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We hypothesized that evoked pain can modulate the muscle compound action potential (CMAP) obtained by DMS possibly due to changes in muscle fibre excitability.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_j.sjpain.2014.05.028_s_002\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Pain was evoked by intramuscular infusion of hypertonic saline in 50 men. Ten control subjects were infused with isotonic saline. The infusions were given distal to the motor end plate region of the dominant brachial biceps muscle (BBM) in a double-blind manner. The nerve CMAP was obtained by stimulating the musculocutaneous nerve and recording from the BBM using surface-electrodes. Muscle CMAPs were obtained by direct muscle stimulation with subdermal electrodes placed subcutaneously in the distal third of the muscle. A stimuli-response curve of the amplitudes from muscle CMAP was obtained by stimulating from 10 to 90 mA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_j.sjpain.2014.05.028_s_003\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      There was a decrease of the nerve CMAP amplitudes after infusion of isotonic saline (from 13.78mV to 12.16 mV),\n                      <jats:italic>p<\/jats:italic>\n                      -value 0.0007 and of hypertonic saline (from 13.35 mV to 10.85 mV),\n                      <jats:italic>p<\/jats:italic>\n                      -value 0.0000. The percent decrease from before to after infusion was larger in the hypertonic saline group (19.37%) compared to the isotonic saline group (12.18%),\n                      <jats:italic>p<\/jats:italic>\n                      -value 0.025.\n                    <\/jats:p>\n                    <jats:p>\n                      There was a decrease of the amplitudes of the muscle CMAP after infusion of both isotonic (at 90 mA from 13.84mV to 10.32 mV,\n                      <jats:italic>p<\/jats:italic>\n                      value 0.001) and of hypertonic saline (at 90 mA from 14.01 mV to 8.19 mV,\n                      <jats:italic>p<\/jats:italic>\n                      value 0.000). The percent decrease was larger in the hypertonic saline group compared to the isotonic saline group for all the stimulations intensities. At 90 mA we saw a 42% decrease in the hypertonic saline group and 24.5% in the isotonic saline group,\n                      <jats:italic>p<\/jats:italic>\n                      value 0.005.\n                    <\/jats:p>\n                    <jats:p>There were no changes in conduction velocity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_j.sjpain.2014.05.028_s_004\">\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>We found a larger amplitude decrease of the muscle and nerve potentials following hypertonic saline infusion compared with that of isotonic saline. We suggest that this deferential outcome of hypertonic saline on muscle CMAP may be linked to the nociceptive effect on muscle fibre membrane excitability.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_j.sjpain.2014.05.028_s_005\">\n                    <jats:title>Implications<\/jats:title>\n                    <jats:p>The study supplies with some evidence of the peripheral effect of muscle pain. However, further trials with other nociceptive substances such as capsaicin should be performed.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1016\/j.sjpain.2014.05.028","type":"journal-article","created":{"date-parts":[[2014,6,16]],"date-time":"2014-06-16T17:14:06Z","timestamp":1402938846000},"page":"55-60","update-policy":"https:\/\/doi.org\/10.1016\/elsevier_cm_policy","source":"Crossref","is-referenced-by-count":1,"title":["Modulation of the muscle and nerve compound muscle action potential by evoked pain"],"prefix":"10.1515","volume":"6","author":[{"given":"L.","family":"Duez","sequence":"first","affiliation":[{"name":"Danish Pain Research Center , Aarhus University Hospital , Aarhus , Denmark"},{"name":"Department of Neurophysiology , Aarhus University Hospital , Aarhus , Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.","family":"Qerama","sequence":"additional","affiliation":[{"name":"Department of Neurophysiology , Aarhus University Hospital , Aarhus , Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.S.","family":"Jensen","sequence":"additional","affiliation":[{"name":"Danish Pain Research Center , Aarhus University Hospital , Aarhus , Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Fuglsang-Frederiksen","sequence":"additional","affiliation":[{"name":"Department of Neurophysiology , Aarhus University Hospital , Aarhus , Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"374","published-online":{"date-parts":[[2015,1,1]]},"reference":[{"key":"2025120909542073977_j_j.sjpain.2014.05.028_ref_001","doi-asserted-by":"crossref","unstructured":"Graven-Nielsen T, Lund H, Arendt-Nielsen L, Danneskiold-Samsoe B, Blid-dal H. 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