NOTE

INFARCT OF THE ANTERIOR LIMB OF THE RIGHT
INTERNAL CAPSULE
CAUSING LEFT MOTOR NEGLECT:
CASE REPORT AND CEREBRAL BLOOD FLOW STUDY
V. de Ia Sayette\ G. Bouvard2, F. Eustache\ F. Chapon 1,
F. Rivaton3, F. Viader\ B. Lechevalier 1
(~Service de Neurologie Dejerine; 2 Service des Radioisotopes; 3Service de

Neuro-radiologie, CHU Cote de Nacre, Caen Cedex)

INTRODUCTION

Unilateral motor neglect (MN) has been described with a variety of cerebral lesions
involving the pre-rolandic cortex, striatum, thalamus or internal capsule. It can occur with
a syndrome of unilateral multimodalities neglect or as an isolated entity, suggesting
relationships between global hemispheric activation and a more specific involvement of
motor function. We report a case of MN caused by an anterior internal capsule infarct with
cerebral blood flow (CBF) measurements before and after motor activation.
CASE PRESENTATION

A right handed 69 year old hypertensive man suddenly presented occipital headache
and ataxia. He was noted to have facial asymmetry and difficulty walking. Admitted on
the same day, he was found to be alert, well oriented, complaining of a left-sided weakness.
His blood pressure was 240/120. The examination showed no spontaneous movement of
the left hemibody, a facial asymmetry (left facial weakness) and a mild dysarthria. The gait
was disturbed by dragging of the left leg and non balance of the left arm, causing the
patient to deviate to the left and to fall frequently. These signs disappeared after verbal
stimulation, that is when the patient was asked with insistance to use his arm and leg.
Under these conditions, no segmental motor deficit was noted. Deep tendon reflexes were
brisk and symmetrical and the plantar reflexes were downgoing. fl_xarninations performed
at different periods never showed sensory deficit. However, nociceptive stimuli caused a
slower withdrawal motor reaction on the left than on the right side. In bimanual motor
activities, for example when the patient was eating, he failed also spontaneously to use his
left hand or took the knife but did not use it. A definite left motor extinction was present
since the patient raised correctly the left or the right arm upon unilateral tactile stimulation
but when bilaterally stimulated, the right arm was initially raised shortly followed by the
left arm. There was no hemianopsia, visual neglect or extinction. Visuo-spatial tests were
correctly executed: clock drawing, complex image description, room drawing, placement
of cities on a map, itinerary description. Body scheme perception and face recognitiori
were normal. Copies of Rey figure and tridimensional constructive praxia showed mild
alteration. Gestual series, dressing and small objects manipulation were correctly exe­
cuted. No frontal signs or memory impairement were detected. Calculation and speech
were normal.
Verbal dichotic listening showed a left sided extinction and the audiogram a mild
bilateral and symmetrical hypoacousia.
Cortical auditory evoked potentials recorded over the temporal and parietal lobes after
stimulation with 95 db at 1000Hz were normal, including the early and late potentials. The
somato-sensory evoked potentials after stimulation of the median nerves were normal. The
EEG showed moderate signs of right frontal damage.
Cortex, (1989) 25, 147-154

148

V. de Ia Sayette and Others

Fig. I - CT scan (axial slice).

Fig. 2- CT scan (coronal slice).

The CT scan (Figures 1 and 2 ) done four days after the onset of symptoms, showed a
small hypodense infarct in the anterior half of the right internal capsule with no obvious
involvement of the caudate nucleus. No cortical lesions were shown before and after
contrast-enhanced ·cT scan.
The motor symptoms regressed markedly over the next three weeks. Three months
later the patient still complained of left sided weakness but the clinical examination as well
as the constructive praxia were normal; only a left extinction was still demonstrated on the
verbal dichotic listening test.

Left motor neglect and CBF study

@@®

149

Fig. 3 - Position of the
scanning probes.

@(j)
@@)

®
In summary, this patient presented on the left side: (1) A reduction of the spontaneous
motricity without any motor deficit. (2) A decreased withdrawal motor reaction to pain.
(3) A reversibility of these symptoms after verbal stimulation. (4) A left motor extinc­
tion.
The present case is not a pure MN since mild constructive apraxia and left sided
extinction on the verbal dichotic listening test were also demonstrated.
MEASUREMENTS OF CEREBRAL BLOOD FLOW (CBF)
Material and Methods

CBF was measured four weeks after the onset of the symptoms by the Xenon 133
Xe) inhalation technique (Obrist, Thompson, Hsioh Shan Wang and Wilkinson, I975;
Risberg, I980). The equipement used (novocerebrograph) has 32 detectors positioned over
both hemispheres. After informed consent, the patient was initially scanned over a 30
seconds Eeriod for a baseline study. Then, the patient inhaled.a gaseous mixture con­
taining 1 3Xe (I 08 Bq/ I) during one minute. The exhaust circuit was then opened and the
patient breathed the room air for 10 minutes. The pC02 and the radioactivity were
recorded. The curve of arterial blood radioactivity was deducted from the end-tidal air
curve and served to compute the tracing of the 32 cerebral activity curves. CBF was
measured from the washout curves by estimation of the initial slope index (lSI) as
described by Risberg (I980).
The positioning of the scanning probes is illustrated on Figure 3.
( 133

Protocol

The patient was submitted to three CBF measurements: rest, right hand activation, left
hand activation, interrupted by one hour each. The resting measurement was done in a
supine position with the eyes closed and the ears occluded. The activation measures were
made over II minutes by having the patient feel different objects with the same hand for 30
seconds each for a total of 22 objects. The left hand was used first, followed by the right
hand one hour later. Adequate palpation of the objects was ascertained by having the
patient enumerate the objects felt after the measurement had been completed and by direct
observation of the patient contact during the examination.

V. de Ia Sayette and Others

!50

TABLE I

Patient; lSI Values at Rest and During Activation: lSI Increases During Activation vs. Rest
Condition

Rest

Activation right hand

Activation left hand

pCOz
(mmHg)

39

38

38.4

LH

RH

LH

RH

LH

RH

Mean CBF

34.3

32.1

36.4

34.6

35.8

35.4

I
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16

41
38
34
37
35
31
32
32
28
32
34
37
34
28
36
41

38
33
35
30
32
33
30
33
28
31
32
32
30
31
32
33

35
38
41**
36
36
32
36
39*
33*
35
35
35
35
39**
35
40

37
34
40*
34
33
33
32
33
32
35
37*
36
33
34
34
37

34
34
44*
37
35
34
36
36
39**
36
34
37
37
35**
33
39

37
34
42*
35*
30
34
30
33
35**
34
37
39**
34
35
33
46*

* .01< p < .05.
** p< .01.
LH = Left hemisphere; RH = Right hemisphere.
TABLE II

Controls (same remarks as Table I)
Condition

Rest

Activation right hand

Activation left hand

pCOz
(mmHg)

42 ± 2.1

40.9 ± 4.2

41.1 ± 3.6

LH
Mean CBF
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16

43.4
44.2
42.2
44.2
44.4
43.3
44.2
44
41.8
42.6
43
44.6
45.6
41.8
40.4
42
46

RH
44.6
44.8
43.2
46.6
45.8
44.6
45.4
44.2
43.2
43.4
44.8
48.4
44.4
44.6
41.8
43.8
43.8

LH
49.4**
48.8
47.8
50.8*
50.8*
51*
49.6*
50.2*
49.6**
47.6*
49.4
51.8
50.6*
50.4*
45
49*
48.4

RH
49.7**
48.8*
46.4
49.8
52.4*
51*
49.4
50.6*
49.4*
46.6
50.6**
50.8
52.4**
51.4*
47
47.8
51.4

LH

RH

49.2**
47
46.8
50.4*
49.4*
48.6
48.8
49.2*
46.6*
49*
50*
54*
52.2**
49.4*
46*
48.8**
50.6*

50.1 **
49.4*
48.2
50.8*
50.6*
49*
50.4*
50.4*
49.6*
48.4
50.6**
53.2
52.6**
50.6*
48.4
47.6*
51.8

Five healthy right handed controls, three men and two women aged from 37 to 75 year
old (mean: 56 y.o) underwent the same protocol for comparison.

Left motor neglect and CBF study

151

Results

The results are shown in Table I for our patient and in Table II for the controls. For the
patient, the lSI differences between baseline vs-activation were considered significant
p<0.05 if above 14.5% and p<O.Ol if above 19%. Controls were studied using the Student
t test on matched series.
Comments

In control subjects, CBF at rest was slightly higher in the frontal and temporal regions
when compared to the rolandic and parietal areas; a significant asymmetry existed in the
postero-inferior region (probe II), the flow being lower on the left side. During activation
studies, the increase in CBF in the hemisphere contralateral to the hand used was similar
on the left and right side. This increase bore both on the mean hemispheric CBF and
regional CBF (rCBF) in the following territories: orbito-frontal and inferior pre-rolandic
(probes 3, 4), superior pre-rolandic (probe 5), rolandic (probes 6, 7, 8), parietal (probes 13,
15) and temporal.
The mean and regional CBF of the hemisphere ipsilateral to the hand used were rather
similar to the contralateral values. The small series of controls could explain this lack of
interhemispheric asymmetry by a "crosstalk" phenomenon, a probe recording activity
contralateral to its position.
In our patient, the mean CBF at rest was slightly lower than in controls in both
hemispheres (lSI of 32.1 on the right, and 34.3 on the left, no significant difference), with
no localized hypoperfusion area.
During activation studies of the right hand, the left hemisphere showed a similar
increase of CBF when compared to controls, but in a smaller area: orbito-frontal (probe 3),
temporal (probe 9) and very high activation on the high rolandic cortex (probe 8) aboye the
primary sensori-motor cortex of the hand and also of the superior parietal cortex (probe
14). There was no superior pre-rolandic activation.
During activation studies of the left hand, significant increases of regional CBF
occurred in the following right hemispheric areas: orbito-frontal (probe 3), inferior pre­
rolandic (probe 4), temporal (probe 9, 11, 12) and occipital (probe 16). There was however
no change in CBF of the rolandic (probe 6, 7, 8) and superior pre-rolandic (probe 5)
areas.
The patient thus showed a low flow at rest whithout regional hypoperfusion nor
inter-hemispheric asymmetry. During manipulation studies of the left hand, there was no
significant activation of neither the rolandic nor the superior pre-rolandic cortex whereas
the activation of the remaining cortex was similar to controls.
DISCUSSION

Usually part of the non dominant hemisphere syndrome (Cambier, Elghozi and
Strube, 1980; Cambier, Masson, Graveleau and Elghozi, 1982; Watson, Valenstein and
Heilman, 1981), pure MN is quite rare and the lesions described have numerous locations,
most of them in the right subcortical areas: parieto-temporal or mid-frontal (Castaigne,
Laplane and Degos, 1970; Castaigne, Laplane and Degos, 1972), thalamic (Schott, Laur­
ent, Mauguiere and Chazot, 1981; Laplane, Escourolle, Degos, Sauron and Massion,
1982), anterior limb of the internal capsule (Viader, Cambier and Pariser, 1982), internal
capsule and lenticulostriate structures (Valenstein and Heilman, 1981).
Considering CBF, an increase in regional CBF (rCBF) in the contralateral primary
sensori-motor cortex after activation of the hand was first demonstrated by Olesen ( 1971)
and further confirmed by subsequent studies done either with an intracarotid injection or
inhalation of Xe 133 (Roland and Larsen, 1976; lngvar and Philipson, 1977; Orgogozo and
Larsen, 1979; Roland, Skinhoj, Lassen and Larsen, 1980; Gelmers, 1980; Meric, Luft,
seylaz and Mamo, 1983). This constant activation is directly proportional to the strength

152

V. de Ia Sayette and Others

(vs. intensity) of the movement. When the executed movement comprises a minimun of
complexity, the rCBF increase may also involve bilateraly the pre-frontal area including
the supplementary motor area (SMA) (Ingvar and Philipson, 1977; Halsey, Blauenstein,
Wilson and Wills, 1979; Orgogozo and Larsen, 1979; Roland, Larsen, Lassen and Skinhoj,
1980; Roland, Skinhoj, Lassen and Larsen, 1980; Eccles, 1982). This activation seems to be
directly related to the movement itself since Larsen, Skinhoj and Lassen (1978) have
shown it in subjects counting out but not when counting mentally. We can then consider in
our patient the failure of activation of the right rolandic area during left hand movements
normally performed as definitely abnormal. No lesion was seen on CT scan in the rolandic
area to explain this failure and if such a lesion existed, abnormalities in the resting rCBF
probably would have been demonstrated. The infarct in the anterior internal capsule could
not explain such a defect by itself since its recording probe is lower situated than the
superior rolandic probe. This could then be a "functional deficit" restricted to the right
primary motor cortex, demonstrated only during movement whitout lack of activation of
the other areas. Such a hemodynamic deficit despite correct motor performance suggests
either a partial cortical inactivation enabling a sufficient level of function for motor
execution, or involvement of different activating circuits.
In other respects, the possible lack of activation of the superior pre-rolandic area and
presumably of the SMA cannot be regarded as definitely abnormal: Roland and Larsen
(1976) found a high inter-subjects variability in this activation during a somesthetic
discrimination protocol being the closest to the one we used (manipulation of prisms of
different sizes). The lesion in the anterior limb of the internal capsule which causes an
interruption of motor thalamic projection to the pre-frontal cortex, could be responsible
for the inactivation of rCBF in the right superior pre-rolandic and then rolandic areas and
therefore set up the physiopathological basis of the MN in our patient. Indeed the SMA is
considered as the motor programming area initiating and supervising the execution of
voluntary movements (Orgogozo and Larsen, 1979; Roland et al., 1980a; Roland et al.,
1980b) and its removal in animal creates a picture of transient MN (Eccles, 1982). In
addition experimental MN in the monkey has been ascribed to a break in a specific
activating motor system which integrates the mesencephalic reticular formation, central
structures of the thalamus and the ventrolateral and ventroanterior nuclei, the basal
ganglia, the prefrontal cortex and anterior cingulum (Watson and Heilman, 1979; Watson,
Valenstein and Heilman, 1981 ; Rizzolatti, Matesi and Pavesi, 1983; Watson, Valenstein,
Day and Heilman, 1984). Finally we did not find any preferential rCBF increase of speech
areas while the left hand was stimulated, making unlikely interference by interior speech
when this hand was moving. Actually, the left hemisphere dominance for both speech and
voluntary movement is thought to explain the dissociation between spontaneous motor
function and intentional movement. This dissociation is the clue to MN, which is observed
more frequently with right sided lesions, and could explain the reversible deficit under
verbal stimulation (Laplane, Escourolle, Degos, Sauron and Massion, 1982) and its
transient nature.
Regarding the present case, the association between auditory extinction and MN
possibly reflects the interrelations of different mechanisms for hemispheric activation.
Even though a specialized loop for the motor activation exists, the functional and ana­
tomical relationships with the system conducting one's attention and integrating sensory
informations are numerous. Thus "the thalamo-frontal connections can be seen as the true
activation pathway for the motor response in a hemisphere already activated by sensory
inputs" (Viader et al., 1982). This would explain why MN is usually observed when a
complete sensory neglect is present. This observation is not absolute since Dehen and
Cambier ( 1980) reported a case of somatosensory, auditory and visual neglect whitout any
MN.
In conclusion CBF sudies in our patient give a hemodynamic and functional corre­
lation to the MN syndrome. In a study of patients with permanent motor deficit after
capsular lesions, Takano, Kimura, Nakamura et al. (1985) have demonstrated, using the
intra-carotid 133Xe technique, areas of hypoperfusion limited to the central cortex, which
were present at rest. Our study, on the contrary, shows a dissociation between a normal
resting flow and a localized hypoperfusion restricted to a specific cortical area which

Left motor neglect and CBF study

153

appears only upon activation of this specific area. This dissociation reflects a dynamic
phenomenon which correlates well with the neglect entity.
ABSTRACT

A sixty-nine year old hypertensive man had left motor neglect following an infarct of
the anterior limb of the right internal capsule. He also had left auditory extinction on
verbal dichotic listening and a sligh constructional apraxia. Regional cerebral blood flow
(CBF) was measured at rest with Xenon 133 inhalation and was found to be slightly
decreased in a diffuse fashion. Motor activation of the right hand resulted in an increase of
CBF in the contralateral superior rolandic area, whereas no such increase was found
during motor activation of the left hand. This lack of cortical CBF increase on contralate­
ral motor activation is interpreted as a consequence of the failure of some corticosub­
cortical connexions involved in motor arousal. The specifically d)'namic appearance of
regional CBF abnormalities, i.e. during selective activation as opposed to rest measure­
ments, is consistent with the functional character of neglect.
Acknowledgement. We thank Ernst Meyer and Gilles Marshall from Montreal Neu­
rological Institute and Hospital for their support help and advices and Carole Levert for
typing the manuscript.

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V. de Ia Sayette, Service de Neurologie Dejerine, CHU Cote de Nacre. 14040 Caen Cedex, France.