BRAIN

AND

COGNITION

8, 348-378 (1988)

The Neuropsychology

of Paramedian Thalamic Infarction

D. T. STUSS, A. GUBERMAN,

R. NELSON, AND S. LAROCHELLE

Schools of Medicine (Neurology) and Psychology, and Human Nearosciences Research
unit, University of Ottawa; Ottawa General Hospital, Ottawa, Ontario, Canada
A longitudinal study of three patients with CT-scan documented paramedian
thalamic infarctions (bilateral, primarily right, unilateral left) is reported and the
neuropsychology of human paramedian thalamic infarction is reviewed. The
neuropsychological deficits following these selected lesions, the nature of the
clinical memory disorder, and the neuroanatomy of memory are discussed. The
significance of cortical/subcortical relationship in explaining observed behavioral
changes is emphasized. Brain damage with maximum involvement in the dorsomedial nuclei and mamillothalamic tracts appears to cause primarily a memory
disorder and frontal-limbic behavioral changes, the severity and profile of deficits
depending on lesion extent and location. Both anterograde and remote memory
loss may be present. Asymmetry in memory at the level of the thalamus was
observed, following the left-verbal, right-nonverbal dichotomy.
6 1988 Academic
Press. Inc.

Two distinct forms of human amnesia have been distinguished in the
last 15 years (Huppert & Piercy, 1978, 1979; Lhermitte & Signoret, 1972;
Mattis, Kovner, & Goldmeier,
1978; Signoret, 1983; Squire, 1980, 1981,
1982; Squire & Cohen, 1982; Squire & Zola-Morgan,
1983): diencephalic
and bitemporal amnesia. Diencephalic amnesia is typified by Korsakoff
patients (Victor, Adams, & Collins, 1971) and by cases of trauma or
infarction such as NA (Squire & Moore, 1979; Teuber, Milner, & Vaughan,
1968). Bitemporal
amnesias are exemplified by surgical cases such as
H.M. (Milner, 1966, 1972; Scoville & Milner, 1957), and by patients who
Funding for this research was provided by the Medical Research Council of Canada to
the senior author. M. Lecompte and L. Stethem are thanked for assistance in preparation
of the manuscript and figures. The University of Ottawa Medical Communications Department
is acknowledged for its assistance in preparation of several of the figures. We gratefully
thank E. Murray and J. Saint-Cyr for comments on an early draft. The memory encoding
task was borrowed with permission from the doctoral dissertation of G. Lalltche (manuscript
in preparation). Address reprint requests and correspondence to Dr. Donald T. Stuss,
Human Neurosciences Research Unit, Faculty of Health Sciences, University of Ottawa,
451 Smyth Road, Ottawa, Ontario, Canada KIH 3M5.
348
0278-2626188 $3.00
Copyright
0 1988 by Academic
Press, inc.
All rights of reproduction
in any form reserved.

NEUROPSYCHOLOGY

OF

PARAMEDIAN

THALAMIC

INFARCTS

349

have received electroconvulsive
therapy (Squire, 1981, 1982; Squire &
Zola-Morgan,
1983).
Anatomical investigations have probed the role of damage to various
brain areas in the two clinical types of amnesia. In bitemporal amnesia,
lesions in both the amygdala and hippocampus appear necessary to produce
an obvious memory deficit (Andersen, 1978; Andy, Jurko, & Hughes,
1975; Duyckaerts et al., 1985; Halgren, 1981; Milner, 1966; Mishkin,
1978; Sarter & Markowitsch,
1985; Saunders, Murray, & Mishkin, 1984;
Scoville & Milner, 1957; Squire & Zola-Morgan,
1983; Woods, Schoene,
& Kneisley, 1982; Zola-Morgan,
Squire, & Mishkin, 1982). Controversy
surrounds the role of various diencephalic regions in memory, in particular
the dorsomedial
(DM) nucleus and the mamillary bodies (MB). Many
publications
emphasize the role of the MB or mamillothalamic
tract
(bundle of vicq d’Azyr which runs from the MB to the anterior thalamic
nuclei), particularly in patients with Korsakoff’s disease (e.g., Brierly,
1977; Brion & Mikol, 1978; Brion, Mikol, & Plas, 1983; Castaigne et al.,
1966, 1981; Delay & Brion, 1954; Delay, Brion, & Elissalde, 1958, a,b;
Gruner, 1956; Grunthal, 1939; Jarho, 1973; Mair, Warrington, & Weiskrantz, 1979; Pierrot-Deseilligny,
Chain, & Lhermitte,
1982; Swanson &
Schmidley, 1985). The anterior thalamic nuclei themselves have also been
implicated in memory functioning (Barbizet, Degos, Louam, Nguyen, &
Mas, 1981; Hassler, 1962; Mark, Barry, McLardy, & Ervin, 1970).
The DM nucleus, however, has been suggested most frequently as the
diencephalic area most related to memory (Ignelzi & Squire, 1976; McEntee,
Biber, Perl, & Benson, 1976; Mills & Swanson, 1978; Schott, Maugiere,
Laurent, Serclerat, & Fischer, 1980; Smyth & Stern, 1938; Squire, 1980;
Squire & Moore, 1979; Victor et al., 1971; Williams & Pennybacker,
1954). It has been proposed that lesions of the MB and DM nucleus may
individually
cause some amnesia but that damage to both are necessary
for more profound deficits, the severity correlating with the degree of
involvement (Aggleton & Mishkin, 1983; Riggs & Boles, 1944; Schott et
al., 1980; Speedie & Heilman, 1982, 1983; Squire, 1980, 1982).
In addition to further characterizing diencephalic memory problems,
other issues concerning neuropsychological
changes after pathology in
this region are relevant. If the lesion is unilateral, will asymmetrical
memory deficits be confirmed (verbal-nonverbal)?
Are other functions
disturbed: language, visual-spatial
abilities, attention, etc.? Do lesions
in the diencephalic area result in a “dementia”
and, if so, can this more
general disorder be characterized according to common typologies such
as cortical or subcortical dementia? Because of the intimate interconnections of the dorsomedial nucleus with the frontal lobes, are there
parallels with frontal lobe disturbance?
There remains a need for assessment of patients with well-defined
focal diencephalic lesions to elucidate further the specific role of lesions

350

STUSS ET AL.

in this region in producing specific behavioral abnormalities
(Aggleton
& Mishkin, 1983; Markowitsch, 1982, 1984; Zola-Morgan & Squire, 1985).
Computed tomographic scanning (CT) has allowed more precise localization
of focal brain pathology and has led to progress in the delineation of
brain-behavior
relations. We have studied three patients with isolated
vascular infarcts in the paramedian thalamic areas: one with bilateral
lesions, one with maximal right-sided involvement
and one with only
left-sided damage. These cases provided an opportunity to investigate
the effects of specific subcortical lesions and to assess possible clinical
differences arising from lesions of left versus right thalamic areas. We
also studied specific characteristics of the memory process, including
memory encoding and retrieval, and remote memory. Finally, repeated
assessments yielded information on the prognosis of acute paramedian
thalamic infarction.
METHOD
Subjects
Table 1 outlines the demographic characteristics of the three patients. Details of cases
1 and 2 were originally presented previously (Guberman & Stuss, 1983) and are only
summarized here. In the chronic state, all three patients were fully alert and cooperative
for neuropsychological assessment.
Case 1. This 56year-old man (R.C.) was in excellent health except for long-standing
mild untreated hypertension until one morning he was found unarousable in bed. On
admission, he was deeply stuporous but arousable with vigorous stimulation. The following
day, the level of consciousness fluctuated. Vertical (especially saccadic) gaze was impaired.
For 2 to 3 weeks he was disoriented, hypokinetic, apathetic, and hypersomnolent. CT (see
Fig. 1) at that time showed small ill-defined hypodense areas in both medial thalami. He
was eventually discharged home, where he remains apathetic and unconcerned, under the
care of his wife.
Case 2. This 51-yr-old gentleman (R.M.) with mild untreated hypertension presented
with coma, resolving into hypersomnolence, disorientation, inappropriate behavior, and
both anterograde and retrograde amnesia. Within 2 days, he was alert and oriented, but
slow to respond, with an obvious memory deficit. He eventually returned to work. A CT
scan (see Fig. 1) done 19 months after admission revealed a discrete low density lesion
in the right paramedian thalamus. A coronal view suggested a barely discernible hypodense
area in the left thalamus.
Case 3. This 70-yr-old right-handed female (I.G.) was in good health until December 5,
1981. She had had one episode of vertigo a year previously for which she saw a neurologist.
A CT scan at that time was normal. On the day of the present admission, she felt unwell.
She was unable to follow a recipe to bake a cake. Later her husband noted that she had
trouble finding words and was using inappropriate words. On admission to hospital, her
blood pressure was 170/90, but later 130/60. Heart rate and rhythm were normal but she
had an early systolic click. No bruits were heard in the neck. She appeared confused,
said she was in a hospital in another city and gave the year initially as 1941 but later
corrected herself. The neurological examination was otherwise normal.
A CT scan completed 48 hr after the onset of symptoms revealed a low density lesion
in the left thalamus adjacent to the genu of the internal capsule. Four days later, the lesion
was not seen on a contrast enhanced study but reappeared on a subsequent scan and was
still noted 1 year later (see Fig. 1). The EEG was normal and cerebral angiography did

Sex

M

M

F

Patient

1. R.C.

2. R.M.

3. LG.

70

51

54

Age

DATA

R

R

R

Handedness

DEMOGRAPHIC

OF THREE

B.A.

1 year
university
5

Education

WITH

TABLE
PATIENTS

THALAMK

Retired

Truck driver

Disability

Present
employment

PARAMEDIAN

1

School principal

Business analyst;
civil servant
Truck driver

Previous
employment

INFARCTIONS

O-3 weeks; 6, IS, 24
months
O-2 weeks; 10, 27
months
O-l week;
7, 9 months

Assessment
dates

5
CA

%
$
ij
2
2

2

z

E
g

%
7

2

s

8

i3
2
2

352

STUSS ET AL.

NEUROPSYCHOLOGY

OF

PARAMEDIAN

THALAMIC

353

INFARCTS

not show any occlusive
disease. Both posterior
cerebral arteries were noted to arise mainly
from the posterior
communicating
arteries.
Echocardiogram
demonstrated
no mitral valve
prolapse.
On discharge
from hospital,
she returned
to her regular schedule.

Neurological

Investigations

The neurological
symptoms
and investigations
are summarized
in Table 2. Part A (top)
outlines
the presenting
and early states; Part B (bottom)
summarizes
the chronic
stage.
The CT scans (top) and the schematic
localizations
(bottom)
are presented
in Fig. I.
For each patient,
the level best demonstrating
the lesion was selected.
For purposes
of
localization,
a horizontal
brain section from a CT scan atlas (DeArmond,
Fusco, & Dewey,
1976, p. 28) was selected as the diagram
most representative
of all three scans. For patient
2 (R.M.),
an additional
coronal cut was used to approximate
the left thalamic
lesion. For
each CT scan, two neurologists
(A.G.. R.N.) independently
outlined the lesion on a schematic
drawing.
These two independent
approximations
were then overlapped
(darker
area) to
yield the composite
schematic
localization
on the bottom
of Fig. I. and indicate
close
agreement
in localization.
In Fig. 2, the level of the horizontal
view and the thalamic
area,
in enlarged
format
without
lesion demarcation.
are presented
to facilitate
localization
in
Fig. I.
The schematic
diagram based on analysis of the CT scans suggests the following
localized
maximum
thalamic
involvement.
Involvement
of other proximal
areas, such as the internal
medullary
lamina and thalamic
inflow and outflow pathways
cannot be definitely
ruled out
due to the limitations
of volumetric
analyses of CT scan. especially for subcortical
structures.
I. Dorsomedial
nucleus:
This nucleus is damaged
in all three patients.
In patient R.C..
there is maximum
left DM involvement,
and apparently
only minimal
right DM nucleus
damage. In patient R.M., the dorsomedial
pathology
appears more bilateral.
with maximum
involvement
on the right. Patient I.G. has unilateral
left damage,
the DM involvement
apparent
only at the rostra1 tip of the nucleus.
2. Mamillothalamic
tracts:
In all three patients,
the mamillothalamic
tract.
between three thalamic
regions (dorsomedial.
ventral anterior,
and ventral lateral)
from the mamillary
bodies to the thalamus appears to be involved,
either bilaterally
or unilaterally
(R.M.-on
the right; I.G.--on
the left).
3. Ventral
anterior
be involved
bilaterally
R.M. has no evidence

coursing
en route
(R.C.).

thalamic
nucleus:
The ventral
anterior
thalamic
nucleus appears to
in patient R.C. and unilaterally
on the left for patient I.G. Patient
of ventral
anterior
involvement.

4. Vemral
lateral thalamic
nucleus:
The involvement
of this nucleus is variable.
In all
patients, there is some involvement.
For example.
in patient R.C. there is minimal bilateral
involvement.
In patient R.M. there is minimal
suggestion
of involvement
of this nucleus.
In patient I.G.. there is evidence
of some unilateral
left ventral
lateral involvement.
5. Centromedian,
ventral
posterolateral,
pathology.
There is a suggestion
of minimal
patients KC. and R.M.

and pulvinar
involvement

have little if any
of the centromedian

evidence
nucleus

of
in

Involvement
of each of these brain areas, in each of the three patients,
is schematically
represented
in Table 3. using a rating of 0 to 5 to provide
an approximation
of zero to
maximum
involvement.

FIG. I. CT scan and schematic
representation
of localization
of lesions in the three
patients
with paramedian
thalamic
infarcts.
The top half illustrates
the actual CT scan
results; the lower half depicts the location
of the lesion according
to a CT scan atlas. The
procedure
is described
in the text. The left thalamic
lesion in patient
R.M. is a barely
discernible
hypodense
area seen only on a coronal
cut. suggesting
that there is primarily
right pardmedian
thalamic
involvement
in this patient.

Confusion

Alert,

Normal

Normal

3. I.G.

I. R.C.

2. R.M.

3. I.G.

abulid

Coma+

2. R.M.

apathy,

Coma+
Stupor-,
Fluctuating
levels
of consciousness,
hypersomnolence

1. R.C.

Arousal

Normal

Normal

Normal

Early
incontinence;
normal
Normal

Normal

state
Minimal
vertical
saccadic gaze
deficit
Normal

Normal

and early findings
Absence
of
voluntary
vertical
gaze
SC
oculocephalic
movements
Eye movement
limitation

B. Chronic

A. Presenting
Bilateral
asterixis;
normal

Cranial

General
physical,
neurological
nerves

TABLE
2
SYMPTOMS AND INVESTIGATIONS

NEUROLCGICAL

status

Limited
memory
impairment
Limited
memory
disturbance

Severe memory,
initiation
deficit

Confusion

Slow mentation,
confusion

Not testable-,
drifting
attention,
confabulation

Mental

Normal

Diffuse

slowing

Diffuse slowing,
with minimal
a in arousal

EEG

E
F

2

NEUROPSYCHOLOGY

OF PARAMEDIAN

THALAMIC

355

INFARCTS

FIG. 2. On the left, the level of the horizontal cut is shown (DeArmond et al., 1976).
On the right, a schematic blowup of the paramedian thalamic area is illustrated, for more
precise lesion localization of the areas depicted in Fig. I. See Table 3.

Neuropsychological

Znvestigations

Commonly used clinical tests are summarized in Table 4. Experimenter-devised procedures
are described below. The latter were all administered after the patient had stabilized (after
6 months).

Learning

of Spatial Mazes

Following Milner (1964), two simplified manual forms were devised (see Fig. 3). For
each, holes were drilled in a wooden board at equal intervals for either a 10 x 10 or 4
x 4 grid. The subject was told that there was one correct path leading from the bottom
left to the top right. The subject had to learn the path by trial and error by placing pegs
in the holes. Feedback was given for each response. If an error was made, all pegs were
removed, and the patient restarted the test. Because of the patients’ difficulty (particularly
R.C.) in successfully completing the 10 x 10 grid, the 4 x 4 grid was used for comparison
across ail three patients. Thirteen trials were administered to each patient; the score was
the number of correct pegs placed in each trial. The patients were compared to three
normal control subjects of the same mean age and educational level.

Memory

Encoding

and Retrieval

Two different conditions were used. In the free encoding condition, a list of 12 words,
3 words from four different semantic categories, were presented at a rate of 1 every 2 set
TABLE
L~G%IZATION

OF LESION

IN THE THREE

3

SUBJECTS

ACCORDING

R.C.

TO BRAIN

STRUCTURE

R.M.

I.G.

Patient:
Thalamic region

L

R

L

R

L

R

Mamillothalamic
tract
Dorsomedial
Ventral anterior
Ventral lateral
Ventral posterolateral
Pulvinar
Centromedian

5
5
1
2
0
0
1

3
1
2
1
0
0
0

0
2
0
1
0
0
2

2
5
0
1
0
0
2

5
1
2
1
0
0
0

0
0
0
0
0
0
0

Note. 0 = normal; 5 = maximum involvement.

356

STUSS ET AL.
TABLE
NEUROPSYCHOLOGICAL

4
F~XEDURES

A. Attention, mental control
1. Arousal level (Plum & Posner, 1980).
2. Digit span.
3. Wechsler Memory Scale (WMS) mental control (Wechsler, 1945).
4. Trail Making Test (Army Individual Test Battery, 1944).
B. Speech and language
1. Boston Diagnostic Aphasia Examination (BDAE) fluency and content (Goodglass &
Kaplan, 1972).
2. Boston Naming Test (Kaplan, Goodglass, & Weintraub, 1983).
3. F-A-S verbal fluency (Spreen & Benton, 1969).
4. Western Aphasia Battery (Kertesz, 1982).
C. Cognitive tests
1. Wechsler Adult Intelligence Scale (WAIS) (Wechsler, 1955).
D. Planning and executive control functions
1. Wisconsin Card Sorting Test (WCST) (Grant & Berg, 1948).
2. Porteus Maze (Porteus, 1933/1965).
3. Color-Form Sorting (Goldstein & Scheerer, 1941).
E. Memory
1. Wechsler Memory Scale (WMS) (Wechsler, 1945).
2. Benton Visual Retention Test (Benton, 1974).
3. Three word memory.
4. Consonant Trigrams (Brown, 1958; Peterson & Peterson, 1959).
5. Retrograde Amnesia Test (Ottawa General Hospital French Version, developed by
SLR).
F. Visual-spatial
1. WAIS Block Design, Object Assembly
2. WMS Copy
3. BDAE Parietal Lobe Drawings

with immediate free recall required. The patient was then told what the four categories
were, and recall was again requested (category recall). In condition two, the two types of
recall were identical, Before the presentation of the list of 12 different words from four
other semantic categories, however, the patient was informed what the four categories
were (category encoding). Comparisons were possible between type of recall within and
across the two acquisition conditions. On this test, the three patients were compared to
12 normal subjects (age = 58.9 (6.9); education = 14.3 years (2.3)).

Retrograde

Amnesia

One patient (R.C.) was administered a series of measures of retrograde amnesia. All
tests were devised, since no valid test existed for a French Canadian population. Twentytwo items constituted a measure of autobiographical remote memory covering work, school
history, family history, and personal preferences. Knowledge of generic facts was assessed
by the WAIS-R information subtest, and 10 additional questions (where does the sun
rise? what is the color of snow?). Ten questions addressed memory of singular facts (who
sculpted the Pieta and painted the Sistene chapel?; who invented the airplane?). Finally,
50 questions spanning five decades from 1930 to 1980 were presented, based on expected
knowledge for an educated individual with a French-Canadian background. Spontaneous
recall and multiple choice responses were requested. Three normal control subjects
of the
same approximate age (range 52-57), education (completed high school to 3 years university),

NEUROPSYCHOLOGY

OF PARAMEDIAN

THALAMIC

INFARCTS

357

3

FIG. 3. The dotted path depicts the simplified route the patients had to learn in a trial
and error fashion, moving from bottom left to top right. The inset illustrates the very
reduced 4 x 4 grid and route.
cultural background (all French-Canadian),
were tested for comparison.

and socioeconomic status (upper middle-class)

RESULTS

General Neuropsychological
Tests
Data gathered are described below, and summarized

in Table 5.

General Observations, Arousal, Attention
Two (R.C., R.M.) of the three patients presented with coma, evolving
into hypersomnolence
and fluctuating levels of consciousness. Patient
I.G. presented with confusion, evolving into an unconcerned state, with
elements of denial. In the chronic (see Table 5 for definition) state, all
three were alert, pleasant, and cooperative. R.M. had returned to work,
with some lack of insight. I.G. was somewhat distractible, anxious, with
a tendency to minimize any residual deficits. R.C. remained at home,
apathetic, unaware, unconcerned, distractible,
slow in response, with
flat affect, good humor, occasionally aggressive outbursts, and little spontaneous initiation. His wife, however, noted improvement in daily activities
3 years postonset. The patient took limited walks by himself and became
involved in at least minimal social interaction.
Attentional capabilities as measured by digit span (see Table 5), remained
relatively stable after the acute period. In the early stage, other clinical
tests used to measure attention capabilities revealed a tendency for errors
and slowness in response. All patients, particularly R.C., continued to
have extreme difficulty with the Trail Making Test, particularly in Part
B, which requires alternating between numbers and letters (l-A-2-

Comp
Arith
Simil
D. span
VOC

MO

VIQ

Repetition
Comprehension
BNT-’
Word generation
General intelligence’
WAIS

Content

Attention
Digit Span
FWD
BWD
Mental Ctl
20-I
147
Trail malting
A
B
I-wwage
Speech

83
6
5
8
6
7
9

Low vol., no
spontaneous
output
Confab., persev.,
redupl.
paramnesia
8.8/10
7.5110
5/18
0
20/40

Confab., persev . ,
redupl.
paramnesia
IO/IO

Low vol.; normal

Normal

STAGES

89
I3
6
IO
7
8
I4

Confab., pcrsev.
redulp.
paramnesia
IO/IO
9.3/10
38/84
7

55
300”*

300”*
300”:

5
3
17”
22”(l)

5
4

5
4

I.G.

CHRONIC

37”(2)
56°CI )

R.M.

R.C.

Acute”

TABLE 5
SUMMARYOF NEUROPSYCHOLOGICAL
RESULTSIN THE ACUTE AND

85”
285”

244”
3o(y’*

103
IO
IO
II
9
6
I3

IO/IO
9.7110
lo/l8
2

Low vol. (
increased
output
Mild confab.

IO/IO
IO/IO
29/40
4

Normal

Normal

I2
19”

I5
24”

IU
Y

Ill
I5
II
I2
I2
I2
I7

IO/IO
IO/IO
WM
II

Normal

Normal

33
163”

5
3

7
5

5
5

I.G.

Chronic”

PATIENTS

R.M.

R.C.

FOR THE THREE

3
$

2
C
g

E
00

ass.

2
3
113

0
0

O/3

0
0

O/18
5/6
0
0

l/18

O/3

9
10

2/18
O/18
0
0

4
0
3110
O/3

4118
416
0
0

4
I

6
6

1.5
0

016

76
2
2

71
3
4
5
0
3
9

81
2
5

102
I
9
7
6
7
12

55
3
4.1

8

2

3

Note. Absent data indicates test was not administered.
’ Acute, maximum results in the period O-3 weeks after infarct.
’ Chronic, maximum results in the period 6-12 months after onset.
’ Number in brackets reflects the number of errors. Score is the time required to completion.
’ BNT, Boston Naming Test.
’ Scale scores-a score of 10 for these WAIS subtests would be average.
’ For the WMS, delayed recall was approximately 30 min.
* Maximum time alloted.

Info
Orien
Stories
Immed.
Delayed
Paired assoc.
Easy immed.
Delay
Hard immed.
Delay
Drawings
Immed.
Delay
Benton VRT
3 word

MQ

WMS copy (14)
Memory
WMS

Obj.

Digit symbol.
Pitt. camp.
Block des.
Pitt. arr.

PIQ

Visual-spatial
WAIS

4
4
4110
313

3
1

616

14118

8

I

84
6
4

12

6

6

10
14
lO/lO
O/3

12118
416
3
0

2
4

101
5
5

115
8
9
I
10
12
13

360

STUSS ET AL.

B-3-. . . ). Patient R.C. could never successfully complete this task. Despite
continuing impairment, the overall results indicate an evolving improvement
in the attentive abilities required by this task.
Speech and Language
Two of the three (R.C., R.M.) had diminished voice volume in the
acute stages, which remained permanent for R.C. Neither had had laryngeal
intubation.
None revealed dysarthria or stuttering. Perseveration was
common.
Although all had language disturbance, it is uncertain whether they
can be called “aphasic.”
Repetition in the acute period was impaired
only with longer phrases, and might be attributed to attentional or memory
problems. There was no repetition deficit in the chronic stage. Comprehension was impaired only for sequences or complex ideational questions.
Naming was essentially perfect on the simpler Western Aphasia Battery
subtest for all three patients. However, a naming deficit was identified
by the Boston Naming Test. Patient R.M.‘s performance was primarily
characterized by perceptual errors and educational deficiencies (“I don’t
know”). In the chronic stage, a mild to moderate naming deficit remained,
patient R.C. being more severely impaired. His performance significantly
improved with phonetic cues. Except for R.M., errors were not easily
classifiable. Some were perseveration, others nonaphasic misnaming, and
others paraphasias. Word list generation (number of words generated in
1 min beginning with a specific letter) was impaired for R.C. and R.M.
in the chronic stage. The patient with unilateral left pathology did not
reveal persistent impairment on this test.
General Intelligence
Although the cognitive assessment was not equivalent for all three
patients, there was a consistent trend for impaired functioning soon after
onset, with improvement over time. Patient R.M., with a Grade 5 education,
appeared to have premorbid limited intellectual abilities. Patient I.G.,
the retired school principal, had a definite improvement from low average
to high average functioning. While overall verbal I.Q. abilities increased
from 83 to 103 for patient R.C., suggesting normal functioning in the
chronic state, this likely does not reflect his premorbid abilities. This
conclusion is based on the intertest scatter, superior score (13) on the
test with the highest correlation with overall I.Q. (vocabulary), and
knowledge of his previous occupation. In summary, however, verbal
cognitive abilities, even with bilateral paramedian infarct, recovered to
at least normal levels.

NEUROPSYCHOLOGY

Planning

OF

PARAMEDIAN

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361

and Executive Abilities

In the early stage, all three revealed confabulation and reduplicative
paramnesia of place. Because of overall differences in level of functioning,
examination of planning and executive abilities was completed at different
levels for each patient. Patient, I.G., at both the acute and chronic stages,
despite her high I.Q., had severely impaired performance on the Wisconsin
Card Sorting Test (only two sorting categories), and the Porteus Maze
(test age of 10/17). R.C. and R.M. were administered the simple colorform sorting task, requiring one shift of concept: R.M., despite his lower
I.Q., completed the task successfully, whi1e~R.C. formed one concept,
and continued to perseverate this. He was unable to shift.
Visual-Spatial
Functions
Visual-spatial
functions were assessed by the Performance subtests
of the WAIS (particularly Block Design), related drawings from the Boston
Diagnostic Aphasia Examination (BDAE) Parietal Lobe Battery (performed
to command and copy), and the copy of the Wechsler Memory Scale
(WMS) figures. Patient I.G., with the unilateral left lesion, was only
minimally
deficient on simple drawings in the acute stage. While her
WAIS performance I.Q. was 102 at this time, results were mildly beneath
expected levels. This was confirmed by her above-average results once
recovered. The other two patients, with documented right thalamic infarcts,
had more severe deficits, never recovering to expected levels. Impairment
was most striking in complex tasks and in the spontaneous reproduction
of houses, cubes, etc. Copy of simple designs (WMS) was the least
affected, suggesting that elementary visual-perceptual
functions were
reasonably intact in all three patients.
Memory
Functioning was impaired in all three patients, particularly in the acute
stages. While recovery did occur, two facts were evident in the chronic
stage. First, the patient with bilateral damage had persistent amnesia for
both verbal and nonverbal material. Tactile memory was also severely
impaired. Despite repeated assessments, he never remembered having
seen the examiner before, or having undergone any tests. Even after 3
years, he was disoriented for time, indicating he could never learn the
day, date, or year. Second, there appeared to be hemispheric asymmetry
of memory functions in the two patients who had predominantly
left or
right unilateral pathology: R.M., with the predominant
right thalamic
lesion, was relatively impaired with nonverbal material; I.G., with the
left thalamic lesion, had pronounced difficulty with verbal information
(see Fig. 4).
The results of the 4 x 4 maze learning test for the two separate testing
sessions are illustrated in Fig. 5. Two observations are readily made.

362

STUSS ET AL.
BILATERAL

IRC,

RIQHT

WI

LEFT

UOI

FERCENTUlE
CORRECT

STORIES

FAIRE0

THREE

ASSOCIATES

WRO

VERBAL

NONVERBAL

FIG. 4. Delayed recall on verbal and nonverbal measures of memory for all three
patients with thalamic lesions (bilateral, primarily right, and unilateral left) during the
chronic testing stage. Stories, paired associates, and visual reproductions are derived from
the Wechsler Memory Scale. BVRT refers to the Benton Visual Retention Test, multiple
choice format. For the three-word test, the patient is asked to recall three words after a
5-min delay.

First, the two patients with “unilateral”
(unilateral left; primarily right)
lesions both eventually learned the task on the first session, with greater
success on the second testing session. Patient R.C., on the other hand,
never learned the task. His performance deteriorated over time, his best
results generally occurring on the earlier trials during both the first and
second visits. Second, the learning (or “forgetting”) curve for each patient
frequently showed to a greater or lesser degree a “scalloping”
effect,
with good performance on one trial altering with poor performance on
a subsequent trial.
On the memory encoding test, all three patients were inferior to the
normal control subjects under all conditions (see Fig. 6). There was little
evidence of consistent differences among the three patients in their ability
to use category cues for either recall or encoding. All patients not only
failed to benefit from category recall, but deteriorated in the number of
words recalled. The two patients with more prominent left thalamic
damage benefited at least slightly from category encoding, while the
patient with primarily right thalamic infarction did not improve.
Retrograde amnesia tests were completed only for subject R.C., approximately
3 years postonset. Knowledge of generic facts was 100%.
Knowledge of singular facts was at the 50th percentile for the WAIS
information
subtest (scale score of 10; equivalent to I.Q. of lOO), and

NEUROPSYCHOLOGY

OF PARAMEDIAN

THALAMIC

INFARCTS

363

FIG. 5. First and second testing sessions results on the simplified maze learning test
for all three patients are illustrated. A total of six correct moves are possible for each
trial. Thirteen trials were given to each patient. ‘The results of one testing of three normal
control subjects are illustrated on top for comparison.

60% correct for our 10 questions. He was unable to indicate who painted
the Sistine chapel (although he knew what it was), who invented the
airplane, or what kind of artist Rembrandt was. Twenty-two questions
of autobiographical remote memory (verified by his wife) were 55% correct.
There therefore appears to be a personal remote memory loss. A temporal
gradient cannot be claimed, although descriptively the deficit appears
more severe in the years proximal to the injury, with at least a patchy
loss extending for many years prior.
The results for the verbal retrograde amnesia test for both spontaneous
recall and recognition are illustrated in Fig. 7. Spontaneously, R.C. could
recall only such information as the Prime Minister of England (Thatcher),
the birth place of a Prime Minister of Quebec in the 195Os, Jesse Owens,
and the name of the Dionne quintuplets. As indicated by the figure, the

364

STUSS
MEMORY

ET

AL.

ENCODING
q

/

FREE
ENCODING

ENCODING

FIG.
normal

6.
Illustration
control
subjects

of
on

t.

NC

fnrtnrcitt1 3 1 3 1 3 1 8 1
0

1

1

8

fnrrnrcatt 4

3

6

9

‘:::::’

2

0

8

‘;:;:;;’
CATEGORY

m

the results
this task

on
are

2
the memory
derived
from

encoding
Lafleche

tests.
(1987).

The

results

for

the

recognition procedure improved performance to the level of spontaneous
recall of the control subjects. However, there obviously remains a retrograde amnesia in comparison to the recognition results for the normal
control subjects. With the exception of the improved performance in the
194Os, R.C.‘s profile appears to be relatively constant across decades.
This may be an artifact of test construction.

-spoilt-a

hoall

- - -Recognition

-x)

IWO-Y)
Doeada

FIG. 7.
Results
on the
recognition.
The “control”
matched
in age, education,

verbal
profile
cultural

Remote
Memory
Test for both
is the mean
of three
neurologically
background,
and socioeconomic

spontaneous
recall
and
normal
individuals
status
to patient
R.C.

NEUROPSYCHOLOGY

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365

DISCUSSION
General Discussion
Our results confirm that midline thalamic infarcts, especially when
bilateral, cause a memory impairment.
Our patients were ideal for study
of clinico-anatomical
correlations since they showed no clinical or CT
evidence for brain lesions outside the thalamus. Whether the amnesia
occurs as an isolated disorder or part of a more global dementia associated
with thalamic pathology is open to question (Castaigne et al., 1966, 1981;
Chassagnon, Boucher, Tommasi, Bianchi, & Moene, 1969; Cheek &
Taveras, 1966; Smyth & Stern, 1938; Stern, 1939). Changes in higher
mental functions other than amnesia were noted in our patients. A disorder
in arousal and consciousness was prominent, particularly in the early
stages. This observation has been reported previously in patients with
thalamic lesions, with suggestions of disruption in subthalamic areas,
ascending noradrenergic pathways, and/or the mesencephalic-diencephalic
junction associated with the reticular activating system (Castaigne et al.,
1981; Cox, 1937; Graff-Radford,
Eslinger, Damasio, & Yamada, 1984;
Graff-Radford, Damasio, Yamada, Eslinger, & Damasio, 1985; Magoun,
1958; Mills & Swanson, 1978; Teuber et al., 1968; Von Cramon, Hebel,
& Schuri, 1985). In the chronic stage, this is frequently manifested as a
lethargic, apathetic state, possibly with excessive sleepiness. Closely
allied with the disorder in arousal is the reported attentional impairment
(Archer, Ilinsky, Goldfader, & Smith, 1981; Schott et al., 1980). This
may not be evident on simple tests such as digit span, or mental control
tasks. Certain characteristics appear similar to the selective attention or
executive control disorder of frontal lobe patients (Lezak, 1983; Luria,
1980, 1973; Stuss & Benson, 1984, 1986).
In the acute stage, all three had alterations in personality, mood, and
awareness, including confabulation,
reduplicative
paramnesia, apathy,
and unconcern. The personality change appears to be permanent only
in patient R.C. Several years postonset, he remains unconcerned, unaware,
jovial, and lacking any spontaneous drive or initiation. This apathy extends
to activities of daily living. Other studies have reported similar findings
in the acute or chronic stages (G&f-Radford et al., 1984; Mills & Swanson,
1978; Swanson & Schmidley,
1985; Teuber et al., 1968). Many of the
personality characteristics resemble those described after focal frontal
or frontal-limbic
system damage (Damasio, 1979; Eslinger & Damasio,
1985; Stuss & Benson, 1984, 1986). The type of personality change after
thalamic damage may be dependent on lesion location (Graff-Radford et
al., 1984): anterior thalamic lesions, interrupting connections to the cingulate
gyrus, could result in withdrawal and akinesia; DM lesions, affecting
projections to the frontal (orbitofrontal) cortex, may cause euphoria and
lack of insight.

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STUSS ET AL.

Visual-perceptual
and visual-constructive
disorders were found in all
three patients in the early stages. The relatively intact abilities for our
patient with unilateral left pathology in the chronic stage replicates previous
reports (Speedie & Heilman, 1982; Squire & Moore, 1979; Teuber et al.,
1968). In contrast, Graff-Radford
et al. (1984) reported visual-spatial
impairment in 4/5 thalamic patients, including those with apparent unilateral
left thalamic lesions. Only R.C. (bilateral) and R.M. (primarily right)
revealed persistent problems, but only with more complex tasks such as
block design. Whether the deficit was a premorbid limitation,
as appears
likely in part in the case of R.M., a reflection of lack of initiation,
an
impairment in attention (Graff-Radford et al., 1985; Henderson, Alexander,
& Naeser, 1982), or an organizational,
conceptual deficit similar to those
found in patients with focal frontal pathology (Luria, 1980, 1973; Stuss
& Benson, 1986) cannot be readily determined.
All three patients had a language disturbance that was difficult to
characterize. The language functioning in our patients, typified by our
patient with bilateral lesions, may be summarized as follows: poor initiation
of speech with a general poverty of output that occasionally was contaminated by confabulation and lack of monitoring of output; fluctuation
and variability in performance; relatively intact repetition and comprehension; and naming problems, apparently characterized more by perceptual errors, nonaphasic misnaming,
intrusions, perseverations, and
confabulation than by phonemic and semantic paraphasias. A deficit in
word list generation has been considered a generic sign of aphasia, diffuse
brain dysfunction (Benson, 1979), and focal frontal system lesions (Milner,
1964) including frontal white matter, supplementary motor area, or cingulate
gyrus pathology (Damasio & Van Hoesen, 1980; Freedman, Alexander,
& Naeser, 1984; Kertesz, 1979; Sanides, 1970; Stuss & Benson, 1986).
In most of these cases, the deficit is one of initiation of speech rather
than a true language impairment.
It is noteworthy that the patient with
the unilateral left thalamic lesion does not have significantly deficient
verbal fluency.
Although language deficits have been reported after focal thalamic
lesions (Archer et al., 1981; Bell, 1968; Barraquer-Bordas,
Illa, Escartin,
Ruscalleda, & Marti-Vilalta,
1981; Mohr, Watters, & Duncan, 1975; Walshe,
Davis, & Fisher, 1977), there appears to be lesion specificity, with more
deficits reported after pulvinar, posterolateral, and ventrolateral thalamic
nuclear damage (Brown, Riklin, & Waltz, 1971; Crosson, 1984; Davous
et al., 1984; Eidelberg & Galaburda, 1982; Graff-Radford & Damasio,
1984; Graff-Radford et al., 1984, 1985; Ojemann, 1977; Ojemann, Fedio,
dz Van Buren, 1968; Van Buren & Burke, 1969; Vilkki & Laitinen, 1976).
In general, these are areas that have reciprocal involvement with a cortical
language area (Crosson, 1984; Eidelberg & Galaburda, 1982; Graff-Radford
et al., 1984). In other patients with thalamic lesions, the disturbances in

NEUROPSYCHOLOGY

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PARAMEDIAN

THALAMIC

INFARCTS

367

language (similar to our patients) have been ascribed to alterations in
alerting or in a gate controlling access (Fedio & Van Buren, 1975; Mateer
& Ojemann, 1983; Ojemann, 1977); a deficit in the integration and monitoring of language (Penfield & Roberts, 1959); impaired arousal and
vigilance in a system closely allied with the dominant hemisphere language
system (Luria, 1977); and interaction with other functions such as attention,
concentration,
and memory (Castaigne et al., 1981; Choi, Sudarsky,
Schachter, Biber, & Burke, 1983; Reynolds, Turner, Harris, Ojemann,
& Davis, 1979; Speedie & Heilman,
1982), at least in the early stages
(Graff-Radford & Damasio, 1984; Gratf-Radford et al., 1984). The language
impairment
in our patients may be attributed to multiple dysfunctions
including alteration in alerting, arousal, and monitoring.
While the diencephalic lesions temporarily disrupt performance on I.Q.
tests (WAIS), there is a recovery to average or premorbid levels (Mills
& Swanson, 1978; Squire & Moore, 1979; Teuber et al., 1968; Winocur,
Oxbury, Roberts, Agnetti, & Davis, 1984). In particular, verbal I.Q.
skills are within the normal range in the chronic stage, even for the
patient with bilateral DM damage. It is likely that this does not reflect
this patient’s premorbid abilities. It is uncertain if the deficits that are
observed are primarily cognitive in nature or reflect indirect effects on
behavior due to apathy or lack of organization. Lesion localization may
also play a role, with greater cognitive impairment with damage in caudal
and/or lateral areas (Graff-Radford et al., 1985; Jurko & Andy, 1973;
Wallesch, Komhuber,
Kunz, & Brunner, 1983).
It has been proposed that thalamic lesions may cause dementia (e.g.,
Castaigne et al., 1966; Chassagnon et al., 1969). In some cases small
unilateral lesions result in general but not severe impairment of cognitive
functions (Wallesch et al., 1983). Graff-Radford and colleagues (1984)
proposed that patients with left but not right thalamic lesions meet the
DSM criteria for dementia. Our “unilateral”
patients had impairments
other than memory, but these were not severe, and the disorder is considered limited to memory. Considering as well their return to a relatively
normal life, we conclude that unilateral focal diencephalic lesions do not
result in dementia (Speedie & Heilman, 1982, 1983; Squire & Moore,
1979).
Patient R.C. meets the criteria for dementia, in that he has impaired
functioning in several higher mental functions. Just as clearly, his dementia
has characteristics unlike those described for patients with Alzheimer’s
disease (Cummings & Benson, 1983). With the exception of the amnesia,
the striking slowness in rate of information processing; the absence of
apraxia, agnosia, or a true aphasia; the average I.Q. with impairment in
using his acquired knowledge; the breakdown in organization of new or
complex material; the striking inertia and apathy coupled with unconcern
and a jovial attitude have all been described as characteristics of “sub-

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STUSS ET AL.

cortical dementia” (Albert, 1978; Albert, Feldman, & Willis, 1974; Benson,
1983; McHugh & Folstein, 1975). Many of the symptoms described in
our patient(s) are those reported after frontal and/or anterior limbic
damage (Damasio, 1979; Poirier, Barbizet, Gaston, & Meyrignac, 1983;
Stuss & Benson, 1986). In this respect, the proposed terms fronto-subcortical, frontal system, or frontal-limbic syndrome appear more appropriate
(Albert, 1978; Freedman & Albert, 1985).
The severe memory impairment,
however, is unlike that described
under the generic heading of “subcortical dementia.”
The syndrome of
paramedian thalamic infarct in our patients has its own symptom complex,
characterized by a severe memory disorder and frontal-limbic
behavioral
changes. These deficits may occur with either unilateral or bilateral lesions
depending on the size and location of the damage.
Memory
We have no ready explanation for the deterioration in performance on
the memory encoding test when given category names. A lack of accessibility to the stored information (Tulving & Madigan, 1970) does not
seem feasible to explain the rapid loss of information
that had already
been recalled. Not only is the effectiveness of cueing related to the
memory capacity of the subject tested (Tulving & Pearlstone, 1966), but
additional influences such as inability to maintain working memory in
the face of interference may be a factor.
Laterality
Studies of patients with unilateral thalamic infarction have led to the
proposal that hemispheric specialization extends to the thalamus (Squire
& Moore, 1979; Teuber et al., 1968). In general, left unilateral lesions
resulted in verbal memory problems, while right led to nonverbal memory
deficits (Cappa & Vignolo, 1979; Choi et al., 1983; Jurko & Andy, 1973;
Michel, Laurent, Foyatier, Blanc, & Portafaix, 1982; Reynolds et al.,
1979; Speedie & Heilman,
1982, 1983; Squire, 1982; Squire & Moore,
1979; Squire & Slater, 1978; Vilkki, 1978). In some cases, unilateral left
thalamic dysfunction has been reported as causing verbal memory deficit
or disorientation,
with right-sided lesions showing little evidence of any
deficit (Choi et al., 1983; Graff-Radford et al., 1985). Others report that
left-sided thalamic lesions appear to have a more devastating result,
affecting both verbal and nonverbal memory and/or causing “dementia,”
while unilateral right damage causes only a questionable nonverbal deficit
(Alexander & LoVerme, 1980; Graff-Radford et al, 1984, 1985; Squire,
1982; Squire & Slater, 1978). Finally, Wallesch et al. (1983) did not
demonstrate a laterality effect for patients with lcng-standing unilateral
thalamic lesions, suggesting that differences in the time of assessment
was relevant.

NEUROPSYCHOLOGY

OF PARAMEDIAN

THALAMIC

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369

Our results indicate right-left asymmetries at the level of the thalamus
(see Fig. 4). Testing completed 1 to 2 years following the acute event
suggested a continuing asymmetry. Hemispheric differences were most
apparent only with relatively simple tests; with increasing complexity,
the deficit became more general. At a certain level of complexity, nonspecific functions of the thalamus, such as alerting, vigilance, or directed
attention (Brown, 1974; Luria, 1977; Riklan & Levita, 1969, 1970; Wallesch
et al., 1983), may obscure hemispheric differences. Patient R.M., with
the predominant right thalamic involvement, did have difficulty on verbal
tests such as the paired associates. His minimal left thalamic involvement
may be a factor, as may be his lower intellectual abilities.
The Neuroanatomy
Anterograde

of Memory

vs. retrograde

memory disorders

in diencephalic

amnesia.

Separate roles have been proposed for bitemporal and diencephalic regions
in memory functions (Huppert & Piercy, 1978; Squire, 1981). In these
claims, the bitemporal region has been suggested as being involved in
faulty information storage, while diencephalic zones are hypothesized as
being involved in the encoding operations, the acquisition of information.
Most reports indicate “good” to normal memory for remote events after
acute diencephalic dysfunction (as opposed to Korsakoff’s disease in
which a notable retrograde amnesia is demonstrated) (Michel et al., 1982;
Schott et al., 1980; Von Cramon & Eilert, 1979; Winocur et al., 1984),
with anterograde memory primarily or exclusively affected. The predominance of anterograde over retrograde amnesia has been interpreted
as lending support to the idea that diencephalic amnesia is mainly a
learning deficit, a failure in the initial stages of information processing,
rather than a retrieval deficit (Winocur et al., 1984).
In contrast, two patients with lesions apparently limited to the diencephalic regions appear to have a severe and extensive remote memory
loss in addition to the anterograde amnesia. Patient A.V. (Butters, 1984),
with a paramedian glioma, had a severe and extensive retrograde amnesia,
with no temporal gradient; our patient R.C. has a pronounced remote
memory loss, again with no apparent temporal gradient for historical
facts, but a possible gradient for personal events. Our patient R.C. had
isolated bilateral diencephalic damage secondary to infarction and demonstrated a moderately severe retrograde amnesia.
Diencephalic pathology can cause both an impairment in acquisition
as well as a remote memory deficit. Both of these paramedian thalamic
patients (A.V., R.C.) appear similar in their memory functions to patient
DRB (Damasio, Eslinger, Damasio, Van Hoesen, & Cornell, 1985), who
had herpes simplex encephalitis. Damasio and colleagues argued that a
combination of basal forebrain, lateral temporal, and insular damage were
necessary for major retrograde amnesia. Our findings suggest that, while

STUSS

ET AL.

focal limited DM damage may not cause severe retrograde amnesia,
extension into very proximal corresponding regions or systems may result
in severe remote memory loss in addition to anterograde amnesia. Our
patient had bilateral mamillothalamic
tract, dorsomedial nucleus, and
anterior nucleus damage.
Additional influences on memory functioning.
To establish primacy of
one brain region for memory, it is necessary to demonstrate amnesia
with lesions limited to that area (Butters, 1984). With this precondition,
it is doubtful that human research will unequivocally unravel the role of
different diencephalic areas in memory. In addition to limitations of in
vivo analysis of structural pathology, the two diencephalic systems involved
in memory are intimately linked. As illustrated in Figs. 1 and 2, DM
nucleus is immediately adjacent to the anterior nucleus and mamillothalamic
tract, the outflow of the MB. Involvement of fibers of passage surrounding
the lesion site must be considered (Aggleton & Mishkin, 1983). In addition
to physical proximity, they are usually fed by the same vascular system
(Castaigne et al., 1981). Finally, Speedie & Heilman (1982, 1983), based
on Valenstein and Nauta (1959) and Meibach and Siegel (1977), suggest
that the DM receives input from the MB medial limbic system. While
our quantitive structural analysis would appear to implicate the mamillothalamic tract to a greater extent (Von Cramon et al., 1985), it appears
extremely difficult to selectively damage either the DM nucleus or the
mamillothalamic
tract output of the MB. Moreover, we are unable to
negate possible involvement of other adjoining regions such as the subthalamic zones.
We propose that different brain regions in each of the two systems
contribute to overall memory functioning in a specific way (Aggleton &
Mishkin, 1983; Huppert & Piercy, 1979; Squire, 1981). First, based on
previous animal and human research, both the DM nucleus and MB
systems (including the mamillothalamic
tract and anterior nuclei) contribute
to memory, the severity of the disorder depending on the amount of
damage, with maximum impairment
if both systems are implicated (Aggleton & Mishkin, 1983; Thomas & Gash, 1985; Zola-Morgan & Squire,
1985). Second, in addition to the memory functions, each of these systems
likely adds a unique contribution,
based on its own role in behavior as
well as its connections with more anterior brain regions. Involvement
of the DM nucleus may be responsible for the “frontal lobe” component
observed in the behavior. Much of the prefrontal cortex is defined by
projections from DM (Goldman,
1979; Nauta, 1971). Many prefrontal
signs can be replicated with focal DM pathology (Alexander & Fuster,
1973; Fuster & Alexander, 1973; Kolb, 1977; Schulman, 1964; Speedie
& Heilman,
1982, 1983). This concept would also be compatible with
the suggested frontal lobe or frontal system dysfunction (among other
problems) observed in Korsakoff patients (Butters, 1984; Moscovitch,

NEUROPSYCHOLOGY

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THALAMIC

INFARCTS

371

1982; Oscar-Berman,
1980). The ventral-anterior,
and the surrounding
reticular nuclei, also have important frontal and limbic connections (Akert,
1964; Goldman, 1979; Nauta, 1971), possibly contributing to the arousal,
mood, motivational, and attentional characteristics of behavior (Cummings
& Benson, 1984; Scheibel, 1980; Scheibel & Scheibel, 1967). The medial
limbic circuit, including the mamillary bodies, anterior thalamic nuclei,
frontal connections, and linkage with the brain stem reticular core (Nauta,
1958), is theoretically implicated in activating and feedback control mechanisms (Livingston
& Escobar, 1973). Both the DM nucleus and MB
appear to be involved in memory as well as other functions associated
with the frontal-subcortical
executive and arousal systems and limbic
motivational/emotional
activities.
It may be hypothesized that impairment of these supplementary functions
is sufficient to explain the memory deficit. Our results on the maze test
(a “scalloping”
effect, with an error occurring most often on the very
first trial) suggested that motivational and/or attentional problems influenced
the learning process. However, a true memory deficit, including leftright asymmetry, was revealed on memory tasks that were relatively
simple and/or on tasks that required immediate recall without additional
attentional demands.
Prognosis

We have had the opportunity to follow our three patients for varying
durations up to 3 years. Previous reports have been conflicting, with
evidence of persistent deficits, full recovery, and partial recovery (Mills
& Swanson, 1978; Schott et al., 1980; Swanson & Schmidley, 1985). In
our cases there was a progressive and rapid improvement
in the first 6
months, with some stabilization of performance between 6 and 12 months.
Deficits demonstrated
at this time appear to be relatively permanent
(Aggleton & Mishkin, 1983; Castaigne et al., 1981; Michel et al., 1982;
Zola-Morgan & Squire, 1985). In the case of R.C., the persistent impairment
includes both anterograde and retrograde amnesia.
Summary

Even small infarcts in the paramedian thalamic area can cause devastating
neurobehavioral results. Although the primary deficit is in memory, these
patients have serious problems with motivation,
arousal, initiation,
attention, and executive functions. The memory deficits reflect hemispheric
specialization. Damage to the thalamus can cause persistent impairment
in a number of higher mental functions.
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