Acute Inflammatory Demyelinating Polyradiculoneuropathy Presenting With Multiple Cranial Nerve Palsies and Total Ophthalmoplegia: The Importance of Accurate Diagnosis and Timely Immunotherapy

Abstract

Guillain–Barré syndrome (GBS) is an immune‐mediated disorder of the peripheral nervous system characterized by progressive weakness and often triggered by infections. GBS has an estimated mortality rate of approximately 5%, with a worldwide incidence of 0.81–1.91 cases per 1,00,000 person‐years. This case reported a 23‐year‐old man presented with progressive weakness in all four extremities. An initial neurological examination revealed bilateral total ophthalmoplegia, ptosis on both eyes, bilateral facial palsy lower motor neuron (LMN) type, dysarthria, dysphagia, flaccid tetra‐paresis, gloves, and stocking paresthesia. Lumbar puncture showed cytoalbumin dissociation. Nerve conduction studies showed a demyelinating sensorimotor polyradiculoneuropathy lesion. The patient received intravenous immunoglobulin (IVIG) treatment 0.4 g/kg/day for 5 days, physical rehabilitation therapy, nutritional support, multidisciplinary care involving anesthesiology and intensive care teams, and other symptomatic treatments. At five‐month follow‐up, the patient demonstrated complete recovery. GBS typically presents as an acute ascending sensorimotor neuropathy; however, atypical presentations may occur. Extensive cranial nerve involvement—including complete ophthalmoplegia, bilateral facial palsy, and bulbar dysfunction—in AIDP is uncommon and may mimic other GBS spectrum disorders. Early recognition, prompt immunotherapy, and careful electrophysiological evaluation are essential for optimizing patient outcomes. Because electrodiagnostic classification of GBS may evolve over time, serial nerve conduction studies should be considered whenever feasible to improve subtype classification and diagnostic confidence.