Chronic neuropathic pain components in whiplash-associated disorders correlate with metabolite concentrations in the anterior cingulate and dorsolateral prefrontal cortex: a consensus-driven MRS re-examination.

anterior cingulate cortex choline dorsolateral prefrontal cortex glutamate n-acetyl-aspartate neuropathic pain occipital cortex whiplash injury

Journal

Frontiers in medicine
ISSN: 2296-858X
Titre abrégé: Front Med (Lausanne)
Pays: Switzerland
ID NLM: 101648047

Informations de publication

Date de publication:
2024
Historique:
received: 21 03 2024
accepted: 12 07 2024
medline: 19 8 2024
pubmed: 19 8 2024
entrez: 19 8 2024
Statut: epublish

Résumé

Whiplash injury (WHI) is characterised by a forced neck flexion/extension, which frequently occurs after motor vehicle collisions. Previous studies characterising differences in brain metabolite concentrations and correlations with neuropathic pain (NP) components with chronic whiplash-associated disorders (WAD) have been demonstrated in affective pain-processing areas such as the anterior cingulate cortex (ACC). However, the detection of a difference in metabolite concentrations within these cortical areas with chronic WAD pain has been elusive. In this study, single-voxel magnetic resonance spectroscopy (MRS), following the latest MRSinMRS consensus group guidelines, was performed in the anterior cingulate cortex (ACC), left dorsolateral prefrontal cortex (DLPFC), and occipital cortex (OCC) to quantify differences in metabolite concentrations in individuals with chronic WAD with or without neuropathic pain (NP) components. Healthy individuals ( Participants with WAD-NP presented moderate pain intensity and interference compared with the WAD-noNP group. Single-voxel MRS analysis demonstrated a higher glutamate concentration in the ACC and lower total choline (tCho) in the DLPFC in the WAD-NP versus WAD-noNP group, with no intergroup metabolite difference detected in the OCC. Best fit and stepwise multiple regression revealed that the normalised ACC glutamate/total creatine (tCr) ( This study demonstrates that elevated glutamate concentrations within the ACC are related to chronic WAD-NP components, while higher NAA and lower tCho metabolite levels suggest a role for increased neuronal-glial signalling and cell membrane dysfunction in individuals with chronic WAD-NP components.

Identifiants

pubmed: 39156690
doi: 10.3389/fmed.2024.1404939
pmc: PMC11328873
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1404939

Informations de copyright

Copyright © 2024 Pinilla-Fernández, Ríos-León, Deelchand, Garrido, Torres-Llacsa, García-García, Vidorreta, Ip, Bridge, Taylor and Barriga-Martín.

Déclaration de conflit d'intérêts

MV was employed by company Siemens Healthineers. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer DM declared a shared affiliation with the author AB-M to the handling editor at the time of review. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Auteurs

Irene Pinilla-Fernández (I)

Sensorimotor Function Group, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.
Instituto de Investigación Sanitaria de Castilla La Mancha (IDISCAM), Toledo, Spain.
Grupo de Sistemas Complejos, Universidad Politécnica de Madrid, Madrid, Spain.

Marta Ríos-León (M)

Sensorimotor Function Group, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.
Instituto de Investigación Sanitaria de Castilla La Mancha (IDISCAM), Toledo, Spain.

Dinesh Kumar Deelchand (DK)

Department of Radiology, Center for Magnetic Resonance Research, University of Minnesota, Minneapolis, MN, United States.

Leoncio Garrido (L)

Departamento de Química-Física, Instituto de Ciencia y Tecnología de Polímeros (ICTP-CSIC), CSIC, Madrid, Spain.

Mabel Torres-Llacsa (M)

Instituto de Investigación Sanitaria de Castilla La Mancha (IDISCAM), Toledo, Spain.
Servicio de Radiodiagnóstico, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.

Fernando García-García (F)

Instituto de Investigación Sanitaria de Castilla La Mancha (IDISCAM), Toledo, Spain.
Servicio de Radiodiagnóstico, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.

Marta Vidorreta (M)

Siemens Healthineers, Madrid, Spain.

I Betina Ip (IB)

Wellcome Centre for Integrative Neuroimaging, FMRIB, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom.

Holly Bridge (H)

Wellcome Centre for Integrative Neuroimaging, FMRIB, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom.

Julian Taylor (J)

Sensorimotor Function Group, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.
Instituto de Investigación Sanitaria de Castilla La Mancha (IDISCAM), Toledo, Spain.
Harris Manchester College, University of Oxford, Oxford, United Kingdom.

Andrés Barriga-Martín (A)

Instituto de Investigación Sanitaria de Castilla La Mancha (IDISCAM), Toledo, Spain.
Research Group in Spine Pathology, Orthopedic Surgery and Traumatology Unit, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain.
Faculty of Medicine, University of Castilla La Mancha, Toledo, Spain.

Classifications MeSH