ltal. J. Neurol. Sci. 7:573-580, 1986

Subcortical neglect
Graveleau Ph., Viader F., Cambier J.

Clinique Neurologique,H6pitalBeaujon, Clichy, France

The unilateral neglect syndrome is defined as a lack of directed attention to one
half of the space or the body. It has been reported mainly after cortical lesions of
the right parietal or frontal lobe in man. However, there is strong experimental
and clinical evidencefor the existence of neglect syndromes of subcortical origin.
The unilateral neglect syndrome is not the result of elementary sensory deficits.
The failure in directed attention is dependent on an imbalance of hemispheric
activation.
Key-Words: subcortical neglect -sensory deficit - hemi-inattention - motor neglect

Introduction

In the past few years attention has been paid increasingly neuropsychological effects of subcortical pathology. This has been the case with aphasia
following left thalamic lesions [7, 9, 35], as well as
for the so-called subcortical dementia of progressive supranuclear palsy [1, 8]. Similarly, unilateral
neglect syndromes may follow subcortical lesions,
mainly of the fight cerebral hemisphere.
The unilateral neglect syndrome is defined as a
lack of directed attention to one-half of the space
or body [25]. It may involve one or more following
elements:
I - - Hemi-inattention, that is, failure to respond
to sensory stimulation, whether visual, auditory or
somesthetic from one side of the space or body. In
the least severe cases, there is only extinction on
bilateral simultaneous stimulation. In principle,
the failure to respond must not be ascribable to
any elementary sensory disturbance.
2 -- Failure to orientate towards one side or to
explore one-half of extra-personal space, either
visually or manually (hemispatial akinesia). In severe cases there is also a strong active tendency to
deviate to the side of the lesion. Hemi-inattention
and hemispatial akinesia are commonly associated, leading to unilateral spatial agnosia.
3 -- Motor neglect, or unilateral hypokinesia
(without major motor weakness).
Several behavioral disorders may be associated to
the neglect syndrome: anosognosia, asomatognosia, disorientation, spatial delusions, motor impersistence and constructional apraxia.
The unilateral neglect syndrome has been reported mainly after cortical lesions of the right parietal

[13, 32] or frontal [11, 24] lobes in man. However,
there is at present strong experimental and clinical evidence for the existence of neglect syndromes
of subcortical origin.
As far back as 1934, Van Bogaert [3] reported one
case of right thalamic infarct with disturbances of
the body image. In 1938, De Morisier [16] observed a fight thalamic hemorrhage with features
of the non-dominant hemisphere syndrome.
Since then, several other cases have been reported
[31, 46], but the term "thalamic neglect" was
coined by Watson and Heilman with three
additional cases of fight thalamic hemorrhage
[491.
In animals unilateral neglect has been shown to
occur not only after cortical [47, 52] but also after
discrete subcortical lesions. In cats, visual neglect
was obtained by Orem and co-workers [36] with
destruction of the intralaminar nuclei of the thalamus. In monkeys, Watson and co-workers induced unilateral multimodal neglect through
mesencephalic reticular formation lesions [48]
and unilateral motor neglect by destruction of the
intralaminar nuclei, centrum medianum and parafascicular [50]. In man, the consequences of
stereotactic thalamic surgery on higher cerebral
function have been extensively studied, and they
provide some information about the mechanisms
of subcortical neglect [54] Coagulation of ventrolateral nuclei has mostly induced contralateral motor neglect whichever the side operated. However,
selective impairments of visuo-spatial activities
have been observed after right-sided ventrolateral
thalamotomy [44, 45] for parkinsonism. Similarly,
Hfc~ten and his associates reported disturbances
of the body image following a right thalamotomy
573

The Italian Journal of Neurological Sciences

partly involving the median nuclei [22]. All these
changes were usually transient, perhaps because
the thalamic target was limited.
In human pathology unilateral neglect has been
observed following damage to either the thalamus
or the juxtathalamic structures (including both
basal ganglia and white matter) or both. A hitherto unpublished case will illustrate this topic.

Case report
A 71 year-old hypertensive man was admitted for
left-sided weakness of sudden onset. He had a left
hemiplegia with left hypoesthesia, but full visual
fields on confrontation. He completely denied his
illness. He was desoriented for time and place and
believed he was travelling in Moscow. Despite a
slight tendency to look to the right, he could orient
leftwards on verbal commands. He could not
keep his eyes closed for more than a few seconds.
CT scan showed a right thalamic hemorrhage
(Fig. 1). Formal testing disclosed left neglect in
target cancellation (Fig. 2), picture description
(Fig. 3) and reading words or sentences. When locating cities on a map of France or monumets on
a map of Paris, he showed a tendency to upward
and rightward deviation (Fig. 4). In drawings,
constructional apraxia was marked, together with

Fig. 1. Right thalamic hemorrhage.

574

omission of the left half of models (Fig. 5). There
was left visual extinction, as well as left ear extinction on verbal dichotic testing. Finally, despite a
definite motor improvement, he failed to use his
left limbs spontaneously, showing left motor neglect. These findings are consistent with the reports
of multimodal neglect in three cases of thalamic
hemorrhage by Watson and Heilman [49], in one
case of median thalamic infarction by Watson et
al [51] and in two cases of hemorrhage and one infarction of the thalamus by Cambier et al [4]. In
most cases, anatomical a n d / o r CT data revealed
that the whole thalamus was involved, sometimes
together with neighboring white matter. However,
in two instances at least, the global neglect syndrome was associated with partial thalamic involvement: a thalamic infarction including the
medial nuclear group and portions of the posterior ventral nucleus and of the pulvinar in Watson's
case [51] (CT -- clinical correlation), and, an infarction of the pulvinar, VPL an dorso medial
nuclei in the case 1 of Cambier et al [4] (anatomical data). Predominantly motor neglect has also
been shown to occur in thalamic lesions. Schott et
al [37] reported a case of right thalamic hemorrhage with left motor neglect and left sensory extinction. Only the posterior thalamic region was
involved. Likewise, Laplane et al [29] reported
two cases of pure motor neglect following fight
thalamic damage, predominatly involving lateral
nuclei. In those cases, most of the medial nuclei
seem to have been spared. These observations
emphasize the possibility of dissociated neglect in
thalamic lesions. As shown by Cambier et al [5],
patients with right posterior cerebral artery infarcts involving both the thalamus (deep territory)
and the occipital cortex (superficial territory) also
have an even more conspicuous left neglect syndrome. The comparison with isolated superficial
territory infarcts demonstrates that neglect arises
from the thalamic lesion. The cortical lesion only
appears to enhance the neglect syndrome and to
worsen it, especially in its visuo-spatial aspects.
Neglect syndromes may also occur after
subcortical white matter a n d / o r basal ganglia involvement. Left visual-spatial neglect has been reported by Cambier et al [6] and Ferro and Kertesz
[18] following ischemia of the posterior limb of
the fight internal capsule. One of these patients also had left ear extinction on verbal dichotic testing, but none of them had anosognosia, or asomatognosia. It could not be determined whether motor or somesthetic neglect was present because of
severe motor weakness and dense hypoesthesia.
An interesting feature of these patients was that
they performed better in spontaneous drawings
than in copying or in cancellation tasks [6], a finding which supports an ~attentionab~ mechanism
for that type of neglect syndrome.
Pure motor neglect has been observed following

Graveleau Ph.: Subcortical neglect

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Fig. 2. Left neglect in target cancellation.

Fig. 3. Picture description. The patient descrideb only the right side of the picture.
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575

The Italian Journal o f Neurological Sciences

Ra.r
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Fig. 4. Location o f the principal
towns o f France on a blank map.

Fig. 5. Constructive activities : copy o f a house and o f a bicycle.

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576

Graveleau Ph.: Subcortieal neglect

ischemia of the anterior limb of the internal capsule [52] and hemorrhage of the caudatus nucleus
[41]. Left limb hypokinesia was associated with
left motor extinction, that is enhancement of
akinesia with simultaneous movement on both
sides. Infarction of basal ganglia a n d / o r deep
frontal white matter has been followed by visual
spatial neglect [14, 39]. Finally, Healton et al [21]
reported a case of unilateral left multimodal neglect with asomatognosia and anosognosia casued
by an infarction of striatum and deep white matter, including both limbs of the internal capsule,
but sparing the thalamus.
Subcortical hemispheric lesions may give rise to a
variety of unilateral neglect syndromes. Dissociated types of neglect may occur, either motor or sensory, which are reminiscent of what has been observed in frontal [11, 24] or limited parietal cortical lesions respectively [15]. Similarly, extensive damage to the thalamus or surrounding white matter
and basal ganglia may result in.a global neglect
syndrome, together with anosognosia and asomatognosia, that is hardly distinguishable from the
classical ~parietal>> neglect syndrome.
Both pathways and nuclei involved in transmission of sensory impulses are frequently damaged in patients with neglect syndromes from
subcortical lesions. Thus, the role of elementary
sensory deficits in neglect symptoms has been put
foward. Pure sensory stroke, a condition which
usually includes heavy sensory disturbances on
one side of the body, does not result in unilateral
neglect [10].
Lateral homonymous hemianopia does not result
either in visual-spatial neglect by itself; Willanger
et al [53] found that, in 55 patients with rightsided
cerebral lesions visual neglect was as frequent in
patients with as in patients without visual field defects.
Finally, central nervous system lesions cannot induce unilateral deafness, and dichotic extinction
in neglect syndromes must be interpreted as an
imbalance at a level far higher that of elementary
sensory input. On the other hand, unilateral spatial neglect may occur without any visual field defect or gaze paralysis. Moreover, the hyperactivity
displayed by some neglect patients in or towards
the hemispace ipsilateral to their lesions could not
be explained solely in terms of reduced sensory
input.
Thus, unilateral neglect following subcortical lesions is a specific phenomenon. The relatively few
well-documented cases do not allow definitive
clinico-anatomical correlations. However, it appears that multimodal neglect is usually observed
after either lesions, or disruption of the thalamocortical connections [21]. Isolated visual-spatial
neglect appears to be rare, and so far has been observed only after discrete lesions of the posterior
limb of the internal capsule. Neglect has been in-

terpreted as being the consequence of a disconnection between the posterior thalamus and the
inferior parietal lobule [18], the involvement of
which has been documented in purely attentional
neglect syndromes [15]. However, the thalamic
starting point(s) of the supposedly disrupted pathways remain to be defined. Although it has been
suggested that it could be the pulvinar [18] there is
no documented case to date of lasting visual spatial neglect after isolated pulvinar damage. Motor
neglect is far more common and may be observed
after damage to a variety of subcortical structures
[14, 20, 23, 29, 37, 41,42], all of which are known to
be involved in motor control and activation.
Whereas in thalamic surgery, coagulation of VA
or VL has resulted in motor neglect whichever the
side operated [20], virtually all documented cases
of motor neglect in human pathology involve lesions of the non-dominant hemisphere, either cortical or subcortical. Thus, the mechanisms that are
disrupted in motor neglect seem to be integrated
at different levels, one of which at least belongs
more specifically to the non-dominant hemisphere. Besides the thalamotomy cases, it is logical
to discuss the pathophysiology of motor neglect
together with the other aspects of neglect syndrome.

Pathophysiology
It is admitted that the unilateral neglect phenomenon reflects a failure in directed attention [25].
This failure impairs both attendance to actual stimuli and mental representation of temporally reconstructed structures [2]. The organization of cerebral structures mediating directed attention is debated. According to Watson et al [51], sensory attention on the one hand, and motor activation
and preparation to respond on the other, are
served by reticulo-cortico-limbic loops, involving
the mesencephalic reticular formation, the nucleus reticularis and the medial thalamic nuclei,
and parts of the cortex including cingulate gyrus,
inferior parietal lobule and prefrontal cortex.
Mesulam [33] favors the network model, with
three cortical components (frontal, parietal and
limbic) and a reticular component which provides
for tonic arousal. In both models, the medial thalamic nuclei play a central part in directed attention, a view which is consistent with most clinical
cases of thalamic neglect. Intralaminar thalamic
nuclei receive input from the midbrain reticular
formation and project primarily to the striatum
and frontal cortex [27, 40] but their stimulation involves widespread cortical areas, including frontal, cingulate and parietal cortical association
areas. Thalamic neglect provides a dramatic
clinical demonstration of the physiological importance of these structures. The cases of disso577

The Italian Journal of Neurological Sciences

ciated neglect with different subcortical lesion
sites may stem from selective disruption of distinct thalamocortical activation pathways. The
importance of subcortical structures in neglect
has been further stressed by Deuel and Collins
[17], who have shown by quantitative 2--deoxyglucose autoradiographic studies that unilateral
neglect induced in monkeys by dorsolateral frontal cortex removal was consistently associated
with metabolic depression in selected subcortical
areas, including basal ganglia, parts of nucleus
medialis dorsalis of the thalamus and ventral anterior nucleus of the thalamus. Moreover, these
subcortical metabolic changes disappeared after
recovery from neglect. These data indicate that
several brain areas, both cortical and subcortical,
work together to serve attentional processes, and
that clinical symptoms observed after a single lesion may result from more widespread brain dysfunction. Recovery may be linked to the possibility of using alternate connections, which have
been spared, to re-activate the metabolically depressed distant structures, as observed by Deuel
and Collins.
Unilateral neglect is far more common and more
marked [7, 12, 19, 23, 38] after fight than left brain
damage in man. This assumption holds good for
subcortical as well as for cortical cases, and implies that the fight cerebral hemisphere is in some
way dominant for the function that is failing in the
neglect syndrome, i.e. directed attention [26]. According to this hypothesis, the fight hemisphere is
able to process stimuli from both sides of space,
but the left hemisphere only contralateral stimuli.
The same is true for preparation to act within or
towards one side of space or with one half of
body. After left brain damage, the bilateral attentional abilities of the intact fight hemisphere
would explain the absence or mildness of the neglect phenomena. In fight-sided lesions, left stimuli
cannot be processed any more and neglect appears. It may even be enhanced by the unopposed

activity of the healthy left hemisphere, which is
further stimulated by the activating role of.language [281, therely worsening the interhemispheric imbalance. There is a substantial amount of experimental evidence to support the model of right
attentional dominance [321. This asymmetry for
directed attention processes had not been observed in experimental neglect in animals [52]. It
could result indirectly from the development in
the left cerebral hemisphere of linguistic abilities,
with the correspondig structures taking over directed attention on the right side [30]. This attentional specialization of the right hemisphere, however, depends on extensive connections, both inter -- and intra -- hemispheric. Although directed attention may be more corticalized in humans
than in monkeys or cats [331, it has also been observed that the more lasting cases of neglect follow subcortical lesions in man [34]. Furthermore,
the typical cases of thalamic [4, 49, 51] or juxtathalamic neglect [21] are virtually indistinguishable from the ~classicab~ cortical cases. This does
not appear to be the rule for subcortical and particularly thalamic, aphasia [35]. It is tempting to
compare the left hemispheric dominance for language and fight dominance for directed attention.
In fact, the directed attention processes seem both
to be less corticalized and to depend more on global hemispheric activation than language functions. We have compared the cortical cerebral
blood flow (CBF) in patients with either fight or
left thalamic lesions, and we have observed that
only fight thalamic lesions with a left neglect syndrome led to a significant asymmetry of CBF,
with a diffuse cortical lowering on the side of the
lesion [43]. It will be interesting to find out whether patients with unilateral neglect secondary to
parietal damage have subcortical metabolic depression, especially in the thalamus and/or basal
ganglia. More clinical studies are needed to refine
CT--clinical correlations in neglect syndromes
and to clarify the neural basis of directed attention.

Sommario
La sindrome di in attenzione ~ definita come una mancanza di attenzione diretta, su una meth dello spazio o
sull'emicorpo. E stata descritta soprattutto in relazioni a lesioni corticali situate a destra, in sede parietale o
frontale nell'uomo. Tuttavia vi sono molti elementi sperimentali e clinici sull'esistenza di sindrome di inattenzione di or(gine sottocorticale. Infatti questa sindrome non Oconseguenza di deficit sensoriali elementari, ma
dipende da uno squilibrio di attivazione emisferica.

Address reprint requests to: Gravrleau Ph.
Clinique Neurologique - HrpitalBeaujon
100 bd du Gdnrral Leclerc - 92110 Clichy - France
578

Graveleau Ph. : Subcortical neglect

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