Spinal Cord Injury

Spinal cord injury results in a variety of changes that continue to be cytotoxic to cells that are at risk of dying, both nerve cells and glial cells-cells that are not nerve cells but are critical for normal spinal cord function.  Her group reports that both glial and nerve cells are changed permanently after spinal cord injury. They are in the process of using molecular, behavioral, physiological, immunocytochemical and electrophysiological approaches to study the mechanisms that underlie the permanent changes that will help restore the spinal cord to normal function. Her collaborative manuscripts demonstrate numerous and permanent changes that are many segments above and below the spinal cord injury and persistent changes in neural circuits in these regions that lead to dysfunction. One project is focused on recovery of normal sensory/motor function; another project focuses on improved visceral function, while other projects test the role of transplanted stem cells. For example, her laboratory has demonstrated that molecularly engineered cells transplanted onto the surface of the spinal cord can return the abnormal characteristics of the nerve cells that develop after SCI, to more normal behavior. They hypothesize that persistent neuroinflammation in the spinal cord contributes to permanent alterations in nerve cell circuits, and that the abnormal reaction of microglia and astrocytes after SCI (she calls this “gliopathy”), even many segments away continues to contribute to the neuroinflammation leading to impaired nerve cell function. Insight into these pathways will suggest therapeutic intervention strategies.

Currently, Dr. Hulsebosch is part of the scientific advisory board for both the Neurological Recovery Network and the North American Clinical Trials Network, which are actively involved in advancing clinical trials in spinal cord injury. She serves as scientific advisor to the National Institute of Health for Neuroscience Initiatives, on study section for National Institute of Neurological Diseases and Stroke, on the Craig Neilsen Foundation, the Christopher and Dana Reeves Foundation, the New Jersey Commission for Spinal Cord Injury Research, The Kentucky Initiative for Brain and Spinal Cord Injury Research, The New York Commission for Spinal Cord injury Research and a variety of editorial and review boards for scientific journals. She was a founder and served as Director of Mission Connect from 2005 to 2008 and was the lead for Baylor, UT Houston and UTMB’s involvement during the formative years in the formation of Mission Connect.

How Dr. Hulsebosch’s research relates to Mission Connect

Mission Connect is a multi-institutional research group whose mission is to advance research for recovery after brain and spinal cord injury. This is consistent with the more than 300 publications and presentations from her laboratory. She pioneered the concept of nerve cell process reorganization and the formation of new nerve connections (synaptogenesis) in the spinal cord after injury. She has numerous publications that demonstrate the ability of nerve cells to reorganize after spinal cord injury. In addition, she has several publications examining the ability of nerve fibers to reorganize after brain injury and stroke. Three of the interventions described by her laboratory are in clinical trials, or are in use as an off label clinical strategy to improve function after spinal cord injury. The new discovery of chronic neuroinflammation provides a mechanism for continued research to improve function after spinal cord injury. She served as Mission Connect Director from 2005 to 2008 during which time the Moody Center for Brain and Spinal Cord Injury Research/Mission Connect was established at University Of Texas Medical Branch Galveston; University Of Texas Health Science Center/Mission Connect began its recruitment and development; Baylor recruited three nationally renowned neuroscientists that joined Mission Connect, Project Victory for aggressive rehabilitation and community reintegration for our injured troops returning from the Middle East was initiated and Mission Connect was awarded a 33M grant from the Department of Defense to improve function after mild traumatic brain injury.

Areas of Interest

Research Interests

  • Acute, subacute and chronic models of spinal cord injury
  • traumatic brain injury
  • chronic inflammation
  • neuropathic pain
  • regeneration and repair


Visit the PubMed profile page


  • Hulsebosch, C.E. Mechanisms and treatment strategies for chronic central neuropathic pain after spinal cord injury. Top. Spinal Cord Inj. Rehabil. 8: 76-91, 2003.
  • Hulsebosch, C.E. Central sensitization and pain after spinal cord injury. Sem. Pain Med. 1: 159-170, 2003.

Selected Publications

  • Gliopathy ensures persistent inflammation and chronic pain after spinal cord injury.
  • Hulsebosch CE.
  • Exp Neurol. 2008 Nov;214(1):6-9. doi: 10.1016/j.expneurol.2008.07.016. Epub 2008 Jul 29.
  • Mechanisms of chronic central neuropathic pain after spinal cord injury.
  • Hulsebosch CE, Hains BC, Crown ED, Carlton SM.
  • Brain Res Rev. 2009 Apr;60(1):202-13. doi: 10.1016/j.brainresrev.2008.12.010. Epub 2008 Dec 25. Review.
  • Remote astrocytic and microglial activation modulates neuronal hyperexcitability and below-level neuropathic pain after spinal injury in rat.
  • Gwak YS, Hulsebosch CE.
  • Neuroscience. 2009 Jul 7;161(3):895-903. doi: 10.1016/j.neuroscience.2009.03.055. Epub 2009 Mar 28.
  • Activation of p-38alpha MAPK contributes to neuronal hyperexcitability in caudal regions remote from spinal cord injury.
  • Gwak YS, Unabia GC, Hulsebosch CE.
  • Exp Neurol. 2009 Nov;220(1):154-61. doi: 10.1016/j.expneurol.2009.08.012. Epub 2009 Aug 20.
  • Peripheral and central sensitization in remote spinal cord regions contribute to central neuropathic pain after spinal cord injury.
  • Carlton SM, Du J, Tan HY, Nesic O, Hargett GL, Bopp AC, Yamani A, Lin Q, Willis WD, Hulsebosch CE.
  • Pain. 2009 Dec 15;147(1-3):265-76. doi: 10.1016/j.pain.2009.09.030. Epub 2009 Oct 22.
  • Ionotropic glutamate receptors contribute to maintained neuronal hyperexcitability following spinal cord injury in rats.
  • Leem JW, Kim HK, Hulsebosch CE, Gwak YS.
  • Exp Neurol. 2010 Jul;224(1):321-4. doi: 10.1016/j.expneurol.2010.02.012. Epub 2010 Mar 6.
  • GABA and central neuropathic pain following spinal cord injury.
  • Gwak YS, Hulsebosch CE.
  • Neuropharmacology. 2011 Apr;60(5):799-808. doi: 10.1016/j.neuropharm.2010.12.030. Epub 2011 Jan 7. Review.
  • Neuronal hyperexcitability: a substrate for central neuropathic pain after spinal cord injury.
  • Gwak YS, Hulsebosch CE.
  • Curr Pain Headache Rep. 2011 Jun;15(3):215-22. doi: 10.1007/s11916-011-0186-2. Review.
  • Spatial and temporal activation of spinal glial cells: role of gliopathy in central neuropathic pain following spinal cord injury in rats.
  • Gwak YS, Kang J, Unabia GC, Hulsebosch CE.
  • Exp Neurol. 2012 Apr;234(2):362-72. doi: 10.1016/j.expneurol.2011.10.010. Epub 2011 Oct 21. Review.
  • Special issue on microglia and chronic pain.
  • Hulsebosch CE.
  • Exp Neurol. 2012 Apr;234(2):253-4. doi: 10.1016/j.expneurol.2012.01.009. Epub 2012 Jan 17.
  • Calcium/calmodulin dependent kinase II contributes to persistent central neuropathic pain following spinal cord injury.
  • Crown ED, Gwak YS, Ye Z, Yu Tan H, Johnson KM, Xu GY, McAdoo DJ, Hulsebosch CE.
  • Pain. 2012 Mar;153(3):710-21. doi: 10.1016/j.pain.2011.12.013. Epub 2012 Jan 31.
  • Challenges in the development of rodent models of mild traumatic brain injury.
  • Dewitt DS, Perez-Polo R, Hulsebosch CE, Dash PK, Robertson CS.
  • J Neurotrauma. 2013 May 1;30(9):688-701. doi: 10.1089/neu.2012.2349.
  • Reactive oxygen species contribute to neuropathic pain and locomotor dysfunction via activation of CamKII in remote segments following spinal cord contusion injury in rats.
  • Gwak YS, Hassler SE, Hulsebosch CE.
  • Pain. 2013 Sep;154(9):1699-708. doi: 10.1016/j.pain.2013.05.018. Epub 2013 May 15.
  • Studies of mild traumatic brain injury.
  • Robertson CS, Hulsebosch CE.
  • J Neurotrauma. 2013 May 1;30(9):687. doi: 10.1089/neu.2013.9939. No abstract available.
  • Studies of mild traumatic brain injury.
  • Robertson CS, Hulsebosch CE.
  • J Neurotrauma. 2013 Apr 15;30(8):609. doi: 10.1089/neu.2013.9940. No abstract available.
  • Inflammatory consequences in a rodent model of mild traumatic brain injury.
  • Perez-Polo JR, Rea HC, Johnson KM, Parsley MA, Unabia GC, Xu G, Infante SK, Dewitt DS, Hulsebosch CE.
  • J Neurotrauma. 2013 May 1;30(9):727-40. doi: 10.1089/neu.2012.2650. Epub 2013 May 6.