Guillain-Barre Syndrome: A Review
Sushant M. Ahire1, Prerana S. Pawar2, Sunil K. Mahajan1
1Department of Pharmaceutical Chemistry, Divine College of Pharmacy, Satana, Nashik, Maharashtra, India.
2Department of Pharmaceutics, Divine College of Pharmacy, Satana, Nashik, Maharashtra, India.
*Corresponding Author E-mail: sushantahire071@gmail.com
ABSTRACT:
GBS is a rare but serious neurological disorder in which the immune system mistakenly targets the nerves, causing muscle weakness, tingling, and, in severe cases, paralysis. First identified in 1916, GBS has several variations, including acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and Miller Fisher Syndrome (MFS). Although its exact cause remains unclear, it is often triggered by infections, vaccinations, surgery, or autoimmune conditions. The disorder disrupts nerve communication by damaging either the protective myelin sheath or the nerve fibres themselves, leading to motor and autonomic dysfunction. Diagnosis is based on symptoms, cerebrospinal fluid analysis, and nerve studies. Treatment primarily involves modulating the immune response through intravenous immunoglobulin (IVIG) or plasma exchange, along with supportive care and rehabilitation. While most individuals recover within a year, some may experience persistent weakness or complications. Advances in medical research have significantly improved recovery rates, but further studies are needed to enhance understanding and prevention of the condition.
KEYWORDS: Guillain-Barre syndrome, Infection, Immunity, vaccinations.
INTRODUCTION:
The immune system unintentionally targets the nerves connecting the brain and spinal cord to the rest of the body in GBS, an uncommon neurological disorder. This leads to sudden muscle weakness that can progressively worsen, sometimes within hours, or gradually over days or weeks. Symptoms vary in severity some individuals experience mild weakness, while others may develop severe paralysis, even requiring assistance to breathe.
In the worst situations, GBS can turn fatal, affecting vital signs like blood pressure, heart rate, and breathing. Though some people may still have residual weakness, most people recover, even from severe kinds, so there is hope.1,3,23
History of Guillain-Barre Syndrome:
French neurologists Andre Strohl, Jean Alexandre Barre, and Georges Guillain made the initial identification of GBS in 1916. During World War I, they were caring for two troops when they observed strange symptoms that didn't fit the typical patterns of sickness, such as muscle weakness and irregular reflexes.
High protein levels in the CSF fluid without an increase in white blood cells was a significant finding of their investigation. This discovery developed into a crucial diagnostic hint that physicians still use today to diagnose GBS. However, similar cases had been reported even earlier. In the 19th century, doctors described neurological conditions that resembled GBS, but it was Guillain Barre and Strohl’s work that officially defined it as a distinct disorder. Over the years, scientists learned that GBS is an autoimmune condition, often triggered by infections, vaccinations, or other factors that activate the immune system. The syndrome gained widespread attention in the 1970s when a rise in cases was linked to the swine flu vaccine, bringing more awareness to its potential triggers. While GBS can be severe, medical advancements like intravenous immunoglobulin (IVIG) and plasma exchange have significantly improved recovery rates, offering hope to those affected by the condition.2,20,24,25
Classification of GBS:
Table 1. Classification and types of GBS 5,21
|
Classification |
Subtype |
Key Features |
Affected Nerves |
Common Regions |
|
Demyelinating Type |
Acute Inflammatory Demyelinating Polyneuropathy (AIDP) |
Most common type; immune attack on myelin sheath, leading to muscle weakness and sensory loss. Ascending paralysis (legs → arms). |
Peripheral nerves (myelin sheath) |
North America, Europe |
|
Axonal Types |
Acute Motor Axonal Neuropathy (AMAN) |
Affects motor nerves, causing severe muscle weakness without sensory loss. Strongly linked to Campylobacter jejuni. |
Motor nerve axons |
Asia, Central and South America |
|
Acute Motor and Sensory Axonal Neuropathy (AMSAN) |
More severe than AMAN; affects both motor and sensory nerves, leading to widespread paralysis and sensory disturbances. |
Motor and sensory nerve axons |
Asia, Central and South America |
|
|
Rare Variants |
Miller Fisher Syndrome (MFS) |
Affects eye muscles (ophthalmoplegia), loss of reflexes, and ataxia (unsteady movement). Linked to anti-GQ1b antibodies. |
Cranial nerves (ocular region) |
Worldwide but rare |
|
Bickerstaff’s Brainstem Encephalitis (BBE) |
Severe form of MFS; affects brainstem, causing drowsiness, confusion, and loss of coordination. |
Brainstem and cranial nerves |
Rare, worldwide |
|
|
Pharyngeal-Cervical-Brachial (PCB) Variant |
Weakness in face, throat, neck, and arms, causing difficulty in swallowing and speaking. |
Cranial and upper limb nerves |
Rare, worldwide |
|
|
Chronic Form Related to GBS |
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) |
Chronic form lasting >8 weeks; progressive weakness and sensory loss. Requires long-term treatment. |
Peripheral nerves (myelin sheath) |
Worldwide |
Causes and Risk Factors of GBS:
Although the precise etiology of GBS is unknown, it is thought to occur when the body's own nerves are erroneously attacked by the immune system. Even though GBS is uncommon, there are some things that can make you more likely to get it. These are some of the main triggers that scientists have found. 6, 26
1. Infections (Most Common Trigger): In many cases, GBS is triggered by an infection that sets off the body's immune response. However, sometimes the immune system gets confused and mistakenly attacks the nerves instead of just fighting off the infection. This reaction has been connected to a number of common infections, including:
Bacterial infections:
Campylobacter jejuni (a major cause of food poisoning)
Mycoplasma pneumoniae (which causes respiratory infections)
Cytomegalovirus (CMV)
Epstein-Barr virus (EBV)
Zika virus
Viral infections:
Influenza (flu)
COVID-19
Other respiratory and gastrointestinal viruses.
2. Vaccinations:
Although rare, some vaccines have been linked to GBS, likely because of the way they interact with the immune system. However, the risk is extremely low, and the benefits of vaccines protecting against serious diseases far outweigh the small chance of developing GBS. While a few cases have been associated with certain vaccines, the overall likelihood remains very minimal.
i. Flu vaccine (especially the 1976 swine flu vaccine)
3. Surgery or Trauma:
Although rare, surgery or physical trauma can sometimes trigger GBS. The immune system may become confused by the stress of these occurrences and mistakenly target the nerves rather than the body's healing process.
4. Autoimmune Conditions:
If you have an autoimmune condition where your immune system mistakenly attacks your own body you might have a slightly higher risk of developing GBS. Some autoimmune disorders can increase this risk, including:
i. Lupus
ii. HIV/AIDS
iii. Chronic inflammatory demyelinating polyneuropathy (CIDP)
5. Genetic Factors: Genetics may influence how a person’s body reacts to infections or other triggers that can lead to GBS. While genes aren’t the primary cause, certain genetic traits might make someone more vulnerable to developing the condition.
6. Age and Gender
i. Age: All ages can be affected by GBS, however older folks are more likely to have it. As people age, their risk of acquiring GBS tends to rise.
ii. Gender: While both men and women can develop GBS, men may have a slightly higher chance of experiencing it.
7. Respiratory or Gastrointestinal Illnesses: Illnesses that affect the lungs or digestive system are more likely to trigger GBS. Some of the most common ones include:
i. Gastrointestinal infections caused by Campylobacter jejuni
ii. Respiratory infections like the flu or COVID-19
8. Other Potential Triggers:
There are also a few other conditions and stages in life that could raise the risk of developing GBS.
· Cancer (some cancers, particularly lymphomas and others)
· Pregnancy (though rare, there have been some reports of GBS occurring during pregnancy)
These factors don’t guarantee that someone will develop GBS, but they do increase the risk. It's important to be aware of them, especially if you've recently experienced any of these triggers.
Symptoms of Guillain-Barre Syndrome (GBS):
Fig.1. Signs and Symptoms of Guillain-Barre Syndrome (GBS)10
GBS typically starts with weakness and a tingling sensation in the legs, and these symptoms can progress quickly. While the severity of symptoms can vary, here are the key signs to watch out for:
Weakness or Paralysis
Leg weakness or tingling is frequently the first symptom of GBS, and it can progressively extend to the arms, face, and other areas of the body. In extreme circumstances, it may result in total paralysis.
Tingling or Numbness
The pins-and-needles sensation that many GBS sufferers have in their fingers, toes, or legs can be unsettling or frightening.
Difficulty Moving
The muscle weakness makes it challenging to do basic activities like walking, climbing stairs, or even getting out of bed.
Loss of Reflexes
Reflexes, like the knee-jerk response, may become weak or disappear altogether.
Breathing Issues
In more severe cases, GBS can affect the muscles involved in breathing, leading to shortness of breath or the need for assistance in breathing.
Pain
Muscle pain or aching can occur, especially in the lower back, and it can worsen as the condition progresses.
Problems with Facial Muscles and Eye Movements
If GBS affects facial muscles, it can cause difficulty with things like moving the face, drooping eyelids, and even difficulty speaking or swallowing.
Irregular Heart Rate or Blood Pressure
The autonomic nerve system may be impacted by GBS, causing abrupt variations in blood pressure and heart rate that occasionally leads to major problems.
Extreme Fatigue
As GBS progresses, you may feel increasingly tired and weak, making even routine tasks feel exhausting. (18,26) GBS can progress rapidly, with some people experiencing the most severe symptoms within days or weeks. If you or someone you know begins to show these signs, seeking immediate medical attention is crucial for proper treatment and care. Axons, which serve as electrical signal routes, make up the body's nerves. The myelin sheath, a protective coating that envelops each axon, aids in accelerating nerve signal transmission and facilitating effective brain-body communication. Acute inflammatory demyelinating polyradiculoneuropathy (AIDP), the most prevalent type of GBS, occurs when the immune system unintentionally targets and destroys the myelin sheath. Muscle weakness and problems with coordination result from this disturbance, which slows down nerve signal transmission.
Other types of GBS, such as acute motor axonal neuropathy (AMAN) and acute motor-sensory axonal neuropathy (AMSAN), directly target the axons, damaging nerve fibres. This interference affects how signals travel between the brain and muscles, resulting in weakness and abnormal reflexes. Another variation, Miller Fisher Syndrome, primarily affects the cranial nerves, which control facial, eye, and neck muscles. People with this form of GBS may experience eye muscle weakness or paralysis, balance and coordination difficulties, and absent reflexes. While these symptoms are distinct, they can also overlap with other common signs of GBS, such as muscle weakness.19
Pathophysiology of Guillain-Barre Syndrome:
GBS is an uncommon but dangerous illness when the body's immune system unintentionally targets the nerves. It typically appears following an infection, which sets off an aberrant immune response that harms the myelin sheath that surrounds nerves or, in certain situations, the nerve fibers themselves. Weakness, tingling, and even paralysis result from this damage because it interferes with the brain's ability to communicate with muscles. Although the precise origin isn't always known, GBS is believed to be caused by the immune system overreacting to an infection, attacking the body's own neurological system rather than merely fending off the sickness.7,22
Molecular Mimicry:
An aberrant immune response brought on by some infections, such as Campylobacter jejuni, Cytomegalovirus (CMV), Epstein-Barr virus (EBV), and Mycoplasma pneumoniae, may result in Guillain-Barre syndrome.
The body produces antibodies against bacterial or viral antigens, which resemble components of nerve cells.
These antibodies mistakenly attack gangliosides on nerve cells, leading to nerve damage.
Activation of the Immune System:
Nerve injury is influenced by both T-cell (cellular) and B-cell (humoral) immune responses.
Macrophages invade peripheral nerves and strip away the myelin, resulting in demyelination.
Activation of the complement system triggers inflammation and worsens nerve injury. 11
The most prevalent subtype, Acute Inflammatory Demyelinating Polyneuropathy (AIDP), is caused by macrophages targeting Schwann cells, which results in segmental demyelination and slows the transmission of nerve signals.
The immune system targets axons directly in Acute Motor Axonal Neuropathy (AMAN) and Acute Motor and Sensory Axonal Neuropathy (AMSAN), which causes more severe paralysis.12
Myelin degeneration disrupts saltatory transmission, which causes paralysis, tingling or numbness (paresthesia), and muscle weakness.
There may also be effects on the autonomic nervous system (ANS), which can result in blood pressure instability, irregular heartbeats, and, in extreme situations, respiratory failure.13
If the axons are preserved, Schwann cells can regenerate the myelin, allowing for recovery.
In more severe cases involving axonal damage, the healing process is slower and may not be fully complete.14
Treatment of Guillain-Barre Syndrome:
Recovery support, key function support, and immune attack management are the primary objectives of GBS treatment. The primary methods consist of 8
Since GBS is an autoimmune disorder, treatments focus on stopping the immune system from attacking the nerves:
Plasma Exchange (Plasmapheresis):
Eliminates harmful antibodies from the bloodstream.
It is most effective when started two to four weeks after the onset of symptoms.
Typically performed 5 times over 1-2 weeks.
Intravenous Immunoglobulin (IVIG):
Provides healthy antibodies to neutralize the immune attack.
Given as a 5-day infusion.
Preferred over Plasmapheresis due to easier administration.
Not combined with Plasmapheresis (one or the other is used)15
Since GBS can cause severe muscle weakness, including breathing difficulties, intensive supportive care is essential:
Respiratory Support:
30% of patients may need mechanical ventilation if respiratory muscles are affected.
Frequent monitoring of Forced Vital Capacity (FVC) to assess breathing function.
Pain Management:
Neuropathic pain is common. Treated with:
Gabapentin or Pregabalin (first-line).
Amitriptyline or Duloxetine (alternative options).
Opioids for severe pain.
Blood Clot Prevention:
Patients who have limited movement are more susceptible to deep vein thrombosis (DVT).
Preventive measures include low-dose heparin, enoxaparin, or compression stockings.
Nutritional Support:
If swallowing is affected, a feeding tube may be needed.16
Physical Therapy: Helps restore muscle strength and prevent complications like contractures.
Occupational Therapy: Aids in restoring everyday functional skills.
Speech Therapy: Assists with speech and accepting difficulties.
Psychological Support: Anxiety and depression are common, so mental health support may be necessary.17
80% recover fully within 6–12 months.
10-15% has long-term weakness or disability.
5% mortality rate (usually due to respiratory failure or complications).
Recurrence is rare (~2-5%).
Guillain-Barre syndrome is difficult to prevent because of its unpredictable nature. However, following general health practices can help reduce the risk.
Fig 2. Prevention of GBS9
Proper Hygiene: Washing hands regularly helps prevent infections such as Campylobacter and influenza.
Food Safety: Cooking poultry thoroughly and avoiding cross-contamination reduces the risk of bacterial infections.
Vaccination: Keeping up with recommended vaccines can help protect against infections that may trigger GBS.
Healthy Living: Maintaining a strong immune system is key to defending against infections. 9
REFERENCES:
1. Basuki M, Hamdan M, Fidiana, Fadil, Marjianto IR. Association between transmission season and degree of severity in Guillain-Barre syndrome. Res J Pharm Technol. 2020; 13(11): 5345-8.
2. Kusunoki S. [History of Guillain-Barre syndrome]. Brain Nerve. 2015 Nov; 67(11): 1295-303. Japanese.
3. Hughes RAC. Guillain-Barre syndrome: history, pathogenesis, treatment, and future directions. Eur J Neurol. 2024 Nov; 31(11): e16346.
4. Exploring the incidence and the effectiveness of structured teaching programme on minor disorders of pregnancy and its management among primigravida mothers in a selected rural area in Dharmapuri Dt. Asian J Nurs Educ Res. 2015; 5(1): 118-20.
5. Torres-Vásquez M, Chávez-Bosquez O, Hernández-Ocaña B, Hernández-Torruco J. Classification of Guillain-Barre syndrome subtypes using sampling techniques with binary approach. Symmetry. 2020; 12(3): 482.
6. Gautam H, Kutlehria A, Katoch K, Verma KK. Rhabdoviruses: complex neuropathogenic mechanism, molecular virology, epidemiology and treatment. Asian J Pharm Technol. 2024; 14(1): 59-64.
7. Bellanti R, Rinaldi S. Guillain-Barre syndrome: a comprehensive review. Eur J Neurol. 2024 Aug; 31(8): e16365.
8. Abbassi N, Ambegaonkar G. Guillain-Barre syndrome: a review. Paediatr Child Health. 2019; 29(11): 459-62.
9. Khan SA, Das PR, Nahar Z, Dewan SMR. An updated review on Guillain-Barre syndrome: challenges in infection prevention and control in low- and middle-income countries. SAGE Open Med. 2024; 12: 20503121241239633.
10. Jadhav SP, Ahire SM, Shewale VV, Patil CD, Pagar RY, Sonawane DD, Mahajan SK. Formulation of Tablet of Nifedipine co-crystal for enhancement of solubility and other physical properties. Biotech Res Asia. 2025 Mar 25; 22(1): 191-200.
11. Laman JD, Huizinga R, Boons GJ, Jacobs BC. Guillain-Barre syndrome: expanding the concept of molecular mimicry. Trends Immunol. 2022 Apr; 43(4): 296-308.
12. Dimachkie MM, Barohn RJ. Guillain-Barre syndrome and variants. Neurol Clin. 2013 May; 31(2): 491-510.
13. Chung T, Prasad K, Lloyd TE. Peripheral neuropathy: clinical and electrophysiological considerations. Neuroimaging Clin N Am. 2014 Feb; 24(1): 49-65.
14. Podbielska M, Banik NL, Kurowska E, Hogan EL. Myelin recovery in multiple sclerosis: the challenge of remyelination. Brain Sci. 2013 Aug; 3(3): 1282-324.
15. Liu S, Dong C, Ubogu EE. Immunotherapy of Guillain-Barre syndrome. Hum Vaccin Immunother. 2018; 14(11): 2568-79.
16. Rajabally YA. Immunoglobulin and monoclonal antibody therapies in Guillain-Barre syndrome. Neurotherapeutics. 2022; 19(3): 885-96.
17. Pawar PS, Ahire SM, Shewale VV, Jadhav S, Mahajan SK, Sonawane DD. Silver Nanoparticles: A Comprehensive Review on Synthesis, Properties and Applications. Research Journal of Pharmaceutical Dosage Forms and Technology. 2025 Nov 3; 17(4): 279-85.
18. Susila C. A qualitative assessment on issues among nurses directly involved with women who choose to terminate their pregnancy. Asian J Nurs Educ Res. 2012; 2(3): 107-8.
19. Morell P, Quarles RH. The myelin sheath. In: Siegel GJ, Agranoff BW, Albers RW, et al., editors. Basic neurochemistry: molecular, cellular and medical aspects. 6th ed. Philadelphia (PA): Lippincott-Raven; 1999.
20. Ahire SM, Pawar PS, Sonawane VN, Jadhav SP. Personalized Medicine and Pharmacogenomics: Impact of Genetic variation on Drug Response and Individualized Therapy-A Review. Asian Journal of Pharmacy and Technology. 2026 Jan 27; 16(1): 91-8.
21. Dimachkie MM, Barohn RJ. Guillain-Barre syndrome and variants. Neurol Clin. 2013 May; 31(2): 491-510.
22. Ziganshin RH, Ivanova OM, Lomakin YA, Belogurov AA Jr, Kovalchuk SI, Azarkin IV, et al. The pathogenesis of the demyelinating form of Guillain-Barre syndrome (GBS): proteo-peptidomic and immunological profiling of physiological fluids. Mol Cell Proteomics. 2016 Jul; 15(7): 2366-78.
23. Chang CWJ. Myasthenia gravis and Guillain-Barre syndrome. In: Parrillo JE, Dellinger RP, editors. Critical care medicine: principles of diagnosis and management in the adult. 5th ed. Philadelphia (PA): Elsevier; 2019. p. 1061-74.
24. Katirji B. Disorders of peripheral nerves. In: Jankovic J, Mazziotta JC, Pomeroy SL, Newman NJ, editors. Bradley and Daroff's neurology in clinical practice. 8th ed. Philadelphia (PA): Elsevier; 2022. Chap 106.
25. Sejvar JJ, Baughman AL, Wise M, Morgan OW. Population incidence of Guillain-Barre syndrome: a systematic review and meta-analysis. Neuroepidemiology. 2011; 36(2): 123-33.
26. Gautam H, Kutlehria A, Katoch K, Verma KK. Rhabdoviruses: complex neuropathogenic mechanism, molecular virology, epidemiology and treatment. Asian J Pharm Technol. 2024; 14(1): 59-64.
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Received on 20.09.2025 Revised on 11.11.2025 Accepted on 31.12.2025 Published on 22.04.2026 Available online from April 24, 2026 Res.J. Pharmacology and Pharmacodynamics.2026;18(2):159-164. DOI: 10.52711/2321-5836.2026.00022 ©A and V Publications All right reserved
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