PDF Publication Title:
Text from PDF Page: 026
CHAPTER 1 response to noxious stimuli (hyperalgesia) or pain response to innocuous mechanical or thermal stimuli (allodynia) (Finnerup et al., 2009). Both allodynia and hyperalgesia exist above the level of the injury, at the level of the injury (2-4 segments surrounding the level of the injury), and below the level of the injury (Masri and Keller, 2012). Many studies have endeavoured to understand the mechanism behind chronic pain conditions following spinal cord injury (reviewed in Finnerup et al., 2009; reviewed in Masri and Keller, 2012). Changes in the spinal cord, and at the supraspinal level, have been associated with the development and the maintenance of neuropathic pain. Some of the mechanisms will be explored below. Changes at the spinal cord level are mostly due to central sensitization and spinal cord plasticity (Zhuo et al., 2011). Hyperexcitable neurons arise from both increased excitability and decreased inhibition. Increased excitability may result from ionic imbalance which leads to depolarization (Gwak et al., 2012). Extracellular glutamate accumulation (McAdoo et al., 1999) and reduced GABA inhibition (Drew et al., 2004; Drew et al., 2001) may also contribute to increased neural activity. Apart from neuronal changes, both microglia and astrocytes have been suggested to play essential roles in this process, as they are responsible for recycling neurotransmitters and monitoring cellular environments in the spinal cord (Gwak et al., 2012). Some cytokines and molecules secreted by microglia and astrocytes, e.g. IL1β, TNFα, and NO have been suggested to modulate both presynaptic and postsynaptic terminals to enhance synaptic communication between neurons (Hulsebosch et al., 2009). Abnormal connections resulting from intraspinal sprouting during regeneration has been demonstrated. Primary tactile afferents form connections with demyelinated spinothalamic tract, thus leading to the generation of pain sensation from normally innocuous stimuli (Christensen and Hulsebosch, 1997). Maladaptive forms of activity- dependent plasticity, through alterations of NMDA and AMPA receptors, are also a major player in neuropathic pain (Zhuo et al., 2011). In fact, a contusion injury induces more pain than a hemi- section injury (Christensen and Hulsebosch, 1997). This again suggests that intraspinal sprouting in tracts that remained in a contusion injury, maybe largely responsible for the development of pain. Changes at the supraspinal level, that include anatomical and physiological alterations, have also been observed in the thalamus and the cortex (Gustin et al., 2010; Wrigley et al., 2009). The degrees of the changes in these regions are correlated with the intensity of ongoing pain. Using magnetic resonance imaging, Pattany and colleagues (2002) found that decreased N-acetyl and increased myo-inositol in the thalamic region were correlated with pain in patients following spinal cord injury. N-acetyl is a marker reflecting dysfunction of inhibitory neurons, while myo- inositol is a marker for glial activation (Finnerup et al., 2009). Disinhibition in the thalamus is also thought to alter the firing properties of the neurons, leading to spontaneous firing and evoked bursts (Weng et al., 2000). Thalamic microglial activation through cysteine-cysteine chemokine ligand 21 has been associated with neuropathic pain following spinal cord injury (Zhao et al., 12PDF Image | Effects of Red Light Treatment on Spinal Cord Injury
PDF Search Title:
Effects of Red Light Treatment on Spinal Cord InjuryOriginal File Name Searched:
Thesis_Di Hu_final.pdfDIY PDF Search: Google It | Yahoo | Bing
Cruise Ship Reviews | Luxury Resort | Jet | Yacht | and Travel Tech More Info
Cruising Review Topics and Articles More Info
Software based on Filemaker for the travel industry More Info
The Burgenstock Resort: Reviews on CruisingReview website... More Info
Resort Reviews: World Class resorts... More Info
The Riffelalp Resort: Reviews on CruisingReview website... More Info
CONTACT TEL: 608-238-6001 Email: greg@cruisingreview.com (Standard Web Page)