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Impairment and recovery of postural control in rabbits with spinal cord lesions

Lyalka, VF (författare)
Karolinska Institutet
Zelenin, PV (författare)
Karolinska Institutet
Karayannidou, A (författare)
Karolinska Institutet
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Orlovsky, GN (författare)
Karolinska Institutet
Grillner, S (författare)
Karolinska Institutet
Deliagina, TG (författare)
Karolinska Institutet
visa färre...
 (creator_code:org_t)
American Physiological Society, 2005
2005
Engelska.
Ingår i: Journal of neurophysiology. - : American Physiological Society. - 0022-3077 .- 1522-1598. ; 94:6, s. 3677-3690
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • 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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