Brain (1986), 109,81-97

INFARCTS OF BOTH INFERIOR PARIETAL
LOBULES WITH IMPAIRMENT OF VISUALLY
GUIDED EYE MOVEMENTS, PERIPHERAL
VISUAL INATTENTION AND OPTIC ATAXIA
by CH. PIERROT-DESEILLIGNY, F. GRAY and p. BRUNET
(From the Clinique de Semiologie Neurologique, Unite de Recherches INSERM U. 289 and Laboratoire
de Neuropathologie Charles Foix, Hopital de la Salpetriire, Paris)

SUMMARY

INTRODUCTION

The dorsal part of the inferior parietal lobule (IPL) of the monkey (Brodmann's
area 7) is involved both in visual attention and in the different visually guided eye
movements (Lynch et ai, 1977). In man, it has long been suggested that the
Correspondence to: Dr Ch. Pierrot-Deseilligny, Hopital de la Salpetriere, 47 Bd de l'Hopital, 75651 Paris
Cedex 13, France.
© Oxford University Press 1986

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Clinicopathological correlations are reported in a case with bilateral isolated infarcts in the posterior
part of the parietal lobes, due to nonbacterial thrombotic endocarditis accompanying pancreatic
adenocarcinoma. The initial left-sided infarct induced right visual neglect, impairment of rightbeating optokinetic nystagmus (OKN), optic ataxia, Gerstmann's syndrome and apraxia. After the
right-sided infarct, which occurred six weeks later, bilateral visuo-oculomotor disturbances were
observed, including peripheral visual inattention, disorder of visually guided saccades, severe impairment of foveal smooth pursuit and OK.N slow phase. The lesion on the left involved the upper part
of the angular gyrus and a part of the adjacent superior parietal lobule (SPL). That on the right
involved the supramarginal gyrus and extended posteriorly into the superoanterior extremity of the
angular gyrus, into both margins of the adjacent intraparietal sulcus and into a small part of the
SPL. As the oculomotor deficits and the peripheral visual inattention were bilateral after the second
infarct, they probably resulted from the lesion of homologous areas in both cerebral hemispheres.
The zone damaged in common included a small part of the SPL, the superoanterior extremity of the
angular gyrus, and the adjacent intraparietal sulcus and a small portion of the subcortical white
matter. This restricted cerebral zone could therefore, in man, be implicated both in the control of all
visually guided eye movements and in visual attention. It is further suggested that two corticofugal
pathways are implicated in visually guided saccades, the first arising from the frontal eyefieldsand
projecting directly onto the premotor structures in the brainstem, the second arising from the
posterior parietal cortex (probably mainly the intraparietal sulcus adjacent to the angular gyrus) and
including a relay in the superior colliculus before reaching the premotor structures. Lastly, the
findings support the hypothesis that optic ataxia results from interruption of direct and/or crossed
occipitofrontal pathways coursing in the deep white matter of the parietal lobe.

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posterior part of the parietal lobe is similarly involved (Mesulam, 1981; Sharpe,
1982), but so far clinicopathological cases have been rare and the lesions have not
been limited to the IPL (the angular and supramarginal gyri, namely Brodmann's
areas 39 and 40, respectively), in general largely damaging the parieto-occipital
region. The main interest of the clinicopathological case reported here is to show
that severe deficits in visually guided eye movements (smooth pursuit and saccades)
and peripheral visual inattention can be observed after bilateral infarcts involving
only a restricted part of the IPL on each side. As these two infarcts occurred with
an interval of six weeks, the clinical features of the initial left-sided damage could
be studied first. The case also included other neurological disturbances, such as
optic ataxia which, together with the eye movement disorders and the visual
inattention, formed a syndrome resembling that described by Balint (1909).
CASE REPORT

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A 64-year-old right-handed woman, having stayed at school until 18 years of age but never having
been employed, widowed, with no noteworthy previous medical history, was admitted to hospital
after an initial convulsive seizure. On examination, she was alert and cooperative. Her gait was
normal and she had no motor deficit. The plantar responses were flexor and the tendon reflexes
normal. Postural sense in the right hallux was slightly impaired but other sensory modalities were
normal. There was no astereognosis, but there was tactile inattention over the whole of the right
side of the body.
There was no hemianopia (tested by confrontation at the bedside using a small red sphere) but
right visual extinction was noted. Moreover, the patient showed right visual neglect since, on exploring pictures visually, she looked only at their left halves and noticed none of the objects located on
the right. Saccades to command, visually guided saccades (to a small visual target such as a pencil),
foveal pursuit (stimulated by a smoothly moved pencil) and oculocephalic movement performed in
the lateral and vertical planes appeared clinically normal. It is possible, in the absence of recordings,
that a slight saccadic component of horizontal foveal pursuit was overlooked. Horizontal optokinetic
nystagmus (OKN), elicited by a narrow band of pictures passed in front of the patient (namely
stimulating only the foveal smooth pursuit system) was asymmetric, the amplitude and frequency of
nystagmus being clearly lower when the stimulus was moved leftwards. When eye-hand coordination
was examined (the patient was instructed tofixatestraight ahead while attempting to point at objects
located first peripherally and then centrally in her visual field), a striking optic ataxia was noted:
with the right hand, it was seen in both peripheral visual hemifields as well as when the object was
fixated; with the left hand, it was in the right peripheral visual hemifield only.
There was a complete Gerstmann's syndrome with (1) severe ringer agnosia, the patient being able
to name and to point to her index finger only (or that of the examiner), but having no difficulty in
pointing to and naming the other parts of her body; (2) obvious left-right disorientation (with almost
50 per cent error); (3) marked oral and written dyscalculia, singlefigureadditions being occasionally
right but always wrong with doublefigures;and (4) clear agraphia with almost completely unintelligible spontaneous writing, only slightly improved when copying, whichever hand was used. In
contrast, reading was normal (for words as well as for letters), as was spoken language. Spontaneous
speech was fluent, without paraphasic errors or circumlocutions; she named objects, and repeated
and comprehended oral language without difficulty. In spontaneous drawing, a cube was reduced to
a simple triangle but included two faces when copied. The patient could not perform common
gestures (e.g., a military salute, the sign of the cross, waving goodbye) either spontaneously or by
imitation, regardless of which upper limb was used, although she could recognize and name them

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On the following day the patient developed bronchopneumonia with a pyrexia of 41" C, preventing
oculomotor recordings which had been planned. Her general condition quickly deteriorated and she
died three weeks later, namely nine weeks after the first neurological disturbances.
In summary, the clinical features of this case comprised: (1) after the first lesion, slight impairment
of joint position sense in the right hallux, right tactile inattention, right visual neglect, impairment
of right-beating OKN, optic ataxia (for the right hand in the whole visual field and for the left hand
in the right visual field), Gerstmann's syndrome and various apraxias; (2) after the second lesion,
possible left motor neglect, a dystonic attitude of the left hand, marked disturbance of visual attention
in the whole peripheral visual field, disordered visually guided saccades, severe impairment of foveal
pursuit, abolition of OKN slow phase (in both lateral directions), and persistence of optic ataxia,
apraxia and Gerstmann's syndrome.

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perfectly when they were performed by the examiner. She was unable to light a candle and could
only manipulate everyday objects clumsily (e.g., fork, knife, pen). Memory and judgement were
normal. Further neurological examination revealed no other anomalies.
The patient had lost 5 kg in the previous three months and was anorexic. She had an irregular
hepatomegaly and peritonoscopy confirmed multiple metastases in the liver. General examination
revealed no further abnormalities and the site of origin of the carcinoma was not sought. Left carotid
arteriography showed occlusion of the posterior parietal branch of the left middle cerebral artery
near its origin, but no other abnormalities.
Six weeks after admission, when her apraxia had slightly improved, sudden neurological deterioration was noted. The patient remained alert and cooperative during all the clinical examinations
performed throughout the day. Motility in the limbs was normal on command but motor neglect in
the left upper limb was suspected. Plantar and tendon reflexes were normal. On sensory examination,
left-sided astereognosis was suspected but could not be confirmed because of a dystonic attitude of
the left hand which prevented the manipulation of objects. The fingers were almost always held in
extension, particularly during motor activity of either of the upper limbs. There was no other sensory
loss. When testing stereognosis the patient sat up in bed with her gaze fixated in front of her. She
was allowed to keep her eyes open not only because she apparently did not see objects placed in
either hand, but also because she showed no inclination to move her gaze towards them. She did not
blink when menaced in her peripheral visual field. However, there was no hemianopia since, on both
sides, she could see the fingers of the examiner moving, although this perception was apparently
obtained with much difficulty. She seemed to see only a few dashes on a sheet of paper presented to
her containing numerous scattered dashes. Saccades to command were normal in all directions, but
the patient could not perform a correct saccade from one visual target to another (the results were
the same for two pencils or the faces of two examiners): she fixated the first target for an abnormally
long time (at times a few seconds) and, when she succeeded in releasing her gaze, it wandered in
search of the second target regardless of side. Starting from the first target, the direction of saccade
was often but not always wrong. When correct, however, the amplitude of saccades was inaccurate
(hypometric or hypermetric). Reading was now disturbed, essentially because of these saccadic
disorders: the patient could leave a line and return leftwards but not catch the following line and,
within a line, she missed some words. Foveal pursuit (still stimulated by a smoothly moved pencil)
was absent leftwards. Rightwards, a movement was observed only when the stimulus was moving
very slowly. It is still possible that a saccadic component of the residual rightward foveal pursuit
was overlooked here. OKN was abolished in both lateral directions, the eyes remaining stationary
at the midline. During this stimulation the patient saw and could name the different pictures passed
just in front of her eyes. Vertical foveal pursuit and vertical OKN were not tested. Lateral and
vertical oculocephalic movements were normal. Optic ataxia still existed for the right hand, but could
not be assessed for the left, because of its dystonic attitude. Gerstmann's syndrome and apraxia
persisted. Spoken language, memory and judgement were still normal. There were no other noteworthy neurological anomalies.

#4

CH. PIERROT-DESEILLIGNY, F. GRAY AND P. BRUNET

PATHOLOGICAL FINDINGS
Post-mortem examination was performed 9 h after death. It revealed a pancreatic
adenocarcinoma with hepatic metastases, nonbacterial thrombotic endocarditis
involving the mitral and aortic valves, recent splenic infarction, and multiple distal
pulmonary emboli which were the probable cause of death. Neither stenosis nor
occlusion were found in the cervical arteries.
The brain weighed 1250 g. On macroscopic examination, coronal sections of
the cerebral hemispheres and sections of the brainstem perpendicular to its axis
showed two old bilateral infarcts in the posterior part of the middle cerebral artery
territory.
For microscopic examination, all slices of the cerebral hemispheres affected by
the infarcts were embedded in celloidin, cut serially at 15/im and stained with
haematoxylin and eosin and Loyez's method for myelin. Every 7.5 mm on the left
and every 15 mm on the right, a section stained for myelin (fig. 1) was drawn with
the aid of a camera lucida to define the precise topography of the lesion. Light

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B
FIG. 1. Coronal sections of the cerebral hemispheres. Loyez x 1. A, left side, section 2 (seefigs2 and 4). B, right
side, section 4 (seefigs3 and 4).

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FIG. 2. Coronal sections of the left cerebral hemisphere. Drawn from sections stained by Loyez's method. AG
= angular gyrus; Cc = corpus callosum; ips = intraparietal sulcus; ITG = inferior temporal gyrus; LOG =
lateral occipital gyri; MTG = middle temporal gyrus; OR = optic radiations; PoCG = postcentral gyrus; pos
= parieto-occipital sulcus; PrCG = precentral gyrus; SMG = supramarginal gyrus; SPL = superior parietal
lobule; STG = superior temporal gyrus L; sts = superior temporal sulcus. Shaded area = lesion.

microscopy showed that the infarcts contained numerous gitter cells and rare
siderophages. No arterial occlusion was found.
In the left cerebral hemisphere (fig. 2), the infarct had destroyed the upper part
of the angular gyrus and the posterior and outer part of the superior parietal lobule
(SPL), with an extension terminating in the superior and anterior part of this
lobule. In the subcortical white matter, the lesion extended to the upper and outer
part of the optic radiation, which was barely damaged. The supramarginal gyrus,
the posterior part of the temporal gyri and the lateral occipital gyri were unaffected.

CH. PIERROT-DESEILLIGNY, F. GRAY AND P. BRUNET

86

In the right cerebral hemisphere (fig. 3), the infarct had destroyed almost all the
supramarginal gyrus. It extended posteriorly in the superoanterior extremity of
the angular gyrus, in part of the intraparietal sulcus (both of whose margins were
damaged) and into a small portion of the SPL. The subcortical white matter
was slightly involved by the lesion which did not reach the optic radiation. The
postcentral gyrus, the posterior part of the temporal gyri and the lateral occipital
gyri were unaffected.

PrCG

LOG

FIG. 3. Coronal sections of the right cerebral hemisphere. Drawn from sections stained by Loyez's method. For
abbreviations, seefig.2.

The brain was otherwise normal. No other ischaemic lesions or any metastases
were found.
In summary, there had been two cerebral infarcts (fig. 4). The first damaged the
upper part of the angular gyrus and a part of the SPL in the left cerebral hemisphere; the second damaged, in the right cerebral hemisphere, almost all the
supramarginal gyrus and extended posteriorly into the superoanterior extremity
of the angular gyrus, into the adjacent intraparietal sulcus and into a small part of
the SPL.

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AG

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Left

pos

pos

FIG. 4. Representation of the lesions on the cerebral cortex. The section planes are slightly inclined with respect
to the coronal plane. Note that the cortical zone damaged in common in both hemispheres is clearly defined
on the right side, including all the posterior extremity of the lesion between sections 3 and 5. For abbreviations,
seefig.2.

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Right

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CH. PIERROT-DESEILLIGNY, F. GRAY AND P. BRUNET

DISCUSSION
After the first parietal infarct, this patient had multiple neuropsychological
disturbances including various apraxias and Gerstmann's syndrome resulting
from damage to the left angular gyrus (Gerstmann, 1940; Roeltgen et al., 1983).
These disturbances and some others observed after the second infarct, such as
possible left motor neglect and a dystonic attitude of the left hand resembling
an 'avoiding reaction' (Laplane et al., 1979), were not studied in great detail and
therefore will not be discussed. There were also certain oculomotor and visual disorders which, despite the absence of recordings, were sufficiently clear on bedside
examination, especially after the second infarct, to allow some clinicopathological
correlations.

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Smooth Pursuit Movements
Each parietal lobe controls smooth pursuit movements in all directions and
unilateral parietal lesions affect these movements only partially, with some predominance for those directed ipsilaterally to the lesion (Sharpe, 1982). Foveal
smooth pursuit is then supplemented by catch-up saccades and the slow phase gain
of OKN (velocity of eye movement on apparent velocity of stimulus) is reduced.
In our case, after the left-sided infarct, OKN was impaired when stimulation was
directed leftwards, as is usual with unilateral parietal damage (Carmichael et al.,
1954; Baloh et al., 1980). After the second infarct, leftward foveal smooth pursuit
and OKN slow phase in both lateral directions were abolished. As for the rightward
foveal pursuit, it was elicited only by very slow stimulation and whether this
residual movement was saccadic (without, therefore, persistence of any smooth
movement) is not of critical importance here since the rightward OKN slow phase
was abolished. Indeed, given that the OKN slow phase in our case—namely in the
first seconds of stimulation (Baloh et al., 1980) and with a stimulus essentially
involving foveal vision (Leigh and Zee, 1983)—was probably performed by the
same oculomotor system which produces the foveal smooth pursuit, it may be
concluded that foveal smooth pursuit movements were at least severely impaired
rightwards and abolished leftwards after the second infarct. As foveal smooth
pursuit depends mainly on foveal vision, it may furthermore be considered that
the visual inattention of our patient, essentially for peripheral stimuli, could not
be the actual origin of the severe deficit of this eye movement.
Abolition or striking impairment of horizontal smooth pursuit movements due
to bilateral hemisphere damage has been reported, to our knowledge, in only 6
previous clinicopathological cases (Holmes, 1918, Case 5; Hecaen et al., 1950;
Hecaen and de Ajiuraguerra, 1954, Cases 3 and 4; Michel et al., 1965; Hausser et
al., 1980). Except in the first case (Holmes, 1918), in which the lesion was confined
to the IPL on one side but for which the anatomical description was not very
precise, the lesions of the other cases largely damaged both parieto-occipital regions, namely the IPL as well as the adjacent occipital cortex, and also, in 4 of

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them, the frontal lobes bilaterally. For the clinicopathological case reported by
Balint (1909), in which the lesions also damaged both parieto-occipital regions,
the different eye movements were not specified in detail. In our case, the lesions
lay essentially on both sides in the IPL. On the left, the lesion damaged all the
upper part of the angular gyrus and extended upwards to the paramedian part of
the SPL. On the right, the supramarginal gyrus was damaged and the lesion
extended posteriorly in the superoanterior extremity of the angular gyrus and into
the adjacent intraparietal sulcus and in a small part of the SPL. Given that the
deficit of smooth pursuit movements was bilateral after the second infarct, it may
be deduced that the damaged zone in common in both hemispheres included an
area essential for these movements in man. This area appears very small since the
damaged zone in common involved only the superoanterior extremity of the angular gyrus, both banks of the adjacent intraparietal sulcus, a small portion of the
SPL and a slight portion of the subcortical white matter.
Such a finding correlates with experimental data since, in the monkey, foveal
smooth pursuit was deranged after bilateral damage to the IPL sparing the adjacent
occipital cortex (Lynch and McLaren, 1982), as in our case. On the other hand,
for the OKN elicited by a full-field stimulation to be severely impaired in this
animal, both structures would be involved by the lesion (Lynch and McLaren,
1983), but this would then involve mechanisms other than simple foveal stimulation. Visual tracking neurons have been found in the monkey in the dorsal part
of the IPL (Mountcastle et al., 1975; Lynch et al., 1977; Sakata et al., 1983)—in
the area corresponding in man to the angular gyrus (Eidelberg and Galaburda,
1984)—and they seem to control smooth pursuit movements in both lateral
directions, although mainly responding to ipsilateral stimuli (Kawano et al., 1984)
It must be pointed out that the precise location of these neurons in the dorsal part
of the IPL is not yet well established since Lynch et al. (1977) found them near
the intraparietal sulcus (the anterior border of the IPL), while Sakata et al. (1983)
and Kawano et al. (1984) found them essentially in or near the dorsal extremity
of the superior temporal sulcus (the posterior border of the IPL). The former
location corresponds in man to the upper part of the angular gyrus, damaged on
both sides in our case, but the latter location corresponds to the lower part
of the angular gyrus which, in our case, was partly spared on the left side {see
fig. 2) and undamaged on the right {see fig. 3, sections 3-5). If however, this
latter location is confirmed in the monkey it should be noted that the subcortical
extension of the lesions in our case could have interrupted the efferents from
the lower part of the angular gyrus on both sides {see fig. 2, section 3, and
fig. 3, section 3). Our anatomical data thus allow us merely to suggest that the
cortical area controlling foveal smooth pursuit movements in man is probably
inside the angular gyrus, between the dorsal end of the superior temporal
sulcus and the adjoining intraparietal sulcus. As for damage to the small portion
of the SPL involved by both lesions in our case, it was probably not at the
origin of the different visuo-oculomotor disturbances since in the monkey the

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CH. PIERROT-DESE1LLIGNY, F. GRAY AND P. BRUNET

SPL does not appear to contain neurons involved in such functions (Mountcastle
etal.,\915).

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Visually Guided Saccades
Visually guided saccades appeared clinically normal after the left unilateral
damage. This is not surprising since, in such cases where recordings of eye movements have been made, only a slight increase in the latencies of contralateral
visually guided saccades has been observed (Sundqvist, 1979). After the second
lesion, saccades to command were normal, but visually guided saccades from
one visual target to another were greatly disturbed bilaterally, the patient having
difficulty in transferring gaze from the first target before wandering in search of
the second. Furthermore in reading, the patient skipped lines or words. Therefore,
visually guided saccades had a marked increase in latency and a lack of accuracy
for direction as well as amplitude. It must be emphasized that associated peripheral
visual inattention might play some role in these disturbances of visually guided
saccades.
Analogous disorders of visually guided saccades have been observed previously
in 2 clinicopathological cases having selective bilateral lesions of the parietooccipital regions (Holmes, 1918, Case 5; Hecaen and de Ajiuraguerra, 1954, Case
3) but also in other clinical cases where the lesions most probably involved mainly
the parieto-occipital regions (Godwin-Austen, 1965; Montero et al., 1982). Since
disorders of visually guided saccades were bilateral after the second infarct, our
anatomical data allow us to suggest that in the parietal-occipital region it is also
the superoanterior extremity of the angular gyrus and the adjacent intraparietal
sulcus, damaged in common in both hemispheres, which are mainly involved in
control of these movements. This appears probable since it has been reported in
the monkey that the dorsal part of the IPL near the intraparietal sulcus contains
saccade neurons which discharge just before and during visually guided saccades
and are intermingled with the visual tracking neurons (Lynch et al., 1977; Shibunati
et al.,.\984).
It must be pointed out, however, that visually guided saccades, although greatly
disorganized, still existed after bilateral lesions of the parieto-occipital region. On
the other hand, in 2 cases where bilateral lesions in the region of the frontal eye
fields (FEF) were combined with bilateral lesions of the parieto-occipital region
(Hecaen and de Ajiuraguerra, 1954, Case 4; Hausser et al., 1980), visually guided
saccades were severely impaired or abolished. The FEF of the monkey (Brodmann's area 8) contains neurons involved in visually guided saccades (Goldberg
and Bushnell; Bruce and Goldberg, 1985). Thus, with destruction of both IPLs,
visually guided saccades could still partly be controlled by the FEF: this structure
could receive some visual information from the occipital lobes, but also from the
superficial (visual) layers of the superior colliculus, either directly (Fries, 1984) or
by a pathway passing through the thalamus, in which certain afferent tracts of the
FEF (Barbas and Mesulam, 1981) are perhaps connected with certain efferent

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91

Visual Attention
After the left-sided infarct, the patient clinically did not have a right hemianopia,
but she showed right visual extinction and explored and seemed to see only the
left half of pictures. Such signs are typically those of a marked right visual neglect
(Chain et al., 1979). After the right-sided infarct, the patient was not hemianopic
and post-morten study confirmed that the optic radiations were not involved by
the lesions on the right side and only very slightly damaged on the left. However,
although the fingers of the examiner were at times seen moving in the peripheral
visual field, this perception was obtained with considerable difficulty. Moreover,
the patient seemed to neglect some peripheral visual stimuli. Consequently, despite
the absence of detailed investigation, it may be concluded that some bilateral
peripheral visual inattention existed after the second infarct.

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tracts of the superior colliculus (Benevento and Fallon, 1975). The effect of lesions
of both FEF on visually guided saccades has never to our knowledge been reported
in man, but in the monkey it seems that such a destruction induces only subtle and
transient oculomotor deficits (Schiller et al., 1980). The deep (motor) layers of the
superior colliculus constitute a subcortical area also involved in the control of
visually guided saccades (Wurtz and Albano, 1980; Sparks and Mays, 1981) but
bilateral damage to this structure is followed only by slight oculomotor deficits
(Schiller et al., 1980). On the other hand, bilateral damage to both the FEF and
the superior colliculus leads in the monkey to a long-lasting and severe deficit
paralysis of all saccades (Schiller et al., 1980), as with bilateral lesions
to both the FEF and the IPL in man. As there is in the monkey a direct projection from the IPL—according to Andersen et al. (1985), and Lynch et al. (1985)
especially from the intraparietal sulcus—onto the deep layers of the superior
colliculus (Fries, 1984; Weber and Yin, 1984), which could be involved in triggering saccades (Keating et al., 1983), it may be concluded on both clinical and
experimental grounds that two cortical areas control visually guided saccades
(Pierrot-Deseilligny, 1985). These are (1) the FEF, by direct projections onto
the immediate premotor structures of saccades, namely the paramedian pontine
reticular formation (PPRF) for lateral movements (Leichnetz et al., 1984a;
Schnyder et al., 1985) and the rostral interstitial nucleus of the medial longitudinal
fasciculus (riMLF) for vertical movements (Leichnetz et al., 19846); and (2) the
intraparietal sulcus adjacent to the angular gyrus, by indirect projections, including a relay in the superior colliculus, which also projects onto the PPRF (Graham,
1977; Harting, 1977; Raybourn and Keller, 1977) and onto the riMLF (Benevento
and Fallon, 1975; Harting, 1977; Grantyn et al., 1982). The IPL and the FEF are,
moreover, reciprocally connected in the monkey by direct corticocortical tracts
(Pandya et al.,\91\; Barbas and Mesulam, 1981; Petrides and Pandya, 1984). The
different mechanisms produced in these two cortical areas during the triggering of
visually guided saccades and the nature of their reciprocal functional influences
remain to be determined precisely.

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Optic A taxia
Optic ataxia with the right hand in the whole visual field and with the left hand
in the right visual field was observed after the initial left-sided infarct. After the
second infarct, this disturbance persisted with the right hand but could no longer
be tested with the left because of its dystonic attitude. For this reason, only the
disorder observed after the left infarct will be commented upon here and compared
with previously reported cases in which lesions were certainly or presumably unilateral. Consequently, although the clinical triad observed in our case, namely disorders of visually guided eye movements, peripheral visual inattention and optic
ataxia, was finally close to that in the clinicopathological case described by Balint
(1909), the cases will not be compared because in Balint's case optic ataxia was
associated not only with bilateral lesions of the parieto-occipital regions but also
with another in the right precentral gyrus.
It has been suggested, both on experimental (Haaxma and Kuypers, 1975) and
clinical grounds (Rondot et al., 1977), that optic ataxia results from damage to

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Contralateral visual neglect is now well known in unilateral parietal damage,
usually more marked with lesions of the nondominant cerebral hemisphere
but existing also with lesions of the dominant hemisphere (Brain, 1941; Allen,
1948; Critchley, 1953; Hecaen et al., 1956; Heilman and Valenstein, 1972; Chain
et al., 1979). The comparative anatomical study of the earliest reported cases
allowed Allen (1948) to emphasize that the angular gyrus plays an essential role in
visual attention. In clinical cases, with proven or presumed bilateral parietooccipital lesions, visual inattention involving the whole peripheral visual field has
previously been observed, with on occasions a predominance of the disturbance
on one side (Balint, 1909; Hecaen et al., 1950; Hecaen and de Ajiuraguerra, 1954;
Luria, 1959; Godwin-Austen, 1965; Michel et al., 1965; Hausser et al., 1980;
Montero et ai, 1982; Guard et al., 1984). Since in our case visual inattention was
first unilateral before it affected the whole peripheral visual field after the second
infarct, the zone damaged in common in both hemispheres included the area
essential for peripheral visual attention in the parietal region, possibly the superoanterior extremity of the angular gyrus and the adjacent intraparietal sulcus.
Such a finding appears particularly well correlated with the conclusion of a
recent study in man. This suggested, on cytoarchitectonic criteria, that a very small
zone located in and just below the dorsal portion of the intraparietal sulcus,
overlapping slightly on the upper extremity of the angular gyrus and corresponding
almost exactly to part of the damaged zone in common on both sides in our case,
could be the area involved in visual attention in the parietal lobe (Eidelberg and
Galaburda, 1984). Our finding is also correlated with experimental data, since in
the monkey the dorsal part of the IPL near the intraparietal sulcus contains
neurons involved in visual attention, intermingled with neurons controlling the
different visually guided eye movements (Hyvarinen and Poranen, 1974; Mountcastle et al., 1975; Lynch et al., 1977; Bushnell et al., 1981).

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the visuomotor connections between the occipital and the frontal lobes. These
connections would include (Rondot et al., 1977) (1) a direct pathway, coursing in
the upper half of the white matter of the parietal lobe, possibly through the superior
longitudinal fasciculus according to the anatomical data of Dejerine and DejerineKlumpke (1895, 1901), and (2) a crossed pathway, probably passing through the
splenium of the corpus callosum. Thus, each motor area controlling hand movement would receive visual information from both occipital lobes.
Such an organization is supported by functional and structural correlates in
man. Surgical section at the parieto-occipital junction, just dorsal to the angular
gyrus, has induced an optic ataxia for both hands but only in the visual hemifield
contralateral to the lesion (Rondot et al, 1977). The direct pathway between the
ipsilateral occipital lobe and the ipsilateral frontal lobe and the crossed pathway
between the ipsilateral occipital lobe and the contralateral frontal lobe (before its
decussation through the splenium of the corpus callosum) were then probably
damaged. A lesion of the splenium of the corpus callosum has induced a visuomotor disturbance resembling optic ataxia for both hands but, for each of
them, only in the visual hemifield contralateral to the hand (Gazzaniga et al.,
1965). Both crossed pathways were then damaged. In a lesion involving, as in our
case, the angular gyrus and adjacent superior parietal lobule, or in 2 other cases
mainly involving the posterior part of the superior parietal lobule (Levine et al.,
1978; Auerbach and Alexander, 1981), optic ataxia affecting the contralateral hand
in the whole visualfieldand the ipsilateral hand in the visual hemifield contralateral
to the lesion was observed. Such a syndrome may be explained by the particular
location, in our case, of the lesion which could have damaged (1) the direct pathway
coursing in the deep white matter probably near the junction between the superior
and inferior parietal lobules, (2) the crossed pathway between the ipsilateral occipital lobe and the contralateral frontal lobe, before its decussation since, in the
posteroanterior direction, the lesion began just at the posterior limit of the angular
gyrus and (3) the crossed pathway between the contralateral occipital lobe and the
ipsilateral frontal lobe, after its decussation, since the lesion, in the superior and
inferior parietal lobules, terminated at the anterior limit of the angular gyrus. To
damage both crossed pathways, a unilateral hemisphere lesion must probably be,
as in our case, first, close to the lateral portion of the splenium of the corpus
callosum, namely in the white matter located deeply and medially with respect to
the anterior half of the angular gyrus and, secondly, slightly extended in the
posteroanterior direction in order to involve both types of fibre, before and after
their decussation. Lastly, a lesion of the superior parietal lobule more anteriorly
located (just above the supramarginal gyrus) might induce optic ataxia not only in
the whole visualfieldbut also in the contralateral land, by damaging both the direct
pathway and the crossed pathway, after its decussation. Such a clinicopathological
correlation has not so far been reported to our knowledge, probably because there
is usually a severe associated sensory deficit which prevents the detection of possible
optic ataxia. However, in 2 clinical cases, without definite verification of the

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CH. PIERROT-DESEILLIGNY, F. GRAY AND P. BRUNET

location of the lesions but in which visual and sensori-motor function was preserved, optic ataxia of this last type has been described (Schott et al, 1972.
Conclusion
This clinicopathological case allows us to suggest that the parietal area mainly
involved both in the control of visually guided eye movements and in visual
attention is included in the angular gyrus and in the adjacent intraparietal sulcus.
Furthermore, our data support the hypothesis that optic ataxia results from
damage to direct and/or crossed occipitofrontal pathways coursing in the deep
white matter of the parietal lobe.

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