ARTICLE IN PRESS

Case Studies

Ipsilateral Facial Tactile Hypesthesia in a Patient with Lateral
Medullary Syndrome
Masahiro Katsumata, MD,* Koichi Oki, MD, PhD,* Jin Nakahara, MD, PhD,*
Yoshikane Izawa, MD, PhD,* Takato Abe, MD, PhD,*† Shinichi Takahashi, MD, PhD,*
and Norihiro Suzuki, MD, PhD*

Background: Various sensory impairments have been reported in patients with lateral
medullary syndrome, also known as Wallenberg syndrome. The typical sensory
impairments experienced by patients with this condition are ipsilateral facial and
contralateral trunk and limb thermal hypesthesia and hypoalgesia. Tactile (light
touch) sensation is not generally diminished. Here we report the case of a 35year-old man with lateral medullary infarction who had atypical sensory impairment.
Methods: We examined the results from the neurological examination of the patient
as well as findings from computed tomography of the head and magnetic resonance imaging. Results: Magnetic resonance imaging showed left lateral medullary
infarction caused by left posterior inferior cerebellar artery dissection. Neurological examination revealed both tactile and thermal/pain hypesthesia on the left
side of the patient’s face, and thermal/pain hypesthesia on his right upper and
lower limbs. Conclusion: There are two types of tactile sensation: epicritic and protopathic. Facial tactile sensation is usually thought to be associated with epicritic
tactile sensation, which travels through principal sensory nuclei of the trigeminal nerve. The protopathic pathway travels down through the spinal tract via the
trigeminal nerve and is not considered a primary pathway. However, in this case
the protopathic tactile sensation pathway might be involved, and it caused facial
tactile hypesthesia. Because most of previous case reports and literature reviews
focused only on thermal/pain hypesthesia, we believe that this case provides critical information on the brainstem neuroanatomy, especially for the protopathic
tactile sensation pathway in patients with stroke. Key Words: Lateral medullary
infarction—Wallenberg syndrome—tactile hypesthesia—ipsilateral face.
© 2015 National Stroke Association. Published by Elsevier Inc. All rights reserved.

From the *Department of Neurology, Keio University School of
Medicine, Japan; and †Department of Neurology, Osaka City University Graduate School of Medicine, Japan.
Received June 13, 2015; revision received July 27, 2015; accepted
July 30, 2015.
The authors have reported no conflicts of interest.
Address corresponding to Masahiro Katsumata, Department of
Neurology, Keio University School of Medicine, 35 Shinanomachi,
Shinjuku-ku, Tokyo 160-8582, Japan. E-mail: ktmasahiro@gmail.com.
1052-3057/$ - see front matter
© 2015 National Stroke Association. Published by Elsevier Inc. All
rights reserved.
http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2015.07.027

Case Report
A 35-year-old man with no history of past stroke complained of sudden vertigo, headache, and numbness on
the left side of his face and was admitted to our hospital. Neurological examination revealed both tactile and
thermal/pain hypesthesia on the left side of his face, and
thermal/pain hypesthesia in his right limbs (Fig 1, A,B);
these findings were confirmed by several different neurologists, with the same results for clarity. Difference in
severity of sensory impairment in the areas of three

Journal of Stroke and Cerebrovascular Diseases, Vol. ■■, No. ■■ (■■), 2015: pp ■■–■■

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M. KATSUMATA ET AL.

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Figure 1. Pattern of thermal/pain hypesthesia (A)
and tactile hypesthesia (B) in our case. Left trigeminal and right upper/lower limb thermal/
pain sensations were diminished throughout
hospitalization. Facial hypesthesia persisted throughout hospitalization with no evident limb hypesthesia.
Head MRI on day 3 showed high intensity in the
left lateral medulla both in diffusion weighted
imaging (C) and FLAIR image (D). TOF-MRA
on day 3 (E) showed no remarkable findings in
vertebral and basilar arteries; however, the left PICA
was not detected. TOF-MRA on day 11 (F) showed
vasodilation of the left PICA (arrow). The intimal
flap was not detected in the T2-weighted image.
Abbreviations: FLAIR, fluid attenuated inversion recovery; MRI, magnetic resonance imaging;
PICA, posterior inferior cerebellar artery; TOFMRA, time-of-flight magnetic resonance
angiography.

trigeminal branches was not observed. Tactile hypesthesia in the patient’s limbs was not remarkably evident.
His left corneal reflex was diminished. Horner’s syndrome on the left side and limb ataxia in the right upper
and lower limbs were evident, and a tandem gait test
showed unsteadiness.
His magnetic resonance imaging showed left lateral medullary infarction and dissection of the posterior inferior
cerebellar artery (Fig 1, C-F). Infarction was localized in
only one slice of the brainstem magnetic resonance image
that was taken every 5-mm interval; no other infarction
was found that could explain tactile hypesthesia on the
patient’s face, including the pontine region, where principal sensory nuclei of the trigeminal nerve exist. We
assumed that the posterior inferior cerebellar artery dissection caused the patient’s ipsilateral lateral medullary
infarction and headaches.
On admission, we started intravenous administration
of edaravone (a free radical scavenger) and a rehabilitation program, followed by oral antiplatelet therapy
(cilostazol) 5 days later. Ataxic gait, vertigo, and limb hypesthesia improved several days following admission.
However, left trigeminal hypesthesia, both tactile and
thermal/pain sensations, persisted throughout the patient’s
hospitalization. He was discharged on day 16.

Discussion
Lateral medullary infarction is characterized by sensory
deficits, ipsilateral cerebellar ataxia, ipsilateral Horner’s
syndrome, bulbar palsy, and vertigo. The sensory hypesthesia appears to be ipsilateral facial thermal/pain
hypesthesia and contralateral thermal/pain hypesthesia
in the trunk and limbs, although tactile sensation is usually

not affected.1-9 To the best of our knowledge, only one
case report written in Japanese has indicated ipsilateral
facial tactile hypesthesia in lateral medullary infarction;
however, the sensory tract responsible for this has not
been specified.10
There are two types of tactile sensation: epicritic and
protopathic. Facial epicritic tactile sensory information
travels through the principal sensory nuclei of the trigeminal nerve, crosses the midline, and ascends to the
ventral posteromedial nucleus in the contralateral thalamus. Because this trigeminal lemniscus ascends with the
medial lemniscus, facial tactile sensation is usually thought
to be associated with epicritic tactile sensation. A Japanese textbook written by Hirayama K. has mentioned that
protopathic tactile and thermal/pain sensory information travels down through the spinal tract via the trigeminal
nerve.9 However, this pathway is not considered a primary
pathway because patients with lateral medullary infarction do not usually complain of tactile hypesthesia.
Although numerous reports have analyzed the variation in the distribution pattern of sensory impairment of
pain/temperature in patients with Wallenberg syndrome, few reports focused on tactile hypesthesia in the
face. Usually, tactile sensation in the face is not impaired by the lesions in the medulla because the spinal
tract of the trigeminal nerve is thought to convey only
pain/temperature sensation.8 The existence of the protopathic pathway for light touch in the face,9 which goes
along with the spinal tract of the trigeminal nerve passing
through the lateral medulla, might explain the unusual
facial tactile hypesthesia observed in our case. We speculate that the developmental variation in and dependence
on the protopathic pathway rather than on the pontine
epicritic pathway for the facial tactile sensation

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FACIAL TACTILE HYPESTHESIA IN WALLENBERG SYNDROME

determine whether a patient with Wallenberg syndrome complains of tactile hypesthesia in the face. We
believe that the current case contributes to an understanding of the brainstem neuroanatomy in patients with
stroke; additional case reports and literature reviews that
focus on tactile sensation in Wallenberg syndrome may
be required for further confirmation.

References
1. Kim JS. Pure lateral medullary infarction: clinical
radiological correlation of 130 acute, consecutive patients.
Brain 2003;126:1864-1872.
2. Fukuoka T, Takeda H, Dembo T, et al. Clinical review
of 37 patients with medullary infarction. J Stroke
Cerebrovasc Dis 2012;21:594-599.
3. Kim JS. Sensory symptoms in ipsilateral limbs/body due
to lateral medullary infarction. Neurology 2001;57:12301234.
4. Cerrato P, Imperiale D, Bergui M, et al. Restricted
dissociated sensory loss in a patient with a lateral

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medullary syndrome—a clinical MRI study. Stroke
2000;31:3064-3066.
5. Vrettos A, Fiotaki K, Galati E, et al. A crossed brain
stem syndrome without crossed sensory symptomatology. BMJ Case Rep 2013;doi:10.1136/bcr-2012
-006709.
6. Hongo H, Tanaka Y, Shimada Y, et al. Dermatomal sensory manifestation in lateral medullary
infarction. J Stroke Cerebrovasc Dis 2014;23:182183.
7. Sekine T, Kawabe K, Kawase Y, et al. Cheiro-oral
syndrome associated with lateral medullary infarction.
Neurol Sci 2011;32:321-322.
8. Wilkins RH, Brody IA. Wallenberg’s syndrome. Arch
Neurol 1970;22:379-382.
9. Hirayama K. Ganmen-no-shoukou (Clinical manifestations
in face). In: Hirayama K, ed. Neurological semeiology,
Vol. 1. Revised 2nd ed. Tokyo: Bunko-do, 2010:396-420
[in Japanese].
10. Ooe K, Arai H, Maebeya D, et al. Wallenberg-shoukougun-no-ichirei (A case of Wallenberg
syndrome). Progr Med 2001;21:2868-2869 [in
Japanese].