Experimental neurology
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Experimental neurology · Mar 1998
Quantitative assessment of respiratory function following contusion injury of the cervical spinal cord.
In this study, we describe a new method for quantitative assessment of phrenic inspiratory motor activity in two models of cervical spinal cord contusion injury. Anesthetized rats received contusion injury either to the descending bulbospinal respiratory pathway on one side of the spinal cord alone (C2 lateralized contusion) or to both the descending pathway, as well as the phrenic motoneuron pool bilaterally (C4/C5 midline contusion). Following injury, respiratory-associated phrenic nerve motor activity was recorded under standardized and then asphyxic conditions. ⋯ In C4/5 lesions, the results indicate that this percentage was increased on both sides (77 +/- 4.4%). The results show the feasibility for performing quantitative evaluation of respiratory dysfunction in an animal model of cervical contusion injury. These findings lend to further development of this model for investigations of neuroplasticity and/or therapeutic interventions directed at ameliorating respiratory compromise following cervical spinal cord trauma.
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Experimental neurology · Mar 1998
Extent of nociceptive dermatomes in adult rats is not primarily maintained by axonal competition.
Nociceptive innervation territories of individual peripheral and spinal nerves in the skin of the rat hind paw were investigated. In addition, the hypothesis that competitive interactions among the axons from adjacent dorsal root ganglia (DRG) play an important role in maintenance of dermatomal extent in adult animals was tested. The area of innervation territories of individual spinal and peripheral nerves was determined by nociceptive pinch test of the skin after extirpation of adjacent DRGs or transection of adjacent peripheral nerves, respectively. ⋯ Accordingly, we could find no autonomous innervation area of the sural nerve. Two weeks after extirpation of adjacent DRGs, the area of each of the isolated dermatomes L3, L4, and L5 increased only by about 10%, and it did not change detectably during the next 6 months. The results of our study (a) support the view that innervation fields supplied by the nociceptive (probably A delta) fibers are greater and display more overlap than those supplied by the C-fibers of the same nerve and (b) suggest that axonal competition for innervation territory is not decisive for maintenance of dermatomal borders in the adult rat.
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Experimental neurology · Jan 1998
A neuronal correlate of secondary hyperalgesia in the rat spinal dorsal horn is submodality selective and facilitated by supraspinal influence.
Tissue injury produces hyperalgesia not only in the injured area (primary hyperalgesia) but also outside of it (secondary hyperalgesia). In the present investigation, the submodality selectivity and the contribution of supraspinal influence to a neural correlate of the secondary hyperalgesia induced by neurogenic inflammation was studied in the presumed pain relay neurons of the rat spinal dorsal horn. Mechanically and thermally evoked responses to wide-dynamic range (WDR) neurons of the spinal dorsal horn were recorded under sodium pentobarbital anesthesia in rats. ⋯ The selective mechanical hyperexcitability in spinal WDR neurons, without a change in their spontaneous activity, can be explained by a heterosynaptic facilitatory action on presynaptic terminals mediating mechanical signals to these nociceptive spinal neurons. These findings indicate that brain stem-spinal pathways, involving the RVM, do not only suppress nociception but under some pathophysiological conditions concurrent facilitatory influence may predominate and lead to enhancement of mechanical hyperexcitability. The descending facilitatory feed-back loop to nociceptive spinal neurons may help to protect the wounded tissue and thus promote healing.
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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.