Zusammenfassung
A-Wellen sind reproduzierbare Muskelaktionspotenziale zwischen M-Antwort und F-Welle
oder nach der F-Welle. Sie weisen eine konstante Latenz, Amplitude und Form auf. Motorischer
Axonreflex und die häufigere ektope axonale Nachentladung (EAN) sind die wichtigsten
Spielarten. Es wird allgemein angenommen, dass EAN auf Demyelinisierung zurückgehen.
Diese Interpretation wird in der vorliegenden Arbeit einer kritischen Prüfung unterzogen.
Methoden: Über den Zeitraum von 2001 - 2003 wurden bei 506 F-Wellenuntersuchungen des N. tibialis
von 283 Patienten mit verschiedenen Polyneuropathien (PNP) im Vergleich zu 237 Registrierungen
von 128 Patienten ohne neuromuskuläre Erkrankung die Häufigkeit von A-Wellen untersucht.
Ergebnisse: (A-Wellen pro Nerv ± Standardabweichung; ns: nicht signifikant): Kontrollgruppe 0,4
± 0,7, hereditäre motorische und sensible Polyneuropathien (HMSN) 0,9 ± 1,3 (ns),
Miller-Fisher-Syndrom (MFS) 0,25 ± 0,7 (ns), akutes Guillain-Barré-Syndrom (GBS) 6,8
± 3,5 (p < 0,0005), chronisches GBS 3,0 ± 2,1 (p < 0,0005), sekundär-entzündliche
PNP 1,35 ± 1,6 (p < 0,05), metabolisch-toxische PNP 0,9 ± 1,1 (p < 0,0005). Diskussion: Bei etwa gleicher Nervenleitgeschwindigkeit (35 m/s) war die Anzahl der A-Wellen
beim GBS signifikant erhöht, bei der HMSN nicht. Demyelinisierung per se ist daher
evtl. nicht die alleinige Ursache für das Auftreten von A-Wellen. Neben Unterschieden
der Verlaufsdynamik kommen vor allem humoral-entzündliche Faktoren für die Pathogenese
der A-Wellen vom EAN-Typ beim GBS in Betracht. Ferner scheint das Vorkommen von A-Wellen
zwischen den klinisch verwandten Krankheitsbildern MFS und GBS zu diskriminieren.
Abstract
A-waves are motor unit action potentials that may be registered between M-response
and F-wave or after the F-wave. They have a constant latency, amplitude and shape.
Motor axon reflex or the more frequent ectopic axonal after discharge (EAA) are the
most important representatives. It is generally assumed that EAA are entirely due
to demyelination. This interpretation is challenged in the present report. Methods: Occurrence and frequency of A-waves were analyzed in F-wave curves from 506 tibial
nerves recorded in 283 patients with different types of polyneuropathies (PNP) between
2001 and 2003. 237 F-wave recordings from 128 patients without neuromuscular disorders
served as controls. Results: (A-waves per nerve ± SD; ns: not significant): Control group 0.4 ± 0.7; hereditary
motor and sensory neuropathies (HMSN) 0.9 ± 1.3 (ns), Miller-Fisher syndrome (MFS)
0.25 ± 0.7 (ns), acute Guillain-Barré syndrome (GBS) 6.8 ± 3.5 (p < 0.0005), chronic
GBS 3.0 ± 2.1 (p < 0.0005), secondary inflammatory PNP 1.35 ± 1.6 (p < 0.05), metabolic-toxic
PNP 0.9 ± 1.1 (p < 0.0005). Discussion: Despite of equal values for the nerve conduction velocity (35 m/s), the number of
A-waves per nerve was significantly elevated in patients with GBS and not in HMSN.
Therefore, demyelination does not seem to be the sole precondition for A-waves to
occur. Beside differences in disease dynamics, presumably humoral immune factors may
be involved in the pathogenesis of A-waves of the EAA-type. Furthermore, the occurrence
of A-waves may discriminate between the closely related disease entities of MFS and
GBS.
Key words
A-wave - motor axon reflex - Guillain-Barré syndrome - polyneuropathy - humoral inflammatory
pathogenesis
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PD Dr. med. Malte E. Kornhuber
Klinik und Poliklinik für Neurologie der Universität Halle/Saale · Klinikum Kröllwitz
Ernst-Grube-Straße 40
06097 Halle/Saale
Email: malte.kornhuber@medizin.uni-halle.de
