983
Pure Sensory Stroke
Clinical-Radiological Correlates of 21 Cases
Jong Sung Kim, MD
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Background: Although pure sensory stroke is a relatively common lacunar syndrome, the responsible
lesions are often unidentified because of their small size. I reported 21 cases of pure sensory stroke in
which the lesions could be identified by head computed tomography and/or magnetic resonance imaging
and correlated the clinical findings with the radiological lesions.
Summary of Report: Eleven patients had thalamic strokes. Lacunes confined to the posterolateral part
of the thalamus were found in nine cases, and hemorrhages of relatively large size were found in two. Five
patients showed a loss of all sensory modalities, but six with very small lacunes showed minor or restricted
sensory changes. Seven patients with lacunes or hemorrhages in the lenticulocapsular region or corona
radiata showed abnormalities of spinothalamic tract sensation. Two patients with a small lacune and a
hemorrhage in the pontine tegmentum showed a selective sensory deficit of the medial lemniscal type. One
patient with a small cortical infarct showed a cortical sensory loss that was preceded by cortical sensory
transient ischemic attacks.
Conclusions: Pure sensory stroke can occur with lesions in various areas of the somatosensory system.
Hemisensory deficits of all modalities usually are associated with a relatively large lacune or hemorrhage
in the lateral thalamus, whereas tract-specific or restricted sensory changes suggest very small strokes in
the sensory pathway from the pons to the parietal cortex. (Stroke 1992;23:983-987)
KEY WORDS • computed tomography • magnetic resonance imaging • pure sensory stroke
P
ure sensory stroke (PSS) is a well-defined clinical
entity in which hemisensory symptoms predominate without other major neurological signs.1
While Fisher2 reported PSS to be the most common
lacunar syndrome, more recent studies showed that it is
the second or fourth most common.34 Although thalamic stroke is the most frequent cause of PSS, nonthalamic strokes involving the brain stem,5-16 internal capsule,17-20 or cerebral cortex21 are also reported to
produce PSS.
Because of their small sizes, the lesions producing
PSS are often difficult to identify. Fisher22 previously
analyzed the clinical features of 135 patients with PSS
and allied conditions but could not localize the lesions.
Although computed tomography (CT) may be helpful,23"25 it is often unable to confirm lesions.4-11'20'26 With
the advent of magnetic resonance imaging (MRI), small
strokes causing PSS are more easily identified. However, until recently there has been no clinical-radiological study of PSS, which prompted me to report 21 cases
in which clinical manifestations correlated with radiological (CT and/or MRI) findings.
Subjects and Methods
I identified 24 patients with pure hemisensory stroke
who showed appropriate lesions on head CT (GE/9800)
and/or MRI at Asan Medical Center between SeptemFrom the Department of Neurology, College of Medicine,
University of Ulsan, Asan Medical Center, Seoul, Korea.
Address for correspondence: Jong Sung Kim, MD, Department
of Neurology, Asan Medical Center, 388-1, Poongnap Dong,
Songpa-Ku, Seoul 138-040, Korea.
Received January 1, 1992; accepted March 3, 1992.
ber 1989 and December 1991. The MRI studies were
performed using a 1.5-T superconducting magnet (GE).
Axial T2-weighted (repetition time/echo time [TR/TE],
2,500/80), Tl-weighted (TR/TE, 600/20), and sagittal
Tl-weighted scans were generated with a slice thickness
of 5 mm. Three patients had more than one lesion
contralateral to the sensory deficit and were thus excluded. All 21 patients were examined by the author
(patients 12 and 19 were previously reported16-20). In 14
patients CT identified the lesions. In four of these
patients MRI was performed later to confirm the presence of the lesion and the absence of other lesions,
whereas only MRI was performed in seven patients. The
clinical symptoms and signs were correlated with the
radiological localization. The size of the stroke was
classified as large, small, or very small when the longest
diameter of the lesion was > 1.5 cm, 0.5-1.5 cm, or <0.5
cm, respectively.
Results
Twenty-one patients (12 men and 9 women, aged
46-74 [mean, 57] years) were studied; the details of
each patient are summarized in Table 1. Risk factors for
stroke included hypertension in 16, diabetes mellitus in
three, and hyperlipidemia in three. Patient 2, who had
coronary heart disease, was positive for both lupus
anticoagulant and anticardiolipin antibody, and patient
3 had pancreatic cancer.
Thalamic Strokes
Eleven patients (cases 1-11) had thalamic strokes, of
which nine were ischemic (lacune) and two were hemorrhagic. Eight lesions were demonstrated by head CT
984
TABLE
Stroke
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Vol 23, No 7 July 1992
Clinical Features of 21 Patients With Pure Sensory Stroke
Risk
factors
Case
Sex/Age
1
2
F/52
M/55
3
4
5
6
M/55
M/55
HT
CHD, APL
Cancer
HT
HT
HT
7
M/50
8
Sensory deficits
Nature
I
I
Site
RThal
C
Identification
S
S
Size
+
-
CT
s
nc
CT
+
CT
Pi
T
V
Po
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L
L
nc
CT
I
LThal
RThal
LThal
LThal
RThal
VS
nc
CT
HT, DM
I
LThal
VS
_
MRI
F/64
HT
I
RThal
VS
_
CT
9
F/57
HT
I
RThal
VS
—
MRI
10
11
M/56
DM
HT
I
I
RThal
LThal
VS
M/46
_
MRI
CT
12
M/47
M/61
-
15
M/55
L Post IC
R Post IC
L Post IC
L Post IC
CT, MRI
M/56
I
I
VS
13
14
16
17
M/55
F/59
F/55
F/67
F/74
F/65
HT, HL
HT
HT
HT
HT
HT
HL
HT
HT
DM, HL
18
19
20
21
M/52
F/58
I
H
H
H
H
I
I
VS
s
VS
VS
-
VS
VS
s
s
CT
MRI
MRI
+
MRI
Sensory TIA
-
LCR
Restricted to
digits
Sensory TIA
s
R Pons
R Pons
R Parietal
Faciobrachial
distribution
Faciobrachial
distribution
Cheiro-oral
syndrome
Cheiro-oral
and four toes
-
VS
LCR
I
CT
CT, MRI
CT
MRI
CT, MRI
CT, MRI
LCR
H
I
I
Remark
Pi, pinprick; T, touch; V, vibration; Po, position; C, cortical; F, female; M, male; HT, hypertension; CHD, coronary heart disease; APL,
antiphospholipid antibody syndrome; DM, diabetes mellitus; HL, hyperlipidemia; I, infarct; H, hemorrhage; R, right; L, left; Thai, thalamus;
Post, posterior; IC, internal capsule; CR, corona radiata; S, small; L, large; VS, very small; nc, not checked; CT, computed tomography;
MRI, magnetic resonance imaging; TIA, transient ischemic attack.
and three by MRI. In all ischemic strokes, the lesions
were confined to the posterolateral part of the thalamus
probably involving the ventral posterolateral nucleus
(Figure 1). The two hemorrhagic strokes were relatively
large in size.
Five patients with thalamic stroke showed sensory
deficit of both spinothalamic and medial lemniscal
types, whereas six with very small lacunes (cases 6-11)
did not. Patients 6 and 7 complained of an unpleasant
numbness over the face and arm without an objective
sensory deficit, while patient 10 showed a mildly decreased pinprick sense only. Patient 8, who had decreased pinprick and vibration senses restricted over the
left perioral and cheek area, suffered numbness in those
areas as well as the hard palate and palm. Patient 9 had
painful dysesthesia over the same area as patient 8 but
additionally had numbness in the first four toes. Patient
11, who initially had mildly decreased position and
vibration senses in the right arm and leg, soon showed
sensory changes restricted to the fingertips.
Case 1. A hypertensive 52-year-old woman developed
sudden numbness in the left arm and leg. On admission,
her blood pressure was 160/110 mm Hg with regular
pulse and no carotid bruits. Neurological examination
showed normal motor function and reflexes. There was
a decreased sensation to pinprick, touch, vibration, and
position over the entire left side of her body. Graphes-
thesia and stereognosis were also impaired in the left
limbs. Head CT performed 3 days after the onset
showed an infarct in the posterolateral part of the right
thalamus (Figure 1). The hypesthesia and unpleasant
numbness continued.
Case 11. This 46-year-old hypertensive man suddenly
felt heaviness in his right leg and complained of a gait
difficulty. When he was first examined 2 days later his
blood pressure was 160/100 mm Hg, and he showed
mildly decreased vibration and position senses in his
right arm and leg. The next day he complained of
numbness restricted to the right distal fingers. Sensory
examination showed impaired position sense in all right
fingers and decreased vibration sense restricted to the
area distal to the first interphalangeal joints. However,
pinprick and touch senses were spared. Head CT
showed a small infarct in the left thalamus (Figure 2).
Lenticulocapsular or Corona Radiata Strokes
Four patients (cases 12-15) with lenticulocapsular
strokes were identified. Patients 12 and 13 had lacunes
in the lentiform nuclei abutting the posterior portion of
the posterior limb of the internal capsule, and patients
14 and 15 had very small hemorrhages near the middle
third of the posterior limb of the internal capsule. Three
patients showed very small (cases 16 and 18) or small
(case 17) lacunes in the deep white matter of the middle
Kim
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FIGURE 1. Computed tomography shows infarct in posterolateral part of right thalamus.
cerebral artery territory, probably involving the corona
radiata. All of the patients with lenticulocapsular or
corona radiata stroke showed a decreased sense of
spinothalamic modality and suffered from a long-lasting, unpleasant hemiparesthesia some time after the
initial events. Vibration and position senses were spared
in all of these patients. Patient 18 had suffered repeated
episodes of sensory transient attacks.
Case 13. A 56-year-old hypertensive man awoke with
numbness in the left limbs. Neurological findings were
normal except for decreased pinprick and temperature
senses over the entire left side of his body. His objective
sensory dysfunction gradually improved, but the unpleasant hemiparesthesia continued. Initial brain CT
was negative, but a repeat scan performed 3 months
after the onset showed a small infarct in the right
lentiform nucleus abutting the posterior part of the
posterior limb of the internal capsule (Figure 3).
Pure Sensory Stroke
985
FIGURE 2. Computed tomography shows small infarct in
left thalamus.
Case 21. A 65-year-old hyperglycemic and hyperlipidemic woman developed intermittent abnormal sensation and weak feelings in the left arm 7 days before
admission. These episodes occurred two or three times
a day and lasted usually less than an hour. During those
attacks she could walk, but veered to the left, and the
posture of her left arm became awkward. Neurological
examination showed a normal, obese woman, but during
the attacks she showed a clumsy left hand with markedly
decreased vibration and position senses and abnormal
stereognosis and graphesthesia. However, pinprick and
temperature senses were spared. A similar but less
marked sensory abnormality was present in her left leg.
Brain Stem Strokes
Two women with pontine strokes had PSS. One had a
small hemorrhage, and the other had an infarct in the
tegmentum. Both showed an isolated sensory deficit of
the medial lemniscal type.
Case 19. This 67-year-old hypertensive woman suddenly felt numb in the left half of her body. In the
emergency room her blood pressure was 230/140
mm Hg. Cranial nerve and motor functions were normal. Vibration and position senses in the left limbs were
decreased and were worse in the lower extremity.
Pinprick and temperature were normally perceived.
When standing, she veered to the left. Tl-weighted
MRI performed 2 days after the onset demonstrated a
small hemorrhage in the right pontine tegmentum (Figure 4).
Cerebral Cortical Strokes
One patient with cortical infarct showed PSS. Interestingly, the PSS was preceded by multiple pure cortical
sensory transient ischemic attacks.
FIGURE 3. Computed tomography shows infarct in right
lentiform nucleus bordering posterior limb of internal capsule.
986
Stroke
Vol 23, No 7 July 1992
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FIGURE 4. Tl-weighted magnetic resonance image (repetition time/echo time, 600/20) shows high-signal intensity in
right pontine tegmentum corresponding to location of medial
lemniscus.
In addition, her left arm was observed to assume an
abnormal posture: her elbow became gradually flexed to
90° with her wrist and all fingers slightly flexed. She did
not notice this abnormal posture unless told, after which
she could promptly correct it. During admission, the
recurrent attacks led her to suffer PSS of cortical
sensory deficit, which lasted about 5 days. Three days
after admission T2-weighted and gadolinium-enhanced
Tl-weighted MRIs showed a small, linear, high-signal
intensity in the cortical and subcortical areas of the
right parietal lobe (Figure 5). An angiogram was
refused.
Discussion
As determined in previous investigations, the thalamus was the site most frequently involved in this series.
Five patients showed an impairment of all sensory
modalities including pinprick, touch, vibration, and position senses. Three patients had small infarcts (lacune)
confined to the posterolateral part of the thalamus, and
two had relatively large hemorrhages. Six patients with
very small lacunes showed restricted sensory changes:
paresthesia without objective sensory signs (cases 6, 7,
and 9), mild impairment in pinprick sense only (case
10), and selective impairment in vibration and position
senses (case 11).
Although thalamic strokes were usually reported to
produce deficits of all sensory modalities, Landi et al24
described a patient with decreased pinprick sense only,
whereas Sacco et al27 reported a patient with a selective
loss of the position sense. Therefore, small lacunes
strategically placed in the thalamus may cause tractspecific sensory deficits. According to previous studies,
the medial lemniscal fibers are projected densely to the
caudal division of the ventral posterolateral nucleus,
whereas the spinothalamic fibers diffusely enter the
posterior thalamic nucleus, the ventral posterolateral
FIGURE 5. Gadolinium-enhanced Tl-weighted image (repetition time/echo time, 600/20) shows linear enhancing signal
(arrows) in cortical and subcortical areas of right parietal
lobe. A clinically silent, old lacune is also seen in right basal
ganglia.
nucleus, and the central lateral nucleus.27 Presumably
the small lacune in patient 11 was situated within the
caudal part of the ventral posterolateral nucleus, but
this structure was spared in patients 6, 7, 9, and 10.
The patients with very small lacunes tended to show
restricted distribution of sensory abnormality, in the
faciobrachial area in patients 6 and 7 and the distal
fingertips in patient 11. Patients 8 and 9 showed socalled "cheiro-oral syndrome": numbness restricted
over the corner of the mouth, hard palate, and hand.
The present study and the previously reported thalamic
strokes with cheiro-oral sensory syndrome13-28"34 support the alleged topographic presentation in the ventrolateral nucleus of the thalamus34 in which sensory areas
projected from face and hands are closely related,
although why the first four toes were also affected in
patient 9 remains unexplained.
There have been a few reports of PSS caused by
capsular or corona radiata strokes. Groothius et al17
suggested that to produce PSS, the lesion should occupy
the posterior quarter of the posterior limb of the
internal capsule, where sensory tracts without motor
fibers are believed to be located. In the present study,
four patients with lenticulocapsular stroke with PSS
were identified: two (cases 12 and 13) had lacunes
abutting the posterior quarter of the posterior limb, and
two (cases 14 and 15) showed lesions bordering the
middle of the posterior limb, suggesting that small
lesions in this area could also escape the descending
motor tract. Moreover, in this series three patients had
lacunes in the corona radiata of the middle cerebral
artery distribution. A similar patient with a corona
radiata lacune in the middle cerebral artery territory
was previously reported by Rosenberg and Koller,23 and
Chamorro et al4 described a patient with PSS who had
a CT-identified lacune in the anterior limb of the
internal capsule.
Kim
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It is noticeable that all of the patients in the present
study with capsular or corona radiata stroke showed
decreased pinprick and touch senses without impaired
vibration or position senses. The patient described by
Groothius et al17 who showed an additional deficit in the
medial lemniscal sensory modality had lesions in the
posterior part of the posterior limb adjacent to the
thalamus, whereas the patients in the present study
showed lesions situated in the lateral part of the internal
capsule or corona radiata. Therefore, it may be postulated that the medial lemniscal sensory pathways run
posteriorly and medially within the posterior limb of the
internal capsule, whereas those of spinothalamic modalities ascend more laterally and diffusely into the corona
radiata.
I observed two patients with brain stem stroke, one
with a lacune and another with a hemorrhage in the
pontine tegmentum. Both revealed sensory deficits of
pure lemniscal modality caused by discrete lesions
situated in the medial lemniscus. A patient with similar
clinical features was previously described by Graveleau
et al,8 but patients with isolated spinothalamic modality
impairment1015 or with only subjective sensory symptoms5 have also been described. Therefore, strategically
located small brain stem strokes tend to produce sensory deficit of a single tract type. Recently, brain stem
strokes causing cheiro-oral sensory syndrome were also
described.7*12-'4
Finally, I described a patient with cortical infarct who
showed markedly impaired cortical sensation. Derouesne et al21 reported a similar case with a small
cortical infarct in the middle cerebral artery territory. It
is unique and of interest that patient 21 had pure
cortical sensory transient ischemic attacks. This patient's abnormal posture during the sensory transient
ischemic attack was probably due to a loss of position
sense in the involved limbs.
In conclusion, the clinical-radiological correlation of
21 cases in this study strongly supports the previous
assumption that strokes anywhere in the sensory tract
can produce PSS. Sensory deficits of all modalities in
one half of the body usually are associated with a
relatively large lacune or hemorrhage in the area of the
posterolateral thalamus, whereas tract-specific or restricted sensory abnormalities usually correlate with a
very small lesion located in the sensory pathway.
Acknowledgment
I wish to thank Professor Onyou Hwang for her helpful
suggestions in preparing this manuscript.
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J S Kim
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Stroke. 1992;23:983-987
doi: 10.1161/01.STR.23.7.983
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1992 American Heart Association, Inc. All rights reserved.
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