(Stroke. 1996;27:988-990.)
© 1996 American Heart Association, Inc.
Articles |
From the Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, South Korea.
Correspondence to Jong S. Kim, MD, Department of Neurology, Asan Medical Center, Song-Pa PO Box 145, Seoul 138-600, South Korea.
| Abstract |
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Case Descriptions I describe four patients presenting with restricted sensory disturbances at the proximal parts of the body. The sensory symptoms were restricted to discrete areas of the contralateral proximal arm, shoulder, trunk, and upper thigh. The face and the distal parts of the extremities were largely spared. On MRI, three patients had a small thalamic infarction and one had a putaminal infarction.
Conclusions Strategically located minor strokes can produce restricted sensory syndromes at discrete areas of nonacral parts of the body. These observations highlight the diverse patterns of restricted sensory syndromes after unilateral stroke and support the theory of somatotopic-anatomic proximity of certain parts of the body in the human sensory pathway.
Key Words: cerebrovascular disorders stroke, pure sensory sensation disorders
| Introduction |
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| Case Reports |
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Patient 2
A 60-year-old hypertensive man suddenly developed a sense of
weakness on the left. On admission, the patient was alert, and the
examination of the cranial nerves was unremarkable. He showed slight
clumsiness of the left limbs but without obvious ataxia. On sensory
examination, there was slightly decreased sensation of all modalities
in the left half of his body. He felt paresthesia over discrete areas
of the left thigh, trunk, shoulder, and upper part of the left arm.
Initial brain CT was negative, and brain MRI performed 10 days after
the onset showed a small right thalamic infarction (Fig 2
). At 6 months of follow-up, he still complained of
persistent paresthesia over the above areas but without objective
sensory deficit.
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Patient 3
A 55-year-old hypertensive woman felt, on awakening,
unpleasant numbness over the left leg, more prominent over the
posterior thigh region. The area of the numbness then extended to the
left back and shoulder area. At the emergency department, the patient
was alert, and the examination for cranial nerves, motor strength, and
cerebellar function was unremarkable. On sensory examination, she
complained of unpleasant paresthesia over the left thigh and hip. She
also had slight paresthesia over discrete areas of the left back,
shoulder, upper part of the left arm, and left lower leg. Although she
had intermittent electric-like sensation on touching her posterior
thigh and hip, the objective sensations of pinprick, touch, vibration,
and position remained intact. Brain MRI performed 2 days after the
onset showed a small right thalamic infarction (Fig 3
).
The sensory symptoms persisted, although slightly diminished in
severity, at 1 month of follow-up.
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Patient 4
A 57-year-old hypertensive man developed sudden dull headache
on awakening followed by numbness over the right upper arm, which
spread to the right trunk and upper thigh. On examination, the patient
was alert and slightly dysarthric. His motor function was within normal
limits. The patient had numbness over patchy areas of the
proximal-lateral part of the right upper arm, a part of the right
trunk (between T3 and T10), and the upper-lateral part of the right
thigh. Pinprick and temperature senses were mildly decreased in these
areas. Brain MRI showed an infarct in the left putamen that slightly
involved the anterior limb of the internal capsule (Fig 4
). The patient's sensory symptoms gradually improved
and, at 5 months of follow-up, the sensory abnormality was
restricted to a small area of the upper chest and the
proximal-lateral part of the right arm.
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| Discussion |
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Small thalamic stroke has been well documented to produce pure hemisensory symptoms that usually involve the face, arm, and leg.10 11 12 The symptoms, however, can be limited to certain parts of the body.2 3 Patient 4, with a sizable putaminal infarction, had normal motor function except for slight dysarthria, which seems to agree with the previous theory that small lesions confined to the putamen tend to remain asymptomatic.13 14 15 In this patient, involvement of the ascending sensory fibers at the anterior limb of the internal capsule could explain the sensory symptoms. Previous reports also described pure sensory syndrome due to capsular or corona radiata strokes.16 17 18 19
The pathophysiological mechanism for the
restricted nonacral sensory syndrome remains speculative. The main
pathogenetic mechanisms for restricted acral sensory syndrome are (1)
anatomic proximity of sensory fibers carrying the sensation of the lip,
fingers, and toes and (2) greater representation of the sensory
system of the acral part of the body in the human brain.3
According to previous studies using monkeys, in the ventral
posterolateral nucleus of the thalamus and possibly in the corona
radiata, the sensory projection fibers from the acral parts of the
body are situated in the ventral area, whereas those from the trunk and
proximal parts of the limbs are located in the dorsal
region.20 21 22 It has also been observed that the
somatotopic representation for the sensory fibers subserving
the proximal arm, trunk, and upper thigh are
adjacent.20 21 22 Presumably, the lesions of our patients may
have strategically involved the fibers at the dorsal portion of the
ventral posterolateral thalamic nucleus and thalamocortical sensory
radiation, thereby producing discrete sensory changes at the proximal
body parts (Fig 6
).
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In summary, these four patients demonstrated an unusual nonacral restricted sensory syndrome due to focal stroke, emphasizing diverse patterns of the restricted sensory syndromes. Although the sensory pattern of these patients supports the anatomic proximity theory, it is not necessarily at odds with the second hypothesis described above, considering that the restricted nonacral sensory syndromes appear to be rare compared with the restricted acral sensory syndrome.
Received November 27, 1995; revision received February 1, 1996; accepted February 19, 1996.
| References |
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