A 77-year-old female presented to the neurology department in our hospital with a 5-day history of dysarthria and upper limb weakness with steady progression. She suffered diarrhea 10 days previously and totally recovered before hospitalization. Further medical history of this patient revealed that this was her second occurrence of GBS. At the age of 64, she suffered the first attack, characterized by dysphagia, dysarthria and bilateral upper and lower limb weakness with areflexia. Weakness was more severe in the lower limbs(Medical Research Council [MRC] (grade 0/5)than the upper limbs(MRC grade 3/5). A Nerve conduction study(NCS) during her first presentation revealed axonal motor type polyneuropathy. She was diagnosed with acute motor axonal neuropathy(AMAN) according to Hadden’s criteria  and was treated with 5 days of IVIG and totally recovered. The medical record of the first episode was not available because she was admitted in another hospital in China and the records could not be shared. At this time, weakness was more severe in the upper limbs(MRC grade 2/5) than the lower limbs(MRC grade 4/5). Sensory disturbance and ataxia were not seen and the areflexia persisted. Routine laboratory examinations were normal, including complete blood count, blood chemistry, and immunological examinations. Brain magnetic resonance (MRI) found no abnormalities. NCS performed in another hospital 4days after neurological symptoms occurred revealed reduced motor conduction velocities and amplitudes in median, ulnar, tibial and peroneal nerves. The sensory nerves were normal and decreased F waves were detected in lower limbs. A lumbar puncture was performed 7days after clinical onset. The protein concentration in CSF was 567 mg/L with normal cellularity. A western blot analysis of anti-gangliosides(IgG anti-GM1, GM2, GM3, GM4, GD1a, GD1b, GT1a, GT1b, GQ1b,GD2,GD3,Sulfatide) was performed and GD1a positive(3+), GT1a positive(2+), Sulfatide(+) were found in serum, GD1a positive(3+) in CSF. In this case, the diagnosis of PCB variant, a different subtype from the initial diagnosis 13 years ago, was supported by acute and steadily progressive oropharyngeal, cervical, brachial weakness and mild lower limb weakness, antecedent infective symptoms, and positive for anti-GT1a antibody. Her symptoms were partially improved after the five doses of IVIG and her physical rehabilitation was initiated simultaneously. She did not suffer from any respiratory distress during her hospitalization and her vitals remained stable. She was discharged 10 days later and received regular physiotherapy for the next 3 months. At the 4-month follow-up, she had fully recovered.