Journal of Neuroimaging Vol 13 No 1 January 2003
Kimura et al: Opalski’s Syndrome

Ipsilateral Hemiplegia
in a Lateral Medullary Infarct—
Opalski’s Syndrome

Yasuyuki Kimura, MD
Hiroyuki Hashimoto, MD
Masafumi Tagaya, MD
Yuko Abe, MD
Hideki Etani, MD, PhD

ABSTRACT
A 42-year-old man was admitted complaining of the sudden onset of
headache, vomiting, vertigo, and gait disturbance. The authors found
hemiparesis of his right limbs, right Horner’s syndrome, and decreased
pain and temperature sensation of his right face and left limbs. Diffusionweighted imaging (DWI) showed an acute small infarct located on the
right side of the lateral lower medulla. This is the first report of Opalski’s
syndrome with lower medullary infarction detected by DWI.
Key words: Opalski’s syndrome, ipsilateral hemiplegia, lateral
medullary syndrome, diffusion-weighted imaging.
Kimura Y, Hashimoto H, Tagaya M, Abe Y, Etani H.
Ipsilateral hemiplegia in a lateral
medullary infarct—Opalski’s syndrome.
J Neuroimaging 2003;13:83-84
DOI: 10.1177/1051228402239723

Opalski’s syndrome is a variant of lateral medullary syndrome
with ipsilateral hemiplegia that was first described by Opalski
1
in 1946. Some pathological studies and neuroradiological findings obtained by conventional magnetic resonance imaging
(MRI) have shown that the lesion causing this syndrome is
located lower than in Wallenberg’s syndrome and involves the
2,3
corticospinal fibers caudal to the pyramidal decussation. To
confirm that lower medullary infarction is responsible for this
syndrome, we performed diffusion-weighted imaging (DWI),
which has become available to demonstrate temporal association between clinical signs and infarction.
A 42-year-old man with hypertension was admitted to our
hospital complaining of the sudden onset of headache, vomiting, vertigo, and gait disturbance. He had no recent history of
head and/or neck trauma. On arrival, his consciousness was
clear. The blood pressure was 140/90 mm Hg, and the pulse rate
was 66/min with a regular rhythm. Neither vascular bruits nor

heart murmurs were found. Ocular movements were normal
without nystagmus, and his pupils were equal in size and were
reactive to light and accommodation. The other cranial nerves
were also intact. Slight truncal ataxia was detected, but motor
function, sensation, and reflexes were normal. A few hours later,
he began to complain of right facial pain and difficulty in using
his right arm. Then we found hemiparesis of his right limbs, as
well as right Horner’s syndrome and decreased pain and temperature sensation of his right face and left limbs.
Laboratory tests all gave normal findings, including coagulation and immunological tests. The chest X-ray and the electrocardiogram were also normal.
On the second hospital day, DWI (the average of 3 directions) showed an acute small infarct located on the right side of
the lateral lower medulla (Fig 1A). The apparent diffusion coefficient ratio (ADCr = ADC stroke/ADC contralateral) was 0.47.
Conventional MRI (T2-weighted, T2WI) also showed an infarct
at the same place (Fig 1B). MR angiography of the intracranial
and cervical arteries was normal. Ultrasonography of the
extracranial carotid and vertebral arteries was also normal.
Transesophageal echocardiography showed neither thrombus
in the left atrium and left ventricle nor a patent foramen ovale.
In this patient, we demonstrated acute lower medullary
infarction associated with Opalski’s syndrome by using DWI.
In 1946, Opalski reported 2 patients with ipsilateral facial
loss of pain and temperature sensation, Horner’s syndrome,
hemiplegia, ataxia, and contralateral loss of pain and temperature sensation in the limbs.1 He suggested that these signs were

Received May 30, 2002, and in revised form August 29, 2002.
Accepted for publication September 3, 2002.
From the Division of Stroke and Hypertension, Department of
Internal Medicine, Osaka National Hospital, Japan.
Address correspondence to Yasuyuki Kimura, MD, Department
of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita City, Osaka, Japan, 565-0871. E-mail: yaz@medone.med.osaka-u.ac.jp.

Fig 1.

Axial diffusion-weighted imaging demonstrates hyperintensity, indicating an acute brain infarct, in the lateral lower medulla
(A). Sagittal T2-weighted imaging visualizes the extent of the ischemic
lesion (B).

Copyright © 2003 by the American Society of Neuroimaging

83

related to occlusion of the posterior spinal artery, while Dhamon
et al3 and Hommel et al4 reported that the syndrome was due to
occlusion of the vertebral artery. In the current case, MR
angiography showed no stenosis or irregularity of the right vertebral artery and no significant cardiac disorders were documented. Therefore, we could not find any causative cardiovascular abnormalities contributing to the infarct.
Although there have been some reports on the lesion responsible for Opalski’s syndrome as demonstrated by T2WI, conventional MRI is handicapped by difficulty in differentiating
between new lesions and old asymptomatic infarcts.2-6 In the
current patient, DWI detected an acute infarct located on the
right side of the lateral lower medulla. To the best of our knowledge, this is the first report of Opalski’s syndrome with lower
medullary infarction detected by DWI.

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Journal of Neuroimaging Vol 13 No 1 January 2003

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