Journal of the Neurological Sciences 219 (2004) 167 – 168
www.elsevier.com/locate/jns

Short communication

Sensorimotor hemiparesis with secondary cervical dystonia
following lateral caudal medullary infarction without signs
and symptoms of Wallenberg syndrome
Yoshinori Kajimoto a,*, Hideto Miwa a, Masami Ueno b, Tomoyoshi Kondo a
a

Department of Neurology, Wakayama Medical University, 811-1 Kimiidera, Wakayama City, Wakayama 641-8510, Japan
b
Department of Critical Care Medical Center (Stroke Care Unit), Wakayama Medical University, Japan
Received 4 December 2003; accepted 6 January 2004

Abstract
We report the case of an 84-year-old woman who suddenly developed motor and both superficial and deep sensory hemiparesis on the left
side, and cervical dystonia with a head tilt to the right side. A brain MRI showed an infarct in the left lateral caudal medulla. It is clinically
important to recognize that the lateral caudal medullary infarction appears without signs and symptoms of lower cranial nerve palsies
commonly involved in Wallenberg syndrome.
D 2004 Elsevier B.V. All rights reserved.
Keywords: Cervical dystonia; Lateral caudal medullary infarction; Wallenberg syndrome

1. Introduction
Lateral medullary infarction is one of the most frequently
encountered cerebral infarctions involving the brainstem,
and often manifests as Wallenberg syndrome [1]. If the
ipsilateral pyramidal tract is involved below the decussation
by the caudal extension of the lateral medullary lesion,
ipsilateral hemiparesis may occur, which is known as
Opalsky’s syndrome [2,3]. Recently, we have encountered
a patient with left lateral caudal medullary infarction who
presented sensorimotor hemiparesis and secondary cervical
dystonia without symptoms and signs of lower cranial nerve
palsies commonly seen in Wallenberg syndrome.

2. Case report
An 84-year-old Japanese woman with a medical history
of cardiac ischemic attack (acute myocardial infarction), was
admitted because of the sudden gait disturbance and dysarthria. On admission, her general physical condition was
unremarkable. Neurological examination revealed that she
was alert and well oriented. She had hemiparesis of the left
* Corresponding author. Tel./fax: +81-73-441-0655.
E-mail address: kajimoto@wakayama-med.ac.jp (Y. Kajimoto).
0022-510X/$ - see front matter D 2004 Elsevier B.V. All rights reserved.
doi:10.1016/j.jns.2004.01.002

upper and lower extremities, as well as decreased pain and
touch, and decreased temperature sensations on the left side
of her face, body, and extremities. There was no weakness of
her facial muscles. Her left sternocleidomastiod muscle was
paretic. Decreased deep sensation was noted on the left side
of the body, and extremities. She also complained of pain on
the left side of the neck. Ten days after admission, cervical
dystonia with a head tilt to the right side developed (Fig. 1A).
There was an abnormal sustained muscle contraction of the
right lateral neck muscles, including the sternocleidomastoid
and anterior border of the trapezius muscle. Neuroradiological studies well demonstrated the responsible lesion for her
symptoms. Diffusion-weighted imaging (DWI) and T2weighted imaging (T2WI) showed an infarct located on the
left lateral caudal medulla (Fig. 1B –F). MR-angiography
revealed an absence of blood flow in the left vertebral artery.
Her cervical dystonia gradually improved after several
weeks; however, her left hemiparesis as well as the loss of
deep sensation persisted, and she could not walk without a
support.

3. Discussion
It is rare to see Opalsky’s syndrome, but the clinical
symptoms of our patient are rarer, since her did not

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Y. Kajimoto et al. / Journal of the Neurological Sciences 219 (2004) 167–168

which nucleus cuneatus and nucleus gracilis are located,
spinocerebellar tract, the spinal tract nucleus of the
trigeminal nerve, and the accessory nerve and its nucleus
(Fig. 1G). The lesion of the present patient was more
caudal than the lesions of Wallenberg or Opalsky’s
syndrome. This was the reason the present patient did
not show lower cranial nerves palsies. It is clinically
important to recognize that the occlusion of the vertebral
artery causes the lateral caudal medullary infarction that
presents with hemiparesis and the ipsilateral loss of deep
sensation without signs and symptoms of Wallenberg
syndrome.
Another interesting finding of the present patient is the
associated with cervical dystonia. On the basis of a recent
review of secondary cervical dystonia [4], that is, structural lesions associated with cervical dystonia are most
commonly localized to the brainstem and/or cerebellum; it
is speculated that the dysfunctioning of the cerebellar
afferent pathway, usually that of the olivocerebellar system, plays an important role in generating cervical dystonia [4]. In the present patient, it is unclear whether the
patient had cerebellar symptoms because she had severe
hemiparesis. However, very likely the lesion directly
interrupted the spinocerebellar tract and modified the
function of the olivocerebellar system, supporting such
speculation. Currently, it is uncertain whether the associated secondary cervical dystonia is a chance phenomenon
only seen in the present patient or a significant diagnostic
pointer of this rare syndrome of the lateral caudal
medullary infarction. Further accumulation of similar
cases would be valuable to better understand this rare
clinical syndrome.
Finally, when we see a sudden appearance of sensorimotor hemiparesis of the upper and lower extremities
without facial involvement, the possibility of not only
cervical lesion but also the lateral caudal medullary
infarction should be kept in mind.
Fig. 1. (A) Cervical dystonia of the present patient is demonstrated. (B) – (F)
Brain MRI of the present patient showed an infarct located on the left lateral
caudal medulla. (G) The schematic representations of the location of the
lesion of the present patient are demonstrated. The lesion may involve the
pyramidal tract, the ascending tracts of deep sensation, spinocerebellar tract,
the spinal tract nucleus of the trigeminal nerve, and the accessory nerve
nucleus. Arrowheads indicate the lesion.

present lower cranial nerve palsies usually seen in lateral
medullary infarctions as in Wallenberg or Opalsky’s
syndrome. Based on the findings of MR imaging, the
responsible lesion of our patient probably involved the
pyramidal tract, the ascending tracts of deep sensation in

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