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however, subsequent autopsy studies con rmed that AMSAN is a real disease entity52,53 Clinically and often by early electrodiagnostic studies, patients with AMSAN are indistinguishable from those with AIDP8,28,51 53,82,83 88 Usually, sensory symptoms begin in the hands or feet and later progress Sensation to all modalities is reduced and are exia is usually evident Patients with AMSAN rapidly develop progressive and severe generalized weakness over only a few days, as opposed to progression over a couple of weeks in most patients with AIDP Ophthalmoplegia, dysphagia, and respiratory muscle weakness can occur Blood pressure instability and cardiac arrhythmias may complicate AMSAN as well Recovery of strength and function is slow and often incomplete compared to AIDP87 Only a few children have been reported with AMSAN, and there is some suggestion that the prognosis is better than in adults82,89

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Albuminocytologic dissociation of the CSF protein is usually seen Evidence of a recent infection with C jejuni and antibodies directed against nerve gangliosides, particularly GM1 antibodies, are demonstrated in many patients with AMSAN53,90 92 Nerve conduction studies reveal markedly diminished amplitudes or absent CMAPs and SNAPs within 7 10 days of onset8,24,82,84 88,93,94 As discussed in the AIDP section, low-amplitude CMAPs are one of the earliest electrophysiological abnormalities noted in AIDP; thus, low-amplitude CMAPs do not necessarily imply axonal degeneration Distal conduction block with or without demyelination also leads to low-amplitude distal CMAPs28,83 Initially, it is often impossible to distinguish AIDP from AMSAN by nerve conduction studies; however, serial nerve conduction studies may be helpful83 Most patients with AIDP will eventually develop other features of demyelination (eg, signi cantly prolonged distal latencies and f-wave latencies, slow CVs, more proximal conduction block, or temporal dispersion) The distal latencies of the CMAPs and the nerve conduction velocities, when obtainable, should be normal or only mildly affected in AMSAN Needle EMG demonstrates markedly abnormal reductions in recruitment Several weeks after the presentation of major motor weakness, abundant brillation potentials and positive sharp waves can be detected in most muscles, especially those located in the distal regions of the limbs91,92,95

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oratory, and electrophysiological similarities; however, this is not indicated in clinical practice Nerves biopsied late in the disease course of AIDP or AMSAN may show axonal degeneration, and it can be dif cult to distinguish a primary axonopathy from secondary axonal degeneration Sensory and motor nerve biopsies in several patients with inexcitable motor and sensory conduction studies revealed severe demyelination rather than primary axonal degeneration93,95 98 Nevertheless, some patients with inexcitable CMAPs and SNAPs have features that suggest a primary axonal insult52,53,82,85 Unlike AIDP, demyelination and lymphocytic in ltrates are absent or only minimally present on nerve biopsy or at autopsy in patients with AMSAN; rather, prominent axonal degeneration affecting the ventral and dorsal roots and the peripheral nerves is appreciated As many as 80% of teased bers reveal axonal degeneration, while demyelinating features are rare82,85 A marked loss of both myelinated and unmyelinated axons is evident Grif n and colleagues reported that the autopsies of three patients with AMSAN who died early in the course of their illness demonstrated prominent axonal degeneration of the spinal roots and peripheral nerves without demyelination or signi cant in ammation53 Numerous macrophages were present in the periaxonal space of myelinated internode, as were rare intra-axonal macrophages Similar histological abnormalities are seen in AMAN but are not typically noted in AIDP An autopsy on another patient with AMSAN demonstrated in ammatory cell in ltrates comprising lymphocytes and macrophages in the spinal cord

The pathogenic basis of AMSAN is unknown but is most likely due to an immune-mediated attack directed against epitopes on the axon9,53,59 AMSAN often follows C jejuni infection and may lead to the production of the antibodies directed against various nerve gangliosides (eg, GM1 or GM1a) (Figs 11 2 and 11 3) These gangliosides are present on the nodal axolemma and may be the target of the immune attack due to molecular mimicry91,92 Early in the course or with mild disease, binding of the antibodies to neural epitopes may result in only physiological conduction block However, complement activation on nodal and later internodal axolemma and recruitment of macrophages could result in axonal degeneration

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Nerve biopsy performed early in the course of the disorder is the only way to differentiate axonal GBS from pseudoaxonal GBS because of their clinical, lab-

There have been prospective treatment studies speci cally for AMSAN; however, we treat patients with IVIG or PE

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