Posterior Internal Capsule Infarction
Associated With Neglect
Jos\l=e'\M. Ferro, MD, Andrew Kertesz, MD, FRCP(C)
\s=b\ A persistent hemispatial neglect
developed in a patient following a small
infarction of the posterior limb of the
right internal capsule. This defect was restricted to tasks requiring spontaneous
motor performance on the contralateral
hemispace, especially when carried out

under visual control. It was not associated
with an extinction phenomenon. Verbal
cues improved exploratory behavior, suggesting that hemispatial akinesia in this
case was due to an intentional disorder. A

pulvinar-parietal disconnection, depriving
right parietal cortex from relevant
visuospatial information from the contralateral hemispace, was probably the anatomic basis of hemispatial neglect in this
the

case.

(Arch Neurol 1984;41:422-424)

"Meglect

is

classically associated
with right parietal damage.14
Lesions on a postulated corticolimbicreticular loop5, which mediates selec¬
tive attention, have also been shown
to produce neglect. These include the
dorsolateral frontal lobe,610 cingulate
gyrus,7 striatum,1015 and thalamus.1619
These structures seem to play differ¬
ent roles in hemispheric activation
and preparation to respond. Less

information is available on the role of
the white matter tracts that connect
these anatomic sites.
We report a case of hemispatial
neglect in a patient with a discrete
lesion of the posterior limb of the
right internal capsule.
REPORT OF A CASE

A 61-year-old, right-handed, hyperten¬
sive, diabetic man was admitted to St
Joseph's Hospital, London, Ontario, on
July 28, 1982, because of the sudden onset

of left-sided weakness. His BP was 210/120
mm Hg. Neurologic examination disclosed
a complete left homonymous hemianopia,

Accepted for publication Aug 13, 1983.
From the Department of Clinical Neurological
Sciences, University of Western Ontario, St
Joseph's Hospital, London (Drs Ferro and Kertesz); and the Department of Neurology, Hospital
de St Maria, Lisbon (Dr Ferro).
Reprint requests to Department of Clinical
Neurological Sciences, University of Western
Ontario, St Joseph's Hospital, London, Ontario,
Canada N6A 4V2 (Dr Kertesz).

left-sided facial weakness, and moderate
left hemiparesis. There was a slight
decrease in pinprick sensation on the left
side but position, vibration, and light touch
sensation were normal. There was no
extinction on double simultaneous tactile
stimulation. Reflexes were slightly brisker
on the left and there was a left upgoing toe.
The patient had a history of hypertension
treated with propranolol hydrochloride
and methyldopa. Despite intramuscular
administration of hydralazine, the BP fluc¬
tuated between 200/110 and 160/90 mm
Hg; that evening his hemiparesis wors¬
ened. The next morning there was com¬
plete paralysis on the left, mild left
hypoesthesia, and decreased pinprick posi¬
tion and vibration sense, and the left later¬
al conjugate gaze was impaired. He had
clear-cut left hemispatial neglect on draw¬
ing. A computed tomographic (CT) scan
was performed that showed a small, nonenhancing lucency on the posterior limb of
the internal capsule (Fig 1). This lesion
crossed the line described by Mizukami et
al20 joining the genu of the internal capsule
to the posterior end of the putamen. This
indicated the posterior internal capsular
location of the lesion. The thalamus was
apparently uninvolved as the lesion was
lateral to a line joining the posterior outer
aspect of the frontal horn to the choroidal
plexus.21 A CT scan performed one year
later showed the same lesion with the
lucency extended to the parietal centrum
semiovale. An EEG showed slow waves in
right central leads. Angiograms were not
made. An isotope brain scan performed on
the 15th day after admission was normal.

Neuropsychologic Examination
The patient received a comprehensive
neuropsychologic assessment two weeks
after his stroke. He was alert, fully ori¬
ented, and cooperative. His spontaneous
speech was fluent and his performance on
the language subtests of the Western
Aphasia Battery (WAB)22 was normal. His
aphasia quotient was 96.3 (maximum, 100).
The patient had no trouble reading letters
or words, but reading sentences was labori¬
he tended to omit the first (leftsided) words. Reading comprehension was

ous as

normal when he was instructed to look to
the left edge of the stimulus card. On
writing he tended to use mainly the right
half of the page. On copying a sentence the
patient omitted the left half, while on
dictation he made several neglect-induced
paragraphias, mostly in the form of extra
strokes on letters (with-wuth) or omission
of the left half of letters (hammer-hanmer). Praxis and calculation were not

Downloaded From: by a Western University User on 09/09/2018

impaired. On the drawing subtest of the
WAB he scored 8 of 30 points. He used only
the right half of the page and neglected the
left half of a cube, clock, house, and tree
(Fig 2). The patient could not duplicate any
block designs and his score on the Raven's
Coloured Progressive Matrices (RCPM)
was only in the fifth percentile for his age.
A tendency to neglect correct choices on
the left part of the test pages contributed
to his low score. He had no prosopagnosia
as tested by 20 famous faces and he could
recognize 13 of 15 familiar melodies.
The patient was aware of his defects and
worried about them; he would cry easily
when questioned about his stroke. He could
identify affective speech (18/20). He could
also recognize the emotional category of
"affective situations" in drawings (14/16),
but he was mildly impaired in the identi¬
fication of emotional facial expressions
(8/12).

Neglect Testing

Neglect was further investigated with a
comprehensive neglect testing battery that
included visual, auditory, tactile, and
motor simultaneous stimulation, cancella¬
tion and line bisection tests, tactile search,
spatial representation, and visual spatial
memory tests.
At rest the patient's eyes and head were

midiine, and on verbal command or
pursuit the lateral gaze was full to the
right and the left. Spontaneous gaze was
more often directed to the right. Complete
left hemianopia and left hemiplegia pre¬
on the

cluded motor and visual simultaneous
stimulation testing. Simultaneous audito¬
ry stimulation was tested by placing a
stethoscope on the patient's ears and gent¬
ly tapping the membrane. On ten trials he
reported the sound as bilateral in nine and
as referred to the right ear only in one
trial. He did not show extinction on simul¬
taneous tactile stimulation. On unilateral
right tactile stimulation he reported the
stimuli to the right on five trials and both
to the right and left on the remaining five
trials. A similar behavior that could be
labeled inverted allesthesia was described
by Critchley4 in a man with a right parietal
neoplasm; Critchley suggested that this
was a form of tactile hallucination.
On the cancellation test, where he was
asked to cross out 20 lines distributed
evenly on a test sheet, the patient failed to
cross all the left ones while crossing seven
of ten on the right. The line bisection test
was modified from Schenkenberg et al.23 A
test sheet with six horizontal lines (lengths,
80, 120, 100, 120, 80, and 100 mm) having a
block letter at each end24 was placed in front

Line Bisection Performance

Experimental Condition
2 wk after onset
Lines on center, visual control

Total R Deviation

Mean (SD) R

on 6 Lines, mm

Deviation, mm

70

11.7 ± 8.2

3 mo after onset

Lines on left, visual control'_54, 52_9.0 ± 6.4, 8.7 ± 3.9
0.8 ± 9.1, 6.5 ± 9.7t
Lines on right, visual control·
5, 39t
58
9.7 ± 10.6
Lines on center, visual control
9.2 ± 13.2
Lines on center, somatesthetic control
55
*

Measured on two occasions.

tDeviation was to the left.
pegs. The patient performed well on this
task. The ability to recall spatial details of

Fig 1.—Computed tomographic scan show¬
ing infarction on posterior limb of right inter¬
nal capsule, involving retrolenticular and
part of sublenticular and lenticulothalamic
portions.

a familiar image was tested by asking the
patient to imagine a map of Canada placed
in front of him, and then asking him to
name the provinces on the right and left
parts of this imaginary map. The ability to
recall the spatial location of recently pre¬
sented visual stimuli was assessed by pre¬
senting a card with a horizontal row of six
drawings of objects (used in the WAB).
The patient, after naming all the drawings,
was requested to recall (after a 20-s delay
during which he had to count aloud the
lines of the cancellation test) their spatial
location. His performance was normal on

both tests.

Follow-up Study

Fig 2.—Spontaneous drawing of person and
copying of clock and house demonstrating
left hemispatial neglect (three months after
onset).
of the patient. The patient was asked to
read the letters and then bisect the line.
This procedure ensures that failre to bisect
is not secondary to hemianopia or visual
scanning deficit. The sum of right deviation
on the bisection of the six lines was 70 mm
(mean, 11.7 ± 8.2 mm).
On a tactile search test the patient was
shown a board with nine pegs (three on the
right, three on the left, and three central).
After he counted all of the pegs, he was
blindfolded and asked to pick up the nine

The patient was studied again three
months after onset. He still had complete
hemianopia and hemiplegia on the left, but
his hemisensory loss had improved, espe¬
cially for light touch and position sense. He
did not complain of pain or dysesthesia.
On neuropsychologic examination, read¬
ing and writing were normal, although the
patient continued to use mainly the right
half of the page. The same behavior was
observed on drawing, where his perfor¬
mance was improved, although he still
showed neglect on drawing a person, clock,
and house (Fig 2). He was still impaired on
block design and on RCPM. Recognition of
environmental sounds was perfect (15/15).
He was worried and sad about his de¬
fects.
On the neglect testing battery there was
no auditory or tactile extinction, and per¬
formance on the spatial representation,
visual memory, and tactile search tests
was normal. The patient missed only one
left line on the cancellation task. However,
he was still impaired on line bisection. Line
bisection was worse when the lines were
placed on the left hemispace than when
they were placed on the right. This was
confirmed on two occasions (Table). Somatesthetic cueing (following the lines
with his right index finger before bisecting
them) did not improve his performance.
The patient's ability to use his left hemi¬
space, without visual control and when
explicitly requested to do so, was evaluated
in the following tasks. He was blindfolded
in both tests. In the first test he was asked
to draw two crosses on a blank sheet placed
in front of him, one on the left and the
other on the right. Then he was requested
to draw four other crosses below each of

Downloaded From: by a Western University User on 09/09/2018

the first ones. Crosses were drawn alter¬
nately on the left and right. The patient's
performance was accurate and he did not
demonstrate any tendency to right devia¬
tion. In the second test he was asked (while
blindfolded) to draw three crosses on a
blank sheet of paper placed in front of him.
He succeeded in following the instructions
that required him to draw one cross on the
left, one on the right, and the third at
mid-distance between the first two crosses.
On four trials he only showed a tendency
for right deviation (34 mm) on the central
crosses, but this was within normal con¬
trols range (—5 to 45 mm).
COMMENT

A typical and durable hemispatial
neglect developed in our patient fol¬
lowing a lesion of the posterior limb of
the internal capsule. Hemispatial
neglect disturbed reading and writing
and was impressive on drawing, can¬
cellation, and line bisection tests. This
deficit was restricted to tasks requir¬

ing spontaneous motor performance

under visual control on the contralat¬
eral hemispace and was not associated
with an extinction phenomenon.
Although this patient was hemi¬
anopic, his performance on line bisec¬
tion could not be explained by his
visual field defect, as he had to read
the letters on the left side of each line
prior to bisection. Tracing the lines
with his fingers did not help him
either. It could be argued that,
although he saw the whole line, he
quickly forgot the left part and then
bisected the "remaining" right part.
However, in the present case both
remote and recent visual memory
were spared as spatial details of the
old and recent visual stimuli could be
adequately recollected and described
verbally, suggesting also that his
mental representation of space was
intact.
Heilman and Valenstein24 proposed
that hemispatial neglect is secondary
to a hypokinesia for any act that must
be performed in the neglected hemi¬
spatial field. Like the patients of Heil¬
man and Valenstein, our patient's
performance on line bisection was
worse when the lines were placed in

the left hemispace. Hemispatial aki¬
nesia was present mostly when the
motor

exploratory

activity

was

carried out under visual control.
When direct visual control was
removed and the patient used an
internal representation of space, par¬
ticularly on tasks where verbal
instructions specified that the patient
should describe or explore the left and
right parts of the presented stimuli,
neglect was no longer present. This
superiority of verbal cues over free¬
style performance was also noted by
Diller and Weinberg,25 Laplane et al,"
and Bisiach et al.26 The fact that ver¬
bal cues can act as "external volition"
and improve exploratory behavior
suggests that hemispatial akinesia in
this case is due to an intentional dis¬
order, a defect of the will to explore
the contralateral halfspace and not to
a loss of the motor programs for the
distribution of movements within

extrapersonal space.
Healton et al,13 Bisiach et al,26 and
Kertesz and Dobrowolski10 reported
cases of deep central lesions causing
neglect. In some cases the internal
capsule was damaged in association
with other structures (thalamus, len¬
ticular nucleus). In the present case it
is unlikely that neglect was caused by
temporary dysfunction (diaschisis)27
of neighboring structures such as the
nucleus reticularis (NR) of the thala¬
mus because neglect was still present

three months after onset. Further¬
more, the usual clinical features of the
thalamic syndrome were absent.
Several ascending and descending
pathways run through the posterior
limb of the internal capsule or are in
close anatomic relation to it.28 Those
include the pyramidal, corticorubral,
and temporopontine tracts, and audi¬
tory, visual, and thalamic radiations.
The thalamic radiation includes fibers
connecting the posterior part of the
ventral nuclei of the thalamus with
the somatesthetic sensory cortex,
nonspecific thalamic fibers projecting
from the NR to the multimodal pari¬
etal cortex, and corticothalamic
fibers, namely, collaterals to the NR.17
The retrolenticular portion includes
efferent connections from the pulvinar29 to the multimodal parietal cor¬
tex. Thalamolenticular connections,30
which are important to motor activa¬
tion and preparation to respond, also
cross the internal capsule.
In our patient, the thalamometathalamic connections with the visual
and somatesthetic areas and with the
multimodal parietal cortex appeared
to be important. The internal capsule
lesion probably deprived the postero-

parietal cortex of visual information
from ipsilateral visual associative
areas (by damaging optic radiation)
and the pulvinar. Valenstein et al31
were

able to

produce nonsensory

neglect from parietotemporal lesions
in
monkeys.
Electrophysiologic

studies have demonstrated that some
posteroparietal cells fire before a
motor response to a relevant stimulus
is made.32·33 Based on these findings,
Mountcastle et al33 proposed that the
posteroparietal association cortex
commands operations within extra-

personal space. The principal visual
input to the posteroparietal lobule

comes from the

pulvinar.34 A pulvinarparietal disconnection was probably
the anatomic basis of hemispatial
neglect in our patient. The compensat¬
ing effect of verbal cues suggests that
the left hemisphere is able to activate
the right parietal lobe and the motor
exploratory programs toward the con¬
tralateral halfspace through intact
interhemispheric connections. In the
series by Bisiach et al, patients show¬
ing a disruption of the left half of the
conscious representation of outside
space had large corticosubcortical
lesions involving the parietal lobe.26'35
Preservation of the parietal lobe
explains why our patient could
describe accurately the left half of
recollected images.
This study was supported in part by the Insti¬
tuto Nacional de Investigaçâo Científica, Portu¬
gal (Dr Ferro), and Ontario Heart Foundation
grant 3-33 (Dr Kertesz).

References
1. Brain WR: Visual disorientation with special reference to lesions of the right cerebral
hemisphere. Brain 1941;64:224-272.
2. H\l=e'\caenH, Penfield W, Bertrand C, et al:
The syndrome of apractognosia due to lesions of
the minor cerebral hemisphere. Arch Neurol

Psychiatry 1956;75:400-434.
3. McFie J, Piercy MF, Zangwill OL: Visualspatial agnosia associated with lesions of the
right cerebral hemisphere. Brain 1950;73:167\x=req-\

190.
4. Critchley M: The Parietal Lobes. London,
Edward Arnold Ltd, 1953.
5. Heilman KM: Neglect and related disorders,
in Heilman KM, Valenstein E (eds): Clinical
Neuropsychology. New York, Oxford University
Press, 1979, pp 268-307.
6. Silberpfenning J: Contribution to the problem of eye movements. Confin Neurol 1941;4:1\x=req-\
13.
7. Heilman KM, Valenstein E: Frontal lobe
neglect in man. Neurology 1972;22:660-664.
8. Castaigne P, Laplane D, Degos JD: Trois cas
de negligence motrice par lesion frontale pre-

rolandique. Rev Neurol 1980;18:123-132.
9. Chain F, Chedru F, Leblanc M, et al: Renseignements fournis par l'enrigestrement du
regard dans les pseudo-hemianopsies d'origine
frontale chez l'homme. Rev Electroencephalogr
Neurophysiol Clin 1972;2:223-232.
10. Kertesz A, Dobrowolski S: Right-hemi-$
sphere deficits, lesion size and location. J Clin
Neuropsychol 1981;3:283-299.

Downloaded From: by a Western University User on 09/09/2018

11. Heir DB, Davis KR, Richardson ET, et al:

Hypertensive putaminal hemorrhage. Ann Neurol 1977;1:152-159.
12. Damasio AR, Damasio H, Chui HC:
Neglect following damage to frontal lobe or basal

ganglia. Neuropsychologia 1980;18:123-132.

13. Healton EB, Navarro C, Bressman S, et al:
Subcortical neglect. Neurology 1981;31:62.
14. Valenstein E, Heilman KM: Unilateral
hypokinesia and motor extinction. Neurology

1981;31:445-448.
15. Ferro JM, Martins IP, Pinto F, et al: Apha-

sia following right striato insular infarction in a
left handed child: A clinico-radiological study.
Dev Med Child Neurol 1982;24:173-182.
16. Watson RT, Heilman KM: Thalamic

neglect. Neurology 1979;29:690-694.
17. Watson RT, Valenstein E, Heilman KM:
Thalamic neglect: Possible role of the medial

thalamus and nucleus reticularis in behavior.
Arch Neurol 1981;38:501-506.
18. Schott B, Laurent B, Maugiere F, et al:
Negligence motrice par hematome thalamique
droit. Rev Neurol 1981;137:447-455.
19. Laplane D, Escourolle R, Degos JD, et al:
La negligence motrice d'origine thalamique. Rev

Neurol 1982;138:201-211.
20. Mizukami M, Nishijima M, Kin H: Computed tomographic findings of good prognosis for
hemiplegia in hypertensive putaminal hemorrhage. Stroke 1981;12:648-652.
21. Matsui T, Hirano A: An Atlas of the
Human Brain for Computerized Tomography.

Tokyo, Igaku-Shoin Ltd, 1978.

22. Kertesz A: The Western Aphasia Battery.
New York, Grune & Stratton Inc, 1982.
23. Schenkenberg T, Bradford DC, Ajax ET:
Line bisection and unilateral visual neglect in
patients with neurological impairment. Neurolo-

gy 1980;30:509-517.

24. Heilman KM, Valenstein E: Mechanisms

underlying hemispatial neglect. Ann Neurol
1979;5:166-170.
25. Diller L, Weinberg J: Hemi-inattention in

rehabilitation: The evolution of a rational remediation program, in Weinstein EA, Friedland RP
(eds): Advances in Neurology. New York, Raven
Press, 1977, vol 18, pp 63-82.
26. Bisiach E, Capitani E, Luzzatti C, et al:
Brain and conscious representation of outside

reality. Neuropsychologia 1981;19:543-551.

27. Von Monakow C: Die Lokalisation im Grosshirn und der Abbau der Functionen durch corticale Herde. Wiesbaden, Germany, Bergmann,
1914.
28. Ranson SW, Clark SL: The Anatomy of the
Nervous System. Philadelphia, WB Saunders Co,
1959.
29. Trojanowski JW, Jacobson S: Areal and
laminar distribution of some pulvinar cortical
efferents in rhesus monkey. J Comp Neurol 1976;
169:371-392.
30. Kalil K: Patch-like termination of thalamic fibers in the putamen of the rhesus monkey:
An autoradiographic study. Brain Res 1978;
146:145-150.
31. Valenstein E, Heilman KM, Watson RT, et
al: Nonsensory neglect from parietotemporal
lesions in monkeys. Neurology 1982;32:1198\x=req-\
1201.
32. Hyvarenen J, Poraren A: Function of the
parietal associative area 7 as revealed from
cellular discharges in alert monkeys. Brain 1974;
97:673-692.
33. Mountcastle VB, Lynch JC, Georgopoulos
A, et al: Posterior parietal association cortex of
the monkey: Command functions for operations
within extrapersonal space. J Neurophysiol 1975;
38:875-908.
34. Yin TC, Mountcastle VB: Visual input to
the visuomotor mechanisms of the monkey's

parietal lobe. Science 1977;197:1381-1383.
35. Bisiach E, Luzzatti C, Perani D: Unilateral
neglect, representational schema and consciousness. Brain 1979;102:609-618.