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    The relationship between thalamic GABA content and resting cortical rhythm in neuropathic pain

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    Fulltext not available
    Authors
    Di Pietro, Flavia
    Macey, P.M.
    Rae, C.D.
    Alshelh, Z.
    Macefield, V.G.
    Vickers, E.R.
    Henderson, L.A.
    Date
    2018
    Type
    Journal Article
    
    Metadata
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    Citation
    Di Pietro, F. and Macey, P.M. and Rae, C.D. and Alshelh, Z. and Macefield, V.G. and Vickers, E.R. and Henderson, L.A. 2018. The relationship between thalamic GABA content and resting cortical rhythm in neuropathic pain. Human Brain Mapping. 39 (5): pp. 1945-1956.
    Source Title
    Human Brain Mapping
    DOI
    10.1002/hbm.23973
    ISSN
    1065-9471
    Faculty
    Faculty of Health Sciences
    School
    School of Pharmacy and Biomedical Sciences
    Funding and Sponsorship
    http://purl.org/au-research/grants/nhmrc/G160279
    http://purl.org/au-research/grants/nhmrc/1091415
    URI
    http://hdl.handle.net/20.500.11937/79559
    Collection
    • Curtin Research Publications
    Abstract

    © 2018 Wiley Periodicals, Inc.

    Recurrent thalamocortical connections are integral to the generation of brain rhythms and it is thought that the inhibitory action of the thalamic reticular nucleus is critical in setting these rhythms. Our work and others' has suggested that chronic pain that develops following nerve injury, that is, neuropathic pain, results from altered thalamocortical rhythm, although whether this dysrhythmia is associated with thalamic inhibitory function remains unknown. In this investigation, we used electroencephalography and magnetic resonance spectroscopy to investigate cortical power and thalamic GABAergic concentration in 20 patients with neuropathic pain and 20 pain-free controls. First, we found thalamocortical dysrhythmia in chronic orofacial neuropathic pain; patients displayed greater power than controls over the 4–25 Hz frequency range, most marked in the theta and low alpha bands. Furthermore, sensorimotor cortex displayed a strong positive correlation between cortical power and pain intensity. Interestingly, we found no difference in thalamic GABA concentration between pain subjects and control subjects. However, we demonstrated significant linear relationships between thalamic GABA concentration and enhanced cortical power in pain subjects but not controls. Whilst the difference in relationship between thalamic GABA concentration and resting brain rhythm between chronic pain and control subjects does not prove a cause and effect link, it is consistent with a role for thalamic inhibitory neurotransmitter release, possibly from the thalamic reticular nucleus, in altered brain rhythms in individuals with chronic neuropathic pain.

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