Central Plasticity of Cutaneous Afferents Is Associated with Nociceptive Hyperreflexia after Spinal Cord Injury in Rats.

Hyun Joon Lee,Jumi Chung,Natalee Wilson,Jason Tidwell,Jason M White,Keith E Tansey,Patrick S Malone

doi:10.1155/2019/6147878

Hyun Joon Lee, Jumi Chung + Show 5 more

Open Access

https://doi.org/10.1155/2019/6147878

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Abstract

Electrical stimulations of dorsal cutaneous nerves (DCNs) at each lumbothoracic spinal level produce the bilateral cutaneus trunci muscle (CTM) reflex responses which consist of two temporal components: an early and late responses purportedly mediated by Aδ and C fibers, respectively. We have previously reported central projections of DCN A and C fibers and demonstrated that different projection patterns of those afferent types contributed to the somatotopic organization of CTM reflex responses. Unilateral hemisection spinal cord injury (SCI) was made at T10 spinal segments to investigate the plasticity of early and late CTM responses 6 weeks after injury. Both early and late responses were drastically increased in response to both ipsi- and contralateral DCN stimulations both above (T6 and T8) and below (T12 and L1) the levels of injury demonstrating that nociceptive hyperreflexia developed at 6 weeks following hemisection SCI. We also found that DCN A and C fibers centrally sprouted, expanded their projection areas, and increased synaptic terminations in both T7 and T13, which correlated with the size of hemisection injury. These data demonstrate that central sprouting of cutaneous afferents away from the site of injury is closely associated with enhanced responses of intraspinal signal processing potentially contributing to nociceptive hyperreflexia following SCI.

Highlights

Spinal cord injury (SCI) often results in devastating pain that largely impacts the quality of life in patients
We have previously shown that cutaneus trunci muscle (CTM) reflex responses varied by dorsal cutaneous nerves (DCNs) stimulations with different stimulation frequencies at different spinal levels and sides [21]
T10 hemisection SCI produced cutaneous nociceptive hyperreflexia measured with significantly increased size of both early and late responses of the evoked CTM reflex at both sides of injury both above and below the injury site at T6, T8, T12, and L1

Summary

Introduction

Spinal cord injury (SCI) often results in devastating pain that largely impacts the quality of life in patients. A longitudinal study for 5 years demonstrated that somatic pain is the most common type of pain in SCI patients regardless of the type of injury, the injury severity, and the onset time of pain-related symptoms [1] This implies that damage at the spinal cord of any size may cause early or late changes in nociceptive signal pathways which result in persistently enhanced pain sensitivity, e.g., nociceptive hyperreflexia. This maladaptive plasticity appears to be a consequence of central changes that include loss of supraspinal inhibitory control [2], death of inhibitory propriospinal interneurons [3], reduced GABA (GAD65) synthesis [4], interrupted chloride equilibrium in spinal neurons [5], and sprouting of nociceptive afferents [6,7,8]. These changes mostly occur at the level of SCI but may expand away, both above and below the level of injury, generating hyperreflexia in nociceptive circuitries that are not directly affected by that injury.

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