Mechanisms of chronic central neuropathic pain after spinal cord injury

Claire E. Hulsebosch, Bryan C. Hains, Eric D. Crown, Susan M. Carlton

Research output: Contribution to journalArticle

172 Citations (Scopus)

Abstract

Not all spinal contusions result in mechanical allodynia, in which non-noxious stimuli become noxious. The studies presented use the NYU impactor at 12.5 mm drop or the Infinite Horizons Impactor (150 kdyn, 1 s dwell) devices to model spinal cord injury (SCI). Both of these devices and injury parameters, if done correctly, will result in animals with above level (forelimb), at level (trunk) and below level (hindlimb) mechanical allodynia that model the changes in evoked somatosensation experienced by the majority of people with SCI. The sections are as follows: 1) Mechanisms of remote microglial activation and pain signaling in "below-level" central pain 2) Intracellular signaling mechanisms in central sensitization in "at-level" pain 3) Peripheral sensitization contributes to "above level" injury pain following spinal cord injury and 4) Role of reactive oxygen species in central sensitization in regional neuropathic pain following SCI. To summarize, differential regional mechanisms contribute to the regional chronic pain states. We propose the importance of understanding the mechanisms in the differential regional pain syndromes after SCI in the chronic condition. Targeting regional mechanisms will be of enormous benefit to the SCI population that suffer chronic pain, and will contribute to better treatment strategies for other chronic pain syndromes.

Original languageEnglish (US)
Pages (from-to)202-213
Number of pages12
JournalBrain Research Reviews
Volume60
Issue number1
DOIs
StatePublished - Apr 2009

Fingerprint

Neuralgia
Spinal Cord Injuries
Pain
Chronic Pain
Central Nervous System Sensitization
Hyperalgesia
Equipment and Supplies
Forelimb
Contusions
Wounds and Injuries
Hindlimb
Reactive Oxygen Species
Population

Keywords

  • Central sensitization
  • Chronic pain
  • Cytokine
  • Pain
  • Peripheral sensitization
  • Reactive oxygen species
  • Regional pain syndrome

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology

Cite this

Mechanisms of chronic central neuropathic pain after spinal cord injury. / Hulsebosch, Claire E.; Hains, Bryan C.; Crown, Eric D.; Carlton, Susan M.

In: Brain Research Reviews, Vol. 60, No. 1, 04.2009, p. 202-213.

Research output: Contribution to journalArticle

Hulsebosch, Claire E. ; Hains, Bryan C. ; Crown, Eric D. ; Carlton, Susan M. / Mechanisms of chronic central neuropathic pain after spinal cord injury. In: Brain Research Reviews. 2009 ; Vol. 60, No. 1. pp. 202-213.
@article{e2c498451b1f42508c5939425d97f8ec,
title = "Mechanisms of chronic central neuropathic pain after spinal cord injury",
abstract = "Not all spinal contusions result in mechanical allodynia, in which non-noxious stimuli become noxious. The studies presented use the NYU impactor at 12.5 mm drop or the Infinite Horizons Impactor (150 kdyn, 1 s dwell) devices to model spinal cord injury (SCI). Both of these devices and injury parameters, if done correctly, will result in animals with above level (forelimb), at level (trunk) and below level (hindlimb) mechanical allodynia that model the changes in evoked somatosensation experienced by the majority of people with SCI. The sections are as follows: 1) Mechanisms of remote microglial activation and pain signaling in {"}below-level{"} central pain 2) Intracellular signaling mechanisms in central sensitization in {"}at-level{"} pain 3) Peripheral sensitization contributes to {"}above level{"} injury pain following spinal cord injury and 4) Role of reactive oxygen species in central sensitization in regional neuropathic pain following SCI. To summarize, differential regional mechanisms contribute to the regional chronic pain states. We propose the importance of understanding the mechanisms in the differential regional pain syndromes after SCI in the chronic condition. Targeting regional mechanisms will be of enormous benefit to the SCI population that suffer chronic pain, and will contribute to better treatment strategies for other chronic pain syndromes.",
keywords = "Central sensitization, Chronic pain, Cytokine, Pain, Peripheral sensitization, Reactive oxygen species, Regional pain syndrome",
author = "Hulsebosch, {Claire E.} and Hains, {Bryan C.} and Crown, {Eric D.} and Carlton, {Susan M.}",
year = "2009",
month = "4",
doi = "10.1016/j.brainresrev.2008.12.010",
language = "English (US)",
volume = "60",
pages = "202--213",
journal = "Brain Research Reviews",
issn = "0165-0173",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Mechanisms of chronic central neuropathic pain after spinal cord injury

AU - Hulsebosch, Claire E.

AU - Hains, Bryan C.

AU - Crown, Eric D.

AU - Carlton, Susan M.

PY - 2009/4

Y1 - 2009/4

N2 - Not all spinal contusions result in mechanical allodynia, in which non-noxious stimuli become noxious. The studies presented use the NYU impactor at 12.5 mm drop or the Infinite Horizons Impactor (150 kdyn, 1 s dwell) devices to model spinal cord injury (SCI). Both of these devices and injury parameters, if done correctly, will result in animals with above level (forelimb), at level (trunk) and below level (hindlimb) mechanical allodynia that model the changes in evoked somatosensation experienced by the majority of people with SCI. The sections are as follows: 1) Mechanisms of remote microglial activation and pain signaling in "below-level" central pain 2) Intracellular signaling mechanisms in central sensitization in "at-level" pain 3) Peripheral sensitization contributes to "above level" injury pain following spinal cord injury and 4) Role of reactive oxygen species in central sensitization in regional neuropathic pain following SCI. To summarize, differential regional mechanisms contribute to the regional chronic pain states. We propose the importance of understanding the mechanisms in the differential regional pain syndromes after SCI in the chronic condition. Targeting regional mechanisms will be of enormous benefit to the SCI population that suffer chronic pain, and will contribute to better treatment strategies for other chronic pain syndromes.

AB - Not all spinal contusions result in mechanical allodynia, in which non-noxious stimuli become noxious. The studies presented use the NYU impactor at 12.5 mm drop or the Infinite Horizons Impactor (150 kdyn, 1 s dwell) devices to model spinal cord injury (SCI). Both of these devices and injury parameters, if done correctly, will result in animals with above level (forelimb), at level (trunk) and below level (hindlimb) mechanical allodynia that model the changes in evoked somatosensation experienced by the majority of people with SCI. The sections are as follows: 1) Mechanisms of remote microglial activation and pain signaling in "below-level" central pain 2) Intracellular signaling mechanisms in central sensitization in "at-level" pain 3) Peripheral sensitization contributes to "above level" injury pain following spinal cord injury and 4) Role of reactive oxygen species in central sensitization in regional neuropathic pain following SCI. To summarize, differential regional mechanisms contribute to the regional chronic pain states. We propose the importance of understanding the mechanisms in the differential regional pain syndromes after SCI in the chronic condition. Targeting regional mechanisms will be of enormous benefit to the SCI population that suffer chronic pain, and will contribute to better treatment strategies for other chronic pain syndromes.

KW - Central sensitization

KW - Chronic pain

KW - Cytokine

KW - Pain

KW - Peripheral sensitization

KW - Reactive oxygen species

KW - Regional pain syndrome

UR - http://www.scopus.com/inward/record.url?scp=63449106099&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=63449106099&partnerID=8YFLogxK

U2 - 10.1016/j.brainresrev.2008.12.010

DO - 10.1016/j.brainresrev.2008.12.010

M3 - Article

VL - 60

SP - 202

EP - 213

JO - Brain Research Reviews

JF - Brain Research Reviews

SN - 0165-0173

IS - 1

ER -