We report three cases showing body lateropulsion as the sole or predominant symptom of caudal lateral medullary infarction. All of them presented a small infarction on the lateral surface of the caudal medulla corresponding to the dorsal spinocerebellar tract (DSCT). IntroductionLateropulsion is known to be one of the symptoms of lateral medullary infarctions (LMIs). Although it is usually associated with ipsilateral Horner syndrome, ipsilateral limb ataxia, superficial sensory disturbance of the ipsilateral face and contralateral limbs, dysarthria, dysphagia, and vertigo, isolated body lateropulsion is rare. Although the lesion responsible for lateropulsion is controversial (1), recent studies (2-4) have identified possible corresponding lesions for lateropulsion. Here, we present three cases of caudal LMIs in which lateropulsion was the sole or predominant manifestation. Although lateropulsion due to LMIs is reported to improve within a few weeks (4), the condition of one of our patients progressed to typical Wallenberg syndrome. Case Report Case 1A 78-year-old woman noted acute lateropulsion to the right on June 16, 2002. She had diabetes mellitus and angina pectoris. On examination, there was no vertigo, nystagmus, hearing deficit, dysarthria, dysphagia, deficit in either superficial or deep sensation, ophthalmoplegia, Horner syndrome, hemiparesis, or limb ataxia. Magnetic resonance imaging (MRI) showed a fresh small infarction selectively involving the right superficial lateral portion of the caudal medulla (Fig. 1A). MR angiography showed stenosis of the right vertebral artery. Her symptom slowly resolved within two weeks. Case 2A 76-year-old man experienced lateropulsion to the right on January 9, 2003. He was receiving medication for hypertension. He showed no vertigo, nystagmus, hearing loss, dysarthria, dysphagia, sensory loss, ophthalmoplegia, Horner syndrome, or hemiparesis. MRI showed a fresh small infarction situated in the same position as in Case 1 (Fig. 1B). MR angiography showed weak flow in the vertebral arteries. Three days later, vomiting, decreased temperature sensation on the right face and the left limbs and trunk, and right Horner syndrome appeared abruptly. MRI revealed expansion of the infarct area (Fig. 1C). The lateropulsion itself improved within two weeks. Case 3An 84-year-old man presented with acute onset of veering of his body to the right on February 20, 2004. He was receiving medication for hypertension and diabetes mellitus. He did not have vertigo, nausea, or tinnitus, nor did he have hoarseness, dysphagia, or dysarthria. There was no ophthalmoplegia, Horner syndrome, limb ataxia, or hemiparesis. Pain and thermal sensations were decreased on his right face and over the contralateral side of his body. MRI showed a
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