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dc.creatorXin, D. L.
dc.creatorHadrevi, J.
dc.creatorElliott, M. E.
dc.creatorAmin, M.
dc.creatorHarris, M. Y.
dc.creatorBarr-Gillespie, A. E.
dc.creatorBarbe, Mary
dc.date.accessioned2023-06-22T15:11:20Z
dc.date.available2023-06-22T15:11:20Z
dc.date.issued2017-03-29
dc.identifier.citationXin, D.L., Hadrévi, J., Elliott, M.E. et al. Effectiveness of conservative interventions for sickness and pain behaviors induced by a high repetition high force upper extremity task. BMC Neurosci 18, 36 (2017). https://doi.org/10.1186/s12868-017-0354-3
dc.identifier.issn1471-2202
dc.identifier.doihttp://dx.doi.org/10.34944/dspace/8687
dc.identifier.urihttp://hdl.handle.net/20.500.12613/8723
dc.description.abstractBackground: Systemic inflammation is known to induce sickness behaviors, including decreased social interaction and pain. We have reported increased serum inflammatory cytokines in a rat model of repetitive strain injury (rats perform an upper extremity reaching task for prolonged periods). Here, we sought to determine if sickness behaviors are induced in this model and the effectiveness of conservative treatments. Methods: Experimental rats underwent initial training to learn a high force reaching task (10 min/day, 5 days/week for 6 weeks), with or without ibuprofen treatment (TRHF vs. TRHF + IBU rats). Subsets of trained animals went on to perform a high repetition high force (HRHF) task for 6 or 12 weeks (2 h/day, 3 days/week) without treatment, or received two secondary interventions: ibuprofen (HRHF + IBU) or a move to a lower demand low repetition low force task (HRHF-to-LRLF), beginning in task week 5. Mixed-effects models with repeated measures assays were used to assay duration of social interaction, aggression, forepaw withdrawal thresholds and reach performance abilities. One-way and two-way ANOVAs were used to assay tissue responses. Corrections for multiple comparisons were made. Results: TRHF + IBU rats did not develop behavioral declines or systemic increases in IL-1beta and IL-6, observed in untreated TRHF rats. Untreated HRHF rats showed social interaction declines, difficulties performing the operant task and forepaw mechanical allodynia. Untreated HRHF rats also had increased serum levels of several inflammatory cytokines and chemokines, neuroinflammatory responses (e.g., increased TNFalpha) in the brain, median nerve and spinal cord, and Substance P and neurokinin 1 immunoexpression in the spinal cord. HRHF + IBU and HRHF-to-LRLF rats showed improved social interaction and reduced inflammatory serum, nerve and brain changes. However, neither secondary treatment rescued HRHF-task induced forepaw allodynia, or completely attenuated task performance declines or spinal cord responses. Conclusions: These results suggest that inflammatory mechanisms induced by prolonged performance of high physical demand tasks mediate the development of social interaction declines and aggression. However, persistent spinal cord sensitization was associated with persistent behavioral indices of discomfort, despite use of conservative secondary interventions indicating the need for prevention or more effective interventions.
dc.format.extent17 pages
dc.languageEnglish
dc.language.isoeng
dc.relation.ispartofFaculty/ Researcher Works
dc.relation.haspartBMC Neuroscience, Vol. 18, Iss. 36
dc.relation.isreferencedbyBMC
dc.rightsAttribution CC BY
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectRepetitive loading
dc.subjectWork-related musculoskeletal disorders
dc.subjectUpper extremity
dc.subjectSocial interaction
dc.subjectAggression
dc.subjectMechanical hypersensitivity
dc.subjectVon Frey
dc.subjectInflammation
dc.subjectCytokines
dc.titleEffectiveness of conservative interventions for sickness and pain behaviors induced by a high repetition high force upper extremity task
dc.typeText
dc.type.genreJournal article
dc.description.departmentAnatomy and Cell Biology
dc.relation.doihttps://doi.org/10.1186/s12868-017-0354-3
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.description.schoolcollegeLewis Katz School of Medicine
dc.creator.orcidBarbe|0000-0002-5235-9803
dc.temple.creatorAmin, M.
dc.temple.creatorHarris, M. Y.
dc.temple.creatorBarbe, Mary F.
refterms.dateFOA2023-06-22T15:11:20Z


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