Experimental neurology
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Experimental neurology · Dec 1997
Comparative StudyCentral cord syndrome of cervical spinal cord injury: widespread changes in muscle recruitment studied by voluntary contractions and transcranial magnetic stimulation.
Muscle recruitment after central cord syndrome (CCS), a cervical spinal cord injury leading to a weaker motor function in the upper limbs versus the lower limbs, was examined in 14 individuals by means of voluntary muscle contractions and transcranial magnetic stimulation (TMS). Previously obtained data from able-bodied (AB) and non-CCS spinal cord injured subjects were used for comparison. Surface EMG was recorded from as many as six pairs of affected muscles. ⋯ The delays in muscle responses were not significantly different from those observed in subjects with more severe cervical injury. Despite improvement in EMG scores, repeated measurements of TMS-evoked muscle response latencies in the same CCS subjects did not reveal significant shortening in central conduction latency. This argues against remyelination as an important contributor to the recovery process.
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Experimental neurology · Dec 1997
Muscle weakness, paralysis, and atrophy after human cervical spinal cord injury.
Muscle weakness and failure of central motor drive were assessed in triceps brachii muscles of individuals with chronic cervical spinal cord injury (SCI) and able-bodied controls. Electrical stimuli were applied to the radial nerve during rest and during triceps submaximal and maximal voluntary contractions (MVCs). The mean forces and integrated EMGs generated by SCI subjects during MVCs were significantly less than those produced by controls (P < 0.01), with 74 and 71% of muscles generating <10% control force and EMG, respectively. ⋯ Thus central motor drive was probably maximal to these muscles, and the force evoked during MVCs by below-lesion stimulation must come from activation of paralyzed muscle. SCI subjects also had significantly longer mean central nervous system (CNS) conduction times to triceps (P < 0.01) suggesting that the measured deficits reflect CNS rather than peripheral nervous system factors. Thus, the weak voluntary strength of these partially paralyzed muscles is not due to submaximal excitation of higher CNS centers, but results mainly from reduction of this input to triceps motoneurons.
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Experimental neurology · Dec 1997
Truncated trkB receptors on nonneuronal cells inhibit BDNF-induced neurite outgrowth in vitro.
The function of truncated trkB receptors during nervous system plasticity and regeneration is currently unknown. The extensive nonneuronal localization of truncated trkB-T1 receptors, coupled with their up-regulation by CNS glial cells in response to injury, has led to the speculation that these receptors may sequester BDNF and NT-4/5 to reduce their local availability and, thus, limit axonal sprouting. Conversely, trkB-T1 receptors could bind and present neurotrophins to injured axons and facilitate their regeneration in a manor analogous to that proposed for p75(NTR) receptors on Schwann cells. ⋯ This ability of trkB-T1 receptors on the nonneuronal substratum to inhibit BDNF-induced neurite outgrowth can be overcome by the addition of high concentrations of BDNF (1 microg/ml). Binding assays using 125I-BDNF suggest that this inhibitory effect could be mediated via binding and internalization of BDNF by the trkB-T1 receptors on the 3T3 cells. These results provide strong support for the hypothesis that the up-regulation of trkB-T1 receptors on astrocytes following CNS lesions enhances the sequestration of the trkB ligands, BDNF and NT- 4/5, at the site of reactive gliosis and, thus, contributes to the inhibition of CNS axonal regeneration from neurons expressing trkB-kinase receptors by removing their ligands from the extracellular environment.
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Experimental neurology · Dec 1997
Endogenous repair after spinal cord contusion injuries in the rat.
Contusion injuries of the rat thoracic spinal cord were made using a standardized device developed for the Multicenter Animal Spinal Cord Injury Study (MASCIS). Lesions of different severity were studied for signs of endogenous repair at times up to 6 weeks following injury. Contusion injuries produced a typical picture of secondary damage resulting in the destruction of the cord center and the chronic sparing of a peripheral rim of fibers which varied in amount depending upon the injury magnitude. ⋯ These cells may contribute to the development of cellular trabeculae that provide a scaffolding within the lesion cavity that provides the substrates for cellular infiltration and regeneration of axons. Together, these observations suggest that the endogenous reparative response to spinal contusion injury is substantial. Understanding the regulation and restrictions on the repair processes might lead to better ways in which to encourage spontaneous recovery after CNS injury.