Lateropulsion Due to a Lesion of the Dorsal Spinocerebellar Tract

Abstract

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

Body lateropulsion as an isolated or predominant symptom of a pontine infarction

“…Body lateropulsion as the main clinical manifestation of posterior circulation stroke is rare. We are aware of only five previously reported cases of lateral medullary infarction, [3][4][5] infarction of the superior and inferior cerebellar peduncle, 6 and midbrain infarction involving the red nucleus. 7 There are no prior reports of isolated body lateropulsion due to a pontine stroke.…”

Isolated body lateropulsion caused by a lesion of the rostral vermis

“…Furthermore, although the ventral spinocerebellar tract (VSCT) also convey unconsciousness proprioceptive information from the leg and the lower trunk, the VSCT conveys the proprioception of the contralateral lower limb and the VSCT neurons are being more related to attempted movements rather than to pure sensory signals [17]. Considering the lesion on the brain MRI of my patient showed the selective involvement of the centralis of Larsell's lobules II, that the ascending DSCT conveying posture, gait, and muscle tone of the lower limb and the trunk terminate in the rostral vermis [16], and that previous reports of an isolated lateropulsion due to a lesion of the DSCT exist [10,11], I speculated that a lesion of the ascending DSCT at the rostral vermis in my patient is responsible for the observed lateropulsion. A recent functional MRI study, which showed that the leg movement activated area is found within the central lobule of Larsell's lobules II-III, also supports our hypothesis [18].…”

“…I have identified seven previously reported cases with different kinds of lesions in the English literatures: lateral medullary infarction [9][10][11], infarction of the superior and inferior cerebellar peduncle [12], midbrain infarction involving red nucleus [13], and cerebellar infarction [14,15]. Cerebellar lesion commonly results in a postural instability from mild veering to severe gait ataxia with sudden falling (i.e., axial or body lateropulsion), and the other neurological symptoms or signs are usually associated with gait ataxia.…”

Isolated axial lateropulsion with ipsilesional subjective visual vertical tilt in caudal lateral medullary infarction

“…Lesions in lateral medulla [13], paramedian pons [20], cerebellum [16] was associated with their symptoms. In other studies, the lateropulsion without limb ataxia was reported to result from the DSCT involvement [12,14,17]. But SVV tilt or ocular torsion in patients with DSCT involvement without vestibular nuclei complex involvement has not been reported.…”

“…In classic LMI, axial lateropulsion is ascribed to the involvement of vestibulo-spinal or vestibulo-ocular reflex (VOR) pathway and is usually accompanied by ocular tilt reaction (OTR). However, isolated axial lateropulsion without any sign of OTR has been well described in caudal lateral medullary infarction (CLMI) [12,14,17]. The dorsal spinocerebellar tract (DSCT) is at the lateral surface of the caudal medulla and is reported to be responsible for the isolated axial lateropulsion without limb ataxia in CLMI [17].…”