Consideration about “sonographic evaluation of peripheral nerves in subtypes of Guillain-Barré syndrome”

We have highly appreciated the paper by Mori and colleagues entitled “Sonographic evaluation of peripheral nerves in subtypes of Guillain-Barré syndrome”, investigating ultrasound (US) features of acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy/acute motor and sensory axonal neuropathy (AMAN/AMSAN) [1]. The authors examined 14 patients (5 with AIDP and 9 with AMAN/AMSAN) performing an extensive clinical and neurophysiological evaluation and antiganglioside antibody analysis. US assessment of media and ulnar nerves in different sites (from wrist to axilla), tibial nerve (at ankle and popliteal fossa) and C5-C7 roots was performed. The authors found higher US enlargements of the proximal nerve sites and cervical roots in AIDP patients, while a greater distal involvements in AMAN/AMSAN. From our point of view, the paper by Mori and colleagues is very important and remarkable for several reasons. In this study, the authors show a possible usefulness of US evaluation, which may help differentiation between demyelinating and axonal subtypes of Guillain-Barré syndrome (GBS), on the basis of the more involved sites. At the same time, the results show the convenience to perform a wide US evaluation of the examined nerves, up to axilla, like the authors did. Another important point is the association of US with clinical and neurophysiological exams. This practice should always be considered in the management of patients with peripheral neuropathies. In fact, only a comprehensive evaluation can provide the essential information for diagnosis, therapy and rehabilitation. Finally, probably the most significant result, showed by Mori and colleagues, is the increase of nerve cross sectional area (CSA) in AMAN/AMSAN. The presence of this enlargement in axonal neuropathies demonstrates the non-direct couple CSA enlargement/demyelination. Indeed, as the authors correctly introduced, the real significance of CSA increase may be different and is linked to specific pathological conditions and pathomechanisms. Thus, in cases of some hereditary (e.g. Charcot-Marie-Tooth) and immune-mediate (e.g. chronic inflammatory demyelinating polyneuropathies) neuropathies, nerve enlargement is linked to demyelination [2]. On the other hands, in traumatic nerve injuries the axonal damage is associated with CSA enlargements [3].The authors correctly discussed this point and underlined the real importance of the disease features, which may explain this different significance of nerve enlargement. This topic again stresses the necessary neurophysiological examination to real understand the neuropathy nature and characterize the nerve function impairment. We consider suitable authors' explication of CSA increase in AMAN/ AMSAN. For this reason, we would like to suggest a larger investigation about the pathomechanisms and morphological alterations in the two GBS subtypes. In particular, further perspective studies could shed light on this issue. An extensive US follow-up evaluation in a larger sample, performed from the hyperacute phase and repeated at short intervals, associated with neuropathological findings (e.g. biopsies) and other morphological evaluation, like magnetic resonance, could be useful to better characterize the substantial differences of GBS subtypes. We would like to ask the authors their opinion about our suggestions.