Experimental neurology
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Experimental neurology · Aug 2010
Voluntary ankle flexor activity and adaptive coactivation gain is decreased by spasticity during subacute spinal cord injury.
Although spasticity has been defined as an increase in velocity-dependent stretch reflexes and muscle hypertonia during passive movement, the measurement of flexor muscle paresis may better characterize the negative impact of this syndrome on residual motor function following incomplete spinal cord injury (iSCI). In this longitudinal study Tibialis Anterior (TA) muscle paresis produced by a loss in maximal voluntary contraction during dorsiflexion and ankle flexor muscle coactivation during ramp-and-hold controlled plantarflexion was measured in ten patients during subacute iSCI. Tibialis Anterior activity was measured at approximately two-week intervals between 3-5 months following iSCI in subjects with or without spasticity, characterized by lower-limb muscle hypertonia and/or involuntary spasms. ⋯ In contrast contraction-dependent TA coactivation gain decreased from 2.4+/-0.3 to 1.4+/-0.1 during spasticity. In conclusion the adaptive increase in TA coactivation gain observed in this pilot study during subacute iSCI was also sensitive to the presence of spasticity. The successful early diagnosis and treatment of spasticity would be expected to further preserve and promote adaptive motor function during subacute iSCI neurorehabilitation.
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Experimental neurology · Aug 2010
Anti-IL-6-receptor antibody promotes repair of spinal cord injury by inducing microglia-dominant inflammation.
We previously reported the beneficial effect of administering an anti-mouse IL-6 receptor antibody (MR16-1) immediately after spinal cord injury (SCI). The purpose of our present study was to clarify the mechanism underlying how MR16-1 improves motor function after SCI. Quantitative analyses of inflammatory cells using flow cytometry, and immunohistochemistry with bone marrow-chimeric mice generated by transplanting genetically marked purified hematopoietic stem cells, revealed that MR16-1 dramatically switched the central player in the post-traumatic inflammation, from hematogenous macrophages to resident microglia. ⋯ Consistent with these findings, we observed significantly decreased tissue damage and reduced levels of myelin debris and Nogo-A, the axonal growth inhibitor, by MR16-1 treatment. Moreover, we observed increased axonal regeneration and/or sprouting in the MR16-1-treated mice. Our findings indicate that the functional improvement elicited by MR16-1 involves microglial functions, and provide new insights into the role of IL-6 signaling in the pathology of SCI.