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Guillain-Barre Syndrome

Author: Andrew C Miller, MD, Chief Resident and Clinical Assistant Instructor, Departments of Emergency Medicine and Internal Medicine, State University of New York Downstate Medical Center, Kings County Hospital Center
Coauthor(s): Razi M Rashid, MD, MPH, Intern, Department of Internal Medicine, St John's Hospital and Medical Center, Detroit, Michigan; Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Contributor Information and Disclosures

Updated: Jul 1, 2009

Introduction

Background

In 1859, Landry published a report on 10 patients with an ascending paralysis.1 This was followed by a report in 1916 written by 3 French physicians working in the Sixth Army camp during the First World War; they described 2 French soldiers with motor weakness, areflexia, and albuminocytological dissociation in the cerebrospinal fluid.2 In this report Guillain, Barr é, and Strohl carefully recorded and interpreted the tendon reflexes of their patients and recognized the peripheral nature of the illness. The identified syndrome was later named Guillain-Barr é syndrome (GBS). Historically, GBS was a single disorder; however, current practice acknowledges several variant forms.

GBS is a heterogeneous grouping of immune-mediated processes generally characterized by motor, sensory, and autonomic dysfunction. In its classic form, GBS is an acute inflammatory demyelinating polyneuropathy characterized by progressive symmetric ascending muscle weakness, paralysis, and hyporeflexia with or without sensory or autonomic symptoms; however, variants involving the cranial nerves or pure motor involvement are not uncommon. In severe cases, muscle weakness may lead to respiratory failure, and labile autonomic dysfunction may complicate the use of vasoactive and sedative drugs.

Pathophysiology

Although the clinical syndrome of Guillain-Barré syndrome classically presents as a rapidly progressive acute polyneuropathy, several pathologic and etiologic subtypes exist. Most patients with Guillain-Barré syndrome exhibit absent or profoundly delayed conduction in action nerve fibers. This aberrant conduction results from axon demyelination occurring primarily in peripheral nerves and spinal roots, but cranial nerves may be involved as well.

Guillain-Barré syndrome is believed to result from autoimmune humoral- and cell-mediated responses to a recent infection or any of a long list of medical problems. Its relation to antecedent infections and the identification of various antiganglioside antibodies suggest that molecular mimicry may serve as a possible mechanism.3,4  Antibodies formed against ganglioside-like epitopes in the lipopolysaccharide (LPS) layer of some infectious agents have been shown in both necropsy and animal models to cross-react with the ganglioside surface molecules of peripheral nerves.3 Symptoms generally coincide pathologically with various patterns of lymphocytic infiltration and macrophage-mediated demyelination, depending on the subtype in question. Recovery is typically associated with remyelination. In a subset of patients, GBS is associated primarily with myelin-sparing axonal damage resulting from a direct cellular immune attack on the axon itself.

The acute inflammatory demyelinating polyneuropathy (AIDP) subtype is the most commonly identified form in the United States. It is generally preceded by a bacterial or viral infection. Nearly 40% of patients are seropositive for Campylobacter jejuni. Lymphocytic infiltration and macrophage-mediated demyelination of peripheral nerves is present. Symptoms generally resolve with remyelination.

The acute motor axonal neuropathy (AMAN) subtype is a purely motor subtype that is more prevalent amongst pediatric age groups. Nearly 70-75% of patients are seropositive for Campylobacter. One third of these cases may actually be hyperreflexic. The hyperreflexia mechanism associated with AMAN is not known, but dysfunction of the inhibitory system via spinal interneurons may increase motor neuron excitability. Hyperreflexia is significantly associated with the presence of anti-GM1 antibodies.1 Inflammation of the spinal anterior roots may lead to disruption of the blood-CNS barrier.3 AMAN is generally characterized by a rapidly progressive weakness, ensuing respiratory failure, and good recovery.

Acute motor-sensory axonal neuropathy (AMSAN) is an acute severe illness differing from AMAN in that AMSAN also affects sensory nerves and roots.5  Patients are typically adults with both motor and sensory dysfunction, marked muscle wasting, and poor recovery.

Miller-Fisher syndrome (MFS) is a rare variant that typically presents with the classic triad of ataxia, areflexia, and ophthalmoplegia. Acute onset of external ophthalmoplegia is a cardinal MFS feature.3 The ataxia tends to be out of proportion to the degree of sensory loss. Patients may also have mild limb weakness, ptosis, facial palsy, or bulbar palsy. Anti-GQ1b antibodies are prominent in this variant, and patients have reduced or absent sensory nerve action potentials and absent tibial H reflex.6  Patients with acute oropharyngeal palsy carry anti-GQ1b/GT1a IgG antibodies.3 Recovery generally occurs within 1-3 months.

Acute panautonomic neuropathy is the rarest of all variants and involves both the sympathetic and parasympathetic nervous systems. Cardiovascular involvement is common, and dysrhythmias are a significant source of mortality in this form of the disease. The patient may also experience sensory symptoms. Recovery is gradual and often incomplete.

Frequency

United States

The incidence of Guillain-Barré syndrome (GBS) is 1-3 per 100,000 inhabitants, making GBS the most common cause of acute flaccid paralysis in the United States.1,2,7

International

AMAN and AMSAN occur mainly in northern China, Japan, and Mexico, and they comprise 5-10% percent of GBS cases in the United States.8

AIDP accounts for up to 90% of cases in Europe, North America, and the developed world.

Epidemiologic studies from Japan indicate that, in this region, a greater percentage of GBS cases are associated with antecedent C jejuni infections and a lesser number are related to antecedent cytomegalovirus infections compared with that in North America and Europe.

A study in Iran showed that 47% of pediatric GBS cases had evidence of recent C jejuni infection.9

Mortality/Morbidity

Most patients (up to 85%) with GBS achieve a full and functional recovery within 6-12 months. Recovery is maximal by 18 months past onset.10

  • Patients may have persistent weakness, areflexia, imbalance, or sensory loss. Approximately 7-15% of patients have permanent neurologic sequelae including bilateral footdrop, intrinsic hand muscle wasting, sensory ataxia, and dysesthesia.
  • The mortality rate varies but may be less than 5% in tertiary care centers with a team of medical professionals who are familiar with GBS management. Causes of death include adult respiratory distress syndrome, sepsis, pneumonia, pulmonary emboli, and cardiac arrest.
  • Despite intensive care, 3-8% of patients die.
  • GBS can rarely be a recurrent disorder.11     

Race

No racial preponderance exists.

Sex

The male-to-female ratio of Guillain-Barré syndrome is 1.5:1. A Swedish epidemiologic study indicated that the incidence of Guillain-Barré syndrome is lower during pregnancy and increases in the months immediately following delivery.12

Age

Guillain-Barré syndrome occurs at all ages, but a bimodal distribution with peaks in young adulthood (15-35 y) and in elderly persons (50-75 y) appears to exist. Rare cases have been noted in infants.13

Clinical

History

The typical patient with Guillain-Barré syndrome (GBS) (likely AIDP) presents 2-4 weeks after a relatively benign respiratory or gastrointestinal illness complaining of dysesthesias of the fingers and lower extremity proximal muscle weakness. The weakness may progress over hours to days to involve the arms, truncal muscles, cranial nerves, and muscles of respiration. The illness progresses from days to weeks, with the mean time to the nadir of clinical function being 12 days and 98% of patients reaching a nadir by 4 weeks. A plateau phase of persistent, unchanging symptoms then ensues followed days later by gradual symptom improvement. The mean time to improvement and clinical recovery are 28 and 200 days, respectively.

  • Up to one third of patients require mechanical ventilation during the course of their illness. Causes for this include cranial nerve involvement affecting airway maintenance and respiratory muscle paralysis.
  • Motor dysfunction
    • Symmetric limb weakness typically begins as proximal lower extremity weakness and ascends to involve the upper extremities, truncal muscles, and head.
    • Inability to stand or walk despite reasonable strength, especially when ophthalmoparesis or impaired proprioception is present.
    • Respiratory muscle weakness with shortness of breath may be present.
    • Cranial nerve palsies (III-VII, IX-XII) may be present. Patients may present with facial weakness mimicking Bell palsy, dysphagia, dysarthria, ophthalmoplegia, and pupillary disturbances. The Miller-Fisher variant is unique in that this subtype begins with cranial nerve deficits.
    • Lack of deep tendon reflexes is a hallmark sign.
  • Sensory dysfunction
    • Paresthesia generally begins in the toes and fingertips and progresses upward but generally not extending beyond the wrists or ankles.
    • Pain is most severe in the shoulder girdle, back, buttocks, and thighs and may occur with even the slightest movements.
    • Loss of vibration, proprioception, touch, and pain distally may be present.
  • Autonomic dysfunction
    • Cardiovascular signs may include tachycardia, bradycardia, dysrhythmias, wide fluctuations in blood pressure, and postural hypotension.
    • Urinary retention due to urinary sphincter disturbances may be noted.
    • Constipation due to bowel paresis and gastric dysmotility may be present.
    • Facial flushing and venous pooling secondary to abnormal vasomotor tone may be present.
    • Hypersalivation
    • Anhydrosis
    • Tonic pupils
  • Papilledema secondary to elevated intracranial pressure is present in rare cases.
  • Miller-Fisher variant presents with a predominance of cranial nerve findings, ataxia, and areflexia. Facial weakness, ophthalmoplegias, dysarthria, and dysphagia may precede ataxia, areflexia, and weakness.14  

Physical

  • Vital signs
    • Patients may have tachycardia or bradycardia, hypertension or hypotension, or hyperthermia or hypothermia.
    • Low oxygen saturation may be present with advanced respiratory muscle involvement.
  • Cranial nerves: Patients may present with facial weakness mimicking Bell palsy, dysphagia, dysarthria, ophthalmoplegia, and pupillary disturbances.
  • Dysreflexia
    • Patients with manifest weakness are invariably hyporeflexic or areflexic in the involved areas.
    • Respiratory symptoms
    • Poor inspiratory effort or diminished breath sounds
  • Motor
    • Symmetric limb weakness typically begins as proximal lower extremity weakness and ascends to involve the upper extremities, truncal muscles, and head.
    • Inability to stand or walk despite reasonable strength, especially when ophthalmoparesis or impaired proprioception is present.
    • Hypotonia
    • Wasting of limb muscles is not an acute finding.
  • Abdominal
    • Paucity or absence of bowel sounds suggests paralytic ileus.
    • Suprapubic tenderness or fullness may be suggestive of urinary retention.
  • Sensory: Patients may experience numbness, paresthesias, impaired proprioception, and pain.
  • Papilledema secondary to elevated intracranial pressure is present in rare cases.

Causes

Guillain-Barré syndrome (GBS) has been associated with antecedent bacterial and viral infections, administration of certain vaccinations, and other systemic illnesses. Case reports exist regarding numerous medications and procedures; however, whether any causal link exists is unclear.

  • Bacterial infections include C jejuni, Haemophilus influenzae, Mycoplasma pneumoniae, and Borrelia burgdorferi.1,7
  • Viral infections include cytomegalovirus, Ebstein-Barr virus, and during seroconversion with the human immunodeficiency virus (HIV).1,7
  • Vaccines
    • A study reviewing the cases of Guillain-Barré syndrome (GBS) during the 1992-1993 and 1993-1994 influenza seasons found an adjusted relative risk of 1.7 cases per 1 million influenza vaccinations.15
    • Epidemiologic studies from Finland and southern California failed to validate an earlier retrospective study from Finland suggesting a cause-effect relationship between oral polio vaccination and GBS,16,17  while a Brazilian study suggested that, based on a temporal association between the vaccine and the onset of GBS, the vaccine may rarely trigger GBS.18
    • Data from a large-scale epidemiologic study found that fewer cases of GBS occurred following administration of tetanus toxoid containing vaccinations than occurred in the baseline population.19
    • An epidemiologic study failed to show any conclusive epidemiologic association between GBS and the hepatitis B vaccine.20
    • A large Latin American study of more than 2000 children with GBS following a mass measles vaccination program in 1992 and 1993 failed to establish a statistically significant causal relationship between administration of the measles vaccine and GBS.21
    • A recent report from the Centers for Disease Control and Prevention (CDC) suggests that an increased incidence of GBS may exist amongst recipients of the Menactra meningococcal conjugate vaccine.22
    • A recent study found no evidence of an increased risk of Guillain-Barré syndrome after seasonal influenza vaccine.23
    • Case reports exist regarding group A streptococci vaccines, the rabies vaccine, and the swine flu vaccine; however, conclusive statistically significant evidence is lacking.
  • Medications24
    • A case-controlled study showed that patients with Guillain-Barré syndrome had used antimotility drugs and penicillins more often and oral contraceptives less often. No definite cause-effect relationship has been established.
    • Case reports of Guillain-Barré syndrome associated with tumor necrosis factor antagonist agents used in rheumatoid arthitis.25,26,27
    • Case reports exist regarding streptokinase, isotretinoin, danazol, captopril, gold, heroin, and epidural anesthesia among others.
    • Case reports cite associations between bariatric and other gastric surgeries.28
  • Anecdotal associations include systemic lupus erythematosus, sarcoidosis, lymphoma, surgery, renal transplantation, and snake bite.

More on Guillain-Barre Syndrome

Overview: Guillain-Barre Syndrome
Differential Diagnoses & Workup: Guillain-Barre Syndrome
Treatment & Medication: Guillain-Barre Syndrome
Follow-up: Guillain-Barre Syndrome
References
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Further Reading

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Keywords

Guillain-Barre syndrome, Guillain-Barré syndrome, GBS, nervous system, myelin sheath, neuropathy, nerves, causes, symptoms, treatment, viral infection, weakness, autoimmune disease, acute inflammatory demyelinating polyneuropathy, AIDP, acute motor axonal neuropathy, AMAN, acute motor-sensory axonal neuropathy, AMSAN, Miller-Fisher syndrome, MFS, acute panautonomic neuropathy, pharyngeal-brachial-cervical variant, pure sensory variant, Campylobacter jejuni, IVIG, plasmapheresis, acute flaccid paralysis

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Contributor Information and Disclosures

Author

Andrew C Miller, MD, Chief Resident and Clinical Assistant Instructor, Departments of Emergency Medicine and Internal Medicine, State University of New York Downstate Medical Center, Kings County Hospital Center
Andrew C Miller, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians, American Medical Association, Emergency Medicine Residents Association, Islamic Medical Association of North America, Medical Society of the State of New York, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Razi M Rashid, MD, MPH, Intern, Department of Internal Medicine, St John's Hospital and Medical Center, Detroit, Michigan
Disclosure: Nothing to disclose.

Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Edward A Michelson, MD, Program Director, Associate Professor, Department of Emergency Medicine, University Hospital Health Systems in Cleveland
Edward A Michelson, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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