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Guillain-Barre Syndrome

Original Editor -Nitisha Sethi
Top Contributors - Oshomoji Olawale, Vidya Acharya, Surinder Singh, Garima Gedamkar, Kim Jackson, Jonathan Wong, Redisha Jakibanjar, Andeela Hafeez, Wendy Walker, Lucinda hampton, Rachael Lowe, Nitisha Sethi, Eugenie Lamprecht, Chelsea Mclene, Evan Thomas, Admin, WikiSysop, Alex Kin Ming NG, Claire Knott, Alexandra Stead, Wout Van Hees, Naomi O'Reilly, Oyemi Sillo, Khloud Shreif, Sai Kripa and Mason Trauger

Introduction

Guillain-Barré syndrome (GBS) is an acute, immune-mediated polyradiculoneuropathy and a neurological emergency.[1][2] GBS was first described in 1916 by the French neurologists Georges Charles Guillain and Jean Alexandre Barré, along side with the physiologist André Strohl.[3] It can involve sensory, motor, and autonomic nerves and it's the most common cause of rapid progressive flaccid paralysis.[2][4]

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Aetiology

Most cases of GBS are preceded by upper respiratory tract infections or diarrhoea six weeks prior to their onset.[6] The most common infections causing GBS include Campylobacter jejuni, Mycoplasma pneumoniae, Epstein-Barr virus, and Cytomegalovirus. Campylobacter jejuni is responsible for about a third of GBS cases, and the ensuing GBS is usually more severe than that due to other causes. Recent infection with Campylobacter jejuni is strongly associated with developing Acute Motor Axonal Neuropathy (AMAN).[7]

Coronavirus disease 2019 (COVID-19) vaccination and severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) infection are both recognised triggers of GBS.[8] A 2025 systematic review comparing 295 confirmed post-vaccination GBS cases against GBS following other infections (including Campylobacter jejuni and Zika virus) found out that COVID-19-associated GBS was associated with a significantly higher rate of prolonged hospitalisation and substantial respiratory involvement, suggesting a more severe clinical course than GBS arising from other infectious triggers.[9] These findings were further supported by a 2026 multicentre retrospective observational study conducted in China, which additionally identified higher rates of cranial nerve involvement in this population.[10]

Herpes zoster also has been identified as a potential antecedent infection in GBS, with epidemiological evidence demonstrating a significantly increased short-term risk following infection.[11] Molecular mimicry by the bacterial agents is thought to cause the autoimmunity with the development of anti-GQ1b IgG antibodies.[12] [13]

Alternative predisposing factors include recent surgery, lymphoma, and systemic lupus erythematosus (SLE).[3]

Pathophysiology

The pathophysiology of GBS is complex. GBS is considered to be an autoimmune disease triggered by a preceding bacterial or viral infection.[12][14]

The body's immune response causes a cross-reaction with neural tissue through molecular mimicry, a phenomenon whereby microbial antigens share structural similarities with gangliosides found on peripheral nerve tissue, triggering the production of cross-reactive antibodies that attack the host's own nerves. [15] [16] [17] The pathophysiology differs on the subtype of GBS. For example in Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP), the most common subtype in Western countries, the immune response destroys the myelin sheath, accompanied by endoneurial oedema and inflammation.[18] [19] These acute inflammatory lesions are present within several days of the onset of symptoms. Nerve conduction is slowed and may be blocked completely, there's also distal motor latency.[18] In AIDP axons are intact unlike in AMAN and acute motor and sensory axonal neuropathy (AMSAN), where the immune response targets the axons directly, causing primary axonal degeneration.[19] After 2-3 weeks of demyelination, the Schwann cells begin to proliferate, inflammation subsides, and re-myelination begins.[20]

Subtypes

GBS can be split up into two types according to electrophysiologic and pathologic features: the demyelinating type, and the axonal type.[21] Subtypes in line with these include:

  1. AIDP: most common form, characterised by T-cell activation and cytokine elevation, leading to demyelination and slower nerve conduction.[12]
  2. Axonal subtypes: AMAN (historically Chinese paralytic syndrome) and AMSAN. Both of which are driven by anti-ganglioside M1 (anti-GM1) antibodies and complement activation, causing axonal degeneration.[12]
  3. Regional GBS syndromes: Miller Fisher variant (MFS/MFV), characterised by ataxia, ophthalmoplegia, and areflexia without weakness, anti-ganglioside Q1b (anti-GQ1b) antibodies are present in most cases.[22] MFS is associated with anti-GQ1b Immunoglobulin G (IgG) antibodies and form part of a broader spectrum known as the anti-GQ1b antibody syndrome.[23] Bickerstaff brainstem encephalitis (BBE) is a rare anti-GQ1b antibody–associated disorder characterised by ophthalmoplegia, ataxia, and impaired consciousness, and is considered to overlap with GBS within a shared autoimmune spectrum.[23]

Epidemiology

  • Incidence: The annual incidence of GBS is 1.2–2.3 per 100,000 person-years.[22] A 2023 systematic review, which included 72 studies, reported a global incidence of 0.30–6.08 per 100,000 person-years between 1985 and 2020.[24] Incidence in some Asian populations has been reported as notably lower, including 0.44 per 100,000 person-years in Japan and 0.63 per 100,000 person-years in Korea.[25] A meta-analysis of urban China reported incidence rates ranging from 0.41 (95% confidence interval [CI]: 0.27 to 0.58) to 0.58 (95% CI: 0.38 to 0.82) per 100,000 person-years between 2013 and 2017.[25] Globally, incidence is higher in Western Europe, South Asia, and Northern Europe, and lower in Australia and New Zealand, South-East Asia, and North Africa.[25]
  • Age: The annual mean rate of hospitalisations related to GBS increases with age. A national population-based study in China (2016–2019) confirmed this pattern, recording incidence of 0.233 per 100,000 person-years in children, rising to 0.829 per 100,000 in adults, and peaking in the 70–74 age group at 1.806 per 100,000 person-years (95% CI 1.741–1.870). This is consistent with US hospitalisation data, which records 1.5 cases per 100,000 in children under 15, peaking at 8.6 cases per 100,000 in people aged 70–79 years.[26][27] However, a large self-controlled case series of over 1.1 million Herpes zoster cases demonstrated a significantly increased short-term risk of GBS following infection across adult age groups (relative risk [RR] = 6.3, 95% CI: 1.8–21.9 in those aged 18–64; RR = 4.1, 95% CI: 1.9–8.7 in those aged ≥65).[11] This suggest that while baseline incidence is higher in older adults, the relative impact of specific infectious triggers may be more pronounced in younger populations.[28]
  • Sex: Men are more likely to develop GBS than women; the relative risk for men is 1.78 compared to women.[29][30]

Clinical presentation

Typically, GBS symptoms present 2-4 weeks after a relatively benign gastrointestinal or respiratory illness.[31] The first neurological sign of GBS is usually paraesthesia of the toes, followed by a sudden onset (hours to days) of symmetrical, progressive bilateral weakness and sensory loss distal to proximal throughout the body. This dysfunction may impact the muscles of respiration, and even cranial nerves. In most forms of GBS, there is a greater loss of motor function than sensory function.[14][13]

GBS patterns: Pattern can be sensory, motor or mixed. There can be greater motor or sensory function as explained above.
Disease Course and Recovery

The mean time to the peak of symptoms is 12 days (from first neurological symptoms), with 98% of patients reaching a peak by 4 weeks.[32] More recent evidence corroborates this timeline, reporting that the nadir is reached within 4 weeks in more than 95% of cases.[33] A plateau phase of persistent, unchanging symptoms then ensues, followed days later by gradual symptom improvement.[34] Recovery usually begins 2-4 weeks after the progression ceases.[35] Overall, most patients with GBS do well, however, 20% of patients continue with morbidity.[2] More than 80% of patients achieve independent ambulation within six months.[36]

Pain

Pain is an often under-recognised symptom of GBS.[37] [38] In a study following 55 patients with GBS, 89% reported pain, with 47% grading it as severe.[39] Another study following 223 patients with GBS found that 55% experienced pain, with 70% experiencing pain before the onset of weakness.[40] Pain was described as deep and achy in the lower back and legs, and patients also described dysesthesia in their extremities.[39] The pain improved with time, but the dysesthesia (burning, aching, electrical shocks) remained in a small group of patients.[39] Another study suggested that pain may last up to 2 years for some patients.[41]

Two types of pain can be classified in GBS. The first type of pain is more acute, beginning before onset of muscle weakness and lasts until discharge from hospital. It presents as mainly radicular, muscle pain and dysesthesia of the extremities. The second type is observed during the chronic stage - patients complain of dysesthesia, muscle pain and arthralgia in the limbs; and these are associated with weakness and disability.[37]

Autonomic dysfunction

A study in 2023, concluded that autonomic dysfunction is a common complication GBS, occurring in about one-third of patient population, and may present with cardiovascular instability (hypertension, hypotension, tachycardia), enteric (intestinal) dysmotility, and need for vasopressor support.[22] It is associated with more severe disease, increased need for intensive care and mechanical ventilation, and poorer functional outcomes, including delayed recovery of independent walking.[22]

Fatigue

Fatigue is another underreported clinical presentation of GBS.[38] It occurs in 35-80% of persons with GBS,[6] showing that it affects majority of the population of GBS.[42] A 2024 systematic review shows that the frequency of fatigue is more reduced in population of GBS in low-middle income countries than high income countries.[42]

Psychosocial

The psychosocial aspect is an important and underreported area in GBS clinical presentation. Feelings of guilt, sadness, and unhappiness related to the loss of ability to ambulate and functional independence are important considerations. Persistent fatigue is not solely a physical phenomenon; it is also associated with reduced quality of life, low mood, and social withdrawal.[42] Patients with GBS often experience a sense of loss in the context of a changing life, and dissatisfaction with healthcare services, which may contribute to depression, post-traumatic stress, and anxiety.[43] [38]

Post-traumatic stress disorder (PTSD) is a recognised psychological sequela of GBS, and is particularly prevalent in patients who have required ICU admission or mechanical ventilation, where the experience of sudden paralysis, loss of communication, and dependence on life-sustaining equipment can be profoundly distressing.[44]

Differential diagnosis

Diagnostic procedures

GBS is considered a clinical diagnosis and a diagnosis can be made at the bedside in most cases. For atypical cases or unusual subtypes, ancillary testing can be useful.[45]

These include:

  • Cerebrospinal fluid (CSF) investigation: CSF protein may be normal in the early stages; albumino-cytological dissociation (elevated protein with normal cell count) is found in the majority of cases, increasing in frequency with time from onset. There may be lymphocytosis (< 50 cells/µL).[46]
  • Electrophysiological studies: it includes nerve conduction studies and electromyography. They are normal in the early stages but show typical changes after a week or so with conduction block and multifocal motor slowing, sometimes most evident proximally as delayed F-waves.[4]
    The only way to classify a patient as having the axonal or nonaxonal type is electrodiagnostically.
  • Further investigative procedures can be undertaken to identify an underlying cause
    For example:
    • Chest X-ray , stool culture and appropriate immunological tests to rule out the presence of cytomegalovirus or mycoplasma
    • Antibodies to the ganglioside GQ1b for MFV.[23]
  • MRI: Not routine for typical presentations in GBS, but should be considered in atypical cases. Whole spine MRI with contrast helps exclude mimics such as spinal cord compression, transverse myelitis, and tumours. Nerve root enhancement supports GBS but lacks specificity and a normal MRI does not rule it out. Findings must always be interpreted alongside clinical, CSF, and electrophysiological data.[6]
  • Lumbar Puncture: Most, but not all, patients with GBS have an elevated CSF protein level (>400 mg/L), with normal CSF cell counts. Elevated or rising protein levels on serial lumbar punctures and 10 or fewer mononuclear cells/mm3 strongly support the diagnosis.[46]

Prognosis

GBS can be a devastating disorder because of its sudden and unexpected onset. In addition, recovery is not necessarily quick. Typically, improvement occurs after a number of weeks to months.[3][6]

The majority of people recover completely or nearly completely.[47] However, some have mild residual effects such as foot drop or abnormal sensation in the feet and hands that may persist for two years or more. Persistent fatigue and pain may also present. While most patients recover well, a minority may experience substantial long-term disability requiring mobility aids such as a cane, walker, or wheelchair, and approximately 15% experience long-term weakness affecting their daily functioning and quality of life.[38]

Predictive factors for poor outcome for GBS include:[48][49][50] [33][51]

  • Older age
  • Cranial nerve impairment
  • Recent surgery
  • Elevated level of liver enzymes
  • Diabetes
  • High blood pressure at admission
  • Uroschesis (urinary retention)
  • Fever
  • Ventilator support during hospitalisation
  • Impaired consciousness
  • Absence of preceding respiratory infection

It's also important to note that high levels of anti-GM1 antibodies in AMAN and AMSAN are associated with more severe axonal damage and poorer recovery.[12][52] These markers can help predict prognosis and guide therapeutic decisions. Early management is an indication of better prognosis.[30]

Most patients with GBS have a good long-term prognosis; while death during hospitalisation is uncommon (less than 5%), some individuals may be left with persistent neurological deficits.[53]

Outcome measures

  • GBS Disability Scale
    • The GBS disability scale (Hughes Disability Scale) is a common outcome measure used to determine the severity of GBS. The scale is a seven-point functional grading scale with scores from 0 (healthy) to 6 (death), widely used to assess disease severity, guide treatment decisions, and monitor recovery in patients with Guillain-Barré syndrome; a score of 3 or more generally indicates the need for hospitalisation and immunotherapy.[54]
  • Modified Erasmus GBS Respiratory Insufficiency Score (mEGRIS)
    • The mEGRIS is a validated clinical prediction tool used to estimate the risk of mechanical ventilation in patients with Guillain-Barré syndrome. It is initially scored using three clinical variables: time from onset of weakness to admission, presence of bulbar palsy, and weakness of neck flexion and hip flexion. Each variable is scored and summed to generate a total score, with higher scores indicating a greater risk of requiring mechanical ventilation. It can be reassessed at multiple time points, making it useful for ongoing risk monitoring; a high score should prompt early consideration of intensive care admission and ventilatory support. The tool was internally validated within the full International Guillain-Barré syndrome Outcome Study (IGOS) cohort, achieving an area under the curve (AUC) of 0.83, and within separate regional subgroups with an AUC of 0.85, demonstrating consistent and reliable predictive performance across different geographical regions and patient populations.[6] An AUC value of 1.0 represents perfect predictive accuracy; values above 0.80 are considered strong.
  • Functional Independence Measure (FIM)
    • Beyond disease severity and respiratory risk, functional independence is a key goal in GBS rehabilitation. The FIM is a common outcome measure used to determine the ability to perform activities of daily living. It is made up of 18 individual items consisting of motor and cognitive functioning, that are scored from 1 (total assistance) to 7 (independent). Each item is added together to get an overall level of independence between 18-126. The FIM is considered time-consuming but an easy-to-use, valid and reliable method that can be trusted in clinical settings to assess patients with various conditions.[55] [56] It captures both motor and cognitive aspect, with a motor total sub-score of 91 and cognitive total sub-score of 35.
  • 10-meter walk test
    • The 10-meter walk test is a useful tool to measure gait speed and functional mobility. The tool uses the amount of time a patient takes to walk 10 meters, to provide a speed in m/sec. This can be compared to normative data to determine risk of falls and if a gait aid is indicated. The 10-meter walk test is a common tool used by clinicians and is seen as reliable and valid for a number of neurological conditions.[57]  
  • Medical Research Council Sumscore
    • The Medical Research Council Sumscore is a common tool used to measure muscle strength. This tool considers six main muscle groups (bilaterally) and assesses their strength using a scale of 0-5. These six scores can then be added together to create a total sum ranging from 0 to 60.[58] It has shown to be a clinically useful tool for physiotherapists for neurological conditions. This tool has high intra-rater reliability, indicating it needs to be repeated by the same physiotherapist to assess change.[59]
  • Depression Anxiety Stress Scale (DASS)
    • The DASS is a validated screening tool used to measure the severity of depression, anxiety, and stress. It is particularly relevant in GBS given the high prevalence of psychological sequelae, including post-traumatic stress disorder.[43]
  • World Health Organisation Quality of Life Assessment with 100 items (WHOQOL-100)
    • The WHOQOL-100 is a quality of life questionnaire developed by the World Health Organisation. It assesses six domains including physical health, psychological wellbeing, and social relationships, making it a comprehensive tool for monitoring recovery beyond physical function alone.
  • Fatigue Severity Scale (FSS)
    • The FSS is a 9-item scale which measures the severity of fatigue and its effect on a person's activities and lifestyle in patients with a variety of disorders. It is particularly relevant in GBS given the high prevalence of fatigue as a clinical presentation.[42][60]

Management

There is no known cure for GBS, but therapies that lessen the severity of the illness and accelerate the recovery in most patients exist. GBS is primarily managed with Intravenous (IV) immunoglobulin (Ig) or plasmapheresis (plasma exchange) along with supportive measures, which can hasten recovery.[3][6]

For dosage, the 2023 European Academy of Neurology/Peripheral Nerve Society Guideline,[6] stated that "The task force recommends intravenous immunoglobulin (IVIg) 0.4 g/kg for 5 days, in patients within 2 weeks (good point practice also within 2–4 weeks) after onset of weakness if unable to walk unaided, or a course of plasma exchange (PE) 12–15 L in four to five exchanges over 1–2 weeks, in patients within 4 weeks after onset of weakness if unable to walk unaided."

Further medical management

  • Ventilatory support
    • Atelectasis leads to hypoxia.[61]
    • Hypercarbia later finding; arterial blood gases may be misleading.
    • Vital capacity, tidal volume and negative inspiratory force are the best indicators of diaphragmatic function.[61]
    • Progressive decline of these functions indicates an impending need for ventilatory assistance. Forced Vital Capacity (FVC) should be monitored three to six times daily; ventilation should be considered when FVC falls to ≤20 mL/kg, and is almost inevitable at ≤10 mL/kg. Ultimate risk is also influenced by age, concurrent lung disease, aspiration risk, and respiratory muscle fatigue.[6]
    • Intubation may be necessary for patients with substantial oro-pharyngeal dysfunction to prevent aspiration.
    • Tracheostomy may be needed in patients intubated for 2 weeks who do not show improvement. This is important to reduce complications with prolonged translaryngeal intubation and facilitate weaning (extubation).[62][61]
    • Weaning readiness can be assessed using the Rapid Shallow Breathing Index (RSBI): RSBI = respiratory frequency (f) ÷ tidal volume in litres (VT); an RSBI <105 breaths/min/L predicts successful weaning.[63]
    • A spontaneous breathing trial (SBT) on minimal ventilator support for 30–120 minutes should be conducted, monitoring accessory muscle recruitment, paradoxical breathing, tachycardia, desaturation, and patient-reported distress.[64]
  • Autonomic dysfunction
    • Autonomic dysfunction[22] may be self-limited; do not over-treat.
    • Sustained hypertension managed by angiotensin-converting enzyme inhibitor or beta-blocking agent. Use short-acting intravenous medication for labile hypertension requiring immediate therapy.
    • Postural hypotension treated with fluid bolus or positioning.
    • Urinary difficulties may require intermittent catheterisation.
  • Nosocomial infections usually involve pulmonary and urinary Tracts.
    • Occasionally central venous catheters become infected.[61]
    • Antibiotic therapy should be reserved for those patients showing clinical infection rather than the colonisation of fluid or sputum specimens.
  • Venous thrombosis due to immobilisation poses a great risk of thromboembolism
    • Prophylactic use of subcutaneous heparin and compression stockings.[61]

Physiotherapy management

Physiotherapy plays a central role across all phases of GBS management, aiming to prevent secondary complications, restore function, and support the patient's return to independence, guided by the patient's current disease prognosis.

Role of exercise

Exercise can positively influence outcomes such as mobility, fatigue levels and even mental function in patient with GBS.[65][66] [67] [6] However, over-exercise for patients with GBS of partially denervated muscles can cause further damage, including a loss of functioning motor units,[68] [69] hence the need to closely monitor exercise intensity to avoid over-exercising partially denervated motor units.[69] [70][71] Exercise prescription in GBS should follow the frequency, intensity, time, and type (FITT) principle, with all the FITT components carefully matched to the patient's current status and phase of recovery.

Aims of physiotherapy

Physiotherapy in GBS targets several interconnected aims, spanning functional recovery, respiratory health, musculoskeletal health, neurological health, and psychological wellbeing[72] [73] [74] . The aims of physiotherapy management includes:

  1. Regaining the patient's independence with everyday tasks.
  2. Retraining normal movement patterns.
  3. Improving patient's posture.
  4. Improving the balance and coordination
  5. Maintaining clear airways
  6. Preventing lung infection
  7. Supporting joint in functional position to minimize damage or deformity
  8. Prevention of pressure sores
  9. Maintaining peripheral circulation
  10. Providing psychological support for the patient and relatives.
Approach to physiotherapy management

A tri-phasic approach is suggested for physiotherapy management based on disease progression[74]. This approach includes:

  1. Acute/Ascending Phase (first 2-3 weeks): Prevention of complications of immobilisation (contracture, pressure injury, etc.), supporting pulmonary function, and pain management.
  2. Plateau Phase: Increasing upright posturing, improving pulmonary function while avoiding fatigue/overexertion, gentle stretching and active-assisted and active range of motion as tolerated for gradual improvements in mobility.
  3. Recovery/Descending Phase (~2-4 weeks after the plateau phase): Increased upright posturing, weight-bearing, rhythmic stabilisation on high sitting, encouraging a high-intensity rehabilitation approach utilising active resistance training and neuromuscular facilitation techniques.[74][6][73]

Psychosocial Support

The psychological burden of GBS extends beyond the patient; family members and carers may frequently experience significant anxiety, emotional exhaustion, and disruption to their own daily lives, and should be included in psychosocial assessment and support planning. It should be noted that the evidence base specific to carer burden in GBS remains limited, and further research in this area is needed.

Where family members participate in physiotherapy treatment, enhanced levels of patient participation and functional gains have been reported.[75] In contrast, where there is no family participation, reduced functional gains have been observed. The importance of involving relatives and family in treatment of person's with GBS cannot be overemphasised.

The role of the physiotherapist is to ensure clear communication regarding prognosis, identify barriers to physiotherapy treatment, consider the financial impact of care[75] particularly where ICU admission is required and facilitate goal-setting and graded return to function. It is also important for physiotherapists to acknowledge the psychosocial and cultural limitations that may impact management.

Where signs of anxiety, depression, or post-traumatic stress are identified, timely referral to a psychologist or liaison psychiatrist should be considered.

Respiratory Care

The common respiratory complications in the rehabilitation setting include incomplete respiratory recovery including chronic obstructive pulmonary disease, restrictive respiratory disease (pulmonary scarring, pneumonia), and tracheitis from chronic intubation and respiratory muscle insufficiency. Sleep hypercapnia and hypoxia, which worsens during sleep can be the result of a restrictive pulmonary function.[76][77]

Treatment methods are:

  • Night-time saturation records with a pulse oximeter and bilevel positive airway pressure (BiPAP) may be indicated for the patients.
  • Physiotherapy measures (chest percussion, breathing exercises, resistive inspiratory training) may be required to clear respiratory secretions to reduce the work of breathing.
  • Special weaning protocol to prevent over-fatigue of respiratory muscles can be recommended for more severe patients with tracheostomy. Patients with cranial nerve involvement need extra monitoring as they are more prone to respiratory dysfunction.
  • Patients should be encouraged to cease smoking.
  • Postural drainage to areas of lung tissues, 2-hourly turning into supine or side-lying positions.
  • 2-4 litre anaesthetic bag can be used to enhance chest expansion. Therefore, 2 people are necessary for this technique, one to squeeze the bag and another to apply chest manipulation.
  • Rib springing to stimulate cough.
  • After the removal of a ventilator and adequate expansion, effective coughing must be taught to the patient.
  • Once patient is extubated, establish mean inspiratory pressure (MIP) and commence inspiratory muscle training (IMT) at 30% MIP, progressing to 50% MIP; a protocol of 3 sets of 6-10 breaths with 2-minute rest periods once or twice daily is recommended.[78]
  • Reassess MIP weekly and titrate load upward; monitor for respiratory fatigue (accessory muscle use, SpO₂ decline) and reduce intensity if present
  • Where the patient remains too weak for active IMT, Intermittent positive pressure breathing (IPPB) serves as a bridging intervention until active participation is possible.

Neurological Monitoring

According to the European Academy of Neurology/Peripheral Nerve Society Guideline,[6] in severe cases of GBS, there's cranial nerve involvements (especially bilateral facial palsy). To examine the extent of cranial involvement, there's a need for cranial nerve assessment and also monitoring of intracranial pressure.[79]

Maintain Normal Range of Movement

Gentle passive movements through full range of motion (ROM) at least three times a day especially at the hip, shoulder, wrist, ankle, and feet.

Orthoses

Use of Orthoses/light splints (e.g., using Plastazote) may be required for the following purpose listed below:

  • Support the peripheral joints in a comfortable and functional position during flaccid paralysis.
  • To prevent abnormal movements.
  • To stabilise patients using sandbags, and pillows.

Prevention of Pressure Sores

  • Patient's re-positioning every 3 hours.[80]
  • Use air, or water mattress.[81]
  • Use ripple bed
  • Providing soft padding in the pressure-areas
  • Providing good skin care by keeping the skin clean and dry

Maintenance of Circulation

  • Passive movements
  • Effleurage massage to lower limbs

Relief of Pain

  • Transcutaneous electrical nerve stimulation (TENS)
  • Massage with passive ROM
  • The patient can demonstrate increased sensitivity to light touch, a cradle can be used to keep the bedsheet away from the skin. Low-pressure wrapping or snug-fitting garments can provide a way to avoid light touch.
  • Reassurance and explanation of what to expect can help in the alleviation of anxiety that could compound the pain.

Electrotherapy in GBS

The evidence base for electrotherapy use in GBS remains limited, with the majority of available studies comprising case reports. While clinical reasoning can be appreciated within individual cases, findings cannot be readily generalised given the specificity of the patient population and the inherent risk of bias associated with this study design.[82] Current recommendations are therefore extracted from the broader neurological and critical care rehabilitation literature, and should be applied with appropriate clinical caution.

Three GBS-specific clinical considerations necessitate careful electrotherapy dose selection and close skin monitoring throughout treatment: reduced or absent cutaneous sensation,[13] heightened susceptibility to fatigue[42], and autonomic dysfunction, which occurs in approximately one-third of patients.[22]

Transcutaneous Electrical Nerve Stimulation (TENS) may be used for its analgesic effect, particularly in patients with preserved cutaneous sensation, and is the most established electrotherapy modality in GBS pain management.[83][72]

Neuromuscular Electrical Stimulation (NMES) and Functional Electrical Stimulation (FES) may facilitate muscle activation and attenuate denervation-related atrophy at a stage when voluntary exercise is not yet possible. A pilot randomised controlled trial demonstrated NMES to be safe and feasible in the early phase of GBS with no adverse effects recorded.[84] Additionally, a 2023 systematic review found that NMES added to usual care reduced ICU-acquired muscle weakness in critically ill patients;[85] however, it should be noted that in GBS, significant weakness typically precedes ICU admission, which may limit direct interpretation of these findings.

Surface Electromyography (sEMG) Biofeedback may support motor relearning during the recovery phase by providing patients with real-time visual feedback on muscle activation at a stage when contraction is not yet clinically detectable. In the analogous peripheral nerve injury population, sEMG biofeedback has been shown to improve motor outcomes and patient motivation during rehabilitation.[86][87][88]

There is currently no high-quality evidence supporting the use of Electrical Muscle Stimulation (EMS) in GBS. Theoretically, EMS using longer pulse durations may be considered in axonal GBS subtypes (AMAN/AMSAN) where peripheral nerve conduction is severely disrupted, necessitating direct muscle fibre depolarisation rather than nerve-mediated contraction. Whole-body Electrical Muscle Stimulation (WB-EMS) suits are contraindicated in GBS across all phases and subtypes. The combination of reduced sensation, autonomic instability, and fatigue susceptibility presents an unacceptable safety risk..

Transcranial Direct Current Stimulation (tDCS) remains experimental in GBS, with no direct evidence base at present. Its use cannot be recommended outside of a structured research protocol.

Two significant research gaps are identified: first, there are no high-quality trials examining electrotherapy modalities specifically in the GBS population; second, there is no evidence examining potential interactions between electrotherapy and the pharmacological effects of Intravenous Immunoglobulin (IVIg). Both areas represent priorities for future research.

Strength and Endurance Training

Strengthening exercises can involve isometric, isotonic or isokinetic exercises, while endurance training involves progressively increasing the intensity and duration of functional activities such as walking or stair-climbing.[72] [89] [67] Supervised exercise has been shown to be more effective than unsupervised home exercises.[67]

Functional Training

Retraining of dressing, washing, bed mobility, transfers, and ambulation activities comprise a big part of the rehabilitation process. Balance and proprioception retraining in all these functional activities should also be included, while motor control can be achieved by doing Proprioceptive Neuromuscular Facilitation (PNF) techniques.[72]

Research shows that high-intensity relative to lower intensity exercise significantly reduced disability in patients with GBS, as measured with the FIM (p<0.005, r=0.71).[66] Overall, various types of exercise programmes improve physical outcomes such as functional mobility, cardiopulmonary function, isokinetic muscle strength, and work rate and reduce fatigue in patients with GBS.[66] [73][67]

Assistive devices

Assistive devices such as wheelchairs, walking sticks and quadrupeds should be made available to individuals if required in order to facilitate safe and effective ambulation.[72]

A study of 35 patients (27 with classic GBS and 8 with Acute Motor Axonal Neuropathy [AMAN]), reported GBS-related deficits included:

  • Neuropathic pain requiring medication therapy (28 patients)
  • Foot drop necessitating ankle-foot orthosis (AFO) use (21 patients)
  • Locomotion difficulties requiring assistive devices (30 patients)

At 1-year follow-up, the authors found continued foot drop in 12 of the AFO patients. However, significant overall functional recovery had occurred within the general cohort[90] level of evidence (LoE) 1B.

Nehal and Manisha (2015) suggest a functional goal-oriented multidisciplinary rehabilitation programme for daily 1 hour sessions for 12 weeks.[72]

Future of GBS management

Eculizumab has been investigated as a potential therapeutic option for GBS; however, a placebo-controlled clinical trial (NCT04752566) demonstrated that, despite good tolerability, it did not significantly improve motor recovery.[91] Its role in future management therefore remains uncertain, and further research is required. In terms of rehabilitation, Robot-Assisted Therapy (RAT) and Virtual Reality are considered areas of future research.[92][93] RAT works on principle of neuroplasticity by delivering task-specific exercises that promote neural reorganisation and consequently, motor function.[92]

Summary of GBS

GBS is an autoimmune disease that typically begins following a gastrointestinal or respiratory illness, with neurological symptoms appearing 2–4 weeks later. It is characterised by ascending weakness, with clinical features including pain, fatigue, and autonomic dysfunction. Diagnosis involves CSF investigation and electrophysiological studies. Medical management includes IVIg and plasma exchange, while physiotherapy management encompasses prevention of complications, maintaining circulation, pain management, prescription of orthoses, and strength, endurance, and functional training. Respiratory care and psychosocial assessment are also indicated.

References

  1. ↑ Abbassi N, Ambegaonkar G. Guillain-Barre syndrome: a review. Paediatrics and child health. 2019 Nov 1;29(11):459-62.
  2. ↑ 2.0 2.1 2.2 Nguyen TP, Taylor RS. Guillain-Barre Syndrome.[Updated 2023 Feb 7]. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. 2025.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 Radiopedia Guillain-Barré syndrome (accessed 25.9.2022)
  4. ↑ 4.0 4.1 Bellanti R, Rinaldi S. Guillain‐Barré syndrome: a comprehensive review. European journal of neurology. 2024 Aug;31(8):e16365.
  5. ↑ Guillain-Barre Syndrome (GBS) Explained - causes, symptoms, pathophysiology, types, diagnosis, treatment, recovery
  6. ↑ 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 van Doorn PA, Van den Bergh PY, Hadden RD, Avau B, Vankrunkelsven P, Attarian S, Blomkwist‐Markens PH, Cornblath DR, Goedee HS, Harbo T, Jacobs BC. European Academy of Neurology/Peripheral Nerve Society guideline on diagnosis and treatment of Guillain–Barré syndrome. Journal of the Peripheral Nervous System. 2023 Dec;28(4):535-63
  7. ↑ Finsterer J. Triggers of Guillain–Barré syndrome: Campylobacter jejuni predominates. International journal of molecular sciences. 2022 Nov 17;23(22):14222.
  8. ↑ Keh RY, Scanlon S, Datta-Nemdharry P, Donegan K, Cavanagh S, Foster M, Skelland D, Palmer J, Machado PM, Keddie S, Carr AS. COVID-19 vaccination and Guillain-Barré syndrome: analyses using the National Immunoglobulin Database. Brain. 2023Feb 1;146(2):739–48.
  9. ↑ Rajput J, Rajput P, Mohanty E, Saini GK. The impact of preceding infections on the clinical presentation and prognosis of Guillain-Barré Syndrome: A focus on post-COVID-19 GBS. Brain Disorders. 2025 Mar 1;17:100196.
  10. ↑ Zhang J, Guo Y, Wei L, Liu J, Li S, Zhang S. Post-COVID-19 surge in Guillain-Barré syndrome during the Omicron wave in China with clinical characteristics and potential immune-mediated pathways. Scientific Reports. 2026 Mar 13.
  11. ↑ 11.0 11.1 Anderson TC, Leung JW, Harpaz R, Dooling KL. Risk of Guillain-Barré syndrome following herpes zoster, United States, 2010–2018. Human Vaccines & Immunotherapeutics. 2021 Dec 2;17(12):5304-10.
  12. ↑ 12.0 12.1 12.2 12.3 12.4 Oshomoji OI, Ajiroba JO, Semudara SO, Olayemi MA, Adeoye SO. Autoimmune mechanisms in Guillain-Barré syndrome subtypes: a systematic review. Bulletin of Faculty of Physical Therapy. 2024 Dec;29(1):1-1.
  13. ↑ 13.0 13.1 13.2 Leonhard SE, Papri N, Querol L, Rinaldi S, Shahrizaila N, Jacobs BC. Guillain–Barré syndrome. Nature Reviews Disease Primers. 2024 Dec 19;10(1):97.
  14. ↑ 14.0 14.1 Dimachkie MM, Barohn RJ. Guillain-Barré syndrome and variants. Neurol Clin [Internet]. 2013;31(2):491–510.
  15. ↑ National Institute of Neurological Disorders and Stroke.Guillain-Barré Syndrome.ninds.nih.gov. [cited 2026 May 9].
  16. ↑ Suliman BA. Potential clinical implications of molecular mimicry‐induced autoimmunity. Immunity, inflammation and disease. 2024 Feb;12(2):e1178.
  17. ↑ Elendu C, Osamuyi EI, Afolayan IA, Opara NC, Chinedu-Anunaso NA, Okoro CB, Nwankwo AU, Ezidiegwu DO, Anunaso CA, Ogbu CC, Aghahowa SO. Clinical presentation and symptomatology of Guillain-Barré syndrome: A literature review. Medicine. 2024 Jul 26;103(30):e38890.
  18. ↑ 18.0 18.1 Berciano J. The pathophysiological role of endoneurial inflammatory edema in early classical Guillain-Barré syndrome. Clinical Neurology and Neurosurgery. 2024 Feb 1;237:108131.
  19. ↑ 19.0 19.1 Berciano J. Axonal pathology in early stages of Guillain-Barré syndrome. Neurología (English Edition). 2022 Jul 1;37(6):466-79.
  20. ↑ Joshua AM, Misri Z. Peripheral nerve disorders. InPhysiotherapy for Adult Neurological Conditions 2022 Jun 21 (pp. 621-729). Singapore: Springer Nature Singapore.
  21. ↑ Lv J, Zhaori G. Collaborative studies of U.S.-China neurologists on acute motor axonal neuropathy. Pediatr Investig. 2022 Mar 22;6(1):1-4.
  22. ↑ 22.0 22.1 22.2 22.3 22.4 22.5 Bazán-Rodríguez L, Ruiz-Avalos JA, de Saráchaga AJ, Martinez-Jimenez E, López-Hernández JC, Vargas-Cañas S. Dysautonomia and related outcomes in Guillain-Barre syndrome. Autonomic Neuroscience. 2023 Mar 1;245:103070.
  23. ↑ 23.0 23.1 23.2 Noioso CM, Bevilacqua L, Acerra GM, Valle PD, Serio M, Pecoraro A, Rienzo A, De Marca U, De Biasi G, Vinciguerra C, Piscosquito G. The spectrum of anti-GQ1B antibody syndrome: beyond Miller Fisher syndrome and Bickerstaff brainstem encephalitis. Neurological Sciences. 2024 Dec;45(12):5657-69
  24. ↑ Wachira VK, Farinasso CM, Silva RB, Peixoto HM, de Oliveira MR. Incidence of Guillain-Barré syndrome in the world between 1985 and 2020: A systematic review. Global Epidemiology. 2023 Dec 1;5:100098.
  25. ↑ 25.0 25.1 25.2 Xu L, Zhao C, Bao Y, Liu Y, Liang Y, Wei J, Liu G, Wang J, Zhan S, Wang S, Fan D. Variation in worldwide incidence of Guillain-Barré syndrome: a population-based study in urban China and existing global evidence. Frontiers in Immunology. 2024 Sep 10;15:1415986.
  26. ↑ Zheng P, Tian DC, Xiu Y, Wang Y, Shi FD. Incidence of Guillain-Barré syndrome (GBS) in China: a national population-based study. The Lancet Regional Health–Western Pacific. 2022 Jan 1;18.
  27. ↑ Prevots DR, Sutter RW. Assessment of Guillain-Barré syndrome mortality and morbidity in the United States: implications for acute flaccid paralysis surveillance. J Infect Dis. Feb 1997;175 Suppl 1:S151-5
  28. ↑ Nadeem ZA, Ashraf H, Ashfaq H, Fatima E, Larik MO, Ur Rehman O, Ashraf A, Nadeem A. Temporal trends and regional variations in mortality related to Guillain-Barré syndrome in the United States: a retrospective study from 1999 to 2020. International Journal of Neuroscience. 2025 Dec 2;135(12):1469-78.
  29. ↑ Sejvar JJ, Baughman AL, Wise M, Morgan OW. Population incidence of Guillain-Barré syndrome: a systematic review and meta-analysis. Neuroepidemiology. 2011;36(2):123-33.
  30. ↑ 30.0 30.1 Grelowska M, Logoń K, Dziadkowiak E. Prognostic factors associated with worse outcomes in patients with GBS: A systematic review. Advances in Clinical and Experimental Medicine. 2025;34(3):457-67.
  31. ↑ Nelson L, Gormley R, Riddle MS, Tribble DR, Porter CK. The epidemiology of Guillain-Barré Syndrome in U.S. military personnel: a case-control study. BMC Res Notes. Aug 26 2009;2:171
  32. ↑ Italian Guillain-Barré Study Group. The prognosis and main prognostic indicators of Guillain-Barre syndrome A multicentre prospective study of 297 patients. Brain. 1996 Dec 1;119(6):2053-61.
  33. ↑ 33.0 33.1 Hunter J, English WA, Wiegers EJ, Jacobs BC. Guillain–Barré syndrome. BJA education. 2025 Aug 1;25(8):309-16.
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  35. ↑ El Mhandi L, Calmels P, Camdessanché JP, Gautheron V, Féasson L. Muscle strength recovery in treated Guillain-Barré syndrome: a prospective study for the first 18 months after onset. Am J Phys Med Rehabil. Sep 2007;86(9):716-24
  36. ↑ 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 Aug;10(8):469-82.
  37. ↑ 37.0 37.1 Umapathi T, Yuki N. Pain in Guillain-Barré syndrome. Expert review of neurotherapeutics. 2011;11(3):335–9.
  38. ↑ 38.0 38.1 38.2 38.3 Laparidou D, Curtis F, Akanuwe J, Jackson J, Hodgson TL, Siriwardena AN. Patients’ experiences and perceptions of Guillain-Barré syndrome: A systematic review and meta-synthesis of qualitative research. PloS one. 2021 Feb 3;16(2):e0245826.
  39. ↑ 39.0 39.1 39.2 Moulin DE, Hagen N, Feasby TE, Amireh R, Hahn A. Pain in Guillain-Barré syndrome. Neurology. 1997 Feb;48(2):328-31.
  40. ↑ Ruts L, van Koningsveld R, Jacobs BC, van Doorn PA. Determination of pain and response to methylprednisolone in Guillain-Barré syndrome. Journal of neurology. 2007 Oct;254:1318-22.
  41. ↑ Forsberg A, Press R, Einarsson U, de Pedro-Cuesta J, Holmqvist LW, Network Members of the Swedish Epidemiological Study Group. Impairment in Guillain–Barré syndrome during the first 2 years after onset: a prospective study. Journal of the neurological sciences. 2004 Dec 15;227(1):131-8.
  42. ↑ 42.0 42.1 42.2 42.3 42.4 Zuluaga Lotero D, Ortiz Munoz D, Acero-Garces DO, Arango GP, Parra B, García-Perdomo HA. Frequency of residual fatigue in the recovery phase of Guillain-Barré syndrome: a systematic review and meta-analysis. Neurological Research. 2025 Nov 2;47(11):1023-33
  43. ↑ 43.0 43.1 Levison LS, Thomsen RW, Andersen H. Increased risk of depression after Guillain‐Barré syndrome. Muscle & Nerve. 2023 Jun;67(6):497-505.
  44. ↑ Susanti V, Trisyani Y, Nuraeni A. Patient Experiences of the Biopsychosocial Impact of Guillain-Barré Syndrome: A Scoping Review. Patient preference and adherence. 2025 Dec 31:3755-67.
  45. ↑ Leonhard SE, Mandarakas MR, Gondim FA, Bateman K, Ferreira ML, Cornblath DR, van Doorn PA, Dourado ME, Hughes RA, Islam B, Kusunoki S. Diagnosis and management of Guillain–Barré syndrome in ten steps. Nature Reviews Neurology. 2019 Nov;15(11):671-83.
  46. ↑ 46.0 46.1 Al-Hakem H, Doets AY, Stino AM, Zivkovic SA, Andersen H, Willison HJ, Cornblath DR, Gorson KC, Islam Z, Mohammad QD, Sindrup SH. CSF findings in relation to clinical characteristics, subtype, and disease course in patients with Guillain-Barré syndrome. Neurology. 2023 Jun 6;100(23):e2386-97.
  47. ↑ National Organization for Rare Disorders. Miller-Fisher Syndrome. rarediseases.org. [cited 2026 May 9].
  48. ↑ Wen P, Wang L, Liu H, Gong L, Ji H, Wu H, Chu W. Risk factors for the severity of Guillain-Barré syndrome and predictors of short-term prognosis of severe Guillain-Barré syndrome. Sci Rep. 2021 Jun 2;11(1):11578.
  49. ↑ Seta T, Nagayama H, Katsura KI, Hamamoto M, Araki T, Yokochi M, Utsumi K, Katayama Y. Factors influencing outcome in Guillain–Barré Syndrome: comparison of plasma adsorption against other treatments. Clinical neurology and neurosurgery. 2005 Oct 1;107(6):491-6.
  50. ↑ Zhang Y, Zhao Y, Wang Y. Prognostic factors of Guillain-Barré syndrome: a 111-case retrospective review. Chinese Neurosurgical Journal. 2018 Sep 10;4(03):145-53.
  51. ↑ Busl KM, Fried H, Muehlschlegel S, Wartenberg KE, Rajajee V, Alexander SA, Creutzfeldt CJ, Fontaine GV, Hocker SE, Hwang DY, Kim KS. Guidelines for neuroprognostication in adults with Guillain–Barré syndrome. Neurocritical care. 2023 Jun;38(3):564-83.
  52. ↑ Shang P, Zhu M, Wang Y, Zheng X, Wu X, Zhu J, Feng J, Zhang HL. Axonal variants of Guillain-Barré syndrome: an update. J Neurol. 2021Jul;268(7):2402–19.
  53. ↑ Weiss N, Marois C, Le Guennec L, Rohaut B, Demeret S. Critical insights for intensivists on Guillain-Barré syndrome. Annals of Intensive Care. 2025 Jan 1;15(1):67
  54. ↑ van Koningsveld R, Steyerberg EW, Hughes RA, Swan AV, van Doorn PA, Jacobs BC. A clinical prognostic scoring system for Guillain-Barré syndrome. The Lancet Neurology. 2007 Jul 1;6(7):589-94.
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  57. ↑ Moore JL, Potter K, Blankshain K, Kaplan SL, O'Dwyer LC, Sullivan JE. A core set of outcome measures for adults with neurologic conditions undergoing rehabilitation: a clinical practice guideline. Journal of neurologic physical therapy. 2018 Jul 1;42(3):174-220.
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  62. ↑ Rose L, Messer B. Prolonged mechanical ventilation, weaning, and the role of tracheostomy. Critical care clinics. 2024 Apr 1;40(2):409-27.
  63. ↑ Shamil PK, Gupta NK, Ish P, Sen MK, Kumar R, Chakrabarti S, Gupta N. Prediction of weaning outcome from mechanical ventilation using diaphragmatic rapid shallow breathing index. Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine. 2022 Sep;26(9):1000.
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  65. ↑ Bussmann JB, Garssen MP, van Doorn PA, Stam HJ. Analysing the favourable effects of physical exercise: relationships between physical fitness, fatigue and functioning in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy. Journal of rehabilitation medicine. 2007 Mar;39(2):121-5.
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  82. ↑ Murad MH, Sultan S, Haffar S, Bazerbachi F. Methodological quality and synthesis of case series and case reports. BMJ evidence-based medicine. 2018 Feb 2.
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  93. ↑ Torres-Reyes AB, Reyes-Hernández I, Domínguez-Ramírez OA, Tellez-Lopez AM. Use of biomedical engineering for rehabilitation of patients with disability caused by guillain-barre syndrome: a systematic review. Revista mexicana de ingeniería biomédica. 2024 Apr;45(1):43-59
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