Thalamic activity and biochemical changes in individuals with neuropathic pain after spinal cord injury
Neuropathic pain following spinal cord injury is associated with altered thalamic biochemistry, structure and function, which may disturb central processing and play a key role in the persistent experience of pain. There is increasing evidence relating thalamic changes to the generation and/or maint...
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| Published in | Pain (Amsterdam) Vol. 155; no. 5; pp. 1027 - 1036 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article Web Resource |
| Language | English |
| Published |
Philadelphia, PA
Elsevier B.V
01.05.2014
International Association for the Study of Pain Elsevier |
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| Online Access | Get full text |
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| Abstract | Neuropathic pain following spinal cord injury is associated with altered thalamic biochemistry, structure and function, which may disturb central processing and play a key role in the persistent experience of pain.
There is increasing evidence relating thalamic changes to the generation and/or maintenance of neuropathic pain. We have recently reported that neuropathic orofacial pain is associated with altered thalamic anatomy, biochemistry, and activity, which may result in disturbed thalamocortical oscillatory circuits. Despite this evidence, it is possible that these thalamic changes are not responsible for the presence of pain per se, but result as a consequence of the injury. To clarify this subject, we compared brain activity and biochemistry in 12 people with below-level neuropathic pain after complete thoracic spinal cord injury with 11 people with similar injuries and no neuropathic pain and 21 age- and gender-matched healthy control subjects. Quantitative arterial spinal labelling was used to measure thalamic activity, and magnetic resonance spectroscopy was used to determine changes in neuronal variability quantifying N-acetylaspartate and alterations in inhibitory function quantifying gamma amino butyric acid. This study revealed that the presence of neuropathic pain is associated with significant changes in thalamic biochemistry and neuronal activity. More specifically, the presence of neuropathic pain after spinal cord injury is associated with significant reductions in thalamic N-acetylaspartate, gamma amino butyric acid content, and blood flow in the region of the thalamic reticular nucleus. Spinal cord injury on its own did not account for these changes. These findings support the hypothesis that neuropathic pain is associated with altered thalamic structure and function, which may disturb central processing and play a key role in the experience of neuropathic pain. |
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| AbstractList | There is increasing evidence relating thalamic changes to the generation and/or maintenance of neuropathic pain. We have recently reported that neuropathic orofacial pain is associated with altered thalamic anatomy, biochemistry, and activity, which may result in disturbed thalamocortical oscillatory circuits. Despite this evidence, it is possible that these thalamic changes are not responsible for the presence of pain per se, but result as a consequence of the injury. To clarify this subject, we compared brain activity and biochemistry in 12 people with below-level neuropathic pain after complete thoracic spinal cord injury with 11 people with similar injuries and no neuropathic pain and 21 age- and gender-matched healthy control subjects. Quantitative arterial spinal labelling was used to measure thalamic activity, and magnetic resonance spectroscopy was used to determine changes in neuronal variability quantifying N-acetylaspartate and alterations in inhibitory function quantifying gamma amino butyric acid. This study revealed that the presence of neuropathic pain is associated with significant changes in thalamic biochemistry and neuronal activity. More specifically, the presence of neuropathic pain after spinal cord injury is associated with significant reductions in thalamic N-acetylaspartate, gamma amino butyric acid content, and blood flow in the region of the thalamic reticular nucleus. Spinal cord injury on its own did not account for these changes. These findings support the hypothesis that neuropathic pain is associated with altered thalamic structure and function, which may disturb central processing and play a key role in the experience of neuropathic pain.There is increasing evidence relating thalamic changes to the generation and/or maintenance of neuropathic pain. We have recently reported that neuropathic orofacial pain is associated with altered thalamic anatomy, biochemistry, and activity, which may result in disturbed thalamocortical oscillatory circuits. Despite this evidence, it is possible that these thalamic changes are not responsible for the presence of pain per se, but result as a consequence of the injury. To clarify this subject, we compared brain activity and biochemistry in 12 people with below-level neuropathic pain after complete thoracic spinal cord injury with 11 people with similar injuries and no neuropathic pain and 21 age- and gender-matched healthy control subjects. Quantitative arterial spinal labelling was used to measure thalamic activity, and magnetic resonance spectroscopy was used to determine changes in neuronal variability quantifying N-acetylaspartate and alterations in inhibitory function quantifying gamma amino butyric acid. This study revealed that the presence of neuropathic pain is associated with significant changes in thalamic biochemistry and neuronal activity. More specifically, the presence of neuropathic pain after spinal cord injury is associated with significant reductions in thalamic N-acetylaspartate, gamma amino butyric acid content, and blood flow in the region of the thalamic reticular nucleus. Spinal cord injury on its own did not account for these changes. These findings support the hypothesis that neuropathic pain is associated with altered thalamic structure and function, which may disturb central processing and play a key role in the experience of neuropathic pain. There is increasing evidence relating thalamic changes to the generation and/or maintenance of neuropathic pain. We have recently reported that neuropathic orofacial pain is associated with altered thalamic anatomy, biochemistry, and activity, which may result in disturbed thalamocortical oscillatory circuits. Despite this evidence, it is possible that these thalamic changes are not responsible for the presence of pain per se, but result as a consequence of the injury. To clarify this subject, we compared brain activity and biochemistry in 12 people with below-level neuropathic pain after complete thoracic spinal cord injury with 11 people with similar injuries and no neuropathic pain and 21 age- and gender-matched healthy control subjects. Quantitative arterial spinal labelling was used to measure thalamic activity, and magnetic resonance spectroscopy was used to determine changes in neuronal variability quantifying N-acetylaspartate and alterations in inhibitory function quantifying gamma amino butyric acid. This study revealed that the presence of neuropathic pain is associated with significant changes in thalamic biochemistry and neuronal activity. More specifically, the presence of neuropathic pain after spinal cord injury is associated with significant reductions in thalamic N-acetylaspartate, gamma amino butyric acid content, and blood flow in the region of the thalamic reticular nucleus. Spinal cord injury on its own did not account for these changes. These findings support the hypothesis that neuropathic pain is associated with altered thalamic structure and function, which may disturb central processing and play a key role in the experience of neuropathic pain. Neuropathic pain following spinal cord injury is associated with altered thalamic biochemistry, structure and function, which may disturb central processing and play a key role in the persistent experience of pain. There is increasing evidence relating thalamic changes to the generation and/or maintenance of neuropathic pain. We have recently reported that neuropathic orofacial pain is associated with altered thalamic anatomy, biochemistry, and activity, which may result in disturbed thalamocortical oscillatory circuits. Despite this evidence, it is possible that these thalamic changes are not responsible for the presence of pain per se, but result as a consequence of the injury. To clarify this subject, we compared brain activity and biochemistry in 12 people with below-level neuropathic pain after complete thoracic spinal cord injury with 11 people with similar injuries and no neuropathic pain and 21 age- and gender-matched healthy control subjects. Quantitative arterial spinal labelling was used to measure thalamic activity, and magnetic resonance spectroscopy was used to determine changes in neuronal variability quantifying N-acetylaspartate and alterations in inhibitory function quantifying gamma amino butyric acid. This study revealed that the presence of neuropathic pain is associated with significant changes in thalamic biochemistry and neuronal activity. More specifically, the presence of neuropathic pain after spinal cord injury is associated with significant reductions in thalamic N-acetylaspartate, gamma amino butyric acid content, and blood flow in the region of the thalamic reticular nucleus. Spinal cord injury on its own did not account for these changes. These findings support the hypothesis that neuropathic pain is associated with altered thalamic structure and function, which may disturb central processing and play a key role in the experience of neuropathic pain. |
| Author | Rae, C.D. Gustin, S.M. McIndoe, L. Siddall, P.J. Henderson, L.A. Wrigley, P.J. Youssef, A.M. Wilcox, S.L. Edden, R.A.E. |
| AuthorAffiliation | Pain Management Research Institute, Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales, Australia Department of Anatomy and Histology, University of Sydney, Sydney, New South Wales, Australia Neuroscience Research Australia, Randwick, NSW 2031, Australia Sydney Medical School–Northern, University of Sydney, Sydney, New South Wales, Australia Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, MD, USA F.M. Kirby Research Center for Functional MRI, Baltimore, MD, USA Department of Pain Management, HammondCare, Greenwich Hospital, Greenwich, New South Wales, Australia |
| AuthorAffiliation_xml | – name: Pain Management Research Institute, Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales, Australia Department of Anatomy and Histology, University of Sydney, Sydney, New South Wales, Australia Neuroscience Research Australia, Randwick, NSW 2031, Australia Sydney Medical School–Northern, University of Sydney, Sydney, New South Wales, Australia Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, MD, USA F.M. Kirby Research Center for Functional MRI, Baltimore, MD, USA Department of Pain Management, HammondCare, Greenwich Hospital, Greenwich, New South Wales, Australia |
| Author_xml | – sequence: 1 givenname: S.M. surname: Gustin fullname: Gustin, S.M. email: sagustin@anatomy.usyd.edu.au organization: Pain Management Research Institute, Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales, Australia – sequence: 2 givenname: P.J. surname: Wrigley fullname: Wrigley, P.J. organization: Pain Management Research Institute, Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales, Australia – sequence: 3 givenname: A.M. surname: Youssef fullname: Youssef, A.M. organization: Department of Anatomy and Histology, University of Sydney, Sydney, New South Wales, Australia – sequence: 4 givenname: L. surname: McIndoe fullname: McIndoe, L. organization: Pain Management Research Institute, Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales, Australia – sequence: 5 givenname: S.L. surname: Wilcox fullname: Wilcox, S.L. organization: Department of Anatomy and Histology, University of Sydney, Sydney, New South Wales, Australia – sequence: 6 givenname: C.D. surname: Rae fullname: Rae, C.D. organization: Neuroscience Research Australia, Randwick, NSW 2031, Australia – sequence: 7 givenname: R.A.E. surname: Edden fullname: Edden, R.A.E. organization: Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, MD, USA – sequence: 8 givenname: P.J. surname: Siddall fullname: Siddall, P.J. organization: Sydney Medical School–Northern, University of Sydney, Sydney, New South Wales, Australia – sequence: 9 givenname: L.A. surname: Henderson fullname: Henderson, L.A. organization: Department of Anatomy and Histology, University of Sydney, Sydney, New South Wales, Australia |
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| Snippet | Neuropathic pain following spinal cord injury is associated with altered thalamic biochemistry, structure and function, which may disturb central processing... There is increasing evidence relating thalamic changes to the generation and/or maintenance of neuropathic pain. We have recently reported that neuropathic... |
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| SubjectTerms | Adult Aged Aspartic Acid - analogs & derivatives Aspartic Acid - metabolism Aspartic Acid/analogs & derivatives/metabolism Biological and medical sciences Female Functional Neuroimaging Fundamental and applied biological sciences. Psychology Gamma amino butyric acid Humans Life sciences Magnetic Resonance Imaging Magnetic Resonance Spectroscopy Male Medical sciences Middle Aged MRI Nervous system involvement in other diseases. Miscellaneous Neuralgia - etiology Neuralgia - metabolism Neuralgia - physiopathology Neuralgia/etiology/metabolism/physiopathology Neurology Neuropathic pain Pain Measurement Sciences du vivant Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors Spin Labels Spinal Cord Injuries - complications Spinal Cord Injuries - metabolism Spinal Cord Injuries - physiopathology Spinal Cord Injuries/complications/metabolism/physiopathology Spinal cord injury Thalamus Thalamus - metabolism Thalamus - physiopathology Thalamus/metabolism/physiopathology Vertebrates: nervous system and sense organs |
| Title | Thalamic activity and biochemical changes in individuals with neuropathic pain after spinal cord injury |
| URI | https://dx.doi.org/10.1016/j.pain.2014.02.008 https://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00006396-201405000-00026 https://www.ncbi.nlm.nih.gov/pubmed/24530612 https://www.proquest.com/docview/1516722050 http://orbi.ulg.ac.be/handle/2268/235984 |
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