Guillain–Barré syndrome
Updated: 12/16/2025, 8:55:54 PM Wikipedia source
Guillain–Barré syndrome (GBS) is a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system. Typically, both sides of the body are involved, and the initial symptoms are changes in sensation or pain often in the back along with muscle weakness, beginning in the feet and hands, often spreading to the arms and upper body. The symptoms may develop over hours to a few weeks. During the acute phase, the disorder can be life-threatening, with about 15% of people developing respiratory muscle weakness requiring mechanical ventilation. Some are affected by changes in the function of the autonomic nervous system, which can lead to dangerous abnormalities in heart rate and blood pressure. Although the cause is unknown, the underlying mechanism involves an autoimmune disorder in which the body's immune system mistakenly attacks the peripheral nerves and damages their myelin insulation. Sometimes this immune dysfunction is triggered by an infection or, less commonly, by surgery, and by vaccination. The diagnosis is usually based on the signs and symptoms through the exclusion of alternative causes and supported by tests such as nerve conduction studies and examination of the cerebrospinal fluid. There are several subtypes based on the areas of weakness, results of nerve conduction studies, and the presence of certain antibodies. It is classified as an acute polyneuropathy. In those with severe weakness, prompt treatment with intravenous immunoglobulins or plasmapheresis, together with supportive care, lead to good recovery in the majority of cases. Recovery may take weeks to years, with about a third having some permanent weakness. Globally, death occurs in approximately 7.5% of patients. Guillain–Barré syndrome is rare, at 1 or 2 cases per 100,000 people every year. The syndrome is named after the French neurologists Georges Guillain and Jean Alexandre Barré, who, together with French physician André Strohl, described the condition in 1916.
Infobox
Other names
Guillain–Barré–Strohl syndrome, Landry's paralysis, postinfectious polyneuritis, Acute Inflammatory Demyelinating Polyneuropathy
Pronunciation
mw- UK: /ˌɡiː(j)æn ˈbæreɪ, ˌɡiːlæn -/ GHEE-(y)an BARR-ay, GHEE-lan -US: /ɡiːˌjæn bəˈreɪ, ɡiːˌ(j)æn -/ ghee-LAN bə-RAY, ghee-(y)AN -French: [ɡilɛ̃ baʁe]
Specialty
Neurology
Symptoms
Muscle weakness beginning in the feet and hands, usually ascending
Complications
Breathing difficulties, heart and blood pressure problems
Usual onset
Rapid (hours to weeks)
Causes
Typically triggered by an infection; occasionally by surgery
Diagnostic method
Based on symptoms, nerve conduction studies, lumbar puncture
Treatment
Supportive care, intravenous immunoglobulin, plasmapheresis
Prognosis
Weeks to years for recovery
Frequency
2 per 100,000 people per year
Deaths
7.5% of those affected
Named after
Georges GuillainJean Alexandre Barré
Tables
· Diagnosis › Clinical subtypes
Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)
Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)
Type
Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)
Symptoms
Sensory symptoms and muscle weakness, often with cranial nerve weakness and autonomic involvement
Population affected
Most common in Europe and North America
Nerve conduction studies
Demyelinating polyneuropathy
Antiganglioside antibodies
No clear association
Acute motor axonal neuropathy (AMAN)
Acute motor axonal neuropathy (AMAN)
Type
Acute motor axonal neuropathy (AMAN)
Symptoms
Isolated muscle weakness without sensory symptoms in less than 10%; cranial nerve involvement uncommon
Population affected
Rare in Europe and North America, a substantial proportion (30–65%) in Asia and Central and South America; sometimes called "Chinese paralytic syndrome"
Nerve conduction studies
Axonal polyneuropathy, normal sensory action potential
Antiganglioside antibodies
GM1a/b, GD1a & GalNac-GD1a
Acute motor and sensory axonal neuropathy (AMSAN)
Acute motor and sensory axonal neuropathy (AMSAN)
Type
Acute motor and sensory axonal neuropathy (AMSAN)
Symptoms
Severe muscle weakness similar to AMAN but with sensory loss
Population affected
—
Nerve conduction studies
Axonal polyneuropathy, reduced or absent sensory action potential
Antiganglioside antibodies
GM1, GD1a
Pharyngeal-cervical-brachial variant
Pharyngeal-cervical-brachial variant
Type
Pharyngeal-cervical-brachial variant
Symptoms
Weakness particularly of the throat muscles, and face, neck, and shoulder muscles
Population affected
—
Nerve conduction studies
Generally normal, sometimes axonal neuropathy in arms
Antiganglioside antibodies
Mostly GT1a, occasionally GQ1b, rarely GD1a
Miller Fisher syndrome
Miller Fisher syndrome
Type
Miller Fisher syndrome
Symptoms
Ataxia, eye muscle weakness, areflexia but usually no limb weakness
Population affected
This variant occurs more commonly in men than in women (2:1 ratio). Cases typically occur in the spring and the average age of occurrence is 43 years old.
Nerve conduction studies
Generally normal, sometimes discrete changes in sensory conduction or H-reflex detected
Antiganglioside antibodies
GQ1b, GT1a
| Type | Symptoms | Population affected | Nerve conduction studies | Antiganglioside antibodies |
| Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) | Sensory symptoms and muscle weakness, often with cranial nerve weakness and autonomic involvement | Most common in Europe and North America | Demyelinating polyneuropathy | No clear association |
| Acute motor axonal neuropathy (AMAN) | Isolated muscle weakness without sensory symptoms in less than 10%; cranial nerve involvement uncommon | Rare in Europe and North America, a substantial proportion (30–65%) in Asia and Central and South America; sometimes called "Chinese paralytic syndrome" | Axonal polyneuropathy, normal sensory action potential | GM1a/b, GD1a & GalNac-GD1a |
| Acute motor and sensory axonal neuropathy (AMSAN) | Severe muscle weakness similar to AMAN but with sensory loss | — | Axonal polyneuropathy, reduced or absent sensory action potential | GM1, GD1a |
| Pharyngeal-cervical-brachial variant | Weakness particularly of the throat muscles, and face, neck, and shoulder muscles | — | Generally normal, sometimes axonal neuropathy in arms | Mostly GT1a, occasionally GQ1b, rarely GD1a |
| Miller Fisher syndrome | Ataxia, eye muscle weakness, areflexia but usually no limb weakness | This variant occurs more commonly in men than in women (2:1 ratio). Cases typically occur in the spring and the average age of occurrence is 43 years old. | Generally normal, sometimes discrete changes in sensory conduction or H-reflex detected | GQ1b, GT1a |
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