European Journal of Neurology 2007, 14: e8–e9

doi:10.1111/j.1468-1331.2006.01606.x

LETTER TO THE EDITOR
Unusual triad due to a bilateral medial
medullary infarction in a 35-year-old
man
K. B. Alstadhaug and R. Salvesen
Department of Neurology,
Nordlandssykehuset, Bodo, Norway
Correspondence: Karl Bjørnar Alstadhaug, Department of Neurology, Nordlandssykehuset, 8092 Bodo, Norway
(tel.: +47 755 340 23; fax: +47 755 347 37;
e-mail: karl.bjornar.alstadhaug@
nordlandssykehuset.no).
Keywords: dysphagia, medial medullary
infarction, paresthesia, vertical nystagmus
Received 10 May 2006
Accepted 26 June 2006
Sirs,
A 35-year-old man with a previous diagnosis of migraine with visual aura arrived
at the emergency room 3 h after he had
experienced sudden onset of severe
oscillopsia shortly followed by paresthesia
involving the trunk and all four extremities. During transport to the hospital
he noticed difficulty in swallowing. On
admission he had his eyes closed and
complained of dizziness, nausea and tingling. Blood pressure was 147/68 and he
had a regular pulse of 83. He was alert and
responsive, slightly dysarthric, and was
not able to swallow. There was a pronounced spontaneous upbeat nystagmus.
Pupil reflexes were normal and there were
no ophthalmoplegia. Palatal movement
was normal and the pharyngeal sensation
was not lost, but gag reflex was absent.
Tongue movement was normal. Sensation
and power in all extremities were normal,
but there was a mild dysmetria in the
extremities. Reflexes were symmetrically
augmented, but no Babinski sign was
present. Gait was not tested due to his
pronounced vertigo.
Magnetic resonance imaging (MRI)
18 h after the incident (Fig. 1) demonstrated bilateral infarction in the medial
portion of the upper medulla oblongata.
Triplex ultrasound of precerebral arteries
and MRI-angiography were normal. A
thorough examination with regard to
aetiologic and risk factors was performed
with a negative result.
The patient was initially treated with
low molecular heparin, later with acetylsalicylic acid 160 mg daily. Two days after
the stroke the vertigo disappeared. After

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3 weeks he suddenly regained ability to
swallow and was able to eat. His tingling
was still present, though less troublesome.
Comment
Spiller proposed a symptom-complex due
to a postulated medial medullary infarction (MMI) in which Ôwe should expect to
find paralysis of all the limbs, trunk and
neck, whereas the reflexes necessary to life
would be preservedÕ [1]. Several patients
have since been reported [2–4]. Motor
deficit has been considered the hallmark of
MMI, and as far as we are aware of, only
two patients with bilateral MMI without
hemiparesis or quadriparesis have been
reported [2,5]. The present patient
demonstrated three main symptoms
which matched both clinical and radiological examination.
First there was oscillopsia due to a
prominent upbeat nystagmus in the
straight ahead position of gaze. Such a
nystagmus has according to Pierrot-Deseilligny and Milea [6] not been reported
after pure bilateral lesion of the medial
longitudinal fasciculus. However, lesions
involving the medullary tegmentum both
clinically end experimentally give ocular
motor abnormalities [4,6,7]. In our patient
there was no ophthalmoplegia, and after
2 days nystagmus faded away. Radiologically the medial longitudinal fasciculus, and the perihypoglossal nuclei may
have been affected at least on the initial
diffusion-weighted image. Lesions in the
cell groups of the paramedian tract (PMT)
may perhaps also give upbeat nystagmus
[4]. PMT was almost certainly affected in
our patient. Shortly after the first symptom the patient experienced tingling which
still persists. In 15 of 18 patients reported
by Kim et al. [3], tingling and a numb
sensation were reported. This was attributed to affection of the medial lemniscus,
and the partial involvement in our patient
may explain the symptoms and the slight
sensory dysmetria despite an otherwise
normal sensory modalities test.
The third prominent symptom in our
patient was severe dysphagia which is
regarded a common symptom in lateral
medullary infarction [8]. Rostral lesions in
the medulla often result in more severe
dysphagia and may also lead to palatopharyngeal dissociation due to the
viscerotopic organization of the nucleus
ambiguus [9]. Our patient demonstrated
severe dysphagia with a normal phonation, no vocal cord palsy and no oropharyngeal sensory loss. Neither was tongue

weakness found. According to the MRI
nucleus ambiguus would not be affected in
our patient. Kwon et al. [10] have, however, reported that dysphagia may be
common in medial infarction as well, and
that damage to the reticular formation
surrounding nucleus ambiguus perhaps
may explain this phenomenon [9].
One might speculate that an occlusion
of the distal part of an unpaired (anomalous) anteromedial artery (arising from
distal vertebral artery or proximal basilar
artery) due to thrombosis in situ, would be
a possible cause of infarction in our
patient [11].
References
1. Spiller WG. The symptom-complex of a
lesion of the upper-most portion of the
anterior spinal and adjoining portion of
the vertebral arteries. Journal of Nervous
and Mental Disease 1908; 35: 775–778.
2. Ho K, Meyer K. The medial medullary
syndrome. Archives of Neurology 1981;
38: 385–387.
3. Kim JS, Hyeon G, Chung CS. Medial
medullary syndrome: report of 18 new
patients and a review of the literature.
Stroke 1995; 26: 1548–1552.
4. Kim JS, Choi KD, Oh SY et al. Medial
medullary infarction: abnormal ocular
motor findings. Neurology 2005; 25:
1294–1298.
5. Benito-León J, Alvarez-Cermeño JC.
Isolated total tongue paralysis as a
manifestation of bilateral medullary
infarction. Journal of Neurology, Neurosurgery and Psychiatry 2003; 74: 1698–
1699.
6. Pierrot-Deseillingny C, Milea D. Vertical
nystagmus: clinical facts and hypothesis.
Brain 2005; 128: 1237–1246.
7. Kaneko CR. Eye movement deficits after
ibotenic acid lesions of the nucleus prepositus hypoglossi in monkeys. I.
Saccades and fixation. Journal of
Neurophysiology 1997; 78: 1753–1768.
8. Aydogdu I, Ertekin C, Tarlaci S, Turman
B, Kiylioglu N, Secil Y. Dysphagia in
lateral medullary infarction (Wallenberg’s syndrome): an acute disconnection
syndrome in premotor neurons related to
swallowing activity? Stroke 2001; 32:
2081–2087.
9. Broussard DL, Altschuler SM. Brainstem
viscerotopic organization of afferents and
efferents involved in the control of swallowing. American Journal of Medicine
2000; 108(4A): 79S–86S.
10. Kwon M, Lee JH, Kim JS. Dysphagia in
unilateral medullary infarction. Neurology 2005; 65: 714–718.
11. Moon SY, Kim HY, Chung CS. A sequential bilateral medial medullary infarction
separated by 4 months. Neurology 2002;
59: 1814–1815.

Ó 2007 EFNS

Letter to the Editor

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(b)

(c)

(d)

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Figure 1 T2-weighted and diffusion MRI demonstrating a bilateral rostral medial medullary infarction. The schematic drawing is a
modified version after Kim et al. (3, with permission). The light grey on the illustration marks the territory of the anteromedial medullary
artery, while the dark grey marks the territory of the anterolateral artery. CST, corticospinal tract; ML, medial lemniscus; IO, inferior
olivary nucleus; STT, spinothalamic tract; FN, facial nucleus; PMT, cell groups of the paramedian tract; CRF, central reticular formation;
TT, spinal trigeminal tract; RA, nucleus raphes; STN, spinal trigeminal nucleus; ICP, inferior cerebellar peduncle; MLF, medial
longitudinal fasciculus; NPR, nucleus prepositus; NI, nucleus intercalatus; MVN, medial vestibular nucleus; IVN, inferior vestibular
nucleus.

Ó 2007 EFNS European Journal of Neurology 14, e8–e9