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This Article Full Text Full Text (PDF) All Versions of this Article: 94/6/3677    most recent 00538.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (15) Citing Articles via Google Scholar Google Scholar Articles by Lyalka, V. F. Articles by Deliagina, T. G. Search for Related Content PubMed PubMed Citation Articles by Lyalka, V. F. Articles by Deliagina, T. G.

Impairment and Recovery of Postural Control in Rabbits With Spinal Cord Lesions

The Nobel Institute for Neurophysiology, Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.

Submitted 23 May 2005; accepted in final form 5 July 2005

The aim of this study was to characterize impairment and subsequent recovery of postural control after spinal cord injuries. Experiments were carried out on rabbits with three types of lesion—a dorsal (D), lateral (L), or ventral (V) hemisection (HS) at T₁₂ level. The animals were maintaining equilibrium on a platform periodically tilted in the frontal plane. We assessed the postural limb/trunk configuration from video recordings and postural reflexes in the hindquarters from kinematical and electromyographic (EMG) recordings. We found that for a few days after DHS or LHS, the animals were not able to maintain the dorsal-side-up position of their hindquarters. This ability was then gradually restored, and the dynamic postural reflexes reached the prelesion value within 2–3 wk. By contrast, a VHS almost completely abolished postural reflexes, and they did not recover for 7 wk. The DHS, LHS, and VHS caused immediate and slowly compensated changes in the postural limb/trunk configuration as well as gradually developing changes. After DHS, both hind limbs were placed in an abnormal rostral and medial position. After LHS, the limb on the undamaged side was turned inward and occurred at the abnormal medial position; LHS also caused a gradually developing twisting of the caudal trunk. VHS caused gradually developing extension of the ankle and knee joints. These findings show that ventral spinal pathways are of crucial importance for postural control. When a part of these pathways is spared, postural reflexes can be restored rapidly, but not the postural limb/trunk configuration. Spinal and supraspinal mechanisms responsible for postural deficits and their compensation are discussed.

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