Guillain-Barré syndrome (GBS) is a severe immune-driven polyneuropathy marked by the acute onset of flaccid paralysis, areflexia, and in severe cases, life-threatening autonomic or respiratory failure. Although the clinical presentation and diagnostic criteria are widely established, the precise mechanisms underlying GBS are complex and poorly understood. This review summarizes current literature on the interplay of post-infectious triggers, molecular mimicry, and host susceptibility as influenced by genetic and epigenetic variables. Infectious pathogens such as Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, and, more recently, Zika and SARS-CoV-2 operate as initiators via molecular mimicry, in which pathogen antigens imitate peripheral nerve components, triggering the formation of autoreactive antibody and T-cell responses. Acute inflammatory demyelinating polyneuropathy (AIDP) is characterized by demyelination and inflammatory cytokine responses, whereas acute motor axonal neuropathy (AMAN) is associated with ganglioside-targeting antibodies and axonal loss. Genetic polymorphisms, such as those in HLA, TLR4, MMP9, and CD1A, influence vulnerability to the disease and its progression. Given that many patients experience persistent sensory, motor, and autonomic dysfunction despite treatment, the identification of long-term complications highlights the necessity of customized rehabilitation and long-term follow-up. Traditional therapeutic techniques, such as plasma exchange and intravenous immunoglobulin, remain in use, but current trials on complement inhibitors, antibody-degrading enzymes, and mesenchymal stem cell therapies indicate a move toward mechanism-driven approaches. Despite these advances, significant knowledge gaps remain regarding predictors of poor outcomes and underlying causes of persistent disabilities and complications, highlighting the need for continued translational and clinical research.

BACKGROUND Multifocal acquired demyelinating sensory-motor neuropathy (MADSAM) is recognized as a variant of chronic inflammatory demyelinating polyneuropathy. The primary characteristics of MADSAM include multifocal sensory loss and muscle weakness, which are frequently asymmetrical and predominantly affect the upper limbs. Involvement of the lower limbs is less commonly observed in MADSAM. CASE REPORT A 27-year-old female patient presented with recurrent numbness and weakness in her left lower limb was admitted to our hospital. Her medical history included episodes of left peripheral facial paralysis and lower-limb numbness and weakness, which had previously improved after short-term oral steroid therapy. In addition to motor and sensory peripheral nerve impairment in the left lower limb, the neurological examination revealed atrophy of the tongue muscle and a leftward deviation of the tongue. Cerebrospinal fluid examination and magnetic resonance imaging indicated no abnormalities. Electromyography suggested demyelination of motor and sensory nerves in the left lower limb. Sural nerve biopsy demonstrated demyelination changes and axonal degeneration. A diagnosis of multifocal sensory and motor neuropathy was considered, and the patient was administered corticosteroids and tacrolimus. As the condition progressed, electromyography showed gradual involvement of both lower limbs, leading to the consideration of MADSAM. Despite treatment with corticosteroids and tacrolimus, the patient experienced relapse. Rituximab was initiated, resulting in symptoms improvement and reduced recurrence without adverse events. CONCLUSIONS Corticosteroids, plasma exchange, and immunoglobulins have been demonstrated to be effective treatments for CIDP. In our MADSAM case, rituximab proved effective when the patient did not respond to corticosteroids and tacrolimus. We propose that rituximab may serve as an alternative option for patients with MADSAM.

POEMS syndrome is a paraneoplastic condition characterized by peripheral neuropathy and monoclonal plasma cell dysfunction. additional major criteria include sclerotic bone lesions. Malignancies such Hodgkin lymphoma, metastatic prostate cancer, breast cancer, and Paget's disease frequently feature ivory vertebra. A 21-year-old female exhibited symmetric onset of lower motor neuron weakness in both lower limbs, beginning distally and subsequently progressing to proximal involvement, accompanied by sensory loss during the past 8 months. The examination indicated skin hyperpigmentation, pallor, hepatomegaly, and papilledema. Nerve conduction shows axonal sensory-motor neuropathy, whereas bone marrow analysis reveals reactive marrow with 5% plasma cells and variable cellularity. Serum electrophoresis reveals an elevation of M protein in the gamma region. X-ray and MRI spine revealing sclerotic vertebra lesion of body of D11 vertebra, characteristics of ivory vertebra. Ivory vertebra may be a feature of POEMS syndrome in appropriate clinical context. Ivory vertebra is usually associated with various malignancy conditions.

Background and Clinical Significance: Wartenberg's syndrome (cheiralgia paresthetica) is classically described as a pure sensory neuropathy of the superficial branch of the radial nerve (SBRN). However, in rare circumstances, dynamic mechanical irritation around the radial styloid may produce an atypical clinical phenotype with concurrent motor impairment, broadening the clinical significance of recognizing motion-related compression mechanisms. Case Presentation: A 35-year-old woman presented with persistent dorsoradial wrist pain and numbness, accompanied by progressive weakness of thumb extension, five years after a conservatively treated nondisplaced scaphoid fracture. Neurological examination demonstrated sensory loss in the SBRN distribution and Medical Research Council (MRC) grade 3/5 strength of the extensor pollicis longus (EPL). Nerve conduction studies revealed a markedly prolonged EPL motor latency (4.5 ms; normal ≤ 2.5 ms) with preserved sensory conduction. High-resolution ultrasound showed focal enlargement of the SBRN (cross-sectional area 0.13 cm2) and, critically, dynamic snapping of the nerve over the radial styloid that reproduced the patient's symptoms. The patient underwent ten weekly sessions of ultrasound-guided hydrodissection with 5% dextrose. After treatment, the pain Visual Analog Scale improved from 8/10 to 0/10 and EPL strength recovered to MRC 5/5. Follow-up nerve conduction studies demonstrated normalization of EPL motor latency (2.1 ms), and repeat ultrasound confirmed resolution of SBRN enlargement and snapping. Conclusions: This case expands the phenotype of Wartenberg's syndrome to include mixed sensory-motor involvement associated with dynamic SBRN snapping at the radial styloid. Dynamic ultrasound was pivotal for identifying the motion-dependent mechanism, and ultrasound-guided 5% dextrose hydrodissection achieved complete sensory and motor recovery as a minimally invasive and effective treatment option.

Mutations in KIDINS220 are known to cause hereditary spastic paraplegia (HSP) and SINO syndrome. However, the phenotypic and genotypic spectrum of KIDINS220-related disorders remains incompletely understood. Herein, we describe the clinical, electrophysiological, histopathological, and genetic features of a novel KIDINS220 sterile alpha motif (SAM) -like domain mutation identified in a Chinese family with HSP accompanied by severe peripheral neuropathy (PN). Clinical data, electrophysiological characteristics, and sural nerve histopathology were analyzed in a 19-year-old Chinese male. Genetic testing was performed in his family by using whole-exome sequencing, mitochondrial genome testing, and Sanger validation. A comprehensive literature review was conducted to analyze the phenotypic and genetic data of previously reported cases with KIDINS220 variants up to July 2025. The proband exhibited classical signs of autosomal dominant HSP accompanied by severe multifocal sensory-motor PN. The spinal cord MRI showed mild spinal cord thinning, while the brain MRI and nerve ultrasound examinations were normal. Electrophysiological study revealed absent sensory nerve responses and globally reduced motor conduction velocities. Sural nerve biopsy confirmed significantly reduced nerve fiber density, myelin defects, axonal degeneration, and mitochondrial abnormalities. A heterozygous KIDINS220 c.3668A > G (p. Glu1223Gly) mutation, located within the SAM domain, was identified in both the proband and his mother. A total of 42 cases from 11 cohorts were reviewed. We suggest that patients with KIDINS220 SAM domain mutation may present with HSP accompanied by severe, mixed axonal and demyelinating PN, expanding the existing spectrum of the clinical phenotypes and pathogenic variants of KIDINS220.