(Stroke. 2001;32:1696.)
© 2001 American Heart Association, Inc.
Letters to the Editor |
Department of Neurology, Asan Medical Center, Seoul, South Korea
To the Editor:
In a recent article published in Stroke, Cerrato et al1 described a patient with right lateral medullary infarction (LMI) who presented with abnormal spinothalamic sensation in the left arm and impaired dorsal column sensation in the right hand. Although this is an interesting observation, I have several concerns about this report.
First, the authors wrote that "dissociated sensory pattern involving upper limbs has not yet been reported." However, I previously described 3 patients who had ipsilateral dorsal column sensory impairment who had otherwise typical symptoms/signs of LMI.2 Actually, one of them (case 3) showed exactly identical sensory pattern as described by Cerrato et al: dissociated sensory impairment limited to upper extremities. I suggested that involvement of the fibers at the nucleus gracilis/cuneatus or the crossing fibers toward the medial lemniscus may explain this sensory variant, a hypothesis again nearly identical with that raised by Cerrato et al. Therefore, their observation and hypothesis are not new.
Second, their Figure 3 was drawn as if the fibers from the nucleus cuneatus run ventrally and those from the nucleus gracilis dorsally into the contralateral medial lemniscus. Actually, it has been shown that in the medial lemniscus at the medulla level, sensory topography is arranged in such a way that the leg representation area is located ventrally and the arm representation area dorsally.3 Thus, the dorsal column sensory fibers are likely to decussate in a more complex manner than shown in Figure 3. Therefore, I think the lesion may have involved the nucleus cuneatus itself or the proximal portion of the decussating fibers.
Finally, it has been shown that a vertebral artery dissection may cause ipsilateral radiculopathy in the arm by way of the compression of the nerve roots due to enlarged vessels or induction of ischemia in the spinal roots.4 5 Although this is unlikely in the presence of normal MR angiogram findings, one must exclude this possibility with the help of electromyogram when ipsilateral sensory symptoms are encountered in a patient with LMI.
References
1.
Cerrato P,
Imperiale D, Bergui M, Giraudo M, Baima C, Grasso M, Lopiano L,
Bergamasco B. Restricted dissociated sensory loss in a patient with a
lateral medullary syndrome: a clinical-MRI study.
Stroke. 2000;31:30643066.
2.
Kim JS, Lee JH,
Lee MC. Sensory changes in the ipsilateral extremity: a clinical
variant of lateral medullary infarction.
Stroke. 1995;26:19561958.
3. Heines DE. Neuroanatomy: An Atlas of Structures, Sections and Systems. 2nd ed. Berlin, Germany: Urban & Schwarzenberg; 1987:157167.
4. Hetzel A, Berger W, Schumacher M, Lucking CH. Dissection of the vertebral artery with cervical nerve root lesions. J Neurol. 1996;243:121125.[Medline] [Order article via Infotrieve]
5.
Crum B, Mokri B,
Fulgham J. Spinal manifestations of vertebral artery dissection.
Neurology. 2000;55:304306.
Department of Neurology
Department of Neuroradiology, University of Torino, Torino, Italy
Kims letter raises 3 points about our article, "Restricted Dissociated Sensory Loss in a Patient With a Lateral Medullary Syndrome: A Clinical-MRI Study."R1
The first comment is that our report is not so original because he had described 3 patients with similar sensory impairment in 1995.R2 Actually, in those patients the sensory pattern did not involve only the upper limbs, as in our case, but also the face and the trunk and was, therefore, not so "restricted." Moreover, sensory disturbances were not isolated, but there were also other neurological features (Horners sign and ipsilateral weakness of the limbs, ipsilateral limbs ataxia, ipsilateral facial paresis). Finally, the lower medulla ischemic areas in the patients of Dr Kim were much greater than the small area in our case (involving also the cerebellum in 2 of them). Therefore, we think that the actual peculiarity of our report consists in the occurrence of a "truly restricted" dissociated sensory loss as the unique neurological consequence of lateral medullary infarction.
The second comment by Kim regards the anatomy of sensory systems in medulla oblongata. Certainly, the anatomy of lemniscal decussation is more complex than in our scheme.R3 Anyway, the "strategic" location of the ischemic lesion in our patient and the subsequent clinical-anatomical correlation is evident. The simultaneous involvement of the inner spinothalamic fibers and the proximal portion of the lateral archiform fibers (both containing afferents from the upper limbs) clearly explains such a "restricted" and "dissociated" sensory pattern.
In his last comment, Kim raises the hypothesis that a vertebral artery dissection may have caused a compressive or ischemic radiculopathy and may explain the ipsilateral sensory symptoms. In our case, the vertebral artery dissection was ruled out by neuroimaging and ultrasonographic data (MR angiography and extracranial vessel duplex ultrasonography of cervical vessels were normal). Moreover, clinical findings of radiculopathy, such as neck pain and radicular sensory and/or motor deficit and asymmetry of deep tendon reflexes, were absent.
References
1. Cerrato P, Imperiale D, Bergui M, Giraudo M, Baima C, Grasso M, Lopiano L, Bergamasco B. Restricted dissociated sensory loss in a patient with a lateral medullary syndrome: a clinical-MRI study. Stroke. 2000;31:30643066.
2. Kim JS, Lee JH, Lee MC. Sensory changes in the ipsilateral extremity: a clinical variant of lateral medullary infarction. Stroke. 1995;26:19561958.
3. Heines DE. Neuroanatomy: An Atlas of Structures, Sections and Systems. 2nd ed. Berlin, Germany: Urban & Schwarzenberg; 1987:157167.
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