(Stroke. 1996;27:988-990.)
© 1996 American Heart Association, Inc.
Articles |
Restricted Nonacral Sensory Syndrome
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.
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Abstract |
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Background Restricted sensory symptoms due to stroke most often occur at distal parts of the body, manifesting as cheiro-oral or cheiro-oral-pedal syndrome. Sensory symptoms restricted to proximal body parts have rarely been recognized.
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
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Introduction |
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Sensory symptoms due to stroke can be restricted to various parts of the body,1 most often at the acral areas, producing cheiro-oral, cheiro-pedal, or cheiro-oral-pedal syndromes.2 3 Lesions in the central nervous system can also produce atypical sensory disturbances, including a pseudomyelopathic (sensory level at the trunk/extremities)4 5 6 7 or pseudoradicular pattern of sensory disturbance.6 8 9 However, to the best of my knowledge, sensory changes limited to the proximal body parts sparing the acral areas have never been described with concomitant imaging findings, which prompted me to describe the following four patients who presented with sensory symptoms in restricted areas of the proximal body parts.
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Case Reports |
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Patient 1
An 80-year-old hypertensive man underwent brain MRI due to dull headache and dizziness. At this time, his sensory functions were within normal limits. The MRI results were normal except for the presence of a few small, scattered subcortical high signals in T2-weighted images. Five days later, he developed the sudden onset of paresthesia over the right upper arm. At the emergency department, the patient was alert and slightly dysarthric. Other cranial nerve functions and motor strength of the extremities were within normal limits. However, his right arm was slightly clumsy on finger-to-nose and rapid alternating hand tests. On examination of gait, he veered to the right. Tandem gait was difficult because of gait ataxia. On sensory examination, pinprick, touch, and vibration senses were mildly decreased (approximately 70% of the normal side) over discrete areas of the inner side of the right upper arm and the right trunk between the T1 and T10 levels; he also felt numbness over these areas. His face and the distal parts of the arm and leg were spared. Repeated brain MRI performed 3 days after the onset showed a small left thalamic infarction that was not present in the previous MRI (Fig 1
). Although the patient's hospital course was
uneventful, he transiently experienced additional numbness over the
right upper thigh area. However, the area of sensory
disturbances gradually diminished, and at 2 months of
follow-up, the sensory symptoms were restricted to a small area of
the uppermost inner arm and a part of the trunk near the axillary
area.
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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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The four patients described here presented with sensory symptoms almost always restricted to the proximal parts of the body: upper arm, shoulder, trunk, and upper part of the thigh (Fig 5
). Except for patient 3, who had mild and transient
paresthesia over the lower leg, acral parts of the bodies were spared.
Objective sensory deficits, which were mild or often absent, were also
limited to discrete areas of paresthesia except for patient 2, who
initially showed decreased sensation in the broader area. Possibilities
of migraine, peripheral neuropathy, or
myelopathy were virtually excluded by the patients' history,
neurological findings, and imaging results, which revealed discrete
infarcts in the thalamus (patients 1, 2, and 3) and the putamen
(patient 4).
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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.
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References |
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TopAbstractIntroductionCase ReportsDiscussionReferences |
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1. Fisher CM. Pure sensory stroke and allied conditions. Stroke. 1982;13:434-447.
2. Kim JS, Lee MC. Stroke and restricted sensory syndromes. Neuroradiology. 1994;36:258-263. [Medline] [Order article via Infotrieve]
3. Kim JS. Restricted acral sensory syndrome following minor stroke: further observation with special reference to differential symptomatic severity among individual digits. Stroke. 1994;25:2497-2502. [Abstract]
4.
Breuer AC, Cuervo H, Selkoe DJ. Hyperpathia and
sensory level due to parietal lobe arteriovenous malformation.
Arch Neurol. 1981;38:722-724.
5.
Matsumoto S, Okuda B, Imai T, Kameyama M. A
sensory level on the trunk in lower lateral brainstem lesions.
Neurology. 1988;38:1515-1519.
6.
Bassetti C, Bogousslavsky J, Regli F. Sensory
syndromes in parietal stroke. Neurology. 1993;43:1942-1949.
7.
Kim JS, Lee JH, Lee MC. Sensory changes in the
ipsilateral extremity: a clinical variant of lateral medullary
infarction. Stroke. 1995;26:1956-1958.
8. Lapresle J, Haguenau M. Anatomico-clinical correlation in focal thalamic lesions. Z Neurol. 1973;205:29-46. [Medline] [Order article via Infotrieve]
9.
Youl BD, Adams RW, Lance JW. Parietal sensory
loss simulating a peripheral lesion, documented by
somatosensory evoked potentials. Neurology. 1991;41:152-154.
10. Fisher CM. Pure sensory stroke involving the face, arm and leg. Neurology. 1965;15:76-80.
11.
Fisher CM. Thalamic pure sensory stroke: a
pathological study. Neurology. 1978;28:1141-1144.
12.
Kim JS. Pure sensory stroke:
clinical-radiological correlates of 21 cases.
Stroke. 1992;23:983-987.
13. Richardson EP. Striatal syndromes. In: Vinken PJ, Bruyn GW, eds. Handbook of Clinical Neurology, Vol 2. Amsterdam, Netherlands: North Holland; 1969:497-505.
14.
Rudick RA. Asymptomatic
intracerebral hematoma as an incidental
finding. Arch Neurol. 1981;38:396.
15. Kase CS, Mohr JP, Caplan LR. Intracerebral hemorrhage. In: Barnett HJM, Mohr JP, Stein BM, Yatsu FM, eds. Stroke: Pathophysiology, Diagnosis, and Management. 2nd ed. New York, NY: Churchill Livingstone Inc; 1992:561-616.
16. Rosenberg NL, Koller R. Computed tomography and pure sensory stroke. Neurology. 1978;28:1141-1144.
17.
Chamorro A, Sacco RL, Mohr JP, Foulkes MA, Kase CS,
Tatemichi TK, Wolf PA, Price TR, Hier DB. Clinical-computed
tomographic correlations of lacunar infarction in the Stroke Data
Bank. Stroke. 1991;22:175-181.
18. Kim JS. A lenticulocapsular lacune producing pure sensory stroke. Cerebrovasc Dis. 1991;1:302-304.
19. Kim JS, Lee JH, Lee MC. Small primary intracerebral hemorrhage: clinical presentation of 28 cases. Stroke. 1994;25:1500-1506. [Abstract]
20.
Jones EG, Friedman DP. Projection pattern of
functional components of thalamic ventrobasal complex on monkey
somatosensory cortex. J Neurophysiol. 1982;48:521-544.
21. Kaas JH, Nelson RJ, Sur M, Dykes RW, Merzenich MM. The somatotopic organization of the ventroposterior thalamus of the squirrel monkey, Saimiri sciureus. J Comp Neurol. 1984;226:111-140. [Medline] [Order article via Infotrieve]
22.
Loe PR, Whitsel BL, Dreyer DA, Metz CB. Body
representation in ventrobasal thalamus of macaque: a
single-unit analysis. J
Neurophysiol. 1977;40:1339-1355.
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