Enhanced recovery of human spinothalamic function is associated with central neuropathic pain after SCI
Section snippets
Acknowledgments
We would like to thank Martina Spiess for providing support in data analyses and the “European Multicenter Study about Spinal Cord Injury” for support in data collection. This study was financially supported by the Swiss National Center of Competence in Research (NCCR) “Neural Plasticity and Repair” and the Foundation for Research at the Medical Faculty, University of Zurich.
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2022, Neural Repair and Regeneration after Spinal Cord Injury and Spine TraumaAssessments of sensory plasticity after spinal cord injury across species
2017, Neuroscience LettersCitation Excerpt :One limitation of this assessment is that dermatomes that have either decreased sensation or are hypersensitive fall into to the same category of impaired sensation. Only a few studies looked at the relation between the ISNCSCI sensory measures and the development of NP [42,43]. Hari et al. found that patients that suffer from NP have enhanced sensory recovery measured by pinprick sensation in comparison to SCI patients that do not develop NP [42].
Phenotypes and predictors of pain following traumatic spinal cord injury: A prospective study
2014, Journal of PainCitation Excerpt :Two studies have looked at early changes in spinothalamic function and the development of central SCI pain, but the results are contradictory. One study found enhanced recovery of the spinothalamic tract (larger improvement in pinprick score within the first year after SCI) in segments just below the neurological level to be associated with central neuropathic pain,11 whereas another study found higher thermal thresholds indicating more spinothalamic tract damage and gradual worsening of spinothalamic tract function below lesion level in patients who eventually developed central pain compared to those who did not.23 Another possible explanation for the later development of below-level pain is that it may indicate slow neuronal degeneration leading to deafferentation neuronal hyperactivity of supraspinal structures as an underlying mechanism for below-level pain.16
Cortical hyperexcitability in response to preserved spinothalamic inputs immediately after spinal cord hemisection
2011, Experimental NeurologyCitation Excerpt :At a finer level of detail, these two pathways can interact at spinal cord level (Hillman and Wall, 1969; Foreman et al., 1976; Giesler et al., 1984; Giesler and Cliffer, 1985; Cliffer and Giesler, 1989) and show certain anatomical convergence both at thalamic level (Ma et al., 1986, 1987; Yen et al., 1991) and at cortical level (Feldmeyer et al., 2005), creating a delicate balance in the somatosensory system that is necessary for the physiological processing of peripheral signals. Selective injury of the dorsal columns or spinothalamic tract disrupts this delicate balance, leading to long-term reorganization of somatotopic maps and neuropathic pain (Miki et al., 2000; Hains and Waxman, 2007; Wang and Thompson, 2008; Graziano and Jones, 2009; Hari et al., 2009; Masri et al., 2009; Wydenkeller et al., 2009). However, the early pathophysiological mechanisms underlying long-term somatosensory alterations after spinal cord injury remain elusive.