From Meningitis to Guillain-Barré: An Atypical Pediatric Presentation

Background: Guillain-Barré syndrome (GBS) is an acute immune-mediated polyneuropathy and the most common cause of acute flaccid paralysis in children. Typical presentation involves ascending symmetrical weakness and areflexia, atypical forms may mimic other neurologic or infectious disorders. One of the rarest diagnostic challenges is presentation with meningeal signs, which may lead to misdiagnosis as meningitis. Case Presentation: We report the case of an ۱۱-year-old boy previously healthy, admitted with fever, headache, vomiting, photophobia, and positive meningeal signs. His family had a history of Covid-۱۹ infection about a month ago. On examination, he exhibited positive meningeal sign, diffuse myalgia, particularly in the lower limbs, and an antalgic gait. Neurological evaluation revealed bilaterally diminished deep tendon reflexes (۱+) with preserved upper limb strength gag reflex. Initial cerebrospinal fluid (CSF) analysis showed protein ۱۴۸ mg/dL with ۲ WBC/μL. During hospitalization, he developed progressive limb pain, nausea, and bulbar symptoms including dysphagia, dysarthria, and frequent coughing. MRI of the lumbosacral spine with gadolinium demonstrated cauda equina root enhancement. He transferred to pediatric intensive care unit admission for close monitoring and was prophylactically intubated due to worsening respiratory effort and bulbar dysfunction. Repeat CSF later revealed marked protein elevation to ۲۷۲ mg/dL with no leukocytes, consistent with albuminocytologic dissociation. Intravenous immunoglobulin (IVIG) was administered at ۲ g/kg. Following extubation, nerve conduction studies confirmed acute inflammatory demyelinating polyneuropathy (AIDP). With supportive care and physiotherapy, he showed gradual neurological improvement and was discharged for outpatient rehabilitation. Discussion: This case emphasizes the diagnostic challenge of distinguishing GBS from meningitis in children presenting with meningeal irritation and systemic symptoms suggestive of meningitis. While CSF pleocytosis is typical of meningitis, albuminocytologic dissociation with progressive areflexia points toward GBS. MRI findings of cauda equina enhancement and confirmatory electrophysiology further supported the diagnosis. Previous literature has described similar diagnostic pitfalls in pediatric GBS. Conclusion: GBS in children may present with meningeal signs mimicking meningitis, delaying diagnosis and treatment. Clinicians should maintain a high index of suspicion when meningeal signs coexist with evolving hyporeflexia or weakness. Early recognition, IVIG therapy, and supportive rehabilitation are critical for favorable outcomes.