1512

Pure Sensory Stroke Caused
by a Pontine Infarct
Clinical, Radiological, and Physiological Features
in Four Patients
Shuzo Shintani, MD; Shin Tsuruoka, MD; Tatsuo Shiigai, MD
Background and Purpose We conducted this retrospective
study to evaluate the clinical, neuroradiological, and neurophysiological findings in patients with pure sensory stroke due
to pontine lacuna.
Summary of Report Four patients with pontine lacuna,
three men and one woman (mean age, 64.5 years; range, 55 to
75 years), were evaluated. Magnetic resonance images were
obtained with a 0.5-T superconducting magnet using the SE
technique. Short-latency somatosensory evoked potentials
were evaluated by unilateral stimulation of the median nerve
at the wrist. These tests were done at a mean of 22.5 months
(range, 9 to 34 months) after symptom onset. Deep sensory
disturbances were present in one half of the patient's body
with no other neurological deficits found. The sensory deficit
was characterized by a prolonged period of refractory dysesthesia and a discrepancy between the superficial and deep

sensory disturbances. Lesions were localized in the medial
lemniscus of the middle and lower pons, with a sparing of the
spinothalamic tracts. The central conduction times of shortlatency somatosensory evoked potentials were prolonged (patients 1, 2, and 4), and the amplitudes were significantly
reduced (patients 1 and 2) when stimulating the parestheticsided median nerve (contralateral side of the lesion) compared with stimulating the other side.
Conclusions In all cases, the clinical and radiological findings indicated a dysfunction of the medial lemniscal tract in
the pons. The observed somatosensory evoked potentials were
probably related to the persistent refractory dysesthesias
present in these patients. (Stroke. 1994^5:1512-1515.)
Key Words • evoked potentials, somatosensory • pons •
magnetic resonance imaging

ure sensory stroke is a well-defined clinical entity
in which hemisensory symptoms predominate
with the absence of other major neurological
signs.1 Fisher1 attributed this syndrome to a lacunar
infarct in the ventroposterior nucleus of the thalamus.
Although thalamic stroke is the most frequent cause of
pure sensory stroke, nonthalamic strokes involving the
brain stem, 23 internal capsule,6-7 or cerebral cortex8 are
also reported to produce pure sensory stroke.9 We
present the findings in four patients with pure sensory
stroke due to pontine lacuna and discuss their
characteristics.

P

Short-latency somatosensory evoked potentials (SSEPs)
were recorded as follows: SSEPs were elicited by unilateral
stimulation of the median nerve at the wrist according to the
recommendations of the American Electroencephalographic
Society.10 Potentials were recorded from scalp to scalp (C,F,), scalp to ipsilateral Erbs point (C^-EP^, neck to scalp
(SQ-F,), and ipsilateral Erbs point to contralateral Erbs point
(EP,-EP2). Electrodes were located as follows: C,.=N20, Shagass point, cerebral cortex; SC5=N13, fifth cervical vertebral
electrode; and EP=N9, Erbs point, brachial plexus.

Subjects and Methods

A 55-year-old man with a history of hypertension
developed sudden numbness of the left face, neck,
trunk, and extremities at 5 PM, December 24,1990. The
next day on admission, physical examination revealed a
blood pressure of 168/100 mm Hg, regular pulse, and no
carotid bruits. Neurological examination showed normal motor function and reflexes. Babinski's sign was
negative, and cranial nerve palsy was absent. The
dysesthesia involved the breast, cheek, lower jaw, neck,
shoulder, upper arm and forearm, lateral abdomen, and
lower leg on the left side but not tongue or fingers. The
distortion of body schema was not present. Vibration
and position senses were reduced in the left limbs, being
worse in the lower leg. Vibration sense was decreased in
the jaw, neck, and breast also. Pinprick and temperature
were normally perceived. T r weighted MRI (TR, 380
milliseconds; TE, 15 milliseconds) performed 2 weeks
after the onset of symptoms demonstrated a low-intensity lesion in the right paramedian pontine tegmentum

Four Japanese patients with pure sensory stroke who
showed pontine lesions on magnetic resonance imaging (MRI)
were diagnosed and treated at the Toride Kyodo General
Hospital between June 1990 and September 1991. MRI was
performed in each case with a 0.5-T superconducting magnet
(Resona, Yokokawa Medical) using the SE technique. T,weighted (repetition time [TR], 380 milliseconds; echo time
[TE], 15 milliseconds) and T2-weighted (TR, 2000 milliseconds; TE, 100 milliseconds) scans were performed in the axial
plane.
Received January 18, 1994; final revision received March 25,
1994; accepted March 25, 1994.
From the Departments of Neurology (S.S.), Neurosurgery
(S.T.), and Internal Medicine (T.S.), Toride Kyodo General
Hospital, Ibaraki, Japan.
Correspondence and reprint requests to S. Shintani, MD,
Department of Neurology, Toride Kyodo General Hospital,
5901-1 Terada, Toride City, 302 Ibaraki, Japan.
© 1994 American Heart Association, Inc.

Case Reports
Case 1

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Shintani et al Pure Sensory Stroke Due to Pontine Infarct

1513

N20

FIG 1. Axial T,-weighted magnetic resonance image (repetition
time, 380 ms; echo time, 15 ms) in case 1, a 55-year-old man.
Irrfarct is observed in the right pons.

(Fig 1). The deficits in vibration and position senses
gradually improved, but the refractory dysesthesia persisted in the left half of his body, especially in the upper
limb and trunk, even though the patient had been
treated with a variety of pharmacologic agents such as
carbamazepine, imipramine, maprotiline, sulpiride, and
mecobalamin. Two years later the dysesthesias were still
present and severe enough to cause sleep disturbance,
but he had learned to ignore them.
Fasting blood sugar (FBS) concentration was 100
mg/dL. Total cholesterol (TC), high-density lipoprotein
(HDL) cholesterol, and triglyceride (TG) levels were 131
mg/dL, 48 mg/dL, and 82 mg/dL, respectively. The serum
lipoprotein(a) (Lp[a]) concentration was 10 mg/dL.
SSEPs produced by stimulation of the median nerve
were evaluated 28 months after the clinical onset. The
latency of N13 (recorded from the fifth cervical vertebral
electrode) was almost equal on both sides (15.3 milliseconds versus 15.2 milliseconds), but the central conduction time (CCT; N13 to N20) was prolonged (5.70
milliseconds versus 6.42 milliseconds) and the amplitude
was significantly reduced when stimulating the left median nerve as compared with the right (Fig 2).

Fra 2. Tracings of short-latency somatosensory evoked potentials observed 28 months after the clinical onset in case 1, a
55-year-old man. Top, Stimulation of the right median nerve
(N9=11.1 ms, N13=15.3 ms, N20=21.0 ms). Bottom, Stimulation of the left median nerve (N9=10.5 ms, N13=15.2 ms,
N20=21.6 ms). The central conduction time (N13 to N20) was
prolonged (5.70 ms versus 6.42 ms) and the amplitude was
significantly reduced when stimulating the left median nerve
(bottom) compared with stimulating the right (top). EP=N9, Erbs
point, brachial plexus; SC5=N13, fifth cervical vertebral electrode; Q)~N20, Shagass point, cerebral cortex.

ually reduced, but the numbness was still present in the
right forearm and toes despite treatment with a variety of
pharmacologic agents such as carbamazepine, imipramine, mecobalamin, and mexiletine.
FBS concentration was 102 mg/dL. TC, HDL cholesterol, and TG levels were 155 mg/dL, 56 mg/dL, and 56

Case 2

A 63-year-old man with a history of hypertension
developed numbness in the right half of his body early
one morning. His blood pressure was found to be 160/90
mm Hg on the following day, when neurological examination revealed the presence of dysesthesia in the right
face, arm, leg, and upper trunk. The dysesthesias were
especially intense in the forehead, forearm, upper breast,
and foot on the right side. The distortion of body schema
was not present. There was a decrease in vibration and
position senses in the upper breast and limbs on the right
side, but the response to pinprick and temperature
senses was essentially preserved. Motor function and
reflexes were normal, and there was no cranial nerve
palsy. Computed tomography (CT) on the same day
showed normal findings, but 4 days later, Trweighted
MRI (TR, 2000 milliseconds; TE, 100 milliseconds)
demonstrated a lesion of high intensity in the left paramedian pontine tegmentum (Fig 3). Twelve months later
the distribution and intensity of dysesthesias were grad-

FIG 3. Axial T^weighted magnetic resonance image (repetition
time, 2000 ms; echo time, 100 ms) of case 2, a 63-year-old man.
Irrfarct is observed in the left pons.

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1514

Stroke Vol 25, No 7 July 1994

FIG 4. Axial T,-weighted magnetic resonance image (repetition
time, 380 ms; echo time, 15 ms) of case 3, a 75-year-old man.
Irrfarct is observed in the lower right pons.

mg/dL, respectively. The serum Lp(a) concentration
was 52.8 mg/dL. SSEPs were performed 19 months after
the clinical onset. The latency of N13 was almost equal
on both sides (13.6 milliseconds versus 13.9 milliseconds), but the CCT (N13 to N20) was prolonged (7.02
milliseconds versus 6.30 milliseconds) and the amplitude was significantly reduced in response to stimulating
the right median nerve versus the left.
Case 3
This 75-year-old man who had no history of hypertension suddenly developed numbness on the left cheek,
tongue, and fingers when he was playing gateball (the
favorite sport of the elderly in Japan). His blood pressure was 138/80 mm Hg on admission. The next day on
admission, neurological examination revealed marked
dysesthesia and a slight impairment of vibration and
position senses in the corner of the mouth, tongue,
palm, and thumb on the left side. The left fingers,
especially the thumb, felt burned, and the palm felt full,
swollen, and hot. The tongue and lip on the left side also
felt burning dysesthesia. According to the distortion of
body schema, he transiently perceived that his left arm
was attached to the lumbar region for several days.
Response to pinprick, touch, and temperature was
normal. Motor paresis and cranial nerve palsy were
absent. Reflexes were normal, and Babinski's sign was
negative. T,-weighted MRI (TR, 380 milliseconds; TE,
15 milliseconds) performed 2 weeks after symptom
onset demonstrated a lesion of low intensity in the
lower right pons (Fig 4). Three months later the numbness of the left fingers and palm gradually disappeared,
but the dysesthesia and paresthesia in the corner of the
mouth was still present. Fifteen months later the numbness of the face had gradually reduced.
FBS was 114 mg/dL. TC, HDL cholesterol, and TG
levels were 194 mg/dL, 58 mg/dL, and 146 mg/dL,
respectively. The serum Lp(a) concentration was 46.0
mg/dL. SSEPs performed 34 months after the onset of
symptoms showed an essentially equal CCT (N13 to
N20) and amplitudes on both sides.
Case 4
A 65-year-old woman with a history of hypertension
had a sudden onset of numbness on the right side of the

FH3 5. Axial T,-weighted magnetic resonance image (repetition
time, 380 ms; echo time, 15 ms) in case 4, a 65-year-old woman.
Infarct is observed in the left pons.

body, especially her right leg. No other symptoms were
present. The neurological examination on the following
day showed numbness involving the cheek, jaw, arm,
breast, and leg on the right side. Numbness of the limbs
was more severe distally than proximally. Vibration and
position senses were slightly impaired in the right jaw,
elbow, breast, and foot. The distortion of body schema
was not present. There was bilateral hyperreflexia, but
Babinski's sign was absent. Motor function impairment
and cranial nerve palsy were also absent. T,-weighted
MRI (TR, 380 milliseconds; TE, 15 milliseconds) performed 1 week after the onset demonstrated a lesion of
low intensity in the left pons (Fig 5). Two years later the
dysesthesias of face, arm, and breast gradually disappeared, but the burning numbness of the right leg was
still present.
FBS was 88 mg/dL. TC, HDL cholesterol, and TG
levels were 185 mg/dL, 55.3 mg/dL, and 96 mg/dL,
respectively. The serum Lp(a) concentration was 35.6
mg/dL. SSEPs were performed 9 months after the onset
of symptoms. At that time the amplitude was almost
equal on both sides, but the CCT (N13 to N20) was
prolonged (6.48 milliseconds versus 6.18 milliseconds)
in response to stimulation of the right median nerve
compared with that on the left.

Discussion
The characteristics of sensory deficits in pure sensory
stroke due to pontine infarct include a prolonged refractory dysesthesia and a discrepancy between superficial and deep sensory disturbances. In these patients,
the dysesthesia was severe enough to cause sleep disturbances. The deficits of vibration and position senses
gradually improved, but the refractory dysesthesia had
been persistent for a long time. Fisher11 reported that
the objective sensory disturbances were mild in the pure
sensory stroke, and therefore endeavoring neurological
examination revealed faint decreased sensations. Patients with pure sensory stroke suffered primarily from
subjective sensory disturbances, such as dysesthesia and
paresthesia, and suffered in part from objective sensory
disturbances, such as position and vibration sense dis-

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Shintani et al Pure Sensory Stroke Due to Pontine Infarct
turbances. Fisher therefore suggested that the pure
sensory stroke is mainly pure paresthetic stroke.11
Robinson et al12 investigated SEPs in pure sensory
stroke, and reported that SEPs were normal in all 11
cases of pure sensory stroke and that CT was normal in
10. In only one case did CT show a lesion in right
thalamus.12 In our study we used MRI to detect small
brain stem lesions. Because CT is inferior to MRI for
detecting smaller and faint lesions, Robinson et al might
have missed some brain stem, thalamic, and other lesions. Karnaze et al13 evaluated 49 patients who had
suffered hemispheric or thalamic ischemia and reported
that SSEP abnormalities correlated with the presence of
sensory deficit and the degree of neurological deficit.
They discussed the fact that CCT delays and absent
N19-P22 components correlated strongly with the severity of the neurological deficit; the CCT therefore may
prove to have prognostic value in stroke.13 In our SSEP
studies, the CCTs were prolonged in cases 1, 2, and 4,
and the amplitudes were significantly reduced in cases 1
and 2. These neurophysiological findings were probably
related to the characteristics of sensory disturbances in
pure sensory stroke, such as persistent refractory
dysesthesia.
The other characteristic of sensory deficit in pure
sensory stroke due to a pontine infarct is the discrepancy between superficial and deep sensory disturbances. In the four cases presented, vibration and position senses were decreased, but the responses to
pinprick and temperature were essentially preserved.
These clinical symptoms indicated a dysfunction of the
medial lemniscal tract with no dysfunction of the
spinothalamic tract. The lesions in our patients were
localized in the medial lemniscus of the middle pons
(cases 1, 2, and 4) and the lower pons (case 3), with
sparing of the spinothalamic tracts. A discrepancy between the superficial and deep sensory disturbances is
common in pure sensory stroke caused by a pontine
lacuna. It is due to the anatomic location of the medial
lemniscal tract, which is separate from the spinothalamic tract in the pons.14
Fisher15 analyzed 135 patients in which numbness,
either episodic or persistent, involved one side of the
body; he tentatively proposed that isolated paresthesias
of the face, arm, and leg indicate thalamic involvement
and that numbness of cerebrovascular brain stem origin
does not assume any of these patterns. In our patients
with brain stem lesions, the dysesthesias involved face,
arm, leg, and breast in cases 1, 2, and 4. In case 1, the
dysesthesias extended to neck, shoulder, and abdomen.
The characteristic of syndrome-lesion correlation in
pure sensory stroke due to pontine infarct may be the
distribution of its sensory disturbance. The thalamic
lesion causes isolated sensory involvement of all three
parts, face, arm, and leg.15 The pontine lesion causes
sensory involvement that includes trunk (breast and
abdomen) as well as face, arm, and leg. The lesion in
case 3 was quite large, but the syndrome was quite
circumscribed. Case 4 had a small lesion with wide-

1515

spread syndrome and greatest complaints in the leg.
The cause of this disproportion between syndrome and
lesion remains unknown, but the neurophysiological
findings by SSEP may be related to this condition.
SSEPs showed normal findings in case 3, but in case 4
the CCT was prolonged when stimulating the paresthetic-sided median nerve. SSEPs correlate with the
severity of the neurological deficit and sensory abnormalities after cerebral ischemia.13 Case 3, a 75-year-old
man, manifested a cheiro-oral syndrome, which is typically provoked by lesions located in the thalamus and
cortex. Takezawa et al16 reported a 69-year-old woman
with a cheiro-oral syndrome caused by a pontine lacuna.
The onset of the brain stem cheiro-oral syndrome is
thought to involve the medial lemniscus, which has a
body-localization sequence in the upper and lower
limbs.17 It spreads horizontally on both sides of the
paramedian pontine tegmentum. The ascending fibers
from the lower limb are located on the outside, while
those from the upper limb are located on the inside. The
abdominal pathway of the trigeminal nerve, which
transmits the epicritic sensation of the face, ascends
close to the rear inside of these fibers.17

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Pure sensory stroke caused by a pontine infarct. Clinical, radiological, and physiological
features in four patients.
S Shintani, S Tsuruoka and T Shiigai
Stroke. 1994;25:1512-1515
doi: 10.1161/01.STR.25.7.1512
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1994 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628

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