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CRITICALILLNESSNEUROMYOPATHYAbbreviationsHISTORICALREVIEWStudiesaboutAetiologyvariouslyAdaptedwithpermissionfromBolton.AdaptedwithpermissionfromBolton25.Figure.3Schematic,theoreticalpresentationofdisturbancesinthemicrocirculationtovariousorgans,includingbrain,peripheralnerve,andmuscle,inSIRS.Incidence50%–70%SIRS20%–50%ICU•Weaknessoflimbandrespiratorymuscle•Tendonreflexesabsentordecrease•Distallosstopain,temperature,andvibrationThediagnosticcriteriaforCIPareshowninfollowingTableDeclineintheCMAPamplitudefirstly(Fig.4)DclineintheSNAPamplitudeMotorunitpotentialsmaybereducedinnumberSingle-fiberEMGindicatedysfunctionofterminalmotoraxonsMeasurementofcompoundthenarmuscleactionpotentialsattheonsetofsepsis(A)and3weekslater(B).Peripheralaxonaldegeneration.ModeratelossofdorsalrootganglioncellsCentralchromatolysisofanteriorhorncellsNoinflammationintheperipheralnervoussystemAxonalvariantsofGuillain–Barre′syndromeDevelopearlierOftenassociatedwithCJinfectionAbnormalcerebralspinalfluidTreatmentofsepsisandmultipleorgandysfunctionsyndromeManagementofdifficultyinweaningfromtheventilatorAttemptsatdirecttreatmentofCIP(stillunproven)PhysiotherapyandrehabilitationRecoverydependsonthedistanceRecoveryforweeksinmildcasesandmonthsinseverecasesSlowingofnerveconductionmayhaveapoorprognosisIncidenceAtleastone-thirdofICUpatients(treatedforstatusasthmaticus)In7%ofpatientsaftertransplantationDiagnosticcriteriaofCIM●SNAPamplitudes80%ofthelowerlimitofnormal●NeedleEMGwithshort-duration,low-amplitudeMUPswithearlyornormalfullrecruitment,withorwithoutfibrillationpotentials●AbsenceofadecrementalresponseonrepetitivenervestimulationNerveconductionstudiesLow-amplitudeCMAPsLongdurationCMAPsNormalSNAPsPhrenicnerveconductionnormallatenciesdiaphragmCMAPamplitudesreduceFeaturesofthehistopathologyinthickfilamentmyosinloss(Fig.5)Electronmicroscopyrevealsselectivelossofthick(myosin)filaments(Fig.6)InflammatorychangesareconspicuouslyabsentFigure.5Musc