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    Chronic neuropathic pain: It’s about the rhythm

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    Access Status
    Open access
    Authors
    Alshelh, Z.
    Harrington, Flavia
    Youssef, A.M.
    Reeves, J.M.
    Macey, P.M.
    Russell Vickers, E.
    Peck, C.C.
    Murray, G.M.
    Henderson, L.A.
    Date
    2016
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Alshelh, Z. and di Pietro, F. and Youssef, A.M. and Reeves, J.M. and Macey, P.M. and Russell Vickers, E. and Peck, C.C. et al. 2016. Chronic neuropathic pain: It’s about the rhythm. Journal of Neuroscience. 36 (3): pp. 1008-1018.
    Source Title
    Journal of Neuroscience
    DOI
    10.1523/JNEUROSCI.2768-15.2016
    ISSN
    0270-6474
    Faculty
    Faculty of Health Sciences
    School
    School of Pharmacy and Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/79568
    Collection
    • Curtin Research Publications
    Abstract

    © 2016 The Authors. The neural mechanisms underlying the development and maintenance of chronic neuropathic pain remain unclear. Evidence from human investigations suggests that neuropathic pain is associated with altered thalamic burst firing and thalamocortical dysrhythmia. Additionally, experimental animal investigations show that neuropathic pain is associated with altered infra-slow (<0.1 Hz) frequency oscillations within the dorsal horn and somatosensory thalamus. The aim of this investigation was to determine whether, in humans, neuropathic pain was also associated with altered infra-slow oscillations within the ascending “pain” pathway. Using resting-state functional magnetic resonance imaging, we found that individuals with orofacial neuropathic pain have increased infra-slow oscillatory activity throughout the ascending pain pathway, including within the spinal trigeminal nucleus, somatosensory thalamus, thalamic reticular nucleus, and primary somatosensory cortex. Furthermore, these infra-slow oscillations were temporally coupled across these multiple sites and occurred at frequencies similar to calcium waves in activated astrocytes. The region encompassing the spinal trigeminal nucleus also displayed increased regional homogeneity, consistent with a local spread of neural activity by astrocyte activation. In contrast, no increase in oscillatory behavior within the ascending pain pathway occurred during acute noxious stimuli in healthy individuals. These data reveal increased oscillatory activity within the ascending pain pathway that likely underpins increased thalamocortical oscillatory activity, a self-sustaining thalamocortical dysrhythmia, and the constant perception of pain.

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