Subcortical Neglect: Neuropsychological,
SPECT., and Neuropathological Correlations
with Anterior Choroidal Artery
Territory Infarction
Julien Bogousslavsky, MD," Judit Miklossy, MD,f Franco Regli, MD," Jean-Pierre Deruaz, MD,?
Gil Assal, MD,$ and Bernard Delaloye, MD9

In 2 patients with infarction in the territory of the right anterior choroidal artery, hemiparesis, hemihypesthesia (in l),
and hemianopia or superior quadrantanopia were associated with severe multimodal hemineglect, without anosognosia, disorientation, or asomatognosia. Single-photon emission tomography showed that marked hypoperfusion was
not limited to the right posterior capsular region, but also involved the overlying parietal cortex, and to a lesser extent
the frontal cortex. At autopsy in 1 patient, the infarct was nearly limited to the deep white matter of the temporal
isthmus and the retrolenticular part of the internal capsule; only minute lesions were present in the globus pallidus,
body of caudate, and amygdala These findings are consistent with a disconnection phenomenon as the basis for
subcortical neglect with ipsilateral deactivation of the parietofrontal cortex.
Bogousslavsky J, Miklossy J, Regli F, D e w J-P, Assal G, Delaloye B. Subcortical neglect:
neuropsychological, SPECT, and neuropathological correlations with anterior choroidal
artery territory infarction. Ann NeuroI 1988;23:448-452

Infarction in the territory of the anterior choroidal artery (AChA) was not commonly recognized before the
computed tomographic (CT) era, and only 8 unilateral
cases with pathological verification are available in the
literature [G, 8, 10, 11, 15, 17, 22). The main structures supplied by the AChA include the posterior and
retrolenticular parts of the posterior limb of the internal capsule, the inner part of the globus pallidus, the
body and tail of the caudate, the lateral part of the
lateral geniculate body, the optic tract, the amygdala,
and part of the hippocampal region [5, 10, 141. The
classic picture of the AChA territory infarction includes contralateral hemiplegia, hemianesthesia, and
hemianopia 15, 10, 141, but one or two of the elements
of this triad may be lacking 15, lo].
The occurrence of neuropsychological disturbances
has been emphasized recently, with language disturbances similar to thalamic aphasia in left-sided infarction 14, 51, and neglect, constructive apraxia, and
anosognosia in right-sided infarction [4, 5, 7, 141. Because none of the patients with neuropsychological
dysfunction had an autopsy study, the knowledge of
the anatomical structures implicated in the genesis of
dysphasia or neglect remains speculative. We have

studied 2 patients with a right AChA territory infarct
with neuropsychological, CT, single-photon emission
tomography (SPECT), and neuropathological (in 1)
correlations.

From the *Neurology Department, tNeuropathology Division,
SNeuropsychology Center, and §Nuclear Medicine Division, Centre
Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

Received Apr 16, 1987, and in revised form Jul 10, Oct 7, and Oct
26. Accepted for publication Nov 1, 1987.

Case Reports
Patient 1
An 85-year-old right-handed woman with hypertension and
atrial fibrillation was admitted to the hospital after she developed an acute left-sided weakness. O n admission, the patient
was alert and well oriented in time and place. Her head was
turned to the right. There was a complete left homonymous
hemianopia. When closed, the eyes remained in a midposition, but spontaneous gaze was limited to the right hemifield.
Eye tracking of a light spot was smooth and symmetrical
toward both sides. Optokinetic nystagmus testing showed no
quick phase to the left. No motor impersistence was present
for lid closure or for the limbs on the right side. There was a
severe left spastic hemiparesis involving the face, arm, and
leg. Light touch, temperature, pain, position, and vibratory
sensation were decreased on the left side of the body; on
simultaneous stimulation on both sides of the body, only the
right one was recognized. The recognition of numbers written by the examiner's index finger on different parts of the
body was better preserved on the left side than expected
(right: 14/15; left: 10/15). Recognition and localization of the

Address correspondence to Dr Bogousslavsky, Neurology Department, CHUV, 1011 Lausanne Switzerland.

448 Copyright 0 1988 by the American Neurological Association

body parts touched or held by the examiner were moderately
impaired on the left (right: 15/15; left: 8/15). General examination showed atrial fibrillation with a 70/minute pulse;
blood pressure was 160/80 mm Hg.
Five days after
the stroke, the patient remained alert and well oriented. She
was aware of her defects and cooperated well with the examiner. She recalled all the events that had happened to her
after stroke onset. Her spontaneous speech showed no abnormality. All verbal commands had to be given from the
right side, even when the patient closed her eyes, because
she did not pay attention to the commands given from the
left side. She could name 16 animals in I minute (centile 50).
Naming was within normal range (70/75, Boston Naming
Test). The repetition of isolated (or a series of) phonemes or
words, and of short and long sentences, was fully preserved.
Auditory comprehension was normal (34/46, Token Test).
The patient could sing nursery rhymes normally. She had no
trouble writing or reading letters or words, but when reading
a text, she systematically omitted the first three or four words
of the line; however, this abnormality could be corrected
when the patient was instructed to look at the left side of the
page. O n copying a sentence, she also omitted the first three
words, but corrected herself after being cued verbally by the
examiner. Calculation and bucco-linguo-facial and right limb
praxias were normal. Spontaneous drawing of a circle or
square was preserved, but that of a cube showed loss of
perspective; this was unchanged when she attempted to draw
from a copy. When asked to draw or write, the patient used
only the right part of the paper. Recognition of I5 famous
faces was spared. Visuospatial recognition was impaired (19
36, Ghent; 0/4, 1/5, Poppelreuter). The patient had a defective orientation when viewing a map of Switzerland; she did
not visually explore the left part of the map. However, when
the examiner pointed at cities in the left portion of the map
and asked the patient to name them, there was no mistake (5/
5). Her recall of the spatial location of the main cities was
normal. When asked to cross out 20 lines distributed evenly
on a sheet of paper, the patient crossed out only those on the
rght, but when asked to look farther at the left side of the
sheet, she crossed out another two lines. On a line-bisection
test using horizontal lines 30 crn long, the patient bisected
the lines at 8, 10, 10, 11,8, and 10 cm from the right edge of
the sheet on five trials; this was not improved by following the lines with the rlght index finger before bisection.
Brain CT showed an infarct in the posterior part of the
posterior limb of the right internal capsule. Doppler ultrasonography was normal. Ten days after stroke, a SPECT scan
using N-isopropyl-('231)-p-iodo-amphetamine(5 mCi iv,
SPECT performed 50 minutes and 5 hours after injection
with a dual ROTA camera at 6-degree steps of 30 seconds
each) showed marked hypoperfusion (50% compared with
the opposite side) in the right capsular region, with an associated perfusion decrease in the overlying parietal lobe (35%),
and to a lesser extent, the right prefrontal region (25%) (Fig
1).A 30% cerebellar hypoperfusion was present on the left.
A progressive improvement of the hemiparesis and hypesthesia occurred over the following 3 weeks. N o change in
the Poppelreuter test, geographic orientation, cube drawing,
line-bisection test, and reading was observed 10 days after
NEUROPSYCHOLOGICAL EXAMINATION.

Fig 1. SPECT scan of Patient 1, using 1231MP,showing transvwse sections. Five hours after injection, hypoperfusion is visible
in the right lenticulocapsukar region (SO% decrease) (small arrow), werlying parietal lobe (35 %) (large arrow), and frontal
lobe (25%) (middle arrow), compared with the lq5t Jide.

the first assessment. Three weeks after admission, the patient
suffered an acute occlusion of the right common iliac artery,
and she underwent an emergency embolectomy. During supper 1 day later she aspirated massively and died.
A severe atherosclerosis of aorta and
great vessels was found. The heart showed atrial dilatation on
both sides, without thrombus. The formalin-fixed brain
welghed 1,270 gm. The basilar and posterior cerebral arteries showed atheromatous plaques. The AChA was not
examined. The brain was cut in coronal slices 8 mm thick.
Frozen sections from 50 fragments taken from different regions of the cerebral hemispheres were cut at 30 Fm and
stained with cresyl violet and Schroeder's stain. The coronal
brain slices showed an irregularly shaped infarct about 20 x
20 x 6 mm in size in the territory supplied by the right
AChA. This infarct was nearly limited to the white matter.
Anteriorly, it was sharply delineated and extended into the
extreme posterior part of the rght lenticular nucleus, involving only a small part of the globus pallidus (lateral part of the
medial segment and medial part of the lateral segment) (Fig
2A). At this level, the lesion was just lateral to the ventral
part of the posterior limb of the internal capsule (Fig 2B, D).
At the level of the pulvinar (Fig 2C), the lesion extended
from the inferior part of the body of the caudate nucleus to

AUTOPSY FINDINGS.

Bogousslavsky et al: Subcortical Neglect

449

the inferior horn of the lateral ventricle adjacent to the choroidal fissure. The lateral half of the retrolenticular part of
the internal capsule was destroyed. The medial margin of the
lesion was just lateral to the lateral geniculate body, interrupting the optic radiation. Microscopic examination showed
that anteriorly the infarct involved a small part (< 2 mm) of
the basolateral group of the right amygdala. Other structures
usually supplied by the anterior choroidal artery, such as the
optic tract, the hippocampal formation, the tail of the caudate
nucleus, and the lateral geniculate body, were spared. The
cerebral cortex did not show pathological changes.

Patient 2
This 65-year-old man developed left-sided weakness and
dysarthria acutely. He was known to be hypertensive and to
smoke cigarettes. On admission, the patient was oriented to
time and place. Blood pressure was 180/120 mm Hg. H e
had a left superior quadrantanopia and a severe left hemiparesis involving the face, arm, and leg, with increased tendon reflexes and Babinski sign. Touch, pain, temperature,
vibration and position sensation were normal and symmetrical, but on simultaneous stimulation of both sides of the
body, only the right was recognized. Recognition and localization of the body parts was spared.
NEUROPSYCHOLOGICAL EXAMINATION. When examined
4 days after the stroke, the patient was restless in bed but
remained alert and oriented. He was aware of his defects.
The examiner had to stand on the right side of the patient
because he did not cooperate and did not execute orders
whep these were given from his left side. Spontaneous
speech, naming (19/20), repetition (phonemes, words, sentences up to 10 words), and auditory comprehension (35136,
Token Test) were normal. Writing was unimpaired, except
that the patient filled only the right part of the sheet. Also,
reading was impaired by systematic omission of the first two
or three words of the line, except when the patient was
repeatedly instructed to look at the left side of the page. Oral
calculation was normal, but written calculation was perturbed
by misplacement of the numbers. Drawing a cube spontaneously or copying one was impossible; the patient could draw
no better than a square and a triangle attached to each other.
Bucco-linguo-facial and right limb praxia were normal. Recognition of 15 famous faces was spared. Visuospatial recognition was impaired (0/5, Poppelreuter), and orientation on
geographical maps was impossible. On the line-crossing test
(see Patient I), the patient crossed out all lines on the right
but only 2 of 12 on the left; after verbal cueing, he crossed
out another 3 lines on the left. On the 30-cm line-bisection
test, he bisected the lines at 10, 12, 10, 11, and 14 cm from
the right edge of the sheet on 5 trials. Visual learning was
poor (Corsi's block tapping: span of 4 , failure of span + 1
learning; learning of 15 signs: total of 17-2-3-3-5-4).
Brain CT showed an infarct in the posterior part of the
posterior limb of the right internal capsule (Fig 3). Angiog-

V

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Annals of Neurology Vol 23 N o 5 May 1988

Pig 2. Schematic representations of three coronal brain slices from
Patient 1 (A, B, 0,showing the infarct in the territory of the
right anterior choroidzl artery. (0)Macroscopic view of the infarct at the levels shmn in (B). The scale represents 10 mm.

Fig 3. Computed tomographic scan of Patient 2, shwing an
infarct in the posterior part of the posterior limb of the right
internal capsule.

Fig 4. SPECT Jcan of Patient 2, using 1231MP,showing transverse sections (SO minutes afer injection).Hypoperfusion is visible in the right capsukar region (>O% &crease) (small arrow),
werhing parietal lobe (40%) (large arrow), and frontal lobe
(25%) (middle arrow), compared with the lejit side.

raphy showed a plaque at the origin of the right internal
carotid artery; the right AChA was not seen. On SPECT
scan (11 days after stroke, same technique as for Patient I),
there was hypoperfusion in the right capsular region (50%
compared to the left side), overlying parietal lobe (40%),and
frontal lobe (25%) (Fig 4).
On discharge 3 months later, the patient could walk but
severe weakness in the left hand was still present, as well as
the quadrantanopia. Visuospatial recognition, visual learning,
and graphic constructive dyspraxia remained unchanged, but
the left hemineglect had considerably improved (line bisection test: 14, 15, 14, 14, 14 cm; symmetrical response at the
line-crossing test; no touch extinction on the left on simultaneous stimulation of both sides of the body).

sonal space.” This network includes parietal, cingulate,
frontal, and reticular components, in which the inferior
parietal lobule appears to be a critical area. This was
confirmed in a series of patients with stroke occurring
in the right hemisphere, in which the most critical area
for the genesis of neglect was the inferior parietal
lobule 1251. Subcortical neglect has been emphasized
mainly in the right-sided lesions involving the thalamus, in which the motor component of neglect is
usually prominent, with involvement of the paramedian nuclei 13, 271 or the lateral formation 1161. In the
absence of thalamic involvement, subcortical neglect
has rarely been reported in lenticulostriate stroke 124,
261 and in frontal infarction 1231. Neuropathological
examination was done only once, in a 75-year-old
woman who had sensory hemineglect, asomatognosia,
and anosognosia, and who showed an isolated striatal
and deep white matter infarct involving the head of the
caudate, the anterior limb, the genu, and the superior
aspect of the posterior limb of the internal capsule
1121; the authors speculated on a possible thalamoparietal or corticoreticular disconnection, or on
the direct involvement of the striatum, to explain the
neglect syndrome.

Discussion
Our patients showed spatial hemineglect similar to the
neglect syndrome with parietal lobe lesions 113, 191.
Missing features were anosognosia, distractibility, disorientation, motor impersistence, and asomatognosia,
but these disturbances may also be absent in parietal
neglect.
Mesulam 1191 developed a model for neglect in
which there i s dysfunction of an “integrated network
for modulation of directed attention within extraper-

Bogousslavsky et al: Subcortical Neglect

451

Six patients with infarction of the right AChA territory, shown on CT, and hemineglect have been
reported with detailed data 15, 7, 141. None had
cerebral blood flow studies or neuropathological
verification, but it was suggested that a pulvinoparietal
disconnection [5, 7) or involvement of the temporal
isthmus white matter or medial part of the temporal
lobe [141 might have accounted for the hemineglect.
In our first patient, the infarct was nearly limited to
the retrolenticular part of the internal capsule and to
the white matter of the temporal isthmus. The minute
lesions in the globus pallidus, caudate body, and amygdala were probably too small to account for the severe
neglect. The retrolenticular part of the internal capsule
and adjacent deep white matter contain thalamocortical fibers that connect the pulvinar and intralaminar
nuclei to the multimodal parietal cortex 118, 271. Inputs from the brainstem reticular formation to the
parietal cortex may also travel at this level [lS, 21).
Interruption of these reticuloparietal connections by
the infarct could have generated the hemineglect.
With respect to a disconnection phenomenon, we
must emphasize that, in om patients, SPECT revealed
that hypoperfusion was not limited to the deep white
matter, but also affected the parietal cortex and, to a
lesser extent, the frontal cortex. A correlation between
neuropsychological dysfunction associated with deep
hemisphere lesions and ipsilateral cortical hypoperfusion has been emphasized 19, 201 but remains controversial 111. In l patient with a left AChA territory
infarct, neuropsychological testing was normal and
SPECT showed no hypoperfusion of the ipsilateral
cortex 12). The findings in our patients of a severe
ipsilateral parietal diaschisis, together with anatomical
evidence of involvement of thalamoparietal connections in the autopsied case, is consistent with a parietal
deactivation syndrome as the basis for neglect. Frontal
cortex deactivation may also have participated, possibly by involvement of reticuloanterior frontal connections also traveling in the internal capsule.
References
1. Baron JC, DAntona R, Serdaru M, et al: Hypom6tabolim.e
cortical aprss lesion thalamique chez I’homme: etude par la tomographie B positons. Rev Neurol (Paris) 142:465-474, 1986
2. Bogousslavsky J, Regli F, Delaloye B, et al: HCmiataxie et
dkficit sensitif ipsilat6ral. Infarctus du territoire de I’artsre choroidienne ant6rieure. Diaschisis cCr6belleux crois6. Rev Neurol
(Paris) 142:671-676, 1986
3. Cambier J, Elghozi D, Strube E: Usions du thalamus droit avec
syndrome de I’hemisphsre mineur: discussion du concept de
nkghgence thalamique. Rev Neurol (Paris) 136:105-116, 1980
4. Cambier J, Graveleau P, Decroix JP, et al: Le syndrome de
I’artsre choroTdienne anterieure: 6tude neuropsychologique de
4 cas. Rev Neurol (Paris) 139:553-559, 1983
5. Decroix JP, Graveleau P, Masson M, Cambier J: Infarction in

452

Annals of Neurology Vol 23 No 5 May 1988

the territory of the anterior choroidal artery. Brain 109:10711085, 1986
6. Englander RN, Netsky MG, Adelman LS: Location of human
pyramidal tract in the internal capsule: anatomic evidence. Neurology 25:823-826, 1975
7. Ferro JM, Kertesz A: Posterior internal capsule infarction associated with neglect. Arch Neurol41:422-424, 1984
8. Fisher CM, Curry HP: Pure motor hemiplegia of vascular origin. Arch Neurol 13:30-44, 1965
9. Franck G, Salmon E, Sadzot B, Van der Linden M: Etude
hemodynamique et metabolique par tomographie A emission de
positons d‘un cas d’atteinte ischemique thalamo-capsulaire
droite. Rev Neurol (Paris) 142:475-479, 1986
10. Foix C, Chavany JA, Hillemand P, Schiff-Wertheimer S: Obliteration de I’artsre choroidienne antkrieure: Ramollissement c6rkbral, hemiplegie, h6mianesthCsie et hemianopsie. Bull SOC
Ophthalmol Paris 37:221-223, 1925
11. Hanaway J, Young RR:Localization of the pyramidal tract in the
internal capsule of man. J Neurol Sci 34:63-70, 1977
12. Healton EB, Navarro C, Bressman S, Brust JCM: Subcortical
neglect. Neurology 32:776-778, 1982
13. Heilman KM: Localization of lesions in neglect. In Kertesz A
(ed): Localization in Neuropsychology. New York, Academic,
1983, pp 471-492
14. Helgason C, Caplan LR,Goodwin J, Hedges T 111: Anterior
choroidal artery territory infarction: report of cases and review.
Arch Neurol43:681-686, 1986
15. Kolisko A: Ueber die Beziehung der Arteria choroidea anterior
zum hinteren Schenkel der inneren Kapsel des Gehirns.
Vienna, A. Holder, 1891
16. Laplane D, Escourolle R, Degos JD, et al: La negligence motrice
d’origine thalamique: B propos de deux cas. Rev Neurol (Paris)
138:201-211, 1982
17. Ley J: Contribution A I’6tude du ramollissement cerebral. J
Neurol Psychiatr 32:785 and 895, 1932
18. Mesulam M-M, Van Hoesen GW, Pandya DN, Geschwind N:
Limbic and sensory connections of the inferior parietal lobule
(area PG) in the rhesus monkey: a study with a new method for
horseradish peroxidase histochemistry. Brain Res 136:393414, 1977
19. Mesulam M-M: A cortical network for directed attention and
unilateral neglect. Ann Neurol 10:309-325, 1981
20. Olsen TS, Bruhn P, Oberg RGE: Corrical hypoperfusion as a
possible cause of “subcortical aphasia” Brain 109:393-410,
1986
21. Pandya DM, Kuypers HGJM: Cortico-cortical connections in
the rhesus monkey. Brain Res 13:13-36, 1969
22. Poppi U: Sindrome talamo-capsulare per rammollimento nel
territorio dell’ arteria coroidea anteriore. Riv Patol Nerv
33:505-542, 1928
23. Stein S, Volpe BT: Classic “parietal” neglect syndrome after
subcortical right frontal lobe infarction. Neurology 33:797799, 1983
24. Valenstein E, Heilman KM: Unilateral hypokinesia and motor
extinction. Neurology 3 1:445-448, 1981
25. Vallar G, Perani D: The anatomy of unilateral neglect after
right-hemisphere stroke lesions: a clinicaVCT scan correlation
study in man. Neuropsychologia 24:609-622, 1986
26. Viader F, Cambier J, Pariser P: Phenomene &extinction motrice
gauche: lesion ischemique du bras interieur de la capsule interne. Rev Neurol (Paris) 138:213-217, 1982
27. Watson RT, Valenstein E, Heilman KM: Thalamic neglect: possible role of the medial thalamus and nucleus reticularis in behavior. Arch Neurol 38:501-506, 1981