Laboratory findings including cerebrospinal fluid (CSF) examination were normal, except for hypercapnia (PCO2 47

Laboratory findings including cerebrospinal fluid (CSF) examination were normal, except for hypercapnia (PCO2 47.8?mm Hg) on blood gas analysis. and he was admitted to the Department of Neurology, Ishikawa Prefecture Central Hospital, Kanazawa, Japan, 4?days after the onset of weakness. Neurological examination disclosed bilateral facial weakness, poor Itraconazole (Sporanox) elevation of the soft palate, hoarseness, dysarthria, dysphagia, weakness of the tongue, flaccid tetraparesis (grade 4, Medical Research Council scale) and areflexia of deep tendon reflexes. He needed a wheelchair for transfer, and stomach tube for gastrogavage. Laboratory findings including cerebrospinal fluid (CSF) examination were normal, except for hypercapnia (PCO2 47.8?mm Hg) on blood gas analysis. Nerve conduction studies demonstrated a marked reduction of compound muscle action potentials (CMAP) with normal conduction velocity (CMAP was 2.87?mV and motor conduction velocity was 50.6?m/s in the right median nerve), but sensory nerves were normal. The MRI studies of the brain and spinal cord were normal. A diagnosis of GBS was made, and he was given intravenous immunoglobulin (IVIg; 400?mg/kg/day) and intravenous methylprednisolone (500?mg/day) for 5?days, according to the protocol used in the previously reported randomised trial.3 He underwent rehabilitation, and his symptoms gradually improved 1?week after admission. He could stand by himself 2?weeks after admission, Itraconazole (Sporanox) and eat by himself without a Itraconazole (Sporanox) stomach tube 1?month after admission. Nerve conduction studies still showed simple reduction of CMAPs 1?month after admission (CMAP was 1.21?mV and motor conduction velocity was 53.0?m/s in the right median nerve). At 2?months after admission, he could ambulate independently. He returned to work (English teacher at a high school) 3?months after admission. The antibodies to gangliosides (GM1, GM2, GM3, GD1a, GD1b, GD3, GT1b, GQ1b, GA1, Gal\C, and GalNac\GD1a) and GD1a/GD1b complex in the serum obtained on the first day of admission were examined by enzyme\linked Itraconazole (Sporanox) immunosorbent assay, as previously described.1,4 He was positive only to the antibody to GD1a/GD1b complex (anti\GD1a/GD1b antibody). Comment Our patient showed acute progressive axonal motor polyneuropathy involving the cranial nerves 2?weeks after flu\like symptoms. This condition fulfilled the established criteria of GBS, and the results of nerve conduction studies were classified as having acute motor axonal neuropathy (AMAN).5 Anti\GD1a/GD1b antibody was detected in the acute\phase serum; however, there were no antibodies Nt5e to single gangliosides, including GD1a and GD1b. In a recent report,1 8 of 100 patients with GBS had anti\GD1a/GD1b antibodies, and three of these eight did not demonstrate any anti\ganglioside antibodies. These eight patients with anti\GD1a/GD1b antibody tended to have cranial nerve deficits and severe disabilities, and four of these patients required artificial ventilation.1 Of the three anti\GD1a/GD1b antibody\positive patients with available electrophysiological data, two showed an axonal neuropathy pattern, and the remaining one showed an equivocal pattern.1 Of the 12 patients with MFS, 7 had serum antibodies to some GSCs, and anti\GSC antibodies might influence the clinical features, as sensory indicators were infrequent in patients with anti\GQ1b/GM1 antibody.2 These findings may support the theory that anti\GSC antibodies correlate with a certain phenotype of GBS or MFS. The clinical features of our patient were similar to those patients with anti\GD1a/GD1b antibodies,1 such as AMAN\type GBS with cranial nerve deficits and severe disability (the Hughes Functional Grading Scale at the peak of his disability was on grade 4). Although our patient did not require artificial ventilation, his hypercapnia suggested respiratory weakness. The patient received intravenous methylpredonisolone in addition to IVIg. This combination therapy might prevent his case from being aggravated to grade 5. However, a future large\scale study will be needed to clarify this point. Footnotes Competing interests: None declared. Informed consent was obtained for publication of the patient’s details.