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Recent Breakthroughs and Emerging Trends in Gullain Barre
Syndrome
Ms. E. Honey, C. Prapulla
Pharmacology, Dr. Kv Subbareddy Institute of Pharmacy, Kurnool District Dupadu, Andhra Pradesh,
India
ABSTRACT
Guillain-Barré Syndrome (GBS) is an acute autoimmune polyneuropathy causing progressive weakness, loss
of reflexes, and sensory or autonomic dysfunction. It often follows Campylobacter jejuni infection due to
molecular mimicry between microbial and nerve antigens. GBS affects 1–2 per 100,000 people annually,
mainly males and older adults. Subtypes include AIDP, AMAN, AMSAN, and Miller Fisher syndrome.
Diagnosis relies on clinical signs, CSF analysis, and nerve conduction studies. Early treatment with IVIG or
plasma exchange improves outcomes, though some patients face lasting disability or death. Supportive care,
physiotherapy, and new immunotherapies enhance recovery, while infection prevention helps reduce risk.
Polyneuropathy, Acute flaccid paralysis, Autoimmune response, Camphylobacter jejuni.
Guillain-Barré Syndrome (GBS) is an acute autoimmune polyneuropathy causing progressive weakness that
peaks within four weeks. First described by Guillain, Barré, and Strohl in 1916, it remains the leading cause of
acute flaccid paralysis worldwide, affecting 1–2 people per 100,000 annually, more often males and older
adults. In most cases, GBS follows a respiratory or gastrointestinal infection, commonly due to Campylobacter
jejuni, Cytomegalovirus, Zika virus, or SARS-CoV-2, through molecular mimicry between microbial and
nerve antigens. Major subtypes include AIDP, AMAN, AMSAN, and Miller Fisher syndrome. Diagnosis is
based on clinical findings, cerebrospinal fluid analysis, and electrophysiological tests. Although most patients
respond to intravenous immunoglobulin or plasma exchange, 3–10% may die and about 20% experience
residual disability. Ongoing research on complement inhibitors and other immunotherapies shows promise for
improved outcomes.
FIG:1 Guillain Barre syndrome
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Table 1: Summary related to epidemiology of GBS
Annual incidence
1.3cases per 100,000
Age distribution
Elder people are at higher risk
Sex ratio
Males>females (1.5-1.7:1)
Seasonal trend
May increases in certain seasons like (rainy)
Infections
Intestinal infection, respiratory tract infection, campylobacter jejuni
Major variants
AIDP, AMAN
Immune system launches an attack against the peripheral nervous system.
The triggering events begin with infection or vaccination.
The immune system fails to protect against self-tissues because of immunological self-tolerance failure.
The disease produces damage to the protective myelin sheath while also damaging axonal structures during the
demyelinating process, and T-Helper cells produce cytokines.
The immune system produces antibodies which target gangliosides to combat bacterial infections.
The development of disorders at motor nerve terminals and nodes of Ranvier depends on the essential function
of antibiotics.
The complement system becomes active through this process. The disease first attacks the peripheral nervous
system.
This leads to both functional decline and physical harm to the nerves.
The condition produces two main types of nerve damage, which include axonal degeneration and segmental
demyelination.
The antibodies bind at motor nerve terminals, which blocks the release of ACH and stops nerve conduction.
The condition results in conduction block because of membrane damage. The damage process activates both
calcium influx and the complement cascade.
The process leads to proteolytic enzyme activation, which includes calpins and caspases.
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Axonal degeneration occurs.
Research shows that GM1 antibodies have the ability to attack Glial cells.
The damage to Schwann cells leads to axonal degeneration through a secondary process.
The deterioration of demyelization and axonal damage occurs.
FIG:2 Pathophysiology of GBS
GBS has four main subtypes: AIDP, MFS, AMAN, and AMSAN.
AIDP is the most common form (85–90% of cases) and involves demyelination of peripheral nerves, causing
muscle weakness, sensory loss, and complications such as irregular heartbeat or respiratory failure.
MFS mainly affects cranial nerves, leading to double vision, unsteady gait, and facial weakness; it is linked to
anti-GQ1b antibodies.
AMAN damages motor nerve axons, producing severe muscle weakness with minimal sensory loss, often seen
in children and young adults.
AMSAN affects both motor and sensory nerves, resulting in marked weakness and poor recovery.
When to Suspect:
Rapidly progressive limb weakness, reduced reflexes, sensory loss, facial or swallowing weakness, and eye
movement problems.
Diagnosis:
Based on clinical features, CSF analysis (high protein with normal cell count), and nerve conduction studies
after excluding other causes.
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ICU Admission:
Required for rapid progression, autonomic instability, swallowing, or breathing difficulty.
Treatment:
IV immunoglobulin (IVIG) or plasma exchange.
Early Complications:
Arrhythmias, infections, pain, urinary retention, constipation, eye problems, hyponatremia, pressure sores, and
muscle stiffness.
When to Start Treatment:
If unable to walk 10 m unaided, or if weakness, autonomic, or respiratory issues worsen.
Monitoring:
Regularly assess muscle strength, respiration, blood pressure, heart rhythm, and swallowing.
Treatment Fluctuation:
Repeat IVIG or plasma exchange if symptoms recur.
Pharmacological Approaches
FIG:4 Treatment for GBS
Plasma Exchange (PE): Removes harmful antibodies from plasma, speeding recovery and reducing
ventilation needs, especially if started within 2 weeks. Standard regimen: 5 sessions over 2 weeks. Rare risks:
sepsis, viral infections [28,29].
Immunotherapy (IVIG): IV immunoglobulins neutralize antibodies and accelerate recovery when started
early after motor symptoms. Mild cases may not need IVIG [30,31].
Mechanical Ventilation: Needed in ~25% of patients with respiratory failure, rapid progression, bulbar
involvement, or autonomic dysfunction. ICU support and monitoring are crucial for positive outcomes [32].
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MEDICATIONS:
NSAIDs (ibuprofen, naproxen) – relieve mild muscle/joint pain.
Opioids – for severe pain; risk of side effects and dependency.
Gabapentin – reduces nerve pain by inhibiting excitatory neurotransmitter release.
Carbamazepine – eases nerve pain by blocking sodium channels and reducing nerve signalling.
Tricyclic antidepressants (e.g., amitriptyline) – relieve pain and improve mood by increasing serotonin
and norepinephrine.
Additional care – blood clot prevention in immobile or paralyzed patients.
Non- Pharmalogical Approaches
Rehabilitation: Physical and occupational therapy maintain flexibility, prevent complications, and
restore muscle function.
Strengthening: Resistance training or weights to improve muscle power.
Aerobic training: Walking or cycling 2–3 times/week for stamina and cardiovascular health.
Flexibility/stretching: Maintain joint mobility and prevent stiffness.
Gait training: Improve walking patterns using parallel bars or treadmills.
Exercise monitoring: High-intensity exercise can boost recovery but must avoid overworking partially
denervated muscles [36,40].
Future Perspective For Gbs:
Targeting complement activation is a promising new strategy for GBS. Current therapies under trial include
anti-C1q antibodies (Phase 1b, NCT04035135) and IgG-degrading enzymes (Ides) (Phase 2, NCT01582763)
[31–35]. These approaches may help prevent serious and long-term neurological complications.
Etiological Factors Of Guillain Barre Syndrome:
GBS occurs when the immune system attacks peripheral nerves, causing muscle weakness and sensory loss.
Common triggers include bacterial infections (Campylobacter, Mycoplasma), viral infections (Influenza,
CMV, EBV, Zika, Hepatitis, HIV), surgerytrauma, and rarely vaccinations [10–12,22,33].
FIG:5 Etiological factors of GBS
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Management Of Gulliain Baree Syndrome:
Monitoring Stable patients walking >5 m can be managed locally but need close observation of disease
progression, vitals, and respiratory function.
SupportiveCare Essential to reduce mortality from complications.
Immunotherapy IVIG or plasma exchange within the first weeks improves recovery, reduces ventilator
need, and enhances long-term muscle strength. PE sessions should match severity (mild 2, moderate 4,
severe 4), with small-volume PE used in resource-limited settings.
DVTProphylaxis Subcutaneous heparin and compression stockings; oral anticoagulants for prolonged
immobility or tracheostomy
Pain Management Opioids, gabapentin, carbamazepine, NSAIDs, acetaminophen, or tricyclic
antidepressants; monitor for sedation and bowel issues.
Prevention Of Gullain Barre Syndrome:
While GBS is largely unpreventable, risk can be reduced by:
Practicing good hygiene (handwashing, disinfecting surfaces, avoiding contact with sick individuals)
Following food safety (thoroughly cook poultry, avoid unpasteurized milk, wash fruits/vegetables)
Staying healthy (balanced diet, regular exercise, hydration)
Keeping vaccinations up to date and seeking early treatment for infections [12,17,28,33,40]
FIG:6 Prevention for GBS
Complications:
Respiratory failure Weakness may require ventilation (~22% of patients).
Residual weakness or numbness may persist.
Cardiovascular issues Blood pressure changes, irregular heartbeat.
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Nerve pain affects ~1/3 of patients.
Bowel/bladder dysfunction and blood clots from immobility.
Pressure sores from limited movement; prevent with repositioning [7,23,24,27].
FIG:7 Complications of GBS
CONCLUSION
Guillain-Barré Syndrome (GBS) is a serious autoimmune disorder and a leading cause of acute flaccid
paralysis. While infections and molecular mimicry play key roles, early diagnosis via CSF analysis and nerve
studies improves outcomes. Main treatments include IVIG and plasma exchange, though many patients still
face disability, emphasizing the importance of rehabilitation and supportive care. Emerging therapies, like
complement inhibitors, offer future promise. Prevention, early intervention, and multidisciplinary management
are essential to reduce morbidity and mortality.
REFERENCES
1. Sejvar JJ, Baughman AL, Wise M, Morgan OW. Population incidence of Guillain-Barré syndrome: a
systematic review and meta-analysis. Neuroepidemiology. 2011;36(2):123–133.
2. Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barré syndrome. Lancet. 2016;388(10045):717–727.
3. Van den Berg B, Walgaard C, Drenthen J, Fokke C, Jacobs BC, van Doorn PA. Guillain-Barré
syndrome: pathogenesis, diagnosis, treatment and prognosis. Nat Rev Neurol. 2014;10(8):469–482.
4. Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barré syndrome. Ann
Neurol. 1990;27(S1): S21–24.
5. Yuki N, Hartung HP. Guillain-Barré syndrome. N Engl J Med. 2012;366(24):2294–2304.
6. Hughes RAC, Swan AV, van Doorn PA. Intravenous immunoglobulin for Guillain-Barré syndrome.
Cochrane Database Syst Rev. 2014;(9):CD002063.
7. Hughes RAC, Wijdicks EFM, Benson E, et al. Practice parameter: immunotherapy for Guillain-Barré
syndrome. Neurology. 2003;61(6):736–740.
8. Hadden RDM, Cornblath DR, Hughes RAC, et al. Electrodiagnostic criteria for Guillain-Barré
syndrome: a consensus statement. Ann Neurol. 1998;44(5):780–788.
9. Kuwabara S, Yuki N. Axonal Guillain-Barré syndrome: concepts and controversies. Lancet Neurol.
2013;12(12):1180–1188.
10. Jacobs BC, Rothbarth PH, van der Meché FGA, et al. The spectrum of antecedent infections in
Guillain-Barré syndrome: a case-control study. Neurology. 1998;51(4):1110–1115.
ISSN No. 2321-2705 | DOI: 10.51244/IJRSI |Volume XII Issue X October 2025
Page 979
www.rsisinternational.org
11. Wakerley BR, Uncini A, Yuki N. Guillain-Barré and Miller Fisher syndromes—new diagnostic
classification. Nat Rev Neurol. 2014;10(9):537–544.
12. Leonhard SE, Mandarakas MR, Gondim FAA, et al. Diagnosis and management of Guillain-Barré
syndrome in ten steps. Nat Rev Neurol. 2019;15(11):671–683.
13. Shahrizaila N, Lehmann HC, Kuwabara S. Guillain-Barré syndrome. Lancet. 2021;397(10280):1214–
1228.
14. McKhann GM, Cornblath DR, Griffin JW, et al. Acute motor axonal neuropathy: a frequent cause of
acute flaccid paralysis in China. Ann Neurol. 1993;33(4):333–342.
15. Nagashima T, Koga M, Odaka M, Hirata K, Yuki N. Continuous spectrum of pharyngeal–cervical–
brachial variant of Guillain–Barré syndrome. Arch Neurol. 2007;64(10):1519–1523.
16. Dimachkie MM, Barohn RJ. Guillain-Barré syndrome and variants. Neurol Clin. 2013;31(2):491–510.
17. Hughes RAC, Swan AV, Raphaël JC, Annane D, van Koningsveld R, van Doorn PA. Immunotherapy
for Guillain-Barré syndrome: a systematic review. Brain. 2007;130(9):2245–2257.
18. Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group. Randomised trial of plasma
exchange, intravenous immunoglobulin, and combined treatments in Guillain-Barré syndrome. Lancet.
1997;349(9047):225–230.
19. Lawn ND, Wijdicks EFM. Fatal Guillain-Barré syndrome. Neurology. 1999;52(3):635–638.
20. Dhar R, Stitt L, Hahn AF. The morbidity and outcome of Guillain-Barré syndrome associated with
mechanical ventilation. Can J Neurol Sci. 2008;35(4):443–446
21. Sri Ramachandra M, Kavya G, Vijay Teja V, Irshad S. A review on Guillain–Barre syndrome. Int J
Adv Pharm Sci (IAJPS). 2025;12(8):7-13.
