This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
Ulnar tunnel syndrome (UTS) is anuncommon formofulnarentrapmentneuropathyatthewristthatcanbecausedbyseveralintrinsicorextrinsicfactors.1–4)Areviewoftheliterature indicated the following possible causes of UTS:ganglions,5–16) traumaticneuropathies,8) anomalousmuscleor fibrous bands,10,17,18) ulnar artery thromboses or aber-rancy,7,10)wristfracture,5)carpalosteoarthritis,8)pisohamatearch,11) and idiopathic.3) Most previous reports have dealtwith a small number of cases,5–7,11–18) and we previously
reportedfivecasesofUTScausedbyganglion.16) In1861,Guyon19)reportedtheanatomyoftheulnarareaandpredict-ed thatproblemscouldoccurwithentrapmentof theulnarnerve,andin1908Hunt20)describedthreepatientswithoc-cupationalneuritis.Seddon5)andRichmond6)reportedulnarnerve palsy caused by a carpal ganglion. In 1965,Dupontet al.7) used the term ulnar tunnel syndrome and reportedfourcases.AnexactclinicaldiagnosisofUTSanddetectionofthelocationofthecausativelesionaredifficult,andelec-trophysiologicaldiagnosismayhelptoconfirmthediagno-sis.2–4,11,13–16,21–25)Thepurposesofthisstudyweretoassess
Progress in Rehabilitation Medicine 2021; Vol. 6, 20210010doi: 10.2490/prm.20210010
Objectives: The purposes of this study were to assess the clinical features of ulnar tunnelsyndrome(UTS)andtoinvestigatethediagnosticvalueofnerveconductionmeasurementsforUTS.Methods:EighteenpatientswithUTSwerereviewedretrospectively.Fifteenpatientshadintrinsicmuscleatrophyandmotorweakness,and15hadnumbnesswithhypesthesia.Thecom-poundmuscle action potentials (CMAPs) from thefirst dorsal interosseous (FDI)muscle andtheabductordigitiminimi(ADM)muscleandthesensorynerveactionpotential(SNAP)fromthelittlefingerwererecordedandanalyzed.Allpatientsunderwentulnartunnelreleasesurgeryand neurolysis. Static two-point discrimination test results and pinch strengthswere assessedbeforeandaftersurgery.Results:Beforesurgery,FDI-CMAPwasrecordedin17patients,andADM-CMAPin16,andallshoweddelayedlatencyand/orlowamplitude.SNAPwasrecordedineightpatientsandtwoshoweddelayedlatency.Thecausesofulnarnervelesionswereganglioninfivepatients,traumaticadhesioninfour,ulnararteryaberrancyinfour,pisohamatearchinthree,anomalousmuscleinone,andulnarveinvarixinone.Thesitesofthelesionswereinzone1oftheulnartunnelanatomyin12patients,inzone2in2,andinzones1and2in4.Aftersurgery,allpatientsobtainedrecoveryofmotorfunctionandsensation;however,postoperativeFDI-CMAPandADM-CMAPdidnotimprovetothenormalrange.Conclusions:ThecausesofUTSwereganglion,traumaticadhesion,ulnararteryaberrancy,andpisohamatearch.BothFDI-CMAPandADM-CMAPwerevaluableforelectrophysiologicaldiagnosisofUTS.
ORIGINAL ARTICLEClinical Features of Ulnar Tunnel Syndrome and the
Diagnostic Value of Nerve Conduction MeasurementsShingo Nobuta, MD, PhD a Hiroshi Okuno, MD, PhD a Taku Hatta, MD, PhD a Ryo Sato, MD, PhD a
Eighteenhandsfrom18patientswithUTStreatedbetweenMay2008andJuly2016werereviewedafterameanfollow-upof11months(range,5–54months).Detailsofthe18casesareshowninTable 1.Theagesofthepatients(8menand10women)atsurgeryrangedfrom33to80years,withameanageof53years.Therightsidewasaffected in14patients,and the dominant extremity was involved in 12 patients.Themeandurationofsymptomswas9months(range,1–84months).UTSwasdiagnosedbasedonclinical symptoms,electrophysiological evaluations, and magnetic resonanceimaging (MRI) findings. Written informed consent wasobtained from each patient. All patients except for three(cases12,13, and17)hadmotorweakness andatrophyofthe intrinsicmuscleswith a positive Froment’s sign and aclawfingerdeformityofthelittlefinger.Fifteenpatientshadnumbness and hypesthesia in the ulnar nerve distribution;hypesthesiawasseenonlyonthepalmarsideinsixpatients
andonboth thepalmaranddorsalsides innine(Table 1).ATinel-likesignattheulnartunnelwasnotseeninanyofthesepatients.Theintrinsicmusclesincludedthefirstdorsalinterosseous(FDI)and theabductordigitiminimi(ADM).Theresultsofthestatictwo-pointdiscrimination(TPD)testonthelittlefingerrangedfrom5to45mm,withameanof19.6mm.Thepulppinchstrengthrangedfrom0to4.2kg,with amean of 2.1kg (Table 2). T1-weightedMRI of thewrist in 17 patients demonstrated a soft tissue mass in 5patients16) (cases12,14–16,and18),ahigh-signalarea in8(cases1–4,6,8,9,and17),andnormalfindingsin4(cases5,7,10,and13).Nerve conductionmeasurements were performed before
and after surgery.The compoundmuscle action potentials(CMAPs) from the FDI and ADM and the sensory nerveactionpotential(SNAP)fromthelittlefingerwererecordedandanalyzed.WeusedaNicoletVikingelectromyographysystem(NicoletInstruments,Madison,WI,USA)anda10-mmsilverdisc.Thepalmarskintemperaturewasnotallowedto fall below 32°C. FDI-CMAP and ADM-CMAP wererecordedbysupramaximalstimulationoftheulnarnerveatthewrist.Thestimulusdurationwas0.2–0.5ms.SNAPwas
2 Nobuta S, et al: Clinical Features of Ulnar Tunnel Syndrome
1. 34 F L 7m p,d 40 0 6 35 0.32. 38 M R 1 m p,d 15 0 6 5 2.03. 36 M R 2 m p,d 20 2.8 6 5 4.54. 41 F R 84 m none 5 2.5 13 5 3.35. 80 F R 5 m p,d 45 1.8 17 10 3.26. 33 F R 8 m p,d 15 2.6 9 7 3.47. 76 F R 2 m p,d 30 0.8 6 10 3.48. 68 M L 5 m p,d 30 1.5 8 7 3.59. 57 M R 5 m p,d 10 2.4 54 7 4.210. 44 F R 24 m p 15 2.3 7 7 3.511. 58 M R 1 m p 40 2.8 10 15 4.512. 54 F R 1 m p 10 4.2 12 5 4.513. 61 M R 5 m p,d 25 4.2 48 10 4.514. 45 F R 5 m p 10 2.0 5 5 4.015. 56 F L 3 m p 5 0.5 7 5 3.616. 66 F L 2 m none 7 1.3 10 5 4.217. 64 M R 3 m p 25 4.0 7 20 7.018. 56 M R 1 m none 5 2.1 6 5 7.4
recordedwithringelectrodesbyminimalstimulationoftheulnarnerveatthewrist.Accordingtothemeasurementsfor20healthysubjectsatourinstitute,themean±2SDindicatedthe normal values of latency and amplitude. The normalvalueswere:FDI-CMAPlatency<4.2mswithanamplitude>6.6mV,ADM-CMAPlatency<2.9mswithanamplitude>5.3mV,andSNAPpeaklatency<3.5mswithanamplitude>3.4μV.Wediagnoseddelayed latencyand lowamplitudeforCMAPsandSNAPbasedonthesecriteria.Furthermore,toruleoutcubitaltunnelsyndrome,FDI-CMAPandADM-CMAPwererecordedbystimulatingtheulnarnerveattheelbowtoconfirmnoconductiondelayatthecubitaltunnel.Surgerywasindicatedwhenmotorweaknessandatrophy
of the intrinsic muscles were present or there was severenumbnessorpainintheulnarnervedistribution(cases12,13,and17).Allpatientsunderwentulnartunnelreleasebysurgicaldivisionofthevolarcarpalligamentandulnarnerveneurolysis with release of the pisohamate arch (tendinousarch).Atsurgery,weconfirmedthesiteofthelesionwithintheulnartunnelandclassifiedtheminto3zones.12)Zone1istheareaproximaltothebifurcationoftheulnarnerve,zone2encompassesthemotorbranchofthenerveafterbifurcation,andzone3surroundsthesuperficialorsensorybranchoftheulnarnerve.Aspartoftheoutpatientrehabilitationprogram,after surgery,patientswere instructed toperform thepulppinch motion exercise under the supervision of a physio-therapisttwiceaweekfor4weeks.StaticTPDtestresultsonthelittlefinger,thepinchstrength,andFroment’ssignwereevaluatedaftersurgery.Thepresenceofcomplicationssuchasinfection,hematoma,andnerveinjurywerealsoassessed.This research passed the Tohoku Rosai Hospital Ethics
Committee review (approval number Tohoku-Rin 20–20).ThedatawereanalyzedusingStudent’st-testandtheMann-Whitney U test. P values less than 0.05 were consideredstatisticallysignificant.
RESULTS
Before surgery, FDI-CMAPwas recorded in 17 patientsbutwasunrecordablein1,andADM-CMAPwasrecordedin16patientsbutwasunrecordable in1 (Tables 2 and 3).FDI-CMAP showed delayed latency in 14 patients (mean:6.7ms) and low amplitude in 16 (mean: 1.6mV), whereasADM-CMAPrevealeddelayedlatencyin14patients(mean:5.1ms)andlowamplitudein16(mean:1.3mV).SNAPwasrecordedineightpatientsandtwoshoweddelayedlatency.At surgery, the causes of ulnar nerve compression wereganglion infivepatients, traumaticadhesion in four,ulnararteryaberrancy(aberrantbranch)infour,pisohamatearchinthree,anomalousmuscleinone,andulnarveinvarixinone. A ganglion rising from the triquetrohamate joint infivepatientswastracedtoitsoriginandexcised.Histologicexaminationconfirmedthediagnosisofganglion.Traumaticadhesioninfourpatientswascausedbyblunt trauma.Thepisohamatearchwascut,andtheanomalousmusclelocatedatthevolarcarpalligamentasapalmarislongusmusclewasexcised.Theaberrantulnararterybranchandtheulnarveinvarixwereexcised.Thesiteofcompressionwasinzone1in12cases,zone2in2,andzones1and2in4,whereastherewasnocaseofcompressioninzone3(Table 3).Infection,hematoma, and nerve injury are possible complications ofsurgeryforUTS,buttherewerenocomplicationsinour18
patients.After surgery, all patients recoveredmotor function and
sensation.ThemeanTPDimprovedfrom19.6to9.3mm(P<0.05), and themeanpinch strength increased from2.1to3.9kgatfinalfollow-up(P<0.001,Table 3).Asaresultofrehabilitation, themean pinch strength increased to 3.1kg(SD1.4)at2monthsaftersurgery(P<0.05).Exceptforcases1and17,patients showedanegativeFroment’s signat thefinal follow-up. Evaluation of postoperative FDI-CMAPshowed a shortening of latency (mean: 4.6ms, P <0.02)andanincreaseinamplitude(mean:3.1mV).PostoperativeADM-CMAPalso revealedashorteningof latency (mean:3.7ms)andanincreaseofamplitude(mean:2.8mV).FDI-CMAPlatencyrecoveredtothenormalrangeinsixpatientsandtheamplituderecoveredinthree,whereasADM-CMAPlatencyimprovedtothenormalrangeinthreepatientsandtheamplituderecoveredintwo(Tables 2 and 3).Inalmostallcases, residualdelayed latencyand lowamplitudewereseenatthefinalfollow-up.
Case PresentationA 45-year-old right-hand-dominant woman (case 14)
presented with a 5-month history of onset and intrinsicweaknessofherrighthand.Therighthandshowedintrinsicmuscle atrophy and weakness with a positive Froment’ssign and clawing of the little finger. Mild numbness andhypesthesiawereevidentinthelittlefingerandringfinger.TPDwas10mm,andthepinchstrengthwas2.0kg.AxialT1-weightedMRIshowedacysticmass lesionat theulnartunnel (Fig. 1). FDI-CMAP exhibited markedly delayedlatency and low amplitude (Fig. 2A), and ADM-CMAPalso showeddelayed latency and lowamplitude (Fig. 3A).Incontrast,SNAPindicatednormal latencyandamplitude(Fig. 4).Intra-operatively,afterdivisionofthevolarcarpalligament, a22/14/10mmganglionwas found tobemainlycompressing themotorbranchof theulnarnerve in zones1 and 2 (Fig. 5A). The ganglion, which arose from thetriquetrohamatejoint(Fig. 5B),wasexcised,andhistologyconfirmedthediagnosis(Fig. 6).Fivemonthsaftersurgery,motorfunctionandsensationhadrecoveredandthepatienthad a pinch strength of 4.0kg and a TPD of 5mm; FDI-
4 Nobuta S, et al: Clinical Features of Ulnar Tunnel Syndrome
The ulnar tunnel is anatomically classified into threezones12): zone 1 is the area proximal to the bifurcation ofthe ulnar nerve, zone 2 encompasses themotor branch oftheulnarnerve(exceptthebranchtotheADM)afterithas
bifurcated,andzone3surroundsthesuperficialorsensorybranchoftheulnarnerve.Dependingonthesiteofcompres-sion,clinically, thelesionmaybeinthemotor,sensory,ormixedbranch,15)whereas thesensorybranchon thedorsalulnarsideisnormalinUTS.4)However,ifparesthesiaisseenon the dorsal ulnar side of the hand, the likely lesion siteis the cubital tunnel.4) In our series, compression involvedzone1in16cases(89%;12casesinzone1onlyand4casesinzones1and2)andzone2in6cases(2casesinzone2onlyand4casesinzones1and2).Forthetwocaseswithcompressioninzone2only,case4showednosensorylossand case 15 showed palmar side hypesthesia.Hypesthesia
Fig. 2. FDI data for case 14. (A) Preoperatively, FDI-CMAPlatencywas12.6mswithanamplitudeof0.1mV.(B)Fivemonthsaftersurgery,latencywas5.3mswithanamplitudeof4.0mV.
Fig. 3. ADMdata for case14. (A)Preoperatively,ADM-CMAP latencywas 11.8mswith an amplitude of 0.1mV.(B)Fivemonthsafter surgery, latencywas3.9mswithanamplitudeof4.4mV.
wasseenonlyon thepalmarside insixpatients,andbothonthepalmaranddorsalsides inninepatients.Thesehet-erogeneousfindingsunderlinethefactthatanexactclinicaldiagnosisofUTSanddetectionofthelocationofthelesionare often difficult.A possible explanation for the nine pa-tientswho had hypesthesia both on the palmar and dorsalsides is the presence of an aberrant dorsal sensory branchoftheulnarnervewhichdivergedwiththepalmarsensorybranchintheulnartunnel.Murataetal.3)reportedthat90%ofcaseswithUTSwereinzone1.Apreviousreportstated
thatulnarnervelesioninzones1and2arelikelycausedbyganglionsorfracturesofthehamate,andthatlesionsinzone3arecausedbyvascularlesionsresultingfromthrombosisor aneurysm.12)However, inour series, the causesof zone1lesionswereganglions,ulnararteryaberrancy,traumaticadhesion,anomalousmuscle,andulnarveinvarix.Murataetal.3)statedthatsurgicalexplorationistheonlyreliablewaytoclarifythesiteofcompression.Theexpectedtheoreticalsymptomsofcompressionsinthe
Fig. 6. Photomicrograph(hematoxylin-eosinstain,originalmagnification×20)showingtheganglioncystwithathick-walled cystic space and focal myxoid change in the sur-roundingmatrixincase14.
amplitude.OftheeightpatientswhounderwentSNAP,theresults were normal in six (Table 3). Consequently, bothFDI-CMAPandADM-CMAPwerevaluable foradefiniteelectrodiagnosisofUTS;however,SNAPwasnotusefulforconfirmingthediagnosis.Cases12,13,and17showedad-equatepinchstrengths(4.2,4.2,and4.0kg,respectively),butcases13and17hadlowFDI-CMAPamplitudes.Thesetwocasesoriginallyhadadequatepinchstrengthsonthenormalside(5.4and5.2kg,respectively);therefore,thedecreaseinpinchstrengthbeforesurgeryandrehabilitationwassmall.Surgerywasindicatedforthesecaseswithseverenumbnessandpainintheulnarnervedistribution.Lumbrical-interossei motor studies21) and short segment
incrementalstudies (SSIS, inchingmethod)ofFDI-CMAPhavebeenreportedandindicatedthatSSISwasvaluablefordiagnosisofthepreciselocalizationofUTS.22–25)Neverthe-less, SSIS is somewhat time-consuming and technicallydifficult,24)particularlystimulatingasiteonthepalmarside.Accordingly, we performed traditional nerve conductionmeasurementsofCMAPsandSNAP.Murataetal.3)reportednormalvaluesforADM-CMAPlatencyof<3.5mswithanamplitude>2.5mV,andaSNAPlatencyof<2.2mswithanamplitude>15μV.Inthecurrentseries,basedonourcrite-ria,we identifieddelayed latenciesand lowamplitudes forCMAPsandSNAPs.Nerve conductionmeasurements forUTS have been re-
ported,2,3,10,11,13–16)andtheyallindicateddelayedconductionat the wrist. However, few studies have examined nerveconduction before and after surgery.2,11,14) Uriburu et al.11) reported three cases of UTS and found that FDI-CMAPwas recordable in one case after surgery.Moreover, post-operatively, FDI latency was shortened from 7to 4ms inonepatientandfrom24to4msinanother.Ebelingetal.2) describedninecasesofUTSandfoundthatFDIlatencywasshortenedpostoperatively.Erkin et al.14) reported apatientwithaganglionandfoundthattheFDIlatencywasshortenedfrom3.5to3.2msandtheFDIamplitudeincreasedfrom2.1to5.4mVpostoperatively.Inaparthyetal.15)reportedthatthetimeforhypothenarmusclestorecovertothenormalrangewas12to14weeksintheirpatients.Inourseriesof18pa-tients,afterrehabilitation,themeanpinchstrengthincreasedfrom2.1 to3.1kgat2monthsaftersurgery. Inapreviousreport,wedescribedfivecasesofUTScausedbyganglionand found that both FDI-CMAP and ADM-CMAP werevaluableforelectrophysiologicaldiagnosis 16);however,thecurrentstudydescribes18casesofUTSwithvariouscauses,includingganglion,andtheresultswereincidentallysimilartothoseofthepastreport.Inourcurrentseries,FDI-CMAP
and ADM-CMAP did not improve to the normal range,and residual delayed latency and lowamplitudewere seendespite recoveryof the intrinsicmuscles (Tables 2 and 3).Inthesecases,fromtheviewpointofneurophysiology,my-elinizationandaxonalregenerationoffibersintheFDIandADM branches were insufficient, notwithstanding ameanfollow-upof11months.Therewereseverallimitationstothisstudy.First,wedid
not investigate the relationship betweenMRIfindings andthecausesofUTS.Second,wecouldnotclarifytherelation-shipbetweentheelectrophysiologicaldataandtherecoverytimeforintrinsicmuscles.Third,todetectfurtherimprove-mentofFDI-CMAPandADM-CMAP,longerfollow-upisneeded.
CONCLUSIONS
ThecausesofUTSinourserieswereganglion,traumaticadhesion,ulnararteryaberrancy,orpisohamatearch.BothFDI-CMAP and ADM-CMAP were valuable for electro-physiological diagnosis of UTS. Delayed latency and lowamplitudeswere seenat thefinal follow-updespite the re-coveryofintrinsicmuscles.
ACKNOWLEDGMENTS
TheauthorsaregratefultoMs.YumiWatabe,Ms.HiromiTakeda,Ms.YokoKusakari, PathologistNoriyuki Iwama,MD, Fumie Nakayama,MD, and Honorary Director Kat-sumiSato,MD,TohokuRosaiHospital,forassistinginthemanuscriptpreparation.
3. Murata K, Shih JT, Tsai TM: Causes of ulnar tun-nel syndrome: a retrospective study of 31 subjects. JHandSurgAm2003;28:647–651.DOI:10.1016/S0363-5023(03)00147-3, PMID:12877855
5. Seddon HJ: Carpal ganglion as a cause of paralysisof the deep branch of the ulnar nerve. J Bone JointSurg Br 1952;34-B:386–390. DOI:10.1302/0301-620X.34B3.386, PMID:12999919
6. Richmond DA: Carpal ganglion with ulnar nervecompression.JBoneJointSurgBr1963;45-B:513–515.DOI:10.1302/0301-620X.45B3.513, PMID:14058327
8. Vanderpool DW, Chalmers J, Lamb DW, WhistonTB: Peripheral compression lesions of the ulnarnerve. J Bone Joint Surg Br 1968;50-B:792–803.DOI:10.1302/0301-620X.50B4.792, PMID:4303276
9. Hayes JR,Mulholland RC, O’Connor BT: Compres-sion of the deep palmar branch of the ulnar nerve.Case report and anatomical study. J Bone JointSurg Br 1969;51-B:469–472. DOI:10.1302/0301-620X.51B3.469, PMID:5820788
11. UriburuIJ,MorchioFJ,MarinJC:Compressionsyn-drome of the deepmotor branch of the ulnar nerve.(Piso-HamateHiatussyndrome).JBoneJointSurgAm1976;58:145–147. DOI:10.2106/00004623-197658010-00032, PMID:1249106
13. Kuschner SH, Gelberman RH, Jennings C: Ulnarnerve compression at the wrist. J Hand Surg Am1988;13:577–580. DOI:10.1016/S0363-5023(88)80100-X, PMID:3418064
14. Erkin G, Uysal H, Keleş I, Aybay C, Özel S: Acuteulnarneuropathyatthewrist:acasereportandreviewof the literature. Rheumatol Int 2006;27:191–196.DOI:10.1007/s00296-006-0166-8, PMID:16896989
16. Nobuta S, Sonofuchi K, Itoi E: Electrophysiologicalfeatures of ulnar tunnel syndrome caused by gan-glion − a descriptive study. Int J PhysMed Rehabil2018;06:496.DOI:10.4172/2329-9096.1000494
17. HirookaT,HashizumeH,NagoshiM,ShigeyamaY,InoueH:Guyon’s canal syndrome.A different clini-cal presentation caused by an atypical fibrous band.JHandSurgAm1997;22:52–53.DOI:10.1016/S0266-7681(97)80016-2, PMID:9061525
18. Spinner RJ, Lins RE, Spinner M: Compression ofthemedialhalfof thedeepbranchoftheulnarnerveby an anomalous origin of the flexor digiti minimi.A case report. J Bone Joint Surg Am 1996;78:427–430. DOI:10.2106/00004623-199603000-00015, PMID:8613451