Case Report: Neurosyphilis with a paraparetic Guillain-Barré-spectrum phenotype and CSF-detected anti-GT1a IgG: an infection-autoimmunity diagnostic challenge

Background Active central nervous system (CNS) infection can resemble acute immune polyradiculoneuropathy, and the two processes may coexist. We describe a patient with neurosyphilis, rapidly progressive paraparetic weakness, and anti-GT1a IgG detected in cerebrospinal fluid (CSF) but not serum by a qualitative line immunoblot. Case presentation A 41-year-old man developed rapidly progressive paraparesis, urinary retention, and left abducens palsy. On hospital day 2, CSF opening pressure was 260 mmH 2 O, protein 1.56 g/L, white-cell count 272 × 10 6 /L, CSF TPPA was reactive, and CSF RPR was 1:8. Penicillin and methylprednisolone were started after the first lumbar puncture. By day 8, CSF white-cell count and protein had fallen during overlapping antimicrobial and corticosteroid treatment, but opening pressure remained 260 mmH 2 O and neurological deficits persisted. Paired serum-CSF testing showed marked blood-CSF barrier dysfunction (QAlb 17.4 × 10 -3 ), a type IV oligoclonal-band pattern, a Reiber-derived intrathecal IgM fraction of 35%, and anti-GT1a IgG detected in CSF but not serum. Day-11 electrodiagnostic testing showed reduced lower-limb motor amplitudes, preserved sensory responses, and absent F waves; a stable GBS electrophysiological subtype could not be assigned. Initial spinal MRI was normal; repeat lumbar MRI about 20 days later showed smooth enhancement along the ventral conus and cauda equina roots. IVIG was given on days 11-15; improvement was documented by day 30, and at 2 years the patient reported return to normal life and work. Conclusion Neurosyphilis can present with a paraparetic GBS-spectrum phenotype, making it difficult to determine whether syphilitic meningoradiculitis alone explains the syndrome or whether a concurrent immune polyradiculoneuropathy is also present. In this setting, blood-CSF barrier dysfunction, CSF-detected anti-GT1a IgG, and improvement after IVIG should be viewed as hypothesis-generating observations rather than proof of antibody compartmentalization, dual pathology, or treatment causality. In similar cases, longitudinal clinical follow-up, electrophysiology, imaging, and quantitatively validated paired serum-CSF immune testing are needed to distinguish a single infectious process, a concurrent immune neuropathy, and a biologically linked infection-autoimmunity process.