Nrurop,sychologia, Vol. 23. No
Prmted ,n Great Britain.

VISUAL

I. pp I-12, 1985

AGNOSIA

002X 3932/85 $3(x)+00
C 19115Pergamon Preq\ L td

CONTRASTED
WITH
DISCONNECTION*

VISUAL-VERBAL

GLENN J. LARk&BEE,t$ HARVEY S. LEVIN,t F. JACOB HUFF,$ MARILYN C. KAYO and
FAUSTINO C. GUINTO, JR.?
tuniversity

of

Texas Medical

Branch. @Harvard Medical School at the Massachusetts
‘IMedical College of Wisconsin at Milwaukee

General

Hospital

and

(A<,cc/Itrd 30 MU? 1984)
Abstract-Serial
neuropsychologlcal
findings are contrasted
in two cases: one with a syndrome of
visual agnosia, the other with a disorder resulting from visual verbal disconnection.
Both patients
were impaired in confrontation
naming of objects and pictures. but the patient with visual-verbal
disconnection
was able to perform tasks of color object matching and pantomime
recognition.
whereas the patient with visual agnosia could not do so. demonstrating
a failure to establish
meaningful nonverbal visual-visual
association.
Additionally.
the performance
of the patlent with
visual agnosia reflected an evolution from the apperceptive
to associative forms of the disorder,
suggesting
that the various impairments
of visual identification
form a continuum
of related
disorders.

INTRODUCTION
VISUAL agnosia is a rare disorder characterized by a failure to recognize objects visually that
is not associated with aphasia, primary visual disturbance
or dementia (see RUBENS [25] for
an extensive review). There has been controversy over whether visual agnosia is secondary to
a more pervasive cognitive impairment
[ 14,23,25]. BAY [Z, 31 attributed visual agnosia to a
primary
visual disturbance
but others have demonstrated
defects of primary
visual
functions in nonagnosic patients that are comparable to the defects in patients with agnosia
[9,16]. GESCHWIND and F~SILLO [l l] contended that most cases of apparent visual agnosia
represent a confabulatory
visual anomia which interferes with otherwise intact gnostic
capacities. According to this view, the receptive language area of the left hemisphere is
deprived
of visual input by splenio-left
occipital lesions, resulting
in a visual-verbal
disconnection.
Visually mediated deficits that frequently result from such a lesion include
alexia and color anomia, in addition to visual object anomia [I 11.
Since publication
of the study by Geschwind and Fusillo, three cases of visual agnosia
without alexia have been reported that cannot be attributed to a visual -verbal disconnection
[l, 16, IS]. Two of the patients also had preserved color naming in addition to normal
reading, features incompatible
with a visual-verbal
disconnection.
All three cases had
evidence of bilateral occipito-temporal
damage, suggesting visual-limbic
disconnection.

*This study is based in part on a paper presented at the 5th International
Neuropsychological
Society European
Conference, Deauville, France. June 19x1. Preparation
of this paper was supported by the Center for the Study of
Nervous System Injury Grant NS 07377-I I.
IReprint requests should be addressed to: Glenn J. Larrabee, Psychology
Service (116B), James A. Haley VA
Hospital,
13000 North 30th Street. Tampa. FL 33612. U.S.A.

Recent authors [ 14. 751 have adopted LISSAWR’S [ I73 original classitication
of visual
agnosia into apperceptive and associative forms. The apperceptive form, usually associated
with bilateral posterior cerebral disease, is characterized
by a failure of both recognition and
integration
of the features of-a visual stimulus into a unified pet-cept. Concomitant
defects
include inability to relate the stimulus to previousexperience,
to \,isually match objects or to
copy drawings of objects. Associative visual agnosia. which can occur with either bilateral
posterior disease of dominant occipital lobe and splenial lesions, is characterized
by a failure
of recognition
(evidenced by inability to describe or demonstrate
the use of objects) in the
context of preserved ability to match a&or
copy stimuli [25]. RURENS [35] described two
patients whose deficits evolved from associative visual agnosia into visual object anemia OI
“optic aphasia”. which could be explained on the basis of a visual verbal disconnection.
Such cases suggest that there may be a continuum
of disturbance
in Csuul recognition.
In a11
effort to explain the range of observed deficits. RATCLIFF~. and NISYXIMBE
[3]
have
proposed a model of ob.ject recognition,
based on MARR’S computational
theory of vision
[IY]. In Marr’s theory. visual representation
of objects proceeds through successi\.e lel,els of
representation
from a coding ofintensity
changes in the retinal image to a three-dimensional
(physical
and functional
representation
which has access to a “semantic
system”
association) and a “name retrieval” system. According to Ratcliffe and Newcombe’s model.
the various clinical syndromes (apperceptive
and
associative visual ngnosia, visual i,erbal
disconnection)
result from disruption
at different
levels of representation.
The purpose of this communication
is to contrast a case of resolvin g visual agnosia of the
appercepti\,e type with a case ofvisual
verbal disconnection.
Despite the apparent similarit>
of their misnaming
of objects presented visually, these subjects differed in nonverbal visual
recognition
and matching
of objects. .4lthough
both patients were alexic, the cast of
visual verbal disconnection
had splenio-left occipital lesions, whereas the resolving case of
visual apnosia had bilateral lesions. Neither patient had evidence of aphasia or dementia and
their visual acuity was sufficient for the neuropsychological
tasks.

CASE

I

C.E.. a 57-qr-old. right-handed
woman with hyperlcnsion
and diabetes mellitus. but no previous neul-oln~ic~tl
symptoms. was observed to be disoriented
111her own home on 26 June IYXI. She was unable to local fan~har
objects such as light switches. and tended to bump inlo objects situated in her right \lsual field. She complained ufa
headache and was temporally disoriented
Two days aftcr the onset of these symptoms. she was treated in a hospital
emergency room with intramuscular
apresoline and suffered a brief hypotenslve syncopal episode. Subsequently.
her visual symptoms persisted and her gait was unstead!. Several days later. while sllting 111a hospital waiting room.
she suffered a seizure beginnmg with clonic movement of the right leg followed by Ios\ of consciousness.
Blood
pressure and cardiac rhythm were normal. Blood glucose was 3YO mg”,,. Several hour5 later. upon admission to the
neurology servxe. she was alert and oriented to per‘;on. but nor to time or place. Her speech was ilucnt. with
occaGonnl perseverations
but without paraphasias
Repetition and comprehension
of speech were normal. She
could not idenNy objects presented visuall) or tactually nor could she demonstrate
or describe their use. She could
not identify colors and did not recognve the faces ofli~mil> members. She ~asalex~c. and was unable II) manipulate
a pencil appropriately
in order to write (she confused the ends of the pencil). Motor responses to commands were
apraxic bilaterally. more so m the right extremities. A dense right homonymous
hemlanopsla was present. She could
not visually track objects. but produced full saccades on command. Strength was normal. Deep tendon reflcxeh were
symmetric; plantar responses were flexor. Sensation was intact except for intermittent eutlnctlon ofthe right sitlc on
simultaneous
stimulatton.
Her gait was unsteady. wlrh a tendency IO list IO the right O+cr the lirst several hospital
days visual tracking, praxis and gait became normaI. Computed tomography
(CT). which will, performed 7 daq
after the onset of illness.demonstrated
decreased attenuation
in the arcas ofthe Icft occlpltal lobe and the anterior
limb of the internal capsule on the right. Figure I (upper row) deplcls II CT scan ohtalned 20. I months post-onset
(GE XX00 scanner, wlthout contrast) which was compatible with cerebral infarc:ions.
fhe clectroenceph~~lo~rarn
(EEG) was biremporally
slowed. with maximal slowins in the Icft mldtemporal
arc<i.

VISUAL

A<iNOSIA

FIG. 1. Top. Case C.E. Multiple contiguous CT slices show areas of low attenuation
in the anterior
limb of the right internal capsule and the left occipital lobe. consistent with infarction. Bottom. Case
M.W. Contiguous
CT cuts showing a large surgical defect through the left half of the splenium
extending mto ipsilateral occipital lobe. Residual calcification
is just anterior to splenium.

F-I<; 2. (‘ax

M.W. Coronal

CT reveals a large defect of left \plenium

lobe.

and medial aspect of occtpttal

VISUAL

AGNOSIA

5

Evaluation of visual acuity was difficult because of alexia and problems in visual recognition. Within 2 weeks of
her infarction, acuity was estimated to be at least 20/400 by optokinetic nystagmus (OKN), and at least 20/100 by
her response to eye chart stimuli (although she could not read the stimuli, she could indicate when they began to
blur). At 2 months OKN (using a smaller tape) revealed at least 20/100. At 5 months status post, resolution 01
apperceptive deficits allowed training her to discriminate circles. triangles and squares, which was achieved at 2Oi70.
Tactile sensitivity (pressure aesthesiometer)
was relatively preserved.

CASE 2
W.M., a 62-yr-old, right-handed
man presented with a total right homonymous
hemianopsia.
total alexia without
agraphia, object and color naming disturbance
and visuoconstructive
difficulties following surgical division of the
splenium and the posterior 2.5 cm of the body of the corpus callosum to remove a left intraventricular
meningioma.
Prolonged retraction during surgery produced necrosis in the left occipital tip, which was amputated 3.5 cm forward
from the occipital pole. W.M.‘s visual cognitive deficits have remained stable over the 4 yr since his nearly complete
visualLverbal
disconnection
developed
after surgery 1151. Details of the patient’s
preoperative
and early
postsurgical
neuropsychological
and neurological
findings have been reported 1151. A CT scan with contrast (GE
8800) obtained 4 yr after surgery (Figs 1 lower row and 2) demonstrated
the dominant occipital and extensive splenial
damage. Visual acuity, assessed by having him specify the orientation
of the open side of a rotated letter “E”. was
estimated at 20/50 for O.D. Acuity in OS.. assessed by OKN, was at least 20:70.

GENERAL

TESTING

PROCEDURES

The test data for subjects C.E. and W.M. are presented in Tables 1 and 2, respectively. Data on object and
picture naming are presented separately in Fig. 3. and data on pantomime recognition and colorPobject matching
are presented in Fig. 4. References for published tests are cited in Tables 1 and 2 and Figs. 3 and 4.
The object naming test for confrontation
visual naming, tactile naming and for the condition
of visual
confrontation
naming while holding the object was from the Neurosensory
Center Comprehensive
Examination
for
Aphasia
1271. as were the writing-to-dictation
and from-copy
tests. Visual naming of pictures and reading
comprehension
of words and phrases were from the Multilingual
Aphasia Examination
[S]. The visual visual
matching procedure,
which was a series of pictures from the discrimination
section of the Continuous
Visual
Recognition
Memory Test [I 31. consisted of discriminating
a picture which matched a target stimulus (e.g. a beetle)
from five visually similar foil stimuli (other insects). The auditory naming task [ 151 was a verbal analog of the visual
naming of pictures test (e.g. “What is the name for a body of land surrounded
by water‘?“). The tests of facial
recognition and three-dimensional
block construction
were developed by fkNToN
et rd. 16. 73. The verbal memory
for colors test required the subject to state the colors of IO common objects (e.g. banana. snow, etc.) which the
examiner named out loud. Color sorting and color naming were conducted using two sets ofeight jumbo crayons for
matching-to-sample
and confrontation
naming. The various reading tasks (letters. numbers. words vs nonwords)
were constructed
by hand printing the stimuli on X by 5 in. sheets of paper. All performances
are presented as
percentage correct, since some of the performances,
such as confrontation
naming were so impaired that they fell far
below the first percentile of published normative data. Defective performances
were defined as those scores falling
below the fifth percentile of the score distribution
based on normal controls.

RESULTS
Visuul reco~nitim

of djects

C.E.‘s visual identification
of objects markedly improved and changed qualitatively
over
the course of the study (Fig. 3). Initially (IO days post-infarction),
she could not name
common objects presented visually (e.g. bottle) nor could she describe or demonstrate
their
use. Imagined use of objects and symbolic gestures to oral command were intact bilaterally,
excluding ideomotor apraxia as a basis for her inability to use actual objects. The anemic
errors were frequently unrelated to the object, either semantically
or by similarity of visual
form. She was unable to copy drawings or visually match-to-sample
common objects such as
a brush. These features were consistent with apperceptive visual agnosia. By 4X days postinfarction C.E. could match pairs of common objects on the basis of visual cues while verbal
identification
by naming or description
remained
impaired.
Thus, her visual agnosia
apparently
evolved from an apperceptive
to an associative
type. Naming to auditory

description (e.g. “What is a large grey animal with floppy ear5 and a long nose?” .Ans\vcr:
“Elephant”)
was markedly better than visual identification.
Tactile naming of common
objects was impaired
bilaterally
initially (despite normal sensory thresholds
to nylon
filaments), later changing to a left-hand anemia and finally. preserved naming in both hands.
At nearly 1 yr post-infarction,
she continued to misname objects presented visually but could
improve her naming performance
if allowed to hold the object during visual inspection.
Naming objects under the condition
of combined
tactile and visual cues. however. was
notably slowed with occasional errors. Pointing to objects named by the examiner improved
considerably
on the examination
nearly 1 yr post-infarction.
At almost 1 yr post-onset. C.E.
was able to name objects. but still performed at a defective level OII confrontation
naming of
pictures.
As can be seen from Fig. 3. W.M.‘s naming of objects on the basis of visual cues has
remained impaired. In contrast. verbal identification
of objects which he held during visual
inspection was rapid and accurate. Most of W.M.‘s anomicerrors
OII confrontation
naming

VISUAL

Table 2. Visual. cognitive

and related

1

AGNOSIA

neuropsychological

functions
Months

post-surgery
20.9

49

success rate unless otherwise

stated)

I .4

Test
(Figures
Tactile naming [27]
Right hand
Left hand
Visual naming of objects, allowed to
hold and manipulate
1271
Visual visual match of pictures [13]
Auditory naming [IS]
Facial recognition
16. 71
3-D block construction
[6]
Dvorine (tracing) [X]
Farnsworth
Munsell [lo]
Verbal memory for colors
Color sort
Color name
Reading camp.. words and phrases
Reading: letters
numbers
words
words vs nonwords
Writing: Dictation
[27]
From copy

indicate

9.9
percent

75t
371-

I 00
62t
x7.5:

100:

100:
x5:
_~

71

X9.7.t
71

100

100:
100:
20:
15t
10:

[S]

100:
33:

43:
.~
0:

0:
Preserved
Defective

lOOgo60_

IO0
671IO0

100:
79.6

Preserved
Defective

*Tests without references were devised in the course of clinical examination.
tDefective performance
relative to normal controls.
$No data on normal controls. but most literate subjects would be expected

~

for W.M.

----

Preserved
Defective

to approximate

69?

I 00
197
errorst
100:
100:
25:
16.7t
16.7:
16.7:
O$
100:
Preserved
Defective

a perfect

score.

0 VNP. Visual Naming, Pictures
@.VNO. Visual Naming. Objects
CE, Visual Agnosla
VNO
WM. Visual-Verbal
Dlsconnectlon
* Defectwe Performance

P) 7om
:

6Om

0llSZt

1.6

31
Months

FIG. 3. Confrontation

109
Post-Onset

naming

20 9

performance.

were semantically
related to the test object, other objects presented earlier during the
examination
or to his previous responses. W.M.‘s persistent inability to point to objects
named by the examiner
has paralleled
his residual anomia
for visual presentation.
Visual--visual
matching-to-sample
of common objects (e.g. razor) has been consistently
preserved. Description
and demonstration
of the use of objects presented visually were
frequently misdirected by his anemic errors. Naming objects described by the examiner (e.g.
“What is a body of land surrounded
by water called‘?” Answer: “Island”) in the absence of
visual presentation
was preserved. Naming objects palpated by the right hand in the absence
of visual cues was intact, whereas there was a mild anomia for objects placed in the left hand.

The onset of C.E.‘s cerebral vascular insult was followed by a period of resolving
prosopagnosia.
Although
she could recognize her family when examined
IO days postinfarction. she could not identify facial photographs
of famous persons by naming them 01
selecting the target face from a multiple-choice
array. By 3 months. she could identify
famous persons in ;I multiple-choice
format. although
confrontation
naming of these
persons remained impaired. This did not change on examination
almost 2 yr following her
infarction.
In contrast, although W.M. had difficulty in confrontation
naming of familial
faces, at no time did he have difficulty identifying familiar facts in a multiple choice format.
This dissociation
extended to unfamiliar
taces. W.M. was able to match photographs
of
unramiliar
laces [7], while C.E. could not. Both W.M. and C.E. were impaired
in
constructing
designs from three-dimensional
models [S] throughout the serial examinations.
However. W.M. performed better relative to C.E.

Disturbances
in color recognition
can occur in visual agnosia [?I] and in alexia without
agraphia 141. Both C.E. and W.M. displayed preserved color perception [X] and verbal color
memory (e.g. “What color is a banana?“)
despite markedly impaired confrontation
naming
of colors. In contrast to C.E.‘s marked impairments
in ordering hues according to their
saturation
[IO] and matching colors to line drawings ofcommon
objects with characteristic
colors [7Y], W.M.‘s Farnsworth
Munsell performance,
though impaired, was considerably
better relative to C.E., and he achieved a normal level of color-object
matching when
instructed to suppress his misleading verbalizations
of the objects. For example when he first
attempted to match colors with line drawings of objects, he would try to name the color and
the object. When instructed
to perform the task without verbal response (by pointing)
performance
was normalized.
Both patients’
color object matching
performance
is
displayed in Fig. 4.
Keudirty

und pantomime

recognition

Both C.E. and W.M. had alexia without agraphia. W.M.‘s total alexia extended to letters.
\vords and numbers. and improved minimally during the 4-yr study period. C.E.‘s alexia was
also Initially total, but evolved within 3 months to a verbal alexia which persisted during the
20-month follow-up period. At 20 months, she was able to figure out short words (e.g.
“ball”) by spelling them aloud in a letter by letter fashion. True reading of words did not
COM, Color~Ob~ect Matching
PR. Panromlme
Recognltlon

100,

904
G
;

801
70

6

60 i

E
,”

50-1
40

2

20
10
30 I

- CE. “,$“a, Agnom
___-WM. Visual Verbal D~sconnectmn

VISUAL

AGNOSIA

9

return, however. Interestingly,
follow-up examinations
disclosed that both C.E. and W.M.
were able to correctly discriminate a word from two accompanying
nonword anagrams (e.g.
“in” vs “ds”,
“mg”) by pointing, although neither could read the real word. The number of
correct responses varied from 6 out of 10 to 10 out of 10 depending on the type of task. That
is, W.M.‘s discrimination
was maximal when the nonwords did not contain vowels. He could
also distinguish words from nonword homophones
(e.g. “coat” vs “tote”) at a level of 9 out
of 10 correct, but he could not perform synonym or antonym matching tasks nor could he
match simple words with objects (e.g. “baby” with a toy doll). C.E. demonstrated
the same
pattern of performance
in discriminating
words from nonword homophones
(8 out of IO
correct). Her word-nonword
discrimination
was also maximal when the nonwords did not
contain vowels. Matching pictures of common objects while the examiner pantomimed
their
use (e.g. aiming a rifle) [28], was normal for W.M. but impaired for C.E. Pantomime
recognition
performance
for both patients is displayed in Fig. 4.

DISCUSSION
The similarity in the inability of both patients to identify visually presented objects
verbally and in their initial levels of alexia contrasts with the divergence in their nonverbal
visual recognition
performance.
W.M. could not connect a name or description
with its
visual referent, whereas he appropriately
used common objects and he could match them
with their characteristic
color and pantomimed
use. In comparison,
C.E. could not initially
demonstrate
the use of objects nor could she match identical objects on the basis of their
visual cues, interpret
pantomimed
object use of perform color-object
matching.
This
constellation
of features suggests the C.E. was unable to link the contents of her visual
perception with previous experience. The failure of object matching suggests, further, that
the perceptual
aspect of recognition
was impaired. These inferences are supported
by
clinical observations
of C.E.‘s visual disability during the subacute stage after her cerebral
infarction:
she required assistance in using familiar implements and behaved as if “blind”.
C.E.‘s initial visual disturbance,
which included prosopagnosia
and topographic
disorientation, was compatible with the apperceptive type of agnosia [ 171. While C.E. was initially
more visually impaired in daily activities than W.M., her alexia partially resolved during the
early months of her convalescence.
C.E.‘s clinical course was characterized
by marked improvements
in visual matching
performance,
her ability to utilize combined visual and tactile cues for object naming at 11
months post-onset and eventually,
her accurate object naming at 20 months post-onset.
Picture confrontation
naming remained impaired when examined 20 months after the onset
of her symptoms. C.E.‘s residual visual disturbance at 11 months post-onset was compatible
with the associative type of visual agnosia described by Lissauer. This inference is supported
by her recovery of visual matching despite residual defects in meaningful
visual-visual
associations,
i.e. inability to match pictures of objects to their corresponding
color and
pantomimed
use. These sequelae would not be predicted by a visual-verbal
disconnection
[1 I]. At 20 months post-onset, although object naming had recovered, she still experienced
difficulties in picture naming, matching of unfamiliar
faces, color-object
matching and
pantomime recognition. Thus, although her object naming performance was far superior to
W.M.‘s, he performed a variety of complex visual cognitive tasks at a much higher level than
C.E.
We infer that different mechanisms were responsible for each patient’s performances,
i.e.

C’.E.‘s deficits were due to an impairment
in visual recognition,
whereas W.M.‘s deficits lvere
due to ;I disconnection
of generally prescrvcd visual rccogniti0n
functions from language
functions. W.M.‘s alexia without agraphia is characteristic
of previously reported cases 01‘
this clisorcler productd
by splellio-occipitnl
lesions [I 21. As might be predicted from the
surgical division of his splenium. W.M.‘s aleuia was more complete and permanent than the
reading disturbance
typically produced by left posterior cerebral artery disease. Although
W.M shuwd minimal recover! d spontaneous
reading. he could distinguish
between
words and random combinations
of letters.
In view of the surgical division of W..M.‘s splenium and his unresolved
dense right
how can his residual capacity to diacrimmate
\~ords l‘rom
homonymous
hemianopsia,
nonworda be espluined‘! Consistent
with previous studies of patients who have undergone
section of the corpus callosum to relieve epilepsy 1761. wc postulate that W.M.‘s residual
lexic capability
is subserved
bq his right hemisphere.
In fact, UC obser\cd
that 111s
spontaneous
verbalizations
frequently disrupt the silent linguistic operations performed by
his ncmdominant
hemisphere. When asked to point to the picture corrcspondin~
t~l an object
named by the examiner, W.M. was frequently led astray by his anemic errors. This view is
supported by W.M.‘s report of misinterpreting
street signs in his neighborhood.
He would
correctly comprehend
the signs initially.
only to reJect his interpretation
in favor ol
verbalized paralexic errors. The reinterpretations
generally had negative or restrictive effects
(e.g. misinterpreting
‘I sign as reading “Keep off’) and controverted
his past experience.
The contrastin:
clinical courses in C.E. and W.M. suggest that diffcrcnt mechanisms
ot
recovery were involved. In accord with the prr\ailing
concepls of prosopagnosia,
C.‘.E.‘s
acute visual disturbance
ma\; bc attributed
to bilateral disconnection
of \:isual input to the
infcro-medial
temporal lobes [X]. While prcsumptivc
damage
to
C_‘.F. ‘s right
OCCI~I~Otemporal connections
could not be conti~-med h\ computed tomography.
it is possible that
she suffered transient ischemia or it snnaII infarct of the postcrivi- right hcmisphet-c. citlli‘r 4‘
which may bc undetectable
by CT scanning.
liecovcry from impairment
in the postwar
circulation of her right hemi<pherc may account for the evolution of her \ iaual :ugnosia from
the appercepti\e
In the associati\c
type. C‘.E.‘s uI~resnlved dcnsc I-i&t honion~mous
hemianopsia
suggests that clinicxl improvement
\\a5 unrelated
10 changes in her lei‘t
posterior circulation.
A\sociatiLe visual agnosia hux generally been attributed
to bilateral postcrtor cercbrx1
hemisphere Iesions [I. 16. 1311,However, kR7I:SL [ 141 has reported a ca\e in which \ ihua1
agnosia persisted for over 10 yr following a head injury, and a CT scan showed lesions in the
left occipital lobe and deep in the right frontal lobe. probably
representing
coup and
contrecoup inJuries. This patient \vas similar to (‘YE. in many respects. I-fer ability to identil‘h
objects presented visually was severely impaired, although she performed well in discriminnting si/e and shape differences
111objects and drawings.
Because the patient exhibited
prosopagnosia
anti ;I be\cre memor!~ deficit. Kertesz >u,,~~w~ted that bilateral parlctooccipital Icsions ma4 have been present, cvcn though no right pal-icto-occipital
Iesions \vcre
detected on C’T scanning. Ho\+~evcr. since in both Kertes/‘s patient and our patient C’.E. ;I
visual agnosia is correlated with 1cft occipital and deep right frcmtal Icsiona. thr possibility
must be considered that this combination
of lesions may be sufficient to produce visual
agno5ia.
A possible mechanism for the contribution
of deep frontal lesions to agnosia i\ suggested
bj, the recent discor/crh that projections from basal for-ebrain nuclei (principally.
the nucleus
basnlis of Meyncrt) prcrvidc most of the cholinerglz input to the cerebral cortex [2 I. 241. 7 1~

VISUAL AtiNOSIA

II

nucleus basalis is situated ventral to the internal capsule, and in the rhesus monkey some of
its neurons are often found among the fibers of the internal capsule [31]. Although the
projection pathway from nucleus basalis to cortex in man is not known, it is possible that
lesions in deep frontal white matter may interrupt cholinergic fibers projecting to posterior
cerebral cortex. Cholinergic deficiency in the cerebral cortex has been well documented
in
Alzheimer’s disease, in which visual agnosia is a common late and occasional early symptom
[22,24]. Hence, a deficiency of cortical acetylcholine
in posterior right cerebral cortex may
contribute
to the visual agnosia in patients such as Kertesz’s and our case C.E. This
hypothesis is testable by means of postmortem
analysis of regional cholinergic enzyme
activity in cerebral cortex.
In conclusion,
our findings clearly distinguish between visual--verbal
disconnection
and
visual agnosia. Our results in W.M. show that complete deprivation
of visual input to the
language dominant
hemisphere does not impair nonverbal
identification
of objects and
persons, although the “blind” speaking hemisphere can disrupt the lexical performance
of
the nondominant
hemisphere. Secondly, our results suggest that visual agnosic deficits fA
along a continuum
rather than into discrete clinical entities and that considerable evolution
of agnosic symptoms can occur, ranging from appcrceptive
visual agnosia to associative
visual agnosia to recovery of identification
of real objects in spite of persistent agnosia for
pictorial materials. This evolution highlights the importance of longitudinal
examinations
in
the evaluation
of visual agnosia.
ilc.X-,~oIl./~,r/~/mnc~n~r~~the
authors
Marsel Mesulam. The assistance

gratefully acknouledgc
the helpful comments of David N. Levine and Marekof Christina A. Meyers. who helped test the patients, is also appreciated.

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