Case Report
Restricted Dissociated Sensory Loss in a Patient With a
Lateral Medullary Syndrome
A Clinical-MRI Study
Paolo Cerrato, MD; Daniele Imperiale, MD; Mauro Bergui, MD; Marco Giraudo, MD;
Chiara Baima, MD; Maria Grasso, MD; Leonardo Lopiano, MD; Bruno Bergamasco, MD
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Background—Various sensory syndromes in lateral medullary infarctions are described. A small variation in the location
of a lesion may lead to very different clinical features, owing to the complex anatomy of the medulla oblongata. MRI
may identify the location and extent of the ischemic lesions, allowing a clear clinical-anatomical correlation.
Case Description—We describe a man with an ischemic lesion in the right portion of the lower medulla that presented a
contralateral impairment of spinothalamic sensory modalities and an ipsilateral impairment of lemniscal modalities with
a restricted distribution (left forearm and hand, right hand and fingers, respectively). The restricted and dissociated
sensory abnormalities represent the only permanent neurological consequence of that lesion.
Conclusions—The atypical sensory syndrome may be explained by the involvement of the medial portion of spinothalamic
tract and the lateral portion of archiform fibers at the level of the lemniscal decussation. (Stroke. 2000;31:3064-3066.)
Key Words: cerebral infarction 䡲 lateral medullary syndrome 䡲 medulla oblongata
L
ateral medullary syndrome (LMS) is a well-recognized
vascular syndrome of the vertebrobasilar territory. Classically, sensory dysfunction in LMS is characterized by the
dissociated involvement of the spinothalamic sensory modalities (impairment of pain and thermal sensation over the
contralateral hemibody/limbs and over the ipsilateral face).1– 4
Although sensory signs and symptoms may present various
topographic distributions,4 –10 a dissociated sensory pattern
involving upper limbs has not yet been reported. Moreover,
even if ipsilateral upper-extremity symptoms are occasionally
reported, they have never been clearly explained.11 We
describe a patient with a small ischemic area in the right part
of the medulla oblongata, with an impairment of pain and
thermal sensation in the left arm and tactile discrimination
and deep sensation in the right hand. MRI identified the
location and extension of the small ischemic lesion, allowing
a clear clinical-anatomical correlation.
over the right hand; and impairment of thermal and pain sense
over the left hand, forearm, and, to a lesser degree, over the
arm and neck. No other neurological signs were present.
A cranial CT obtained 24 hours from onset was normal.
Extracranial vessel duplex ultrasonography showed a moderate atheromatosis of both internal carotid arteries without
significant stenosis. Transthoracic echocardiography showed
a mild left ventricle concentric hypertrophy, whereas transesophageal echocardiography was normal. MR angiography
was normal, particularly concerning the vertebral arteries.
Routine blood analysis highlighted only a mild increase in
hematocrit level and red blood cell count. Immunologic
investigations, fasting lipid profile, and homocyst(e)ine
plasma levels were all normal.
MRI showed a small, diagonal lesion in the dorsolateral
portion of the right lower medulla, between the retro-olivary
sulcus and the inferior cerebellar peduncle, sparing the most
lateral portion (Figures 1 and 2). The lesion was consistent
with an infarction in the territory of the perforating arteries
arising from the vertebrobasilar junction.
The condition of the patient improved within a few days.
Neurological examination at discharge revealed only an
impairment of the temperature sense involving the left hand
and forearm. He continued to complain of numbness and
paresthesia of the right fingers (a described symptom of the
proprioceptive pathways involvement),12 even though the
abnormalities of 2-point discrimination, vibration, and joint
Case Report
A 54-year-old man was admitted to our inpatient department
because of the abrupt occurrence of gait and postural imbalance, dizziness, nausea, vomiting, and numbness of the right
hand and fingers. Regarding vascular risk factors, mild
hypertension and cigarette smoking were present. Upon
admission, neurological examination revealed gait ataxia with
falling to the right side; vertical nystagmus on downward
gaze; decrease of vibration sense and 2-point discrimination
Received June 20, 2000; final revision received August 7, 2000; accepted August 28, 2000.
From the First Division of Neurology and the Service of Neuroradiology (M.B.), University of Torino, Torino, Italy.
Correspondence to Paolo Cerrato, MD, First Division of Neurology, Department of Neuroscience, Via Cherasco 15, 10126 Torino, Italy. E-mail
[email protected]
© 2000 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org
3064
Cerrato et al
Atypical Sensory Loss in Lateral Medullary Syndrome
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Figure 1. MRI, T2-weighted coronal scan (spin-echo, repetition
time 2800 ms, echo time 98 ms, 2 excitations). A small, hyperintense lesion is located in the lower portion of the right medulla.
position/movement sense were no longer evident. Although
sensory symptoms and signs were unchanged at a 2-month
follow-up examination, the patient was fully independent and
able to work.
Discussion
The case here reported broads the spectrum of the LMS.
Sensory abnormalities in our patient may represent an undescribed variant of LMS. The dissociated sensory impairment
involving upper limbs (pain and thermal sense in the contralateral hand and forearm, tactile discrimination and deep
sense in the ipsilateral hand and fingers) is explained by the
site of the lesion (Figures 1 and 2) and by the anatomy of the
lower medulla at the level of the lemniscal decussation
(Figure 3). In the spinal cord and lower medulla, the proprioceptive pathway is located in posterior columns and is
somatotopically organized, being the fibers from the cranial
districts of the body and terminating in the nucleus cuneatus
(NC). From the NC, located in the lateral position, the
Figure 2. MRI, T2-weighted axial enlarged scan at the level of
the lower medulla (spin-echo, repetition time 2800 ms, echo
time 98 ms, 2 excitations). The ischemic lesion involves the dorsal right medulla in the territory of the perforating arteries arising
from the vertebrobasilar junction.
3065
Figure 3. Anatomic drawing of the nervous structure at the level
of the lower medulla, corresponding to the axial scan in Figure
2. The ischemic lesion (dark area) involves the lateral part of the
archiform fibers at the level of the lemniscal decussation and
the medial part of the spinothalamic tract, causing an impairment of the lemniscal sensibilities of the right hand and the spinothalamic sensibilities of the left arm.
secondary proprioceptive fibers (also named “archiform”)
cross the midline (so-called lemniscal decussation) and reach
the opposite side of the medulla constituting the medial
lemniscus (Figure 3). The archiform fibers are also somatotopically organized, being fibers from the upper limb located
in lateral position.
Fibers in the spinothalamic tract in spinal cord and medulla
are arranged in a concentric manner, with the most superficial
coming from caudal districts and the most inner from cranial
districts. Therefore, a lesion located between the medial
lemniscus and spinothalamic tract in the lower medulla may
explain the restricted dissociated sensory syndrome of our
patient if it involves the lateral portion of archiform fibers and
the medial portion of the spinothalamic tract (Figure 3). An
isolated lesion located between the upper medulla and the
parietal cortex cannot determine a dissociated sensory syndrome because the spinothalamic tract and medial lemniscus
run on the same side. Brain stem ischemic lesions usually
involve the 2 ascending sensory pathways in a separate
fashion: the medial lemniscus is involved in paramedian
medullary infarction and the spinothalamic tract in lateral
medullary infarction because of the different vascular territories. A dissociated impairment of sensory modalities may
be present in spinal cord lesions (the so-called BrownSequard syndrome), but sensory symptoms are almost always
invariably associated with motor deficit.
Ipsilateral impairment of tactile discrimination and deep
sensation may result from lesions of the medial portion of the
medulla below the lemniscal decussation,8,10 but it is rarely
reported in patients with LMS13,14; the Babinski-Nageotte
syndrome, in which the medial lemniscus is occasionally
involved, may represent a medially extended LMS.
In our patient, the sparing of pain and thermal sense over
the left side of the trunk and leg may be related to the lack of
involvement of the superficial layers of the spinothalamic
tract, where the fibers from the caudal districts are located
(Figure 3). Moreover, the incomplete impairment of lemniscal sensory modalities may be explained by the limited
involvement of the proprioceptive fibers and is in agreement
with experimental and clinical observations that lesions of the
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December 2000
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dorsal column may be followed by only limited sensory
losses.15,16
In addition, preservation of the nucleus ambiguus, usually
involved in upper medullary infarction,9 may explain the
absence of hoarseness and dysphagia. The initial occurrence
of ataxia, vertical nystagmus on downward gaze, vertigo, and
dizziness suggest the involvement of vestibular nuclei or
vestibulo-cerebellar connection at the onset. Gait ataxia may
also be related to the initial involvement of the inferior
cerebellar peduncle or the spinocerebellar tracts in the medulla.9 Disappearance of those signs during the course may be
explained by the sparing of the most posterolateral portion of
the medulla in the definitive lesion (Figure 2). Finally, the
absence of sensory impairment in ipsilateral trigeminal districts suggests that the lesion did not involve the most dorsal
portion of medulla, where the descending tract and nucleus of
the fifth nerve are located (Figure 2 and 3).
In conclusion, in this report we described a patient with a
restricted (upper limbs) and dissociated (pain and thermal
hypesthesia in the contralateral left hand and forearm; numbness and decrease of deep sensation in the ipsilateral right
hand and fingers) sensory syndrome related to a small
ischemic lesion in the right portion of the lower medulla, a
location that may explain the dissociated sensory deficits
because it presumably involves the medial portion of the
spinothalamic tract and the lateral part of the archiform fibers
at the level of the lemniscal decussation.
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Restricted Dissociated Sensory Loss in a Patient With a Lateral Medullary Syndrome: A
Clinical-MRI Study
Paolo Cerrato, Daniele Imperiale, Mauro Bergui, Marco Giraudo, Chiara Baima, Maria Grasso,
Leonardo Lopiano and Bruno Bergamasco
Downloaded from http://stroke.ahajournals.org/ by guest on June 16, 2017
Stroke. 2000;31:3064-3066
doi: 10.1161/01.STR.31.12.3064
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 2000 American Heart Association, Inc. All rights reserved.
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