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Sensory Dermatomal Representation in the Medial Lemniscus
Seung-Hoon Lee, MD;
Dong-Eog Kim, MD;
Eun-Cheol Song, MD;
Jae-Kyu Roh, MD, PhD
Arch Neurol. 2001;58:649-651.
ABSTRACT
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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-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.
INTRODUCTION
MEDIAL medullary infarction (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, 5, 6
thalamus,6, 7, 8 or
cortical-subcortical 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 right-sided
hemiparesis and paresthesia. He had 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 right-sided 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
(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.
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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.
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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 medial-ventral 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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Figure 2. T2-weighted magnetic resonance
imaging scan shows a small infarct in the left medial medulla oblongata (arrow).
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COMMENT
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, 5, 6, 7, 8, 9, 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 cortical-subcortical 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 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 arm-representing 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 be applied in the same way to the medial lemniscus in the
human sensory pathway.
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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.
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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.
AUTHOR INFORMATION
Accepted for publication June 30, 2000.
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.
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{at}snu.ac.kr).
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