Das Karpaltunnelsyndrom – eine häufig verbreitete Krankheit mit einigen diagnostischen Fallstricken – Die Nervensonographie (Nervenultraschall) schafft hier zusätzliche Informationen zur Sicherung der Diagnose.

Auf der Informationsseite einer großen deutschen Krankenkasse für Patienten zum Thema Karpaltunnelsyndrom ist, obwohl diese Informationen medizinisch geprüft und zertifiziert ist, die Nervensonographie zur Diagnostik des Karpaltunnelsyndroms nicht aufgeführt.

Bei Durchsicht der Einträge zum Karpaltunnelsyndrom auf den ersten Google Seiten ist der Nervenultraschall, zur Diagnostik des Karpaltunnelsyndroms, nur selten erwähnt.

Dieses zeigt, wie auch in den meisten zum Thema vorhandenen Artikeln, dass die Nervensonographie bisher noch nicht ihren angemessenen Stellenwert in der oft komplizierten Untersuchung peripherer Nervenerkrankungen gefunden hat.

Die Nervensonographie erhöht die Sensitivität in der Diagnostik des Karpaltunnelsyndroms von 95 % bis auf  98 %. Sie schafft wertvolle Informationen bei Grenzbefunden, Anomalien und anatomischen Varianten.

Im Falle einer anstehenden Operation zur Behandlung des Karpaltunnelsyndroms ist sie somit sehr hilfreich für eine bessere und sicherere Operationsplanung.

Die exakten Ursachen von Kompressionssyndromen wie zum Beispiel des Karpaltunnelsyndrom, der Ulnarisneuropathie, des Tarsaltunnelsyndroms, desSupinatorlogensyndroms oder des Pronatorlogensyndroms, lassen sich auch bei selteneren Auslösern, zum Beispiel eines Tumors, einer knöchernen Ausziehung, einer Entzündung oder eines Orthesematerialanteils sicher erkennen.  

Der Nervenultraschall ist besonders hilfreich für den Fall der Beschwerdepersistenz nach operativen Eingriffen oder auch bei Rezidiven.

Nicht selten kann die Methode der Nervensonographie hier auch eine andere zugrundeliegende Ursache aufzeigen.

Voraussetzung zur Durchführung des Nervenultraschalls sind besondere anatomische Kenntnisse von Knochen-, Muskel-, Gefäß- und Nervenverlauf sowie spezifisches Wissen zur praktischen Anwendung. Ideal ist hierbei die Nutzung eines hochauflösenden Ultraschallgerätes mit einer möglichst breitgefächerten Sendefrequenz von ca. 5 MHz bis 18 MHz. Weiter ist eine ständige Anpassung der Geräteeinstellungen im Verlauf der Untersuchungen je nach Tiefe der zu untersuchenden Nervenstruktur notwendig. Die Methode ist schnell verfügbar, in der Hand des erfahrenen Untersuchers sicher und nebenwirkungsfrei und im Vergleich zu anderen Methoden (MRT, PET, etc.) kostengünstig.

In den folgenden Leitlinien der Deutschen Gesellschaft für Neurologie sind wichtige Hinweise zum Krankheitsbild aufgeführt.

„Zitat“

Leitlinien der DGN 2008

Karpaltunnelsyndrom (KTS)

Was gibt es Neues?

  • • Neue Studien zur Lasertherapie bei KTS zeigen keine positiven Resultate.
  • • Beim operativen Wundverschluss wird von resorbierbaren Vicrylnähten wegen vermehrter Infektionen und Narbengranulome abgeraten.

Die wichtigsten Empfehlungen auf einen Blick

  • • Leichte Fälle (nur Schmerz und Parästhesien) werden mit Schonung und ggf. Schienung behandelt (B).
  • • Symptomatische KTS in der Schwangerschaft können zusätzlich diuretisch behandelt werden (B).
  • • Bei stärkeren Beschwerden kann die lokale Injektion von Steroiden (A) oder ein systemischer Steroidstoß über 2 Wochen erfolgen (B).
  • • Bei Beschwerdepersistenz besteht Operationsindikation. Bei unkompliziertem KTS ohne anatomische Besonderheiten kann je nach Erfahrung des Operateurs endoskopisch oder offen operiert werden. Zusätzliche Epineurotomie ist nicht nötig, eine Tenosynovektomie der Flexoren ist möglich (A).
  • • Bei KTS-Rezidiv sollten Zweitoperationen offen ausgeführt werden.

Definition

Das Karpaltunnelsyndrom (KTS) ist Ausdruck einer chronischen Druckschädigung des N. medianus innerhalb des Karpalkanals. Durch diesen etwa 2 cm langen Tunnel, dessen Basis von den Handwurzelknochen und dessen Dach vom Retinaculum flexorum (Lig. carpi transversum) gebildet wird, ziehen außer dem N. medianus die Beugesehnen der Finger. Eine Nervenkompression innerhalb dieses physiologischen Engpasses erfolgt einerseits bei einer Einengung des Tunnels, häufiger aber durch eine Volumenzunahme des Tunnelinhalts. Das KTS ist das mit Abstand häufigste Engpasssyndrom und macht ca. 45% aller nicht traumatischen Nervenschädigungen aus. Das Erkrankungsrisiko beträgt 8– 10%, wobei Frauen etwa doppelt so häufig erkranken wie Männer. Das Manifestationsalter liegt in der Regel über 30 Jahren; in 76% der Fälle sind 40- bis 70-Jährige betroffen, wobei sich eine bilaterale Manifestation bei etwa 40% der Betroffenen nachweisen lässt.

Symptomatik

Die typische Symptomatik besteht in kribbelnden oder nadelstichartigen Missempfindungen in der betroffenen Hand, die bevorzugt nachts oder bei fixierter Beuge- oder Streckstellung der Hand (Telefonieren, Halten eines Buchs oder Lenkrads …) auftreten und sich durch Schütteln der Hand bessern. Außerdem können manuelle Tätigkeiten wie Stricken, Wringen, repetitive Beuge- und Streckbewegungen im Handgelenk sowie Arbeiten mit stark vibrierenden Werkzeugen die Beschwerden auslösen.  Die Dysästhesien und Schmerzen sind häufig nicht auf das sensible Versorgungsareal des N. medianus begrenzt, sondern greifen auf die ulnare Handpartie und in über einem Drittel der Fälle auf proximal des Handgelenks gelegene Regionen bis hinauf zur Schulter über. Im Initialstadium – das sich über Jahre erstrecken kann – fehlen sensomotorische Ausfälle und erst in einem fortgeschritteneren Stadium findet sich eine Hypästhesie im autonomen Versorgungsareal des N. medianus, einschließlich einer Beeinträchtigung der Stereoästhesie. Dadurch werden feinere manuelle Verrichtungen, wie z. B. das Nähen oder Knöpfen, erschwert. Die funktionell weniger bedeutsame laterale Daumenballenmuskulatur (Mm. abductor pollicis brevis und opponens pollicis) wird paretisch und atrophiert, so dass die Abduktion des Daumens senkrecht zur Handebene und dessen pronatorische Kreiselung beeinträchtigt werden. Trophische Störungen der Haut sowie eine Hyp- oder Anhidrose kommen erst in weit fortgeschrittenen Stadien vor. Der Verlauf variiert in Abhängigkeit von zahlreichen Faktoren. Neben chronisch progredienten oder rezidivierenden Verläufen kommen spontane Besserungen vor, und zwar besonders bei jüngeren Patienten und kurzer Krankheitsdauer, aber auch bei möglicher Reduzierung der manuellen Beanspruchung, Beendigung einer Schwangerschaft bzw. erfolgreicher Behandlung einer relevanten Grundkrankheit.

Ursachen

In den meisten Fällen lässt sich keine besondere Ursache nachweisen, so dass von einem idiopathischen KTS gesprochen wird. In < 10% gehen Traumen im Bereich des Handgelenks, besonders distale Radiusfrakturen, voraus, die durch knöcherne und besonders Weichteilveränderungen den N. medianus komprimieren können. Bei Erkrankungen aus dem rheumatischen Formenkreis findet sich häufig eine Beugesehnen-Synovialitis; etwa 50% der Patienten mit primär chronischer Polyarthritis entwickeln im Verlauf ein KTS, umgekehrt ist das KTS bei ca. 10% Erstmanifestation dieser Erkrankung. Häufig besteht außerdem eine Kombination des KTS mit einer Tendovaginosis stenosans (sog. schnellender Finger) oder mit einer Rhizarthrose. Bei jeder 10. bis 20. Gravidität entwickelt sich meist im 3. Trimenon ein KTS, das auf eine vermehrte Flüssigkeitsretention zurückgeführt wird. Seltene Ursachen sind anatomische Varianten innerhalb des Karpaltunnels, wie z. B. eine persistierende A. mediana oder ein dort gelegener Anteil des M. palmaris longus. Endokrine Störungen wie Myxödem, Hyperthyreose, Akromegalie, Hyper- und Hypoparathyreoidismus können durch Verdickung der Ligamente und Ödembildung ein KTS nach sich ziehen. Bei chronischer Niereninsuffizienz steigt mit zunehmender Dialysedauer die Inzidenz eines KTS auf bis zu 32%, wobei eine urämische Synovialitis der Beugesehnen als pathogenetischer Hauptfaktor anzusehen ist. Da der Shuntarm meist zuerst betroffen wird, werden auch hämodynamische Faktoren angeschuldigt. Bis zu 10% der Diabetiker leiden an einem KTS, wobei eine erhöhte Druckvulnerabilität des Nervs durch die Polyneuropathie postuliert wird. Seltene weitere Ursachen umfassen die Amyloidose, Mukopolysacharidose, Gicht, Chondrokalzinose sowie Raumforderungen wie Ganglien oder Lipome. Eine Sonderstellung nehmen belastungsinduzierte KTS ein, die besonders bei Polsterern und Arbeitern, die mit stark vibrierenden Maschinen beschäftigt sind, vorkommen und dabei als Berufskrankheit anerkannt werden. Eine Häufung von KTS bei Beschäftigten, die viel am Computer arbeiten, besteht demgegenüber nicht.

Diagnostik

Klinische Untersuchung

Diagnostisch wegweisend ist in vielen Fällen die Anamnese, da der neurologische Untersuchungsbefund anfangs meist unauffällig ist. Ein positiver Phalen-Test stützt die Verdachtsdiagnose eines KTS, ist jedoch weniger sensitiv und zuverlässig als die neurographische Diagnostik. In fortgeschritteneren Fällen besteht eine taktile Hypästhesie im autonomen Versorgungsareal des N. medianus, die bei stärkerer Ausprägung mit einer Störung der Stereoästhesie (verzögerte oder aufgehobene Identifizierung einer Münze durch Betasten) einhergeht; weiterhin finden sich eine Schwäche und Atrophie der lateralen Daumenballenmuskulatur. (Da die motorische Funktionsprüfung der lateralen Thenarmuskulatur unzuverlässig ist, sollte ergänzend die Konsistenz des M. abductor pollicis brevis bei maximaler Abduktion des Daumens senkrecht zur Handebene überprüft werden; auf der betroffenen Seite findet sich palpatorisch bei stärkeren Paresen eine weniger pralle Konsistenz.) Eine Hyp- oder Anhidrose der Fingerkuppen I– III stellt ein Spätsymptom dar.

Neurographische Diagnostik

Zum zuverlässigen Nachweis eines KTS sind folgende neurographische Untersuchungen erforderlich:

  • • Sensible Neurographie des N. medianus zwischen Handgelenk und Zeige- oder besser Mittelfinger unter Mitbeurteilung der Amplitude des sensiblen Nervenaktionspotenzials (SNAP). Der validere Messparameter ist allerdings die NLG, bei normaler Amplitude des SNAP, jedoch verlangsamter sensibler Nervenleitgeschwindigkeit spricht dieses nicht gegen ein CTS. Bei Normalbefunden trotz begründeter klinischer Verdachtsdiagnose empfiehlt sich die ergänzende selektive sensible Neurographie des N. medianus zwischen Hohlhand und Handgelenk.
  • • Weniger sensitiv ist die Bestimmung der distalen motorischen Latenzzeit des N. medianus vom Handgelenk zum M. abductor pollicis brevis. Daher empfiehlt sich die vergleichende Bestimmung der motorischen Überleitungszeit zum Medianus-innervierten M. lumbricalis II und zum Ulnaris-innervierten M. interosseus dorsalis II bei identischer Position der Ableitelektroden und gleicher Distanz zur Reizelektrode am N. medianus bzw. N. ulnaris. Durch diese Messmethode wird außerdem die Diagnose eines KTS bei unterlagernder Polyneuropathie erleichtert.
  • • Wegen der Möglichkeit eines beidseitigen KTS bzw. einer systemischen Affektion des peripheren Nervensystems (Polyneuropathie, HMSN usw.) muss stets eine motorische und sensible Neurographie auch des ipsilateralen N. ulnaris und des kontralateralen N. medianus erfolgen.
  • • Wegen der Temperaturabhängigkeit der Impulsleitung muss die Hauttemperatur der Finger bei pathologischen Messwerten auf mindestens 34 °C angehoben werden.

Die nach den oben genannten Kriterien durchgeführte sensible und motorische Neurographie des N. medianus stellt eine valide und reproduzierbare diagnostische Methode dar, die das Vorliegen eines KTS mit einem hohen Grad an Sensitivität und Spezifität bestätigt.

Fakultative Zusatzdiagnostik

  • • Die Nadel-Elektromyographie des M. abductor pollicis brevis ist nur bei technischen Schwierigkeiten erforderlich, z. B. bei Innervationsanomalien, fortgeschrittener Muskelatrophie oder pathologisch erhöhter Reizschwelle des N. medianus, so dass dessen supramaximale Stimulation zur Miterregung des N. ulnaris führt.
  • • Bildgebende Untersuchungen sind bei Verdacht auf bestimmte Begleiterkrankungen oder Anomalien sinnvoll sowie bei Patienten mit klinischem Verdacht auf Karpaltunnelsyndrom und nicht schlüssigen NLG/EMG Untersuchungen, wobei die hochauflösende Sonographie und die Magnetresonanztomographie eingesetzt werden können (Cudlip et al. 2002). Als pathologisch wird sonographisch eine Vergrößerung der Nervenquerschnittsfläche in Höhe des Os pisiforme über 11 mm2 angesehen. Die Angaben schwanken allerdings erheblich zwischen 9 mm2 und 15 mm2 (Wiesler et al. 2006).
  • • Zu weiterführender Diagnostik bei Verdacht auf pathogenetisch relevante Grunderkrankungen siehe „ Ursachen“ .

Pathogenese

Eine Druckerhöhung im Karpalkanal führt zur Kompression der Venolen, später auch der Arteriolen des Epineuriums mit konsekutiver Ischämie des N. medianus und Ausbildung eines intraneuralen Ödems. In der Folge resultieren Nervenfaserläsionen, wobei die dicken markhaltigen Fasern als erste geschädigt werden. Die geläufige nächtliche Symptomzunahme wird auf das Abknicken des Handgelenks bezogen, das den Druck im Karpalkanal erhöht und die Durchblutung weiter drosselt. In den ödematös geschwollenen Nerv sprossen Fibroblasten ein, die zur Fibrosierung und dadurch zur weiteren Schädigung der Nervenfasern mit schließlicher Axondegeneration führen.

Differenzialdiagnose

  • • Zervikale Radikulopathien, wobei Sensibilitätsstörungen in den radialen Fingern bei Läsionen der Nervenwurzeln C 6 und C 7 und eine Daumenballenatrophie bei Läsionen der Wurzeln C 8 und Th 1 vorkommen.
  • • Proximal des Handgelenks gelegene N.-medianus-Läsionen (Pronator-teres-Syndrom und andere seltene Engpasssyndrome, Raumforderungen)
  • • Polyneuropathien, insbesondere initial fokale Immunneuropathien (Schwerpunktneuropathie)
  • • Thoracic-outlet-Syndrom und sonstige untere Armplexusläsionen
  • • Raynaud-Phänomen

Therapie

Konservative Behandlung

Eine konservative Therapie ist in leichten bis mittelschweren Fällen besonders bei jungen Patienten mit kurzer Krankheitsdauer, bei Schwangeren und bei Patienten mit behandelbarer Grundkrankheit bzw. änderbarer manueller Tätigkeit angezeigt und umfasst folgende Maßnahmen:

  • • Manuelle Schonung, eventuell mit beruflicher Umsetzung zur Verminderung der manuellen Beanspruchung (C).
  • • Nächtliche Schienung des Handgelenks in Mittelstellung. Der Erfolg ist mäßig, die Akzeptanz bei Patienten aufgrund des schlechten Schlafkomforts gering (Verdugo et al. 2003). Neuere Studien (Gerritsen et al. 2003, Werner et al. 2005) belegen allerdings einen Effekt über 12 Monate im Vergleich zur Operation in geringer und zur reinen Verhaltensänderung in guter Ausprägung. Sevim et al. (2004) zeigten in einer prospektiven randomisierten einfach blinden Studie, dass die Anwendung einer nächtlichen Schiene der lokalen Steroidinfiltration überlegen war (B).
  • • Bedarfsweise Prednisolon 20 mg morgens über 2 Wochen, danach 10 mg für weitere 2 Wochen. Eine Therapie über 4 Wochen ist der über 2 Wochen nicht überlegen (Chang et al. 2002) (↑).
  • • Injektion von 15 mg Methylprednisolon in den Karpaltunnel. Diese Therapie ist wirksamer als die Gabe von 25 mg Prednisolon oral über 10 Tage, beinhaltet aber das Risiko einer iatrogenen N.-medianus-Läsion. Maximal 3-malige Injektion (Demirci et al. 2002, Hui et al. 2004). Nach 8 Wochen ist keine signifikante Differenz zur Schienung oder Entzündungshemmern vorhanden (Marshall et al. 2007) (A) (↑). Die Wirksamkeit in den einzelnen Studien differierte gravierend.
  • • Diuretika und NSAR sind ohne gesicherte Wirkung bei einem unausgewählten Kollektiv. Bei stärkerer Flüssigkeitseinlagerung, z. B. in der Schwangerschaft, kann eine diuretische Therapie dennoch positiv wirken (B).
  • • Nachdem erste Pilotstudien positive Ergebnisse der Lasertherapie mit niedrigintensivem Rotlichtlaser bei KTS und KTS-Rezidiven zeigten (Naeser et al. 2002), konnten neuere Studien keinen konsistenten Wirksamkeitsnachweis erbringen (Evcik et al. 2007) (C).

Operative Therapie

Eine Indikation zum operativen Vorgehen besteht unter folgenden Bedingungen:

  • • Versagen der konservativen Therapie nach 8 Wochen
  • • Vorliegen funktionell behindernder sensomotorischer Ausfallerscheinungen, wobei besonders eine Beeinträchtigung des Tasterkennens (Stereoästhesie) mit konsekutiver manueller Ungeschicklichkeit von Bedeutung ist.
  • • Als absolute Operationsindikation gelten die seltenen akuten und rasch progredienten Verläufe. Die Operation setzt eine spezielle Expertise des Operateurs voraus, die vor allem bei Neurochirurgen und Handchirurgen gegeben ist.

Zwischenzeitlich sind zwei unterschiedliche operative Verfahren etabliert und als gleichwertig anerkannt (Thoma et al. 2004):

1. Offene Operation mit Durchtrennung des Retinaculum flexorum (A) (↑):

Eine zusätzliche Flexoren-Tenosynovektomie bringt eventuell zusätzlichen Benefit (Ketchum 2004). Zusätzliche Epineurolyse ist nicht erforderlich. Die offene Operation ist vorzuziehen, sofern anatomische Varianten oder lokale Besonderheiten vorliegen (Tenosynovialitis, posttraumatische Veränderungen, Raumforderungen usw.), außerdem bei einges chränkter Handgelenkbeweglichkeit und bei Rezidiveingriffen.Zum Nahtverschluss wird zu Nylonfäden oder Klammern geraten, Vicrylfäden zeigten erhöhte Infektions- und Granulomraten (Menovsky et al. 2004).

2. Endoskopische Spaltung des Retinaculum flexorum (A) (↑):

Die endoskopische Technik ist bei KTS ohne lokale Veränderungen vorteilhaft, da kleinere Narben zurückbleiben und deshalb eine frühzeitigere Belastbarkeit der Hand möglich ist. Das klinische Endergebnis ist bei beiden Verfahren gleich. Sofern die Eingriffe durch versierte Operateure erfolgen, sind die Komplikationsraten beider Verfahren vergleichbar und liegen in der Größenordnung von 1%. Allerdings sind Läsionen der Nn. Medianus und ulnaris sowie deren Äste bei der endoskopischen Technik etwas häufiger (Kiymaz et al. 2002, Park et al. 2004). Aufgrund vermehrter Komplikationen sollten endoskopische Techniken mit 2 Portalen nicht angewandt werden (Uchiyama et al. 2004). Die Kosten des endoskopischen Eingriffs sind wegen des zusätzlich benötigten Instrumentariums höher als die der offenen Operation (ca. 330 € gegenüber 180 € ). Die Eingriffe können in aller Regel ambulant und in Regionalanästhesie durchgeführt werden. Ein stationärer Aufenthalt ist gelegentlich bei Rollstuhlfahrern oder ungünstigen häuslichen Verhältnissen erforderlich. Wichtig ist eine bereits am ersten postoperativen Tag erfolgende funktionelle Nachbehandlung mit Bewegungsübungen ohne Belastung. Das Anlegen einer Schiene ist nicht erforderlich. Bei Diabetikern ist die Prognose nicht schlechter (Mondelli et al. 2004). Bei fehlender Besserung trotz operativer Therapie liegt in etwa der Hälfte der Fälle eine unvollständige Durchtrennung des Retinaculum flexorum zugrunde. Eine seltenere Ursache für ein unbefriedigendes Operationsergebnis besteht in einer iatrogenen Nervenläsion. In beiden Fällen zeigt sich häufig eine atypische Hautinzision als Hinweis auf die mangelnde Qualifikation des Operateurs. Auch bei korrektem Vorgehen kann ein Ast des R. palmaris n. mediani durchtrennt werden, was zur Ausbildung eines schmerzhaften kleinen Neuroms im Narbenbereich führt. Da sich die hierdurch bedingten Schmerzen meist spontan innerhalb eines halben Jahres zurückbilden, kann in vielen Fällen auf eine operative Revision verzichtet werden. Eine weitere Ursache für ein unbefriedigendes Operationsergebnis ist die verspätete Durchführung der Operation mit bereits irreversibler Schädigung des N. medianus. Schließlich kommen echte Rezidive durch Vernarbungsvorgänge, knöcherne Veränderungen, rheumatische Synovialitis und Chondrokalzinose besonders bei Dialysepatienten vor. Auch nach korrekt und erfolgreich durchgeführten Operationen kommt es in der Regel nicht zu einer vollständigen Normalisierung der Impulsleitung, d. h., herabgesetzte sensible Nervenleitgeschwindigkeiten des N. medianus und verlängerte distal motorische Latenzen sind als Residualsymptome und nicht als Ausdruck eines KTS-Rezidivs anzusehen, es sei denn, dass im Vergleich mit den präoperativen Ausgangswerten eine Progredienz der Impulsleitungsverzögerung erkennbar ist.

Expertengruppe

Dr. H. Assmus, Praxis für Neurochirurgie, Dossenheim

Prof. Dr. Ch. Bischoff, Neurologe, München

Priv.-Doz. Dr. A. Hufschmidt, Abt. Neurologie, St.-Elisabeth-Krankenhaus, Wittlich

Dr. O. Kastrup, Neurologische Klinik, Universität Duisburg-Essen,

Prof. Dr. K. Reiners, Neurologische Klinik, Universität Würzburg

Prof. Dr. H.-P. Richter, Neurochirurgische Universitätsklinik, Ulm

Dr. K. Scheglmann, Neurologische Klinik, Klinikum Augsburg

Priv.-Doz. Dr. Th. Vogt, Neurologische Universitätsklinik, Mainz

Für die Schweizerische Neurologische Gesellschaft:Dr. W. Z’ Graggen, Neurologische Klinik, Universitätsklinik Zürich

Für die Österreichische Gesellschaft für Neurologie:Prof. Dr. B. Mamoli, Neurologische Klinik, Universitätsklinik Wien

Federführend: Dr. Oliver Kastrup, Neurologische Klinik, Universität Duisburg-Essen, Hufelandstr. 55, 45122 Essen, Tel.: 0201/7232463,E-Mail: oliver.kastrup@uni-due.de

Dr. Konrad Scheglmann, Neurologische Klinik mit klinischer Neurophysiologie, Klinikum Augsburg, Stenglinstraße 2, 86156 Augsburg, Tel.: 0821/400– 2973, E-Mail: konrad.scheglmann@neurologie.augsburg-med.de

Die Leitlinie wurde abgestimmt mit der Deutschen Gesellschaft für Neurochirurgie, der Deutschen Gesellschaft für Handchirurgie, sowie dem BDN, der Schweizerischen Neurologischen Gesellschaft und der Österreichischen Gesellschaft für Neurologie. Zugrunde liegt dieser Leitlinie die interdisziplinäre AWMF-Leitlinie Diagnostik und Therapie des Karpaltunnelsyndroms der Dt. Ges. f. Handchirurgie, Dt. Ges. für Neurochirurgie, Dt. Ges. f. Neurologie, Dt. Ges. für Orthopädie und Orthopädische Chirurgie unter Beteiligung der Dt. Ges. für Unfallchirurgie, Dt. Ges. f. Klinische Neurophysiologie und Funktionelle Bildgebung, Dt. Ges. f. Plastische, rekonstruktive und Ästhetische Chirurgie.

Literatur

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Assmus H. Korrektur- und Rezidiveingriffe beim Karpaltunnelsyndrom. Nervenarzt 1996;67:998– 1002.

Bagatur AE, Zorer G, Oral B. The role of magnetic resonance imaging in carpal tunnel syndrome. Correlation of clinical, electrodiagnostic, and intraoperative findings and staging. Acta Orthop Traumatol Turc 2002;36(1):22– 30.

Behse F, Masuhr F. Zur elektrophysiologischen Diagnostik des Karpaltunnelsyndroms: Eigene Untersuchungen bei 124 Kontrollpersonen und eine Literaturübersicht. Klin Neurol 2002;33:1– 9.

Borisch N, Haussmann P. Neurophysiological recovery after open carpal tunnel decompression: comparison of simple decompression and decompression with epineurotomy. J Hand Surg 2003;28(5):450– 454.

Chang MH, Chiang HT, Lee SSJ, Ger LP, Lo YK. Oral drug of choice in carpal tunnel syndrome. Neurology 1998;51:390– 393.

Chang MH, Ger LP, Hsieh PF, Huang SY. A randomised clinical trial of oral steroids in the treatment of carpal tunnel syndrome: a long term follow up. J Neurol Neurosurg Psychiatry 2002;73(6): 710– 714.

Cudlip SA, Howe FA, Clifton A, Schwartz MS, Bell BA. Magnetic resonance neurography studies of the median nerve before and after carpal tunnel decompression. J Neurosurg 2002;96(6):1046– 1051.

Dawson DM, Hallett M, Wilbourn AJ. Entrapment neuropathies. Philadelphia: Lippincott-Raven, 1999.

Demirci S, Kutluhan S, Koyuncuoglu HR, Kerman M, Heybeli N, Akkus S, et al. Comparison of open carpal tunnel release and local steroid treatment outcomes in idiopathic carpal tunnel syndrome. Rheumatol Int 2002;22(1):33– 37.

de Pablo P, Katz JN. Pharmacotherapy of carpal tunnel syndrome. Expert Opin Pharmacother 2003;4(6):903– 909

5.027 Gedanken zu „Das Karpaltunnelsyndrom – eine häufig verbreitete Krankheit mit einigen diagnostischen Fallstricken – Die Nervensonographie (Nervenultraschall) schafft hier zusätzliche Informationen zur Sicherung der Diagnose.

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