Guillain–Barré syndrome with overlapping features of acute motor axonal neuropathy and the pharyngeal–cervical–brachial variant: a diagnostic challenge complicated by critical illness and malignancy

The pharyngeal-cervical-brachial (PCB) variant of Guillain–Barré syndrome (GBS) is a rare localized subtype characterized by rapidly progressive oropharyngeal, neck, and upper-limb weakness. Diagnosis becomes challenging when clinical features overlap with generalized forms such as acute motor axonal neuropathy (AMAN). We report a 76-year-old man with advanced gastric cancer who was admitted for chemotherapy but presented with acute-onset muscle weakness. The clinical course was complicated by aspiration pneumonia, acute respiratory decompensation following an endoscopic procedure, and bulbar dysfunction that became clinically apparent during rehabilitation. Although initially diagnosed with generalized GBS, the patient had marked upper-limb-predominant weakness from the outset and developed dysarthria after transfer to rehabilitation, prompting further serological investigation. Testing was positive for anti-GM1 and anti-GD1a and negative for anti-GT1a; because the sample was obtained after IVIG, the serological findings were considered supportive rather than definitive. Serial electrophysiological studies showed evolution from apparent conduction block to electrical inexcitability, favoring an AMAN-type nodal/axonal process. The early block was interpreted as potentially reversible nodal conduction failure, whereas the most severely affected nerves later showed severe axonal degeneration. We interpret this case as an overlap syndrome of AMAN and the PCB variant, while acknowledging that severe AMAN with prominent bulbar and cervicobrachial involvement remains a tenable alternative. Secondary motor deterioration after the critical phase was considered multifactorial: a possible treatment-related fluctuation contributed to the decision to administer a second course of IVIG, while procedure-associated respiratory decompensation, intensive care unit-acquired weakness, and malignancy-related cachexia may also have contributed. This case highlights the complexity of diagnosing overlap syndromes, the importance of recognizing demyelinating-appearing electrophysiological patterns in AMAN, and the difficulty of assessing possible treatment-related fluctuation in critically ill patients, in whom concurrent systemic insults confound the evaluation of secondary deterioration.