Background Acute motor axonal neuropathy (AMAN) and acute motor and sensory axonal neuropathy (AMSAN) are due to an antiganglioside antibody mediated attack, thought to be restricted to motor fibres in AMAN. Sensory symptoms and minor sensory conduction abnormalities, however, have been reported in some AMAN patients.
Objective To verify whether sensory fibres are truly spared in AMAN and whether AMAN and AMSAN represent a continuum.
Methods Serial conduction studies in 13 AMAN and three AMSAN patients were reviewed. To evaluate the variation in sensory nerve action potential (SNAP) amplitude in serial recordings, the least significant change in a test–retest study of 20 controls was calculated. Least significant change for median, ulnar and sural nerves were 44%, 47% and 58%, respectively.
Results In 34% of initially normal sensory nerves of six AMAN patients, SNAP amplitude significantly increased by 57–518%. In three nerves of three AMAN patients, SNAP significantly decreased by 50–69%. Overall, serial recordings allowed detection of sensory fibre involvement in 49% of nerves and in 69% of AMAN patients. In one AMSAN patient, SNAP increased in two nerves by 150–300%; in another patient, SNAPs, unrecordable at baseline in six nerves, reappeared during follow-up and normalised in three nerves. In five nerves of three AMAN and in eight nerves of two AMSAN patients, SNAP amplitudes increased rapidly, suggesting reversible conduction failure of sensory fibres. In other nerves, SNAP increased over months, as for axonal regeneration.
Conclusions Sensory fibres are often involved subclinically in AMAN. Reversible conduction failure may develop in sensory as well as motor fibres in both AMAN and AMSAN. AMAN and AMSAN represent a continuum in axonal GBS.
Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
Funding AU received research support from Kedrion and payment for lectures by Pfizer.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.