We present a patient with pharyngeal-cervical-brachial Guillain-Barré syndrome (PCB-GBS) that progressed to a severe state followed by a quick recovery after treatment. This unique clinical course has not been documented previously and provides a potentially invaluable description of a novel GBS variant. A 42-year-old man arrived at the emergency department with a 24-hour history of dysphagia, weakness in his right arm, and bilateral shoulder weakness. Nerve conduction velocity testing revealed bilateral sensory and motor polyneuropathy, leading to the diagnosis of GBS with the PCB variant. Timely diagnosis and plasmapheresis treatment contributed to a complete recovery of muscle strength and reflexes. In cases resembling ours, it is imperative to contemplate the existence of rare Guillain-Barré variants. This case underscores the necessity of recognizing and addressing rare Guillain-Barré variants in clinical settings with similar presentations.
Guillain-Barré syndrome (GBS) is an aberrant autoimmune response preceded by infections. Progressive limb weakness develops approximately two weeks after the autoimmune stimulation and peaks by the fourth week [1,2]. Campylobacter jejuni is the most frequent causative agent for GBS development; other pathogens, such as Cytomegalovirus, influenza and Zika virus, chikungunya virus, and Mycoplasma pneumoniae, have been reported in the literature; vaccines (e.g., H1N1 influenza vaccine) are other examples of reported causes [3-5]. The association between GBS and C. jejuni infection and a higher incidence of antibodies against GM1 and GD1a gangliosides relate to severe disease with pure motor axonal affection [6,7]. The findings of a prospective study of more than 250 patients with GBS showed that Miller-Fisher syndrome (MFS) (5%) was the most frequent GBS variantand pharyngeal-cervical-brachial (PCB) (3%) the second . The PCB variant of GBS develops a rapidly progressive oropharyngeal and cervicobrachial weakness associated with areflexia in the upper limbs and acute motor axonal neuropathy (AMAN) without acute inflammatory demyelinating polyneuropathy (AIDP) . We present a distinctive case of GBS with an initial clinical course consistent with PCB-GBS that subsequently developed into a severe generalized presentation inconsistent with the previous state, resulting in later ICU admission and successful management.
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