OBSERVATION

Sensory Dermatomal Representation
in the Medial Lemniscus
Seung-Hoon Lee, MD; Dong-Eog Kim, MD; Eun-Cheol Song, MD; Jae-Kyu Roh, MD, PhD

Background: Restricted sensory deficits along the

somatotopic topography of the medial lemniscus rarely
develop in medial medullary infarction. We describe a
patient with medial medullary infarction who presented with dermatomal sensory deficits caused by a
medial lemniscal lesion.
Case Description: A 58-year-old man presented with

sudden right-sided hemiparesis and paresthesia. He had
noticed the paresthesia below the level of the right L5
dermatome, where his vibration and position senses were
mildly diminished. His paresthesia was more severe over
the right calf and foot. Magnetic resonance images of
the brain showed an acute small infarct in the medial-

M

From the Department of
Neurology, College of Medicine,
Seoul National University and
Clinical Research Institute,
SNUMRC, and Neuroscience
Research Institute, Seoul
National University
Hospital, Seoul, Korea.

ventral portion of the left rostral medulla oblongata. A
nerve conduction study and electromyography showed
no abnormalities. At follow-up, the patient’s motor and
sensory deficits had improved considerably.
Conclusions: The patient showed lemniscal sensory deficits below the right L5 dermatome that were caused by
the partial involvement of the medial lemniscus. These
findings suggest that lemniscal sensory dermatomal
representation is preserved at least up to the level of the
medulla oblongata.

Arch Neurol. 2001;58:649-651

EDIAL medullary infarc-

tion (MMI) is a rare occurrence. Although the
detection rate of small
brainstem lesions has
increased since the advent of magnetic resonance imaging (MRI), MMI still accounts
for fewer than 1% of the total number of
strokes.1 In MMI, sensory abnormality is the
second most common manifestation to occur, preceded by motor weakness.1,2 However, sensory deficits that are restricted to
certain parts of the patient’s body have
rarely been described.1,3 Prior studies have
shown that these restricted acral sensory
deficits develop after small infarctions in
the brainstem,4-6 thalamus,6-8 or corticalsubcortical areas.9,10 To our knowledge, only
1 case of MMI has been previously reported with sensory deficits in a dermatomal distribution.1 We describe a patient
with MMI who presented with an unusual
dermatomal sensory manifestation. The
possible pathogenesis is discussed.
REPORT OF A CASE

A 58-year-old right-handed man presented with the sudden onset of rightsided hemiparesis and paresthesia. He had

(REPRINTED) ARCH NEUROL / VOL 58, APR 2001
649

been well until 10 hours before admission, when he suddenly noticed an uncomfortable sensation of tingling in his
right side on walking. His sensory symptoms, which were restricted to his limbs,
especially the right lower extremity, persisted without any change in intensity
before admission. Dysarthria and rightsided hemiparesis followed 5 hours later.
Because of the progressive worsening
of his motor weakness, he was referred
to our hospital. There were no changes in
his mental status. He had a history of
poorly controlled hypertension and diabetes mellitus. He worked as a taxi driver.
He had never smoked and had no history
of excessive alcohol intake.
On admission, his temperature was
36.1°C, his pulse rate was 76/min, and his
blood pressure was 146/95 mm Hg. He was
alert and oriented, with fluent speech. Funduscopic tests showed no hypertensive or
diabetic retinopathy. He had slight dysarthria. The remaining cranial nerve functions were intact. Motor examination revealed right-sided hemiparesis (III/V). His
vibration and position senses were mildly
diminished below the level of the L5 dermatome over the right lower extremity, and
he noticed paresthesia in the same areas

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Figure 2. T2-weighted magnetic resonance imaging scan shows a small
infarct in the left medial medulla oblongata (arrow).

COMMENT
Figure 1. Schematic drawing of lemniscal sensory deficit in the patient.
The gradient of gray to black indicates the degree of sensory deficit below
the level of the L5 dermatome.

(Figure 1). His pain and temperature senses were intact. The dermatomal paresthesia was more severe over
the lateral surface of the calf and the dorsolateral aspect
of the foot. The deep tendon reflexes were normal in all
tested joints, and the results of a Babinski test were positive on the right sole.
The patient’s preprandial and postprandial blood glucose concentrations were 7.1 mmol/L (128 mg/dL) and 13.5
mmol/L (244 mg/dL), respectively. His hemoglobin A1c level
was increased (0.08). Brain MRI scans obtained 1 day after the ictus demonstrated a small infarct in the medialventral portion of the left rostral medulla oblongata
(Figure 2). Magnetic resonance angiography revealed no
abnormalities in the basilar artery or in either distal vertebral artery, with the exception of mild stenosis in the
stems of both middle cerebral arteries. The results of a nerve
conduction study and electromyography to exclude the
possibility of a simultaneous lumbosacral radiculopathy
were normal. The patient was treated with a continous infusion of heparin sodium for 5 days, followed by warfarin
sodium therapy (4 mg/d), and showed a gradual improvement of motor and sensory deficits, without fluctuation.
After 5 months of anticoagulant therapy, the patient’s sensory symptoms had improved to nearly normal, and he
was able to walk without assistance.
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650

The typical neurologic signs associated with MMI, or Dejerine syndrome, include (1) hemiparesis contralateral
to the infarct, (2) hemisensory loss of the posterior column type contralateral to the infarct, and (3) weakness
of the tongue ipsilateral to the infarct.11,12 Before the era
of MRI, there were few case reports of MMI. Frequent
manifestations of pure motor hemiparesis2 or sensorimotor syndrome usually led clinical physicians to misclassify MMI as lacunar infarction. Moreover, pathological diagnosis by autopsy was extremely difficult and rare
because of the relatively favorable prognosis of this disease.2,13 However, the introduction of high-resolution MRI
has led to the clinical radiologic and etiologic correlation of brainstem ischemic strokes, especially strokes in
the medulla and midbrain.1,2,13
Numerous reports have provided evidence to show
that restricted acral sensory deficits frequently occur after
small strokes in the thalamic and cortical areas.4-10,14 Fisher15
stated that isolated paresthesia of the face, arms, and legs
suggests thalamic involvement, whereas selective involvement of some fingers may indicate a cortical localization.
Also, Kim14 observed that dominant sensory involvement
of the upper lip, thumbs, and index fingers occurred with
thalamic and thalamocortical strokes, and that corticalsubcortical strokes usually caused cheiro-oral or restricted finger involvement. Because of these findings, the
somatotopic topography of the ventralis posterior nucleus
of the thalamus is relatively well known. However, it is
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Pyramidal Tract
Medial Lemniscus

S

Inferior Olivary
Nucleus

L
T
C

Spinothalamic
Tract
Nucleus
Ambiguus
Spinal Trigeminal
Nucleus and Tract

Nucleus Cuneatus
Nucleus Gracilis
Nucleus of Hypoglossal Nerve

Figure 3. Sensory topography of the medial lemniscus in the patient.
The gray area indicates the lesion; S, the area of sacral dermatomal
representation; L, lumbar; T, thoracic; and C, cervical.

somewhat unclear in the brainstem. In the medulla oblongata, the medial lemniscus lies in a ventral-dorsal direction, in which the sensory topography is arranged so that
the leg-representing area is located ventrally and the armrepresenting area is located dorsally.16 On the level of the
pons, most of the sacral segments are laterally located, and
the cervical segments are medially located.17 However, the
presence of dermatomal representation in these structures has not been previously reported. Recently, Kim et
al3 described a patient with MMI whose paresthesia was
confined to the lower part of the leg and was not distributed along the dermatomes. Although Bassetti et al1 reported a case involving a patient with a pseudospinal sensory level over the trunk (T-11 level), they did not correlate
it with functional neuroanatomy.
Our patient showed hemiparesis and a restricted lemniscal sensory deficit along the dermatomes. Both symptoms were caused by the involvement of the pyramid and
medial lemniscus, respectively. Because there was no evidence of lumbosacral radiculopathy on electromyography or physical examination, we determined that the involvement of the medial lemniscus probably caused these
peculiar manifestations. These findings suggest that sensory dermatomal representation may be preserved up to
the level of the medulla oblongata, although, to our knowledge, there have been no corresponding reports with regard to the nuclei of the cuneatus or gracilis. Considering the established somatotopic topography of the medial
lemniscus in the medulla oblongata, we speculated that
most of the sacral dermatomes were ventrally located and
that most of the cervical dermatomes were dorsally located (Figure 3). The fact that the patient had more severe paresthesia in the distal area of the lower extremity
than in the proximal area might be explained by the “lowest threshold pattern.”18,19 A previous study on animals
indicated a lower sensory threshold in the fingers and
toes,19 and it is well understood that the acral parts of
the human sensory pathway disproportionately represent the large areas of the cortex.20,21 These concepts can
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651

be applied in the same way to the medial lemniscus in
the human sensory pathway.
Our patient had no other vascular risk factors besides hypertension and diabetes mellitus, and neither
transthoracic echocardiogram nor magnetic resonance angiography showed any remarkable abnormalities. Hence,
thrombotic occlusion of the small perforating branches
in the brainstem was responsible for the pathogenesis of
the stroke in our patient.
In summary, we report the first case (to our knowledge) of MMI with dermatomal lemniscal sensory deficits caused by involvement of the medial lemniscus. Our
findings suggest that sensory dermatomal representation
may be preserved at least up to the level of the medulla
oblongata. Although we were unable to determine the precise somatotopic arrangement of the lemniscal pathway
in this case, it may provide some clues to elucidate the functional neuroanatomy of the medial lemniscus.
Accepted for publication June 30, 2000.
Corresponding author and reprints: Jae-Kyu Roh, MD,
PhD, Department of Neurology, Seoul National University
Hospital, 28 Yongon-dong, Chongno-gu, Seoul 110-744,
Korea (e-mail: rohjk@snu.ac.kr).
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