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Gait Disturbances in Patients With Pontine Medial Tegmental Lesions
Clinical Characteristics and Gait Analysis
Hiroshi Mitoma, MD;
Ryoichi Hayashi, MD;
Nobuo Yanagisawa, MD;
Hiroshi Tsukagoshi, MD
Arch Neurol. 2000;57:1048-1057.
Objective To determine the clinical characteristics of gait disorders in patients with pontine medial tegmental lesions.
Design We compared features of gait disorders between patients with infarcts in the medial tegmentum and those with stroke in other areas of the pons (pathological control subjects) by measuring electromyographic results of lower limb muscles and several biomechanical parameters.
Patients Two patients with infarcts in the rostral medial tegmentum and 4 control subjects. Two of the control patients had lesions in the pontine base, while the lesions in the other 2 were in the pontine tegmentum and base (combined lesions).
Results Patients with rostral medial tegmental lesions and controls with pontine base lesions showed unstable walking characterized by irregular angular displacements and foot pressures. However, they differed by the following 3 features. (1) Rostral medial tegmental lesions elicited truncal ataxia without limb ataxia. In comparison, pontine base lesions elicited limb ataxia without truncal ataxia and caused hemiparesis. (2) Instability was more severe and persistent in patients with the former lesions than in those with the latter lesions. Slowness of walking speed and prolongation of the double-support period were clearly observed in the former group. (3) Electromyographic changes characteristic of cerebellar ataxia were clearly evident in patients with rostral medial tegmental lesions. The electromyographic amplitudes of the gastrocnemius and tibialis anterior muscles were almost constant throughout the gait cycle, resulting in the disappearance of the inherent periodic pattern of each muscle.
Conclusion Medial tegmental lesions in the rostral pons cause prolonged and severe unstable walking that resembles spinocerebellar ataxic pattern, and impairment of the spinocerebellar loop might be the pathomechanism underlying such a gait disturbance.
From the Kakeyu Rehabilitation Research Institute, Maruko-machi, Nagano (Drs Mitoma and Tsukagoshi), and the Department of Medicine (Neurology), Shinshu University School of Medicine, Matsumoto (Drs Hayashi and Yanagisawa), Japan. Dr Mitoma is now with the Mitoma Neurological Clinic, Toshima-ku, Tokyo, Japan.
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