe, G. (1986). Depression and memory impairment in
the aged. In: L.W. Poon (Ed.), Handbook for Clinical Memory
Assessment 99 Older Adults, (pp.226-237). Hyattsville, Md:
American Psychological Association.

 

 

 

Nott, P.N., & Fleminger, J.J. (1975). Presenile dementia:
The difficulties of early diagnosis. Acta Psychiatrica
Scandinavia, 59, 210-217.

 

O'Hara, M.W., Hinrichs, J.V., Kohout, F.J., Wallace, R.B., &
Lemke, J.H. (1986). Memory complaint and memory performance
in the depressed elderly. Psychology and Aging! 9, 208-214.

 

Parkinson, J. (1938) An essay of the shaking palsy, 1817.
Medical Classics, 5, 964-977.

 

Patrick, H.T., & Levy, D.M. (1922). Parkinson's disease: A
clinical study of 146 cases. Archives 99 Neurology 9
Psychiatry, 1, 711-720.

 

 

Peters, B.H. & Levin, H.S. (1979). Effects of Physostigmine
and lecithin on memory in Alzheimer's disease. Annals 99
Neurology, 5, 219-221.

 

Pirozzolo, F.J., Hansch, E.C., & Mortimer, J.A. (1982).
Dementia in Parkinson disease: A neuropsychological
analysis. Brain and Cognition, 9, 71-83.

136

Popkin, S.J. (1985). Laboratory and Real-life correlates of
older adults' metamemory. Paper present at the meeting of
the American Psychological Association, Los Angeles.

Popkin, S.J., Gallagher, D., Thompson, L.W., & Moore, M.E.
(1982). Memory complaint and performance in normal and
depressed older adults. Experimental Aging Research, 5, 141-
145.

 

Prevey, M.L., Delaney, R.C. Mattson, R.H. (1985). Metamemory
in temporal lobe epilepsy: Self monitoring of memory
functions. Paper presented at meeting of the International
NeurOpsychological Society, Denver, Co.

Riklan, M., Whelihan, W., Cullinan, T. (1976). LevodOpa and
psychometric test performance in parkinsonism - 5 years
later. Neurology, 55, 173-179.

 

Robins, A.H. (1976). Depression in patients with
parkinsonism. British Journal 99 Psychiatry, 128, 141-145.

 

 

Rodriguez, M.L. & Levin, B.E. (February, 1987). An analysis
of depression in Parkinson's disease. Paper presented at the
meeting of the International Neuropsychological Society,
Washington, D.C.

Rondot, P., deRecondo, J., Coignet, A., & Ziegler, M.
(1984). Mental disorders in Parkinson's disease after
treatment with L-DOPA. Advances 99 Neurology, 95, 259-269.

 

Russell, E.W., Neuringer, C., & Goldstein, G. (1970).
Assessment 99 Brain Damage: 9 Neuropsychological Key
Approach. New York: Wiley-Interscience.

 

 

 

Santamaria, J., Tolosa, E., Valles, A. (1986). Parkinson's
disease with depression: A possible subgroup of idiopathic
parkinsonism. Neurology, 55, 1130-1133.

 

Schildkraut, J.J. (1973). Neuropharmacology of the affective
disorders. Annual Review 99 Pharmacology, 95, 427-454.

 

 

Shimamura, A.P., Landwher, R.P., & Nelson, T.O. (1981).
FACTRETRIEVAL: A program for assessing someone's recall of
general-information facts, feeling-of-knowing judgements for
nonrecalled facts, and recognition of nonrecalled facts.
Behavior Research Methods and Instrumentation, 95, 691-92.

 

Shimamura, A.P., & Squire, L.R. (February, 1985). Memory
and metamemory: 9 study 99 the feeling-of-knowing phenomenon
99 amnestic patients. Paper presented at the meeting of the
International NeurOpsychological Society, San Diego, Ca.

 

 

Snyder, S.H., and D'Amato, R.J. (1986). MPTP: A neurotoxin
relevant to the pathophysioology of Parkinson's disease.
Neurology, 55, 250-258.

 

137

Spicer, R.B., Roberts, R.J., LeWitt, P.A. (February, 1987).
An investigation of cognitive functioning in asymmetric

Parkinson's disease. Paper presented at the meeting of the
International Neuropsychological Society, Washington, D.C.

Spitzer, R.L., Endicott, J., & Robins, E. (1978). Research
diagnostic criteria: Rationale and reliability. Archives 99
General Psychiatryy 55, 773-782.

 

Squire, L.R., Wetzel, C.D., & Slater, P.C. (1979). Memory
complaint after electroconvulsive therapy: assessment with a
new self-rating instrument. Biological Psychiatry, 99, 791-
801.

Sternberg, D.B., & Jarvik, M.E. (1976). Memory functions in
depression. Archives 99 General Psychiatry, 55, 219-224.

 

Strang, R.R. (1965). Imipramine in treatment of
parkinsonism: A double-blind placebo study. British Medical
Journal, 5, 33-34.

 

Swanda, R.M., & Kaszniak, A.W. (February, 1985).
Differential effects 99 Egg 99 onset and dgpression 99
Parkinson's disease. Paper presented at the International
Neuropsychological Society Meeting, San Diego, Ca.

 

 

 

Sweet, R.D., McDowell, R.H., Feigenson, J.S., Loranger, A.W.
& Goodell, H. (1976). Mental symptoms in Parkinson's disease
during chronic treatment with levodopa. Neurology, 55, 305-
310. '

 

Taylor, A.B., Saint-Cyr, J.A., Lang, A.B., & Kenny, F.T.
(1986). Parkinson's disease and depression: A critical re-
evaluation. Brain, 109, 279-292.

 

Thal, L.J., & Fuld, P.A. (1983). Memory enhancement with
oral physostigmine in Alzheimer's disease. New England
Journal 99 Medicine, 308, 720-721.

 

 

Trahan, D.B., & Larrabee, G.J. (1985). Construct validity
and normative data for some recently developed measures 99
visual and verbal memory. Paper presented at the meeting of
the International Neurological Society, San Diego, Ca.

 

 

Tweedy, J.R., Langer, K.G., & McDowell, F.H. (1982). The
effect of semantic relations on the memory deficit
associated with Parkinson's disease. Journal of Clinical
Neuropsychology, 9, 235-247. _—

 

Weschler, D. (1955).The Wechsler Adult Intelligence Scale.
New York: The Psychological Corporation.

 

Warburton, J.W. (1967). Depressive symptoms in Parkinson
patients referred for thalomotomy. Journal 99 Neurology,
Neurosurgery and Psychiatry, 55, 368-370.

 

 

 

 

138

Weingartner, H. (1986). Automatic and effort-demanding

cognitive processes in depression. In L.W. Poon (Ed.),

Handbook for Clinical Memory Assessment 99 Older Adults
(pp. 218-225). Hyattsville, Md.: American Psychological
Association.

 

Weingartner, H., Burns, S., Diebel, R., Lewitt, P.A. (1984).
Cognitive impairments in Parkinson's disease: Distinguishing
between effort-demanding and automatic cognitive processes.
Psychiatry Research, 99, 223-235.

Wilson, R.S., Kaszniak, A.W., Klawans, H.L., Jr., & Garron,
D.C. (1980). High speed memory scanning in Parkinsonism.
Cortex, 95, 67-72.

Yesavage, J.A., Brink, T.L., Rose, T.L., Lum, 0., Huang, V.,
Adey, M., & Leirer, V.O. (1983). Development and validation
of a geriatric depression screening scale: a preliminary
report. Journal 99 Psychiatric Research, 91, 37-49

 

Yudofsky, S.C, (1979). Parkinson's disease, depression and
electroconvulsive therapy: A clinical and neurobiologic
synthesis. Comprehensive Psychiatry, 55, 579-581.

Zahn, M.A. (1973). Incapacity, Impotence and invisible
impairment: Their effects on interpersonal relationships.
Journal 99 Health and Social Behavior, 99, 115-123.

Zelinski, E.M., Gilewski, M.J., & Thompson, L.W. (1980). Do
laboratory tests relate to self-assessment of memory ability
in the young and old? In L.W. Poon, J.L. Fozard, L.S.
Cermak, D. Arenberg, L.W. Thompson (Eds.), New Directions 99
Memory and Aging: Proceedings 99 the Georgg 99 9999999
Memorial Conference (pp.519-544). Hillsdale, NJ: Lawrence
Erlbaum Associates.

 

   

M'III'IIQ‘I’ILIMIIIfififlnjfiflflifliflflfifufl“