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Acute Motor and Sensory Axonal Neuropathy

Acute Motor and Sensory Axonal Neuropathy (AMSAN) — Comprehensive Disease Characteristics Report

2026-05-07
Falcon MONDO:0020348 Model: Edison Scientific Literature 27 citations

Acute Motor and Sensory Axonal Neuropathy (AMSAN) — Comprehensive Disease Characteristics Report

Target disease: Acute motor and sensory axonal neuropathy (AMSAN) (autoimmune; acute post-infectious immune-mediated peripheral neuropathy; axonal Guillain–Barré syndrome (GBS) variant). (shang2021axonalvariantsof pages 1-2)

High-level definition (current understanding): AMSAN is an axonal form of GBS with acute involvement of motor and sensory axons, typically presenting with rapidly progressive limb weakness plus sensory loss/paresthesia and areflexia/hyporeflexia, often after an infectious trigger. (shang2021axonalvariantsof pages 1-2, leonhard2024guillain–barrésyndrome pages 1-3)

Key abstract-quoted definition (GBS umbrella): Nature Reviews Disease Primers (published 2024-12-19) states: “Guillain–Barré syndrome (GBS) is a rare immune-mediated polyradiculoneuropathy” and notes that “Diagnosis is based on clinical features, supported by cerebrospinal fluid analysis and nerve conduction studies.” (leonhard2024guillain–barrésyndrome pages 1-3)

1. Disease Information

1.1 Overview

AMSAN is a GBS subtype within “axonal variants” (primarily AMAN and AMSAN). AMSAN differs from AMAN by having prominent sensory axonal involvement in addition to motor axonal injury. (shang2021axonalvariantsof pages 1-2)

1.2 Key identifiers / ontology mappings (availability in retrieved sources)

The retrieved literature focused on GBS and axonal variants but did not provide a specific MONDO ID or Orphanet code for AMSAN.

ICD (from real-world claims-based definitions for GBS): - GBS was defined using ICD-9 357.0 and ICD-10 G61.0, G65.0 in a US prescribing-patterns study. (stino2024intravenousimmunoglobulinand pages 1-2)

MeSH / MONDO / Orphanet / OMIM: not explicitly stated in the retrieved texts; thus not reliably reportable here.

1.3 Synonyms / alternative names

1.4 Evidence source type

Most disease-level statements here are derived from aggregated disease resources and reviews (e.g., Nature Reviews Disease Primers; axonal GBS update review; Campylobacter–ganglioside review), supplemented by human clinical case reports illustrating AMSAN phenotypes/triggers and treatment response. (leonhard2024guillain–barrésyndrome pages 1-3, shang2021axonalvariantsof pages 1-2, latov2022campylobacterjejuniinfection pages 1-2, geng2023acutemotorsensoryaxonal pages 3-5)

2. Etiology

2.1 Primary causal factors (mechanistic etiology)

Post-infectious autoimmunity via molecular mimicry is the leading paradigm for axonal GBS/AMSAN, particularly in Campylobacter jejuni–associated disease. (shang2021axonalvariantsof pages 1-2, latov2022campylobacterjejuniinfection pages 1-2, leonhard2024guillain–barrésyndrome pages 1-3)

Abstract quote (Campylobacter–GBS link; published 2022-10-28): Latov writes: “Preceding infection with Campylobacter jejuni (Cj) occurs in approximately 30% of patients with Guillain–Barre syndrome (GBS), and the risk of GBS following Cj infection is increased by 77 to 100-fold. GBS is most often of the axonal subtype and is thought to be mediated by IgG antibodies to peripheral nerve gangliosides … induced by molecular mimicry.” (latov2022campylobacterjejuniinfection pages 1-2)

2.2 Risk factors

Infectious triggers (human clinical + epidemiologic evidence): - Campylobacter jejuni enteritis: strong epidemiologic association and mechanistic evidence via ganglioside mimicry. (latov2022campylobacterjejuniinfection pages 1-2, leonhard2024guillain–barrésyndrome pages 1-3) - Viral and other infectious triggers reported for axonal variants include Zika and other pathogens in review summaries; case literature also reports post–COVID-19 AMSAN. (shang2021axonalvariantsof pages 1-2, geng2023acutemotorsensoryaxonal pages 3-5)

Timing after diarrheal illness: in C. jejuni–associated GBS, neurological symptoms “usually begin at 10 days to 3 weeks after the onset of diarrhea.” (latov2022campylobacterjejuniinfection pages 1-2)

COVID-19 association (case-level, mechanistic hypotheses): AMSAN has been described following SARS-CoV-2 infection, with proposed mechanisms including molecular mimicry and hyperinflammatory para-infectious immune injury; anti-ganglioside antibodies may be absent in some cases. (geng2023acutemotorsensoryaxonal pages 3-5, geng2023acutemotorsensoryaxonal pages 5-6)

2.3 Protective factors

No specific protective genetic variants, environmental protective factors, or proven preventive interventions for AMSAN were identified in the retrieved sources.

2.4 Gene–environment interactions

The retrieved sources emphasize infection-triggered autoimmunity and mention “host genetic predisposition” as an important research direction in GBS broadly, but do not provide validated AMSAN-specific gene–environment interaction loci. (shang2021axonalvariantsof pages 1-2)

3. Phenotypes (clinical features)

3.1 Core phenotype spectrum (suggested HPO terms)

AMSAN typically includes: - Acute/subacute limb weakness (often symmetric), progressing over days (HP:0001324 Muscle weakness; HP:0003674 Motor delay/impairment not specific; consider HP:0003323 Progressive muscular weakness). - Areflexia/hyporeflexia (HP:0001284 Areflexia). (leonhard2024guillain–barrésyndrome pages 1-3) - Sensory symptoms (paresthesia, sensory loss) (HP:0003401 Paresthesia; HP:0000763 Sensory neuropathy). (leonhard2024guillain–barrésyndrome pages 1-3, geng2023acutemotorsensoryaxonal pages 3-5) - Pain (HP:0012531 Pain). (leonhard2024guillain–barrésyndrome pages 1-3) - Cranial nerve involvement may occur in severe GBS phenotypes (facial palsy, bulbar weakness) (HP:0001343 Facial palsy; HP:0002493 Dysphagia). (leonhard2024guillain–barrésyndrome pages 1-3) - Autonomic dysfunction in severe cases (HP:0001278 Orthostatic hypotension; HP:0002013 Vomiting; broader: dysautonomia). (busl2023guidelinesforneuroprognostication pages 1-3, umar2024complexneurologicalsequelae pages 4-6) - Respiratory failure / need for ventilation in severe cases (HP:0002878 Respiratory failure; HP:0002094 Dyspnea). (leonhard2024guillain–barrésyndrome pages 1-3)

3.2 Onset and progression

GBS (including AMSAN) is characterized by rapid progression with a typical nadir within weeks. Neurocritical Care guidelines note symptoms reach maximum “within 2–4 weeks.” (busl2023guidelinesforneuroprognostication pages 1-3)

3.3 Frequency among affected individuals (data availability)

Phenotype frequencies are best described for GBS overall rather than AMSAN specifically in the retrieved sources: - “Around 20% of patients may develop weakness in all four limbs … and respiratory failure requiring mechanical ventilation.” (leonhard2024guillain–barrésyndrome pages 1-3)

3.4 Quality-of-life impact

Nature Reviews Disease Primers emphasizes residual disability: “~20% of patients who received treatment are unable to walk after 6 months.” (leonhard2024guillain–barrésyndrome pages 1-3)

4. Genetic/Molecular Information

4.1 Causal genes

AMSAN is not a monogenic disorder in standard clinical framing; the retrieved sources do not identify causal genes or OMIM disease entries specific to AMSAN. (leonhard2024guillain–barrésyndrome pages 1-3, shang2021axonalvariantsof pages 1-2)

4.2 Key molecular targets (autoantigens)

Gangliosides on peripheral nerves are key immune targets in axonal GBS/AMSAN: - Anti-ganglioside antibodies reported in association with AMSAN include anti-GM1, anti-GM1b, anti-GD1a. (shang2021axonalvariantsof pages 6-7)

4.3 Pathogenic “variants” (not applicable)

Pathogenic DNA variants are not established as causal for AMSAN in the provided evidence.

4.4 Epigenetics / chromosomal abnormalities

Not established for AMSAN in the retrieved sources.

5. Environmental Information

5.1 Infectious agents (key environmental triggers)

5.2 Lifestyle/occupational factors

No AMSAN-specific lifestyle protective/risk factors were established in the retrieved sources.

6. Mechanism / Pathophysiology

6.1 Causal chain (upstream → downstream)

Upstream trigger: infection (especially C. jejuni; also viral triggers). (latov2022campylobacterjejuniinfection pages 1-2, leonhard2024guillain–barrésyndrome pages 1-3)

Immune priming via molecular mimicry: bacterial lipooligosaccharides mimic peripheral nerve gangliosides, producing cross-reactive antibodies. Nature Reviews Disease Primers explicitly summarizes: “For example, in patients with preceding Campylobacter jejuni infection, molecular mimicry causes a cross-reactive antibody response to nerve gangliosides.” (leonhard2024guillain–barrésyndrome pages 1-3)

Effector injury: anti-ganglioside antibodies activate complement at nodes/paranodes and axolemma, causing conduction failure and structural axonal injury/degeneration (axonal variants). (leonhard2024guillain–barrésyndrome pages 5-7, latov2022campylobacterjejuniinfection pages 2-4)

Downstream clinical manifestations: reduced compound muscle action potentials (CMAPs), sensory nerve action potential (SNAP) abnormalities, weakness + sensory loss, and in severe cases bulbar/respiratory/autonomic failure. (geng2023acutemotorsensoryaxonal pages 3-5, leonhard2024guillain–barrésyndrome pages 1-3)

6.2 Immune system involvement

  • Axonal variants are associated with anti-ganglioside antibodies and complement-dependent mechanisms; Latov describes that GBS axonal subtype is “thought to be mediated by IgG antibodies to peripheral nerve gangliosides” cross-reactive with C. jejuni components. (latov2022campylobacterjejuniinfection pages 1-2)

6.3 Suggested GO biological process terms (mechanism-oriented)

6.4 Suggested Cell Ontology terms (CL)

6.5 Molecular profiling / biomarkers (availability)

The retrieved sources highlight a lack of specific biomarkers for GBS broadly (including axonal variants). (leonhard2024guillain–barrésyndrome pages 1-3)

7. Anatomical Structures Affected

7.1 Organ/system level

  • Peripheral nervous system (peripheral nerves and roots; polyradiculoneuropathy). (leonhard2024guillain–barrésyndrome pages 1-3)

7.2 Tissue/cell level (suggested UBERON terms)

7.3 Subcellular (suggested GO Cellular Component)

  • GO:0033267 axon part
  • GO:0043209 myelin sheath (even in “axonal” variants, nerve architecture is involved)
  • GO:0030054 cell junction (node/paranode microdomains; mechanistic target region) (leonhard2024guillain–barrésyndrome pages 5-7)

8. Temporal Development

8.1 Onset pattern

Acute onset with rapid progression; nadir typically within 2–4 weeks in GBS overall. (busl2023guidelinesforneuroprognostication pages 1-3)

8.2 Course

Typically monophasic: Nature Reviews Disease Primers states “GBS is usually a monophasic disease.” (leonhard2024guillain–barrésyndrome pages 1-3)

9. Inheritance and Population

9.1 Epidemiology

Data are primarily for GBS overall; AMSAN-specific incidence is not provided in the retrieved evidence.

  • GBS annual global incidence “1–2 per 100,000 persons per year.” (leonhard2024guillain–barrésyndrome pages 1-3)
  • Axonal-variants review provides a similar range: 0.81–1.89 per 100,000/year. (shang2021axonalvariantsof pages 1-2)
  • Sex/age: males affected ~1.5× more than females; risk rises ~20% per decade of age. (leonhard2024guillain–barrésyndrome pages 1-3)

9.2 Population differences (axonal variants)

Axonal variants (including AMSAN) are discussed as having geographic variability, with higher representation in some regions (review-level). (restrepojimenez2018theimmunotherapyof pages 46-47)

10. Diagnostics

10.1 Diagnostic approach (real-world implementation)

GBS diagnosis is “based on clinical features, supported by cerebrospinal fluid analysis and nerve conduction studies.” (leonhard2024guillain–barrésyndrome pages 1-3)

CSF: - Axonal-variants review: CSF albuminocytologic dissociation is a hallmark “detectable in almost 90%,” with CSF albumin rising from week 2 and present in ~70% by the end of week 2. (shang2021axonalvariantsof pages 1-2)

Electrophysiology (NCS/EMG): - Axonal variants: early studies can be misleading; decreased CMAP amplitudes and reversible conduction failure/block can appear early; electrophysiology “more reliable” at 3–6 weeks than at 1–2 weeks. (shang2021axonalvariantsof pages 1-2) - Nature Reviews Disease Primers emphasizes heterogeneity: mixed axonal–demyelinating or even normal NCS can occur, limiting strict NCS-only subclassification. (leonhard2024guillain–barrésyndrome pages 4-5)

Serology (supportive, not required for all): Anti-ganglioside antibodies support axonal subtype classification (anti-GM1/anti-GD1a and related), but seronegative axonal cases exist. (shang2021axonalvariantsof pages 6-7, geng2023acutemotorsensoryaxonal pages 5-6)

10.2 Differential diagnosis (high-level)

11. Outcome / Prognosis

11.1 Key outcome statistics (GBS overall)

Nature Reviews Disease Primers reports: “~20% of patients who received treatment are unable to walk after 6 months and ~5% die as a consequence of GBS.” (leonhard2024guillain–barrésyndrome pages 1-3)

Neurocritical Care neuroprognostication guidelines provide ICU-relevant statistics: - “10–30% require mechanical ventilation during the acute phase.” (busl2023guidelinesforneuroprognostication pages 1-3) - Mortality “range between 1 and 13%,” with “mortality rates up to 20%” among ventilated patients. (busl2023guidelinesforneuroprognostication pages 1-3)

11.2 Prognostic tools / expert consensus

Busl et al. recommend: - EGRIS (Erasmus GBS Respiratory Insufficiency Score) for predicting ventilation, and - EGOS / modified EGOS for predicting independent ambulation at 3 months and beyond. (busl2023guidelinesforneuroprognostication pages 1-3)

12. Treatment

12.1 Standard of care

Only proven effective disease-modifying treatments for GBS (including AMSAN) remain: - Intravenous immunoglobulin (IVIg) - Plasma exchange (PE/PLEX) (leonhard2024guillain–barrésyndrome pages 1-3)

Nature Reviews Disease Primers (2024) abstract quote: “Effective treatments include plasma exchange and intravenous immunoglobulins.” (leonhard2024guillain–barrésyndrome pages 1-3)

12.2 Treatment strategy and common pitfalls (guidelines + evidence)

A US real-world analysis emphasizes trials showing no benefit from: - Repeat IVIG dosing and - PLEX followed by IVIG (combination therapy) in non-responders. (stino2024intravenousimmunoglobulinand pages 1-2)

Abstract quote (real-world utilization; published 2024-09): Stino et al. state: “Randomized controlled trials show that repeat IVIG dosing and … combination therapy have no additional therapeutic benefit in Guillain-Barre Syndrome (GBS) non-responders.” (stino2024intravenousimmunoglobulinand pages 1-2)

12.3 Recent developments (2023–2024) — complement inhibition (eculizumab)

A key 2024 development is a phase 3 randomized trial of eculizumab (C5 inhibitor) added to IVIg in severe GBS.

Abstract quote (published 2024-07; J Peripher Nerv Syst): “This study evaluated the efficacy and safety of eculizumab add-on therapy to IVIg … in patients with severe GBS.” (kuwabara2024efficacyandsafety pages 1-2)

Results: - Primary endpoint not met (time to Hughes FG ≤1): HR 0.9, 95% CI 0.45–1.97; p = 0.89. (kuwabara2024efficacyandsafety pages 1-2) - Strong target engagement: serum free C5 reduced by 99.99% at 1 hour postdose and sustained to week 5. (kuwabara2024efficacyandsafety pages 1-2)

12.4 MAXO (Medical Action Ontology) suggestions

13. Prevention

No established primary-prevention intervention is specific to AMSAN beyond prevention/management of infectious triggers at the population level.

Vaccine-associated GBS (broader context): The retrieved evidence supports ongoing pharmacovigilance and risk assessment for GBS after vaccination, but does not provide AMSAN-specific prevention guidance. (shang2021axonalvariantsof pages 1-2)

14. Other Species / Natural Disease

Direct naturally occurring AMSAN analogs in non-human species were not identified in the retrieved sources.

15. Model Organisms

Experimental autoimmune neuritis and anti-ganglioside models (mechanistic relevance): Latov reports animal models in which rabbits immunized with GM1 or C. jejuni LPS develop acute axonal neuropathy with anti-GM1 antibodies, supporting the antibody-mediated mechanism relevant to axonal GBS/AMSAN. (latov2022campylobacterjejuniinfection pages 2-4)

2023–2024 “latest research” highlights (prioritized)

  1. 2024 authoritative synthesis: Nature Reviews Disease Primers (Leonhard et al.; 2024-12-19) consolidates contemporary consensus on GBS triggers, diagnosis (CSF + NCS), treatment (IVIg/PE), and residual disability (20% non-ambulant at 6 months; ~5% mortality). (leonhard2024guillain–barrésyndrome pages 1-3)
  2. 2024 mechanism-directed therapy trial: Phase 3 add-on eculizumab to IVIg did not improve functional recovery despite robust complement suppression, suggesting complement blockade alone is insufficient or that patient selection/timing remain unresolved. (kuwabara2024efficacyandsafety pages 1-2)
  3. 2024 real-world implementation gap: A US claims-based cohort (2001–2018) found repeat IVIG use (39.7%) and combination therapy (6.1%) persisted, despite RCT evidence against these approaches in non-responders; diagnostic reclassification to CIDP occurred in 32%. (stino2024intravenousimmunoglobulinand pages 1-2)

Evidence summary table

Table (click to expand)
Domain Evidence summary Key quantitative stats (with values) Primary source (first author, year, journal) PMID if available URL Context citation ID
Definition AMSAN is an axonal Guillain-Barré syndrome (GBS) subtype characterized by acute motor and sensory axonal involvement; axonal GBS variants include AMAN and AMSAN. GBS is an acute, immune-mediated polyradiculoneuropathy with rapidly progressive weakness and sensory deficits. Global GBS incidence: 1–2/100,000/year; males affected ~1.5× more often; risk rises ~20% per decade of age. Leonhard, 2024, Nature Reviews Disease Primers https://doi.org/10.1038/s41572-024-00580-4 (leonhard2024guillain–barrésyndrome pages 1-3, shang2021axonalvariantsof pages 1-2)
Triggers AMSAN is usually post-infectious, with Campylobacter jejuni the best-supported trigger; COVID-19, chikungunya, and other infections have also been reported as antecedents in axonal GBS/AMSAN cases. Molecular mimicry between microbial glycans and nerve gangliosides is the leading mechanism. Preceding C. jejuni in ~30% of GBS; GBS risk after C. jejuni infection increased 77–100-fold; neurologic symptoms usually begin 10 days to 3 weeks after diarrhea. Latov, 2022, Microorganisms https://doi.org/10.3390/microorganisms10112139 (latov2022campylobacterjejuniinfection pages 1-2, latov2022campylobacterjejuniinfection pages 2-4, geng2023acutemotorsensoryaxonal pages 3-5)
Autoantibodies Axonal GBS including AMSAN is associated most often with anti-ganglioside antibodies, particularly anti-GM1, anti-GM1b, and anti-GD1a. Antibodies are often IgG1/IgG3 subclasses and can cross-react with C. jejuni lipooligosaccharides. Anti-ganglioside antibodies reported in 41–85% of GBS following C. jejuni infection. Shang, 2021, Journal of Neurology https://doi.org/10.1007/s00415-020-09742-2 (shang2021axonalvariantsof pages 6-7, latov2022campylobacterjejuniinfection pages 2-4, latov2022campylobacterjejuniinfection pages 1-2)
Pathophysiology The best-supported causal chain is infection → molecular mimicry → anti-ganglioside antibody generation → complement activation at nodes/paranodes/axolemma → conduction failure and axonal degeneration. Pathology in axonal GBS shows antibody/complement deposition on axolemma and macrophage-associated axonal injury. Serum C5 in the eculizumab phase 3 trial was reduced by 99.99% 1 hour post-dose and remained suppressed through week 5, showing effective target engagement. Latov, 2022, Microorganisms https://doi.org/10.3390/microorganisms10112139 (latov2022campylobacterjejuniinfection pages 2-4, leonhard2024guillain–barrésyndrome pages 5-7, kuwabara2024efficacyandsafety pages 1-2)
Diagnostics Diagnosis is primarily clinical and supported by CSF and electrophysiology. For axonal variants, serial NCS/EMG are important because early studies may show reduced CMAPs, reversible conduction failure/block, or equivocal findings; CSF albuminocytologic dissociation is common but may lag. CSF albuminocytologic dissociation in almost 90%; CSF protein elevated in ~70% by end of week 2; electrophysiology more reliable at 3–6 weeks than 1–2 weeks. Shang, 2021, Journal of Neurology https://doi.org/10.1007/s00415-020-09742-2 (shang2021axonalvariantsof pages 1-2, busl2023guidelinesforneuroprognostication pages 1-3, leonhard2024guillain–barrésyndrome pages 1-3)
Prognosis Axonal GBS/AMSAN generally has a more severe course and slower recovery than demyelinating GBS. Across GBS, respiratory failure, bulbar weakness, and severe nadir disability are major poor prognostic features; EGOS and EGRIS are used for outcome and ventilation risk prediction. 10–30% require mechanical ventilation; ~20% of treated GBS patients cannot walk at 6 months; ~5% die; mortality can reach up to 20% among ventilated patients. Busl, 2023, Neurocritical Care https://doi.org/10.1007/s12028-023-01707-3 (busl2023guidelinesforneuroprognostication pages 1-3, leonhard2024guillain–barrésyndrome pages 1-3, umar2024complexneurologicalsequelae pages 4-6)
Treatment Standard evidence-based treatment remains IVIG or plasma exchange; combination therapy and repeat IVIG do not add benefit and can increase adverse events. Supportive ICU care and rehabilitation remain essential, especially in severe axonal cases. Median time to walk without aid: 51 days with IVIG, 49 days with plasma exchange, 40 days with combined treatment in older trial data; repeat IVIG used in 39.7% and combination therapy in 6.1% of a US real-world cohort before newer evidence/guidelines. Kuwabara, 2024, Journal of the Peripheral Nervous System https://doi.org/10.1111/jns.12646 (kuwabara2024efficacyandsafety pages 1-2, stino2024intravenousimmunoglobulinand pages 1-2)
Recent developments 2023-2024 Recent work emphasized 2023 EAN/PNS guideline-based care and mechanism-directed therapy. A 2024 phase 3 trial of eculizumab added to IVIG in severe GBS did not meet its primary endpoint despite strong complement suppression and acceptable safety. Phase 3 eculizumab trial enrolled 57 participants (37 eculizumab, 20 placebo); primary endpoint HR 0.9, 95% CI 0.45–1.97, p=.89. Kuwabara, 2024, Journal of the Peripheral Nervous System https://doi.org/10.1111/jns.12646 (kuwabara2024efficacyandsafety pages 1-2, freiha2026guillainbarrésyndromeprogress pages 7-9)
Real-world implementation Real-world US prescribing data show persistent use of non-recommended repeat IVIG and some IVIG/PLEX combination therapy, suggesting a gap between evidence/guidelines and practice. Diagnostic reclassification from GBS to CIDP also occurs frequently in claims-based care pathways. US cohort n=2325; repeat IVIG 39.7%; combination therapy 6.1%; later reclassified to CIDP 32.0%. Stino, 2024, Muscle & Nerve https://doi.org/10.1002/mus.28265 (stino2024intravenousimmunoglobulinand pages 1-2)

Table: This table condenses the most supported AMSAN findings from the available context into disease knowledge base fields. It highlights what is known specifically for axonal GBS/AMSAN and where evidence comes from broader GBS literature used to inform AMSAN care.

Limitations of this report (evidence availability constraints)

  • AMSAN-specific ontology identifiers (MONDO, Orphanet, OMIM, MeSH term strings) were not available in the retrieved full-text excerpts and therefore are not asserted here.
  • Many epidemiologic and prognosis statistics are reported at the GBS umbrella level; AMSAN-specific incidence, subtype-specific mortality, and antibody-frequency distributions require additional targeted cohort studies not captured in the retrieved evidence subset.

References

  1. (shang2021axonalvariantsof pages 1-2): Pei Shang, Mingqin Zhu, Ying Wang, Xiang-yu Zheng, Xiujuan Wu, Jie Zhu, Jiachun Feng, and Hong-Liang Zhang. Axonal variants of guillain–barré syndrome: an update. Journal of Neurology, pages 1-18, Mar 2021. URL: https://doi.org/10.1007/s00415-020-09742-2, doi:10.1007/s00415-020-09742-2. This article has 93 citations and is from a domain leading peer-reviewed journal.

  2. (leonhard2024guillain–barrésyndrome pages 1-3): Sonja E. Leonhard, Nowshin Papri, Luis Querol, Simon Rinaldi, Nortina Shahrizaila, and Bart C. Jacobs. Guillain–barré syndrome. Nature Reviews Disease Primers, Dec 2024. URL: https://doi.org/10.1038/s41572-024-00580-4, doi:10.1038/s41572-024-00580-4. This article has 48 citations.

  3. (stino2024intravenousimmunoglobulinand pages 1-2): Amro M. Stino, Evan L. Reynolds, Maya Watanabe, and Brian C. Callaghan. Intravenous immunoglobulin and plasma exchange prescribing patterns for guillain‐barre syndrome in the united states—2001 to 2018. Muscle & Nerve, 70:1192-1199, Sep 2024. URL: https://doi.org/10.1002/mus.28265, doi:10.1002/mus.28265. This article has 3 citations and is from a peer-reviewed journal.

  4. (geng2023acutemotorsensoryaxonal pages 3-5): Na Geng, Pengfei Wang, and Yong Zhang. Acute motor-sensory axonal polyneuropathy variant of guillain-barré syndrome with a thalamic lesion and covid-19: a case report and discussion on mechanism. Frontiers in Neurology, Sep 2023. URL: https://doi.org/10.3389/fneur.2023.1227505, doi:10.3389/fneur.2023.1227505. This article has 6 citations and is from a peer-reviewed journal.

  5. (umar2024complexneurologicalsequelae pages 4-6): Anam Umar, Amber E Faquih, Bilal Jawed, and Muhammad Bilal. Complex neurological sequelae: axonal guillain-barré syndrome post covid-19 in a young patient. Cureus, Aug 2024. URL: https://doi.org/10.7759/cureus.67213, doi:10.7759/cureus.67213. This article has 0 citations.

  6. (latov2022campylobacterjejuniinfection pages 1-2): Norman Latov. Campylobacter jejuni infection, anti-ganglioside antibodies, and neuropathy. Microorganisms, 10:2139, Oct 2022. URL: https://doi.org/10.3390/microorganisms10112139, doi:10.3390/microorganisms10112139. This article has 25 citations.

  7. (geng2023acutemotorsensoryaxonal pages 5-6): Na Geng, Pengfei Wang, and Yong Zhang. Acute motor-sensory axonal polyneuropathy variant of guillain-barré syndrome with a thalamic lesion and covid-19: a case report and discussion on mechanism. Frontiers in Neurology, Sep 2023. URL: https://doi.org/10.3389/fneur.2023.1227505, doi:10.3389/fneur.2023.1227505. This article has 6 citations and is from a peer-reviewed journal.

  8. (busl2023guidelinesforneuroprognostication pages 1-3): Katharina M. Busl, Herbert Fried, Susanne Muehlschlegel, Katja E. Wartenberg, Venkatakrishna Rajajee, Sheila A. Alexander, Claire J. Creutzfeldt, Gabriel V. Fontaine, Sara E. Hocker, David Y. Hwang, Keri S. Kim, Dominik Madzar, Dea Mahanes, Shraddha Mainali, Juergen Meixensberger, Oliver W. Sakowitz, Panayiotis N. Varelas, Thomas Westermaier, and Christian Weimar. Guidelines for neuroprognostication in adults with guillain–barré syndrome. Neurocritical Care, 38:564-583, Mar 2023. URL: https://doi.org/10.1007/s12028-023-01707-3, doi:10.1007/s12028-023-01707-3. This article has 52 citations and is from a peer-reviewed journal.

  9. (shang2021axonalvariantsof pages 6-7): Pei Shang, Mingqin Zhu, Ying Wang, Xiang-yu Zheng, Xiujuan Wu, Jie Zhu, Jiachun Feng, and Hong-Liang Zhang. Axonal variants of guillain–barré syndrome: an update. Journal of Neurology, pages 1-18, Mar 2021. URL: https://doi.org/10.1007/s00415-020-09742-2, doi:10.1007/s00415-020-09742-2. This article has 93 citations and is from a domain leading peer-reviewed journal.

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  11. (latov2022campylobacterjejuniinfection pages 2-4): Norman Latov. Campylobacter jejuni infection, anti-ganglioside antibodies, and neuropathy. Microorganisms, 10:2139, Oct 2022. URL: https://doi.org/10.3390/microorganisms10112139, doi:10.3390/microorganisms10112139. This article has 25 citations.

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