close

Вход

Забыли?

вход по аккаунту

?

Amnesia in monkeys after lesions of the mediodorsal nucleus of the thalamus.

код для вставкиСкачать
Amnesia in Monkeys after Lesions
of the Med~odorsalNucleus of the Thalamus
Stuart Zola-Morgan, PhD, and Larry R. Squire, PhD
~
~
Recent successes in developing an animal model of human amnesia in the monkey have made it feasible to try to
identify with certainty the specific structures in the diencephalon and medial temporal region that cause amnesia when
damaged. Monkeys with small lesions restricted largely to the posterior portion of the mediodorsal nucleus of the
thalamus were given a test of memory sensitive to human amnesia and a second test that is analogous to the skill-based
tasks performed normally by amnesic patients. The monkeys exhibited a marked impairment on the first test and
performed normally on the second. The results show that circumscribed lesions of the mediodorsal nucleus can cause
substantial amnesia.
Zola-Morgan S, Squire LR: Amnesia in monkeys after lesions of t h e mediodorsal nucleus of t h e thalamus.
A n n N e u r o l 17:558-564, 198s
Damage to the diencephalic area of the human brain
has been known for nearly a century to cause a profound amnesic syndrome 14, 7 , 10, 15, 45, 471. Although neuropathological evidence has linked the
memory impairment to lesions in the midline diencephalon, the specific structures involved have not yet
been identified with certainty. The two structures most
frequently implicated by clinicopathological data have
been the mammillary bodies of the hypothalamus and
the mediodorsal nucleus of the thalamus.
The idea that the mammillary bodies are important
is based on reports that they are consistently damaged
in Korsakoff's syndrome, the best-studied example of
diencephalic amnesia. This link has been established in
a number of frequently cited single case studies [13,
22, 37) as well as in some well-known multiple-case
studies 16, 12, 19, 20, 23, 25). Yet it is commonly
agreed, both in the case studies cited as well as in the
available neuropathological literature in general, that
the mammillary bodies are not the only site of damage
{ 5 , 25, 26, 381. Accordingly, some uncertainty remains
as to whether mammillary body damage alone can
cause diencephalic amnesia.
The idea that the mediodorsal nucleus is important
in diencephalic amnesia derives from the work of Victor and associates [47]. In their extensive studies of
the neuropathology of Korsakoff's syndrome they
identified 5 patients in whom the mammillary bodies
were damaged, but in whom memory loss was not
observed. All the patients in their series who had
memory loss (n = 38) had lesions in the mediodorsal
nucleus of the thalamus in addition to the mammillary
bodies. These results suggest that damage to the
mediodorsal nucleus, either alone or in combination
with the mammillary bodies, might be required to produce amnesia. A variety of other clinical cases have
provided additional support for the importance of
mediodorsal nucleus lesions in amnesia {273. Tumors
of the third ventricle in the vicinity of the mediodorsal
nucleus have been associated with memory dysfunction [S, 17, 28). Infarction resulting from occlusion of
the thalamosubthalamic paramedian artery can also
produce a severe memory loss 13 1,487, and damage to
the mediodorsal nucleus is common to all the reported
cases (see [14) for review). Left or right unilateral infarctions in the territory of the paramedian artery
cause material-specific disorders of memory involving
verbal or nonverbal material, respectively 130, 36, 39,
40). Finally, in one well-studied case of materialspecific diencephalic amnesia, patient N. A. E21, 461, a
series of computed tomographic scans localized a lesion to the region of the left mediodorsal nucleus 142).
Yet in all of these cases damage to other structures in
addition to the mediodorsal nucleus either has been
demonstrated or can reasonably be presumed. Accordingly, it is still uncertain whether damage to the
mediodorsal nucleus itself can cause diencephalic amnesia.
The available human case reports have identified
candidate structures that may cause diencephalic am-
From the Veterans Administration Medical Center, San Diego, and
the Department of Psychiatry, University of California, San Diego,
School of Medicine, La Jolla, CA 92093.
Received Jul 31, 1984, and in revised form Oct 10. Accepted for
publication Occ 14, 1984.
Address reprint requests to Dr Zola-Morgan, Psychiatry Service, V116, VA Medical Center, 3350 La Jolla Village Drive, San Diego,
CA 92161.
558
nesia when damaged. But these reports have not
identified with certainty any particular structure or
combination of structures. In trying to piece together
from the clinical literature evidence that damage to a
particular structure is responsible for amnesia, one encounters two problems. First, information about the
extent of brain damage is based either on indirect information (e.g., surgeon’s reports or radiographic data)
or on identified lesions that do not neatly honor anatomical boundaries. Second, quantitative data that
would usefully describe the memory impairment are
often not available. When studies report only impressions or the results of informal testing, it is difficult to
know the severity of impairment in an individual case
and impossible to compare impairment across cases.
One promising way to address these issues is to take
advantage of recent successes in the development of an
animal model of human amnesia in the monkey C33,
34,43,44). Several behavioral tests of memory, which
are sensitive to human amnesia, have been adapted for
the monkey 19, 353; such tests have already proved
useful in studying the amnesia associated with medial
temporal lobe lesions [32, 50-52). These tests should
be useful in identifying which specific structures in the
diencephalon must be damaged to produce amnesia.
Two recent studies using this approach demonstrated that medial thalamic lesions in monkeys impaired performance on an object recognition memory
task that is sensitive to human amnesia [l, 2). The
same monkeys were unimpaired on a visual pattern
discrimination task, which is analogous to the skillbased tasks that can be performed normally by human
amnesic patients [41, 431. These findings showed that
medial thalamic lesions alone can cause amnesia, but
some questions remain about the relative contributions
of the structures in that region. In the first of the
studies [l], the lesions were large, including all of the
midline nuclei in addition to the mediodorsal nucleus;
a marked behavioral deficit was reported. In addition,
the anterior nucleus of the thalamus was consistently
damaged, and all animals sustained damage to the
mammillothalamic tract that resulted in cell loss and
gliosis in the mammillary bodies. In the second study
121, the lesions of the mediodorsal nucleus were intentionally smaller, and the behavioral deficit was reported to be less severe. The lesions centered on the
magnocellular portion of the mediodorsal nucleus, but
all of the posterior midline nuclei were also damaged
as well as a portion of the centrum medianum and the
parafascicular nucleus. The extent of damage to the
mediodorsal nucleus was never greater than 50% and
it was always limited to the anterior half of the nucleus.
These studies leave open the question as to whether
lesions restricted entirely to the mediodorsal nucleus
can cause amnesia, and whether lesions that are either
more complete or located in a different portion of the
nucleus might cause a more severe deficit than was
found here. One reason for supposing that the deficit
could be more severe is the report that the impairment
on a different set of behavioral tests was greater after
posterior mediodorsal nucleus lesions than after anterior mediodorsal lesions I181.
Subjects and Methods
Sabjects
Eight cynomolgus monkeys (Macacafascicularis) were used.
Bilateral lesions of the mediodorsal nucleus of the thalamus
were made in 4. Three of the remaining monkeys did not
undergo operation. The fourth monkey underwent the same
surgical procedure as the other monkeys, but the mediodorsal lesion was not made. These latter 4 monkeys made up the
control group.
Swgety
All operations were performed under sodium pentobarbital
anesthesia (30 mdkg). The monkey’s head was held in place
in a stereotaxic instrument, and the mediodorsal lesions were
made using a combination of stereotaxic localization and a
visually guided direct surgical approach. After preparation of
a midline bone flap, the dura mater was opened on the left
side of the midline and the hemispheres were gently retracted to expose the posterior portion of the corpus callosum. The callosum was sectioned longitudinally starting at
the level of the splenium and moving rostrally for about 5
mm. The habenular commissure and the stria medullaris lying on the surface of the thalamus were identified and served
as landmarks. An L-shaped cautery tip ( 3 mm long with a 1
mm uninsulated portion that formed the base of the L) was
then insertqd into the left thalamus, just lateral to the stria
medullaris, to a depth of approximately 3 mm. To make the
lesion, the cauterizing electrode was moved in the anteroposterior plane for a distance of 4 to 5 mm. As the electrode was
moved, a current of approximately 100 milliamperes was
passed through the electrode for 15 seconds. The same procedure was followed on the right side of the brain. The
operated control monkey underwent the same procedure
except for the insertion of the electrode into the thalamus.
Monkeys were allowed 6 to 8 weeks of recovery before the
start of behavioral testing.
Behavioral Testing
Monkeys were experimentally naive at the start of the study.
All testing was carried out in a Wisconsin General Test Apparatus [lb]. During four to six sessions of pretraining, monkeys learned to obtain food by displacing objects that covered any of three food wells. In the trial unique delayed
nonmatching to sample test, monkeys first displaced an object placed over a central food well to obtain a raisin reward;
an opaque door was then lowered to block the monkey’s
view of the food wells. After 8 seconds they saw two objects,
the original one and a new one, and had to displace the new
object to obtain the raisin. Twenty such trials were presented
daily with an intertrial interval of 30 seconds. Each trial used
a new pair of objects selected randomly from a collection of
more than 300 junk objects. After reaching the learning
criterion of 90 correct choices in 100 trials, monkeys were
Zola-Morgan and Squire: Mediodorsal Lesions in Monkeys
559
tested with successively longer delays of 15 seconds, 60 seconds, and then 10 minutes between the sample and choice
trials. One hundred trials were given at each delay.
After completion of this testing, all monkeys were tested
on two pattern discrimination tasks. These tasks, which provide visual pattern information without cues of color, threedimensional shape, or size, are learned gradually by normal
monkeys over many days. Pattern discriminations can be acquired normally by monkeys with con joint hippocampalamygdalar lesions [50].These tasks have therefore provided
a useful way to gauge the selectivity of the behavioral impairment, when lesion studies are designed to model human
amnesia. In the first task, monkeys learned to discriminate a
plus sign from a square, and in the second task they learned
to discriminate an N from a W. In each task, monkeys saw
two blue plaques (7.6 crn2), on each of which was pasted a
cut-out of the pattern to be discriminated. The square (or the
N) was the rewarded stimulus for half the animals, and the
plus sign (or the W) was rewarded for the other half of the
animals. The position of the correct plaque varied on each
trial according to a pseudorandom schedule {ll}.Training
continued until the learning criterion of 2 successive days of
at least 90% correct performance was achieved. Twenty
trials per day were administered for the first task, 30 trials
per day for the second.
Results
Histological Findings
After completion of testing, operated monkeys were
killed with an overdose of sodium pentobarbital and
perfused with 0.7% saline and 10% buffered formalin.
The brains were removed, blocked, dehydrated, and
embedded in albumin. Frozen sections were cut in the
coronal plane at a thickness of 40 bg. Every fifth section was mounted on a glass slide and stained with
cresyl violet for cellular Nissl substance. A photographic enlarger was used to project approximately
every twentieth section onto the corresponding level
of a standard brain atlas, and the outline of the lesion
was traced. A transparent graph paper overlay was
then used for each section to calculate the total area of
a particular nucleus and the total area of lesion within
that nucleus. Based on these calculations, the percentage of tissue destruction was estimated for each nucleus studied.
The lesions of the mediodorsal nucleus in all 4 animals were small and limited to the posterior half of the
nucleus (Fig 1A). The extent of damage to the entire
nucleus averaged 38%. While the lesions in the
mediodorsal nucleus were bilaterally symmetrical,
there was slight to moderate damage to some surrounding structures. The Table provides quantitative
information about the damage to these structures. In
particular, the habenular nucleus was damaged bilaterally in all 4 monkeys (slightly in 2, moderately in the
other 2); the fornix was damaged unilaterally in 2 monkeys and bilaterally in 2. The anterior nucleus of the
thalamus, the mammillothalamic tract, and the mammillary bodies all appeared normal under microscopic
examination. The cingulate cortex also appeared normal. We also found minimal damage in the adjacent
midline thalamic nuclei in 2 monkeys and damage to
the stria medullaris in 2 monkeys, 40% damage for 1
animal and minor unilateral damage (less than 15%) in
another. The stria terminalis was normal in all animals.
The operated control monkey sustained a bilateral
lesion of the fornix that involved approximately 60%
of the structure (Fig l B ) , more damage than was found
in any of the monkeys with mediodorsal lesions. This
monkey had served to locate the anatomical landmarks
used to make the mediodorsal lesion. The greater fornix damage presumably resulted from the repeated
mechanical displacement of midline tissue during identification of these landmarks.
Behavioral Findings
DELAYED NONMATCHING TO SAMPLE. Monkeys
with mediodorsal lesions were impaired at learning the
basic task when a delay of 8 seconds was used and also
when the delays were extended to 15 seconds, 60 sec-
Behavioral Performance and Extent of Lesion in Each Monkey
Monkey
Trials to
Criterion
on
DNMTS
Task
Mean
Percentage
Correct
for 3
Delays"
MD 1
MD 2
MD 3
MD 4
oc 1
NC 2
NC 3
NC 4
140
300
440
380
120
120
140
180
74
67
76
77
81
87
81
89
Extent of Lesion (%)
Mediodorsal
Nucleus
32
37
38
44
0
...
...
...
Fornix
40W)
50
50
30(U)
60
...
...
...
Anterior
Nucleus
0
0
0
0
0
...
Paraventricular
Nucleus
Parafascicular
Nucleus
20
0
0
0
0
0
0
18
0
0
...
...
...
...
...
...
...
...
Centrum
Medianum
Pulvinar
(Medial
Division)
Habenula
0
0
0
0
58
21
27
18
0
0
0
10
8
0
...
...
...
...
...
...
...
...
...
23
"Three delays: 15 sec, 60 sec, 10 min.
DNMTS = delayed nonmatching to sample; MD = mediodorsal nucleus; U = unilateral; OC
560 Annals of Neurology
Vol 17 No 6 June 1985
=
operated control; N C
=
normal control.
onds, and 10 minutes (Table, Fig 2). Figure 2A shows
that the normal group required a mean of only 140
trials to reach learning criterion on the basic task,
whereas the lesion group required a mean of 315 trials
(t [df = 61 = 2.63; p < 0.05). As the delay was
increased from 8 seconds to 10 minutes, the performance of the lesion group deteriorated markedly (Fig
2B). A two-way analysis of variance revealed significant effects of group (F [df = I, 61 = 17.1; p <
O.Ol), delay ( F Cdf = 1, 3) = 47.3; p < O.Ol>, and a
group X delay interaction (F [df = 3, 181 = 6.1;p <
0.01). The single monkey that served as a control for
the surgical procedure performed comparably to the
other 3 control animals (Table).
A 12.1
A 10.8
PATTERN DISCRIMINATION. The two pattern discrimination problems proved to be equally difficult
and, for each monkey, the learning scores for the two
problems were averaged together for purposes of analysis. Figure 2C shows the average number of trials
required to learn the two pattern discrimination problems. The group with the lesions required a mean of
340 trials, and the normal group required a mean of
325 trials (t [df = 61 = 0.37,p > 0.10). The successful performance of monkeys with mediodorsal lesions
cannot be the result of recovery of function. Three
months after completing the pattern discrimination
tasks, the same monkeys remained impaired on the
delayed nonmatching task [49].
In a previous study [ S O ] , monkeys with conjoint
hippocampal-amygdalar lesions were not quite normal
on these same two pattern discrimination tasks, and
their mild impairment resulted entirely from poor performance on the first five trials of each testing day.
Accordingly, in the present study we analyzed separately the scores for the first five trials of each test day
and the scores for the remaining trials of each test day.
Despite the fact that monkeys with mediodorsal lesions performed normally overall, a small but notable
A 9.6
A 8.6
A
B
.
Fig 1. (A) Representative coronal sections through the thalamus
showing the smallest (dark) and the largest (striped) extent of
dzmage in the 4 monkeys with lesions of the mediodorsal nucleus.
Numbers t o the ldt of sections indicate the anteroposterior level
{44a). (B)A coronal section at the level of the thalamus showing
the extent of dzmage t o the fornix in the control monkey that
u n b e n t sham operation.No thakzmic nuclei were damaged
in this monkey. (Cd = caudate nucleus; CM, CM-Pf = centmmedian nucleus; Px = fornix; Hb = habenula; LD =
Lteral dorsal nucleus; LP = lateral posterior nucleus; M D =
mediodorsal nucleus; VLc, VLps = ventral lateral nucleus;
VPLc, VPLo = ventral posterolateral nucleus; VPM = ventral
posteromedial nucleus; CL = claustrum; VPI = ventral postewinferior nucleus; VPMpc = ventral posteromdial nucleus;
THI = habenukzr-intwpedunculartract; Pu1.0 = oral pulvinar nucleus; Pul. = pulvinar.)
Zola-Morgan and Squire: Mediodorsal Lesions in Monkeys
561
500
-
100
400
-
90
z
0
a
w
c
a 300
0
-
2
v)
-J
z
500[
+
8
a
400
a
8
IE0
80-
1
t
a
9
E
-
200
-
w
70
-
60
-
n.
Z
2I
1
50'
A
Lac
B
I
15 sec
60 MC
DELAY
1
10 min
-N
impairment was present in the first five trials. The normal monkeys averaged 76% correct during the first
five trials and 66% correct for the remaining trials.
Monkeys with mediodorsal lesions scored 59 and
71%, respectively ( t {df = 6) = 4 . 1 8 , p < 0.05 for the
first five trials, mediodorsal lesions versus normal; t Edf
= 61 = 0.85 for the remaining trials, mediodorsal
lesions versus normal). This finding supports the suggestion that performance at the beginning of each testing day during pattern discrimination learning depends
on a kind of memory that is sensitive to amnesia {43].
Fig 2. (A) Performanceof 4 control monkeys (N) and 4 monkeys
with lesions of the mediodorsal thalamic nucleus (MD) on initial
learning of the delayed nonmatching t o sample task with 8-second delays. The M D group was impaired as measured by trials
and ewors to criterion. Symbols indicate pedormance of indiddual animals in each group. (B) Mean percentage correct by the N
and M D groups on the delay portion of the nonmatching task.
Compared t o the N group, the M D group was disproportionately
affected by increasing delays. (C) Average scores obtained by the
N and M D groups far two pattern discrimination task. The
M D group was normal as measured by trials and errors to cviterion.
Discussion
Monkeys with small bilateral lesions of the posterior
portion of the mediodorsal nucleus of the thalamus
exhibited a marked deficit on a behavioral test of memory that has been used in recent years to model the
human amnesic syndrome. The same monkeys performed normally on learning pattern discrimination
problems, a finding that is analogous to the preserved
capacity for skill learning in human amnesic patients
{SO]. These findings are in agreement with previous
reports that lesions in this region of the thalamus can
cause amnesia in the monkey [l, 2). These earlier
studies showed that a lesion including both the anterior portion of the mediodorsal nucleus and the anterior nucleus produced a greater memory deficit than a
lesion in either area alone. These results were interpreted to mean that the combined lesion is required to
obtain an appreciable memory deficit. The present
study shows, however, that a small lesion of the posterior portion of the mediodorsal nucleus can also produce an appreciable memory deficit. The deficit was
more severe than that observed after a lesion of the
anterior portion of the mediodorsal nucleus. For example, at a delay of 60 seconds, which was used in
both studies, monkeys with the anterior mediodorsal
lesion achieved a score of 86% correct, and monkeys
with the small posterior lesion achieved a score of
76% correct. Thus, damage to the posterior portion of
the mediodorsal nucleus appears to cause an appreciable loss of memory and a greater loss than is caused by
damage to other portions of the nucleus. A similar
conclusion was reached in a larger study of monkeys
with lesions of the mediodorsal nucleus given different
behavioral tests { 181.
The lesions of the mediodorsal nucleus in the present study were accompanied by unilateral or bilateral
fornix damage and by damage to the habenula (Table).
The involvement of these structures cannot explain the
severity of memory impairment. There was no relationship between the severity of behavioral impairment and the extent of fornix damage in the monkeys
with mediodorsal nucleus lesions (Table). In addition,
the operated control monkey with no damage to the
562
Annals of Neurology
Vol 17 No 6 June 1985
mediodorsal nucleus sustained more damage to the
fornix than did any of the monkeys in the group with
mediodorsal lesions (Fig l), and yet this monkey was
behaviorally unimpaired. Moreover, monkeys with
complete bilateral fornix lesions have been shown previously to be unimpaired on the same delayed nonmatching to sample task used in the present study
(241. Finally, neither the extent of habenula involvement nor the extent of habenula plus fornix involvement was related to the behavioral deficit (Table).
Damage to the midline nuclei occurred in only 2
monkeys with mediodorsal lesions and was limited to
less than 23% of any nucleus (Table). One reason for
considering the possible contribution of damage to the
midline nuclei to memory impairment is the known
connection of these nuclei to the amygdala r3J and to
the hippocampus [29], which have been implicated in
memory functions (32,437. In each case, however, the
portion of the midline nucleus that was damaged was
posterior to the portion of that nucleus known to project to the amygdala and hippocampus. These findings,
together with the fact that 2 monkeys had no involvement of midline nuclei at all, indicate that damage to
these nuclei did not contribute to the behavioral
deficit.
We conclude that damage to the mediodorsal nucleus alone is sufficient to cause an appreciable memory deficit, one presumably severe enough to be clinically significant were it to occur in human patients. It
should be emphasized that these remarks about the
severity of the deficit following mediodorsal lesions are
consistent with the possibility that anterior nucleus lesions, or lesions of other diencephalic structures such
as the mammillary bodies, could add further to the
deficit.
Supported by the Medical Research Service of the Veterans Administration and by USPHS Grant 1 R01 NS19063.
We thank Dr Mark Moss for surgical assistance, Ellen Bulder for
behavioral testing, Janet Kurz for histological assistance, and Dr
David Amaral for help in the histological analysis of the brains.
Our research protocol describing all aspects of the present study
related to the use of animals (care and maintenance, surgery, behavioral testing, and euthanasia) was approved by the Animal Research
Committee of the V.A. Medical Center and University of California
School of Medicine, San Diego.
References
1. Aggleton JP, Mishkin M: Visual recognition impairment following medial thalamic lesions in monkeys. Neuropsychologia
21:189-197, 1983
2. Aggleron JP, Mishkin M: Memory impairments following restricted medial thalamic lesions in monkeys. Exp Brain Res
52:199-209, 1983
3. Amaral DG, Cowan WM: Subcortical afferents to the hippocampal formation in the monkey. J Comp Neurol 188:573592, 1980
4. Barbizet J: Human Memory and Its Pathology. San Francisco,
Freeman, 1973
5. Brierley JB: Neuropathology of amnesic states. In Witty CWM,
Zangwill OL (eds): Amnesia: Clinical, Psychological and
Medicolegal Aspects, ed 2. London, Butterworths, 1977, pp
199-223
6. Brion S, Mikol J: Atteinte du noyau ladral dorsal du thalamus
et syndrome de Korsakoff alcoolique. J Neurol Sci 38:249261, 1978
7. Butters N, Cermak LS: Alcoholic Korsakoff‘s Syndrome. New
York, Academic, 1980
8. Cairns H, Mosberg WH: Colloid cyst of the third ventricle.
Surg Gynecol Obstet 92:545-570, 1951
9. Gaffan D: Recognition impaired and associarion intact in the
memory of monkeys after transection of the fornix. J Comp
Physiol Psychol 86: 1100-1 109, 1974
10. Gamper E: Zur Frage der Polioencephalitis haemorrhagica der
chronischen Alkoholiker. Anatomische Befunde beim chronischen Korsakow und ihre Beziehungen zum klinischen Bild. In
Verhandlungen der Gesellschaft deutscher Nervenartzte, 1928.
Leipzig, Vogel, 1928, pp 352-359
1. Gellerman LW: Chance orders of alternating stimuli in visual
discrimination experiments. J Gen Psychol 42:207-208, 1933
2. Gruner JE: Sur la pathoiogie des encephalopathies alcooliques.
Rev Neurol94:682-689, 1956
3. Grunthal E: Veber das Corpus mamillare und den Korsakowschen Symtomen Komplex. Confinia Neurol2:65-95, 1939
4. Guberman A, Stuss D: The syndrome of bilateral paramedian
thalamic infarcrion. Neurology (Cleveland) 33:540-546, 1983
5. Gudden H : Klinische und anatomische Beitrage zur Kenntnis
der multiplen Alkoholneuritis nebst Bemerkungen uber die Regenerationsvorgange im peripheren Nervensystem. Arch
Psychiatr Nervenkr 28:643-741, 1896
6. Harlow HF Studies in discrimination learning by monkeys. I.
The learning of discrimination series and the reversal of discrimination series. J Gen Psychiatry 30:3-12, 1944
17. Ignelzi RJ, Squire LR: Recovery from anterograde and retrograde amnesia after precutaneous drainage of a cystic
craniopharyngioma. J Neurol Neurosurg Psychiatry 39: 12311235, 1976
18. Isseroff A, Rosvold HE, Galkin TW, Goldman-Rakic PS: Spatial memory impairments following damage to the mediodorsal
nucleus in the thalamus of rhesus monkeys. Brain Res 23297113, 1982
19. Jarho L Korsakoff-like amnesic syndrome in penetrating brain
injury. A study of Finnish war veterans. Acta Psychiatry Neurol
Scand 49(suppl 54):l-156, 1973
20. Kahn EA, Crosby EC: Korsakoff‘s syndrome associated with
surgical lesions involving the mammillary bodies. Neurology
(Minneap) 22:117-125, 1972
21. Kaushall PI, Zetin M, Squire LR: A psychosocial study of
chronic, circumscribed amnesia. J Nerv Ment Dis 169383389, 1981
22. Koeppen AH, Barron KD: Marchiafava-Bignami disease. Neurology (NY) 28:290-294, 1978
23. Lehtonen R Learning, memory, and intellectual performance in
a chronic state of amnesic syndrome. Acta Psychiatry Neurol
Scand 49(suppl 54):l-156, 1973
24. Mahut H, Zola-Morgan S, Moss M: Hippocampal resections
impair associative learning and recognition memory in the monkey. J Neurosci 2:1214-1229, 1982
25. Mair WGP, Warrington EK, Weiskrantz L: Memory disorder in
Korsakoff psychosis. A neuropathological and neuropsychological investigation of two cases. Brain 102:749-783, 1979
26. Malamud N, Skillicorn SA: Relationship between the Wernicke
and Korsakoff syndrome: A clinicopathologic study of sevenry
cases. Arch Neurol Psychiatry 76:585-596, 1956
Zola-Morgan and Squire: Mediodotsal Lesions in Monkeys
563
27. Markowitsch HJ: Thalamic mediodorsal nucleus and memory: a
critical evaluation of studies in animals and man. Neurosci
Biobehav Rev 6:351-380, 1982
28. McEntee WJ, Biber MP, Per1 DP, Benson FD: Diencephalic
amnesia: a reappraisal. J Neural Neurosurg Psychiatry 39:436446, 1976
29. Mehler WR: Subcortical afferent connections of the amygdala in
the monkey. J Comp Neurol 190733-746, 1980
30. Michel D, Laurent B, Foyatier N, et al: Infarctus thalamique
paramedian gauche. Rev Neurol (Paris) 138:533-550, 1982
3 1. Mills RF’,Swanson PD: Vertical oculomotor apraxia and memory loss. Ann Neurol 4:149-153, 1978
32. Mishkin M: Memory in monkeys severely impaired by combined but not by separate removal of amygdala and hippocampus. Nature (Land) 273:297-298, 1978
33. Mishkin M: A memory system in the monkey. Philos Trans Roy
SOCLondon B [Biol] 298:85-95, 1982
34. Mishkin M: Global amnesia in the monkey. In Olton D, Corkin
S, Gamzu E (eds): Conference on Memory Dysfunctions. New
York, New York Academy of Sciences, 1985 (in press)
35. Mishkin M, Delacour J: An analysis of short-term visual memory in the monkey. J Exp Psycho1 [Anim Behav) 1:326-334,
1975
36. Morrell F, de Toledo-Morel1 L, Squire LR, et ak Thalamic amnesia: material specific deficits associated with dorsomedial nucleus infarction. SOCNeurosci (abs) 9:29, 1983
37. Remy M: Contribution i I’etude de la maladie de Korsakow.
Monatssch Psychiatry 106:128-144, 1942
38. R i g s HE, Boles RS: Wernicke’s disease. A clinical and
pathological study of 42 cases. Q J Stud Alcohol 5:361-370,
1944
39. Speedie LJ, Heilman KM: Amnestic disturbance following infarction of the left dorsomedial nucleus of the thalamus.
Neuropsychologia 20:597-604, 1982
40. Speedie LJ, Heilman KM: Anterograde memory deficits for
visuospatial material after infarction of the right thalamus. Arch
Neural 40:183-186, 1983
564 Annals of Neurology Vol 17 No 6 June 1985
41. Squire LR: The neuropsychology of human memory. Ann Rev
Neurosci 5:241-273, 1982
42. Squire LR, Moore RY: Dorsal thalamic lesion in a noted case of
human memory dysfunction. Ann Neurol 6:503-506, 1979
43. Squire LR, Zola-Morgan, S: The neurology of memory: the case
for correspondence between the findings for man and nonhuman primate. In Deutsch JA (ed): The Physiological Basis of
Memory, ed 2. New York, Academic, 1983, pp 200-268
44. Squire LR, Zola-Morgan S: The neuropsychology of memory:
new links between humans and experimental animals. In Olton
D, Corkin S, Gamzu E (eds): Conference on Memory Dysfunctions. New York, New York Academy of Sciences, 1985 (in
press)
44a. Szabo J, Cowan WM: A stereotaxic atlas of the brain of the
cynomolgus monkey (Macaw faJciculans). J Comp Neurol
222265-300, 1984
45. Talland GA: Deranged Memory. New York: Academic, 1965
46. Teuber H-L, Milner B, Vaughan H G Jr: Persistent anterograde
amnesia after stab wound of the basal brain. Neuropsychologia
6~267-282, 1968
47. Victor M, Adams RD, Collins GH: The Wernicke-Korsakoff
Syndrome. Oxford, Blackwell, 1971
48. Winocur G, Oxbury S, Roberts R, et al: Amnesia in a patient
with bilateral lesions to the thalamus. Neuropsychologia
22:123-144, 1984
49. Zola-Morgan S , Squire LR: Two forms of amnesia in monkeys:
rapid forgetting after medial temporal lesions but not diencephalic lesions. SOCNeurosci (abs) 8:24, 1982
50. Zola-Morgan S, Squire LR:Preserved learning in monkeys with
medial temporal lesions: sparing of motor and cognitive skills. J
Neurosci 4:1072-1085, 1984
5 1. Zola-Morgan S , Squire LR: Medial temporal lesions in monkeys
impair memory in a variety of tasks sensitive to amnesia. Behav
Neurosci 9922-34, 1985
52. Zola-Morgan S , Squire LR, Mishkin M: The neuroanatomy of
amnesia: amygdala-hippocampus vs. temporal stem. Science
218:1337-1339, 1982
Документ
Категория
Без категории
Просмотров
2
Размер файла
698 Кб
Теги
mediodorsal, lesions, monkey, thalamus, nucleus, amnesia
1/--страниц
Пожаловаться на содержимое документа