Plasticity of primary afferent neurons and sensory processing after spinal cord injury

Traumatic injury of the spinal cord affects the entire organism directly and indirectly. Primary injury destroys neurons and severs axons which participate in neural circuits. Secondary injuries and pathologies arise from numerous sources including systemic inflammation, consequential damage of cuta...

Full description

Saved in:
Bibliographic Details
Main Author: Jeffrey C. Petruska (auth)
Other Authors: Charles Hubscher (auth), Alexander Rabchevsky (auth)
Format: Book Chapter
Published: Frontiers Media SA 2015
Subjects:
Online Access:Get Fullteks
DOAB: description of the publication
Tags: Add Tag
No Tags, Be the first to tag this record!
LEADER 03624naaaa2200313uu 4500
001 doab_20_500_12854_56389
005 20210211
020 |a 978-2-88919-396-7 
020 |a 9782889193967 
024 7 |a 10.3389/978-2-88919-396-7  |c doi 
041 0 |a English 
042 |a dc 
100 1 |a Jeffrey C. Petruska  |4 auth 
700 1 |a Charles Hubscher  |4 auth 
700 1 |a Alexander Rabchevsky  |4 auth 
245 1 0 |a Plasticity of primary afferent neurons and sensory processing after spinal cord injury 
260 |b Frontiers Media SA  |c 2015 
300 |a 1 electronic resource (221 p.) 
506 0 |a Open Access  |2 star  |f Unrestricted online access 
520 |a Traumatic injury of the spinal cord affects the entire organism directly and indirectly. Primary injury destroys neurons and severs axons which participate in neural circuits. Secondary injuries and pathologies arise from numerous sources including systemic inflammation, consequential damage of cutaneous, muscular, and visceral tissues, and dysregulation of autonomic, endocrine and sensory- motor functions. Evidence is mounting that spinal cord injury (SCI) affects regions of the nervous system spatially remote from the injury site, as well as peripheral tissues, and alters some basic characteristics of primary afferent cell biology and physiology (cell number, size/frequency, electrophysiology, other). The degree of afferent input and processing above the lesion is generally intact, while that in the peri-lesion area is highly variable, though pathologies emerge in both regions, including a variety of pain syndromes. Primary afferent input to spinal regions below the injury and the processing of this information becomes even more important in the face of complete or partial loss of descending input because such spared sensory processing can lead to both adaptive and pathological outcomes. This issue hosts review and research articles considering mechanisms of plasticity of primary afferent neurons and sensory processing after SCI, and how such plasticity contributes to sparing and/or recovery of functions, as well as exacerbation of existing and/or emergent pathologies. A critical issue for the majority of the SCI community is chronic above-, peri-, and below-level neuropathic pain, much of which may arise, at least in part, from plasticity of afferent fibers and nociceptive circuitry. For example, autonomic dysreflexia is common hypertensive syndrome that often develops after SCI that is highly reliant on maladaptive nociceptive sensory input and processing below the lesion. Moreover, the loss of descending input leaves the reflexive components of bladder/bowel/sexual function uncoordinated and susceptible to a variety of effects through afferent fiber plasticity. Finally, proper afferent feedback is vital for the effectiveness of activity-dependent rehabilitative therapies, but aberrant nociceptive input may interfere with these approaches since they are often unchecked due to loss of descending modulation. 
540 |a Creative Commons  |f https://creativecommons.org/licenses/by/4.0/  |2 cc  |4 https://creativecommons.org/licenses/by/4.0/ 
546 |a English 
653 |a sensory systems 
653 |a sensory neurons 
653 |a sensory plasticity 
653 |a spinal cord injury (SCI) 
653 |a sensory perceptions 
856 4 0 |a www.oapen.org  |u http://journal.frontiersin.org/researchtopic/571/plasticity-of-primary-afferent-neurons-and-sensory-processing-after-spinal-cord-injury  |7 0  |z Get Fullteks 
856 4 0 |a www.oapen.org  |u https://directory.doabooks.org/handle/20.500.12854/56389  |7 0  |z DOAB: description of the publication