• Tameto Naoi, Mitsuya Morita, Koki Kosami, Takafumi Mashiko, Tomoaki Kameda, Shunich Okada, Yuka Hayashi, Tadataka Kawakami, Ryota Tanaka, and Shigeru Fujimoto.
• Rehabilitation Center, Jichi Medical University Hospital, Tochigi, Japan. Electronic address: sph89vz9@coda.ocn.ne.jp.
• J Stroke Cerebrovasc Dis. 2020 Oct 1; 29 (10): 105183.

BackgroundIn patients with lower lateral medullary infarction (LMI) located under the vestibular nucleus, proprioceptive impairment due to dorsal spinocerebellar tract (DSCT) is considered a pathological condition for body lateropulsion. In patients with brainstem infarction located at or above the level of the vestibular nucleus, other pathways, such as the crossed vestibulothalamic tract (CVTT), are considered responsible.Research QuestionThe clinical course of body lateropulsion between each anatomical level of infarction remains unclear. Further, whether body lateropulsion refers to a static or a dynamic symptom also remains unclear.MethodsWe examined 47 patients who exhibited body lateropulsion and categorized them into four groups: lower LMI under the vestibular nucleus, LMI at the level of the vestibular nucleus, pontine infarction, and midbrain infarction. The patients' time to acquire static upright standing position and gait in a straight line were statistically analyzed by a log-rank test using the Kaplan-Meier method.ResultsBody lateropulsion in the static upright position was less frequent in the lower LMI group than in the other groups.SignificanceLower LMI primarily affected body lateropulsion in gait. DSCT damage could affect ipsilateral hip joint or leg coordination, causing body lateropulsion in dynamic situation.Copyright © 2020 Elsevier Inc. All rights reserved.

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