AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Guillain-Barré syndrome (GBS) may be described as a collection of clinical syndromes that manifests as an acute inflammatory polyradiculoneuropathy with resultant weakness and diminished reflexes. With poliomyelitis under control in developed countries, GBS is now the most important cause of acute flaccid paralysis. GBS remains a diagnosis made primarily through the assessment of clinical history and findings.

Although the classic description of GBS is that of a demyelinating neuropathy with ascending weakness, many clinical variants have been well documented in the medical literature. Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) is the most widely recognized form in Western countries, but the variants known as acute motor axonal neuropathy (AMAN) and acute motor-sensory axonal neuropathy (AMSAN) also are well recognized. Based on a clinical spectrum of symptoms and findings, many believe that strictly defined subgroups of GBS, although not easily distinguished, nonetheless exist.

See also the following related eMedicine topics:
Guillain-Barré Syndrome [Emergency Medicine]
Guillain-Barre Syndrome in Childhood

Pathophysiology

GBS is a postinfectious, immune-mediated disease. Cellular and humoral immune mechanisms probably play a role in its development. Most patients report an infectious illness in the weeks prior to the onset of GBS. Many of the identified infectious agents are thought to induce antibody production against specific gangliosides and glycolipids, such as GM1 and GD1b, distributed throughout the myelin in the peripheral nervous system.⁷⁰

The pathophysiologic mechanism of an antecedent illness and of GBS can be typified by Campylobacter jejuni infections.^{33, 34} The virulence of C jejuni is thought to be based on the presence of specific antigens in its capsule that are shared with nerves. Immune responses directed against the capsular components produce antibodies that cross-react with myelin to cause demyelination. Ganglioside GM1 appears to cross-react with C jejuni lipopolysaccharide antigens, resulting in the immunologic damage to the peripheral nervous system. This process has been termed molecular mimicry.

Pathologic findings in GBS include lymphocytic infiltration of spinal roots and peripheral nerves, followed by macrophage-mediated, multifocal stripping of myelin. This phenomenon results in defects in the propagation of electrical nerve impulses, with eventual conduction block and flaccid paralysis. In some patients with severe disease, a secondary consequence of the severe inflammation is axonal disruption and loss. A subgroup of patients may have a primary immune attack directly against nerve axons, resulting in a similar clinical presentation.

Variants

Several variants of GBS are recognized. These disorders share similar patterns of evolution, recovery, symptom overlap, and probable immune-mediated pathogenesis.

• The Miller-Fisher syndrome, a common variant of GBS, is observed in about 5% of all GBS cases. The syndrome consists of ataxia, ophthalmoplegia, and areflexia.¹⁸ Ataxia is primarily noted during gait and in the trunk, with lesser involvement of the limbs. Motor strength is characteristically spared. The usual course is one of gradual and complete recovery over weeks or months. A close association exists between antiganglioside antibodies and the Fisher variant. Anti-GQ1b antibodies, triggered by certain C jejuni strains, have a relatively high specificity and sensitivity for the disease.¹² Dense concentrations of GQ1b ganglioside are found in the oculomotor, trochlear, and abducens nerves, which may explain the relationship between anti-GQ1b antibodies and ophthalmoplegia.
• The AMAN variant is associated closely with enteric C jejuni infections and high titers of antibodies to gangliosides (ie, GM1, GD1a, GD1b). Patients with AMAN have pure motor symptoms and appear clinically to be very similar to patients with the demyelinating form of GBS with ascending, symmetric paralysis. AMAN is distinguished by electrodiagnostic study results that are consistent with a pure motor axonopathy.⁴ Biopsies show wallerianlike degeneration without significant lymphocytic inflammation. Many cases have been reported in rural areas of China, especially in children and young adults during the summer months.²⁹ Pure axonal cases may occur more frequently outside of Europe and North America. AMAN cases may also be different from cases of axonal GBS described in the West. Prognosis is often quite favorable. Although recovery for many is rapid, severely disabled patients with AMAN may show improvement over a period of years.
• The axonal form of GBS, also referred to as acute motor-sensory axonal neuropathy (AMSAN), often presents with rapid and severe paralysis with delayed and poorer recovery (in comparison with recovery from electrophysiologically similar AMAN cases). Like AMAN, axonal GBS also is associated with preceding C jejuni diarrhea. Pathologic findings show severe axonal degeneration of motor and sensory nerve fibers with little demyelination.¹¹
• A pure sensory variant of GBS has been described in the medical literature, typified by a rapid onset of sensory loss and areflexia in a symmetric and widespread pattern. Lumbar puncture studies show albuminocytologic dissociation in the cerebrospinal fluid (CSF), and electromyography (EMG) results show characteristic signs of a demyelinating process in the peripheral nerves. Prognosis is generally good, but immunotherapies, such as plasma exchange and the administration of intravenous immunoglobulins (IVIGs), can be tried in patients with severe disease or slow recovery.
• Acute pandysautonomia without significant motor or sensory involvement is a rare presentation of GBS. Dysfunction of the sympathetic and parasympathetic systems results in severe postural hypotension, bowel and bladder retention, anhidrosis, decreased salivation and lacrimation, and pupillary abnormalities.
• The pharyngeal-cervical-brachial variant is distinguished by isolated facial, oropharyngeal, cervical, and upper limb weakness without lower limb involvement. Other unusual clinical variants with restricted patterns of weakness are observed only in rare cases.

See also the following related eMedicine topic:
Intravenous Immunoglobulin

Frequency

United States

According to an epidemiologic survey, the average annual incidence of GBS in the United States is 3.0 cases per 100,000 population. In comparing age groups, the annual mean rate of hospitalizations in the United States related to GBS increases with age, being 1.5 cases per 100,000 population in persons aged less than 15 years and peaking at 8.6 cases per 100,000 population in persons aged 70-79 years.⁵³

International

A widespread syndrome, GBS has been reported throughout the world.⁷¹ Most studies show annual incidence figures that are similar to those in the United States, without geographical clustering.

Mortality/Morbidity

In epidemiologic surveys, the overall death rate related to GBS ranges from 2-12% of patients. GBS-associated mortality rates increase markedly with age. In the United States, the case-fatality ratio ranges from 0.7% among persons younger than 15 years to 8.6% among individuals older than 65 years. Survey data has shown that in patients aged 60 years or older, the risk of death is 6-fold that of persons aged 40-59 years and is 157-fold that of patients younger than 15 years. Although the death rate increases with age in males and females, after age 40 years males have a death rate that is 1.3 times greater than that of females.

GBS-related deaths usually occur in ventilator-dependent patients, resulting from such complications as pneumonia, sepsis, adult respiratory distress syndrome, and, less frequently, autonomic dysfunction.¹⁹ Underlying pulmonary disease and the need for mechanical ventilation increase the risk of death, especially in elderly patients. Length of hospital stays also increases with advancing age, because of disease severity and associated medical complications.

Race

GBS has been reported throughout the international community. In North America, Western Europe, and Australia, most patients with GBS meet electrophysiologic criteria for demyelinating polyneuropathy. In northern China, up to 65% of patients with GBS have axonal pathology.²⁹

Sex

A slight male preponderance is seen in most studies, especially in older patients.

Age

GBS has been reported in all age groups, with the syndrome occurring at any time between infancy and old age. In the United States, the syndrome's age distribution seems to be bimodal, with the incidence of GBS peaking in the elderly population and reaching its second-highest level in young adults. Infants appear to have the lowest risk of developing GBS.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Antecedent illness
• • Up to two thirds of patients with GBS report an antecedent illness or event 1-3 weeks prior to the onset of weakness. Upper respiratory and gastrointestinal illnesses are the most commonly reported conditions.⁶⁹ Symptoms generally have resolved by the time of medical presentation for the neurologic condition.
  • C jejuni is the major causative organism that is identified in most studies and is responsible for AIDP and AMAN cases. In one major study, previous diarrheal illness had occurred in 60% of patients with axonal GBS (by neurophysiologic testing).
  • Vaccinations, surgical procedures, and trauma have been reported to trigger the development of GBS. Much of this information is anecdotal, although vaccination with the swine flu vaccine (administered in 1976) was shown to increase the risk of contracting GBS to a small, but definable, degree. Rabies vaccine prepared from infected brain tissue also was found to have an association with GBS. Studies of other vaccines, however, have not shown a significant relationship between these drugs and GBS.
• Weakness
• • The classic clinical picture of weakness is ascending and symmetrical in nature. The lower limbs are usually involved before the upper limbs. Proximal muscles may be involved earlier than the more distal ones. Trunk, bulbar, and respiratory muscles can be affected as well.
  • Weakness develops acutely and progresses over days to weeks. Severity may range from mild weakness to complete tetraplegia with ventilatory failure. Peak deficits are reached by 4 weeks after the initial development of symptoms.³⁰ The progression of symptoms beyond that point brings the diagnosis under question. Recovery usually begins 2-4 weeks after the progression ceases.¹⁷
• Sensory changes
• • Most patients complain of paresthesias, numbness, or similar sensory changes. Sensory symptoms often precede the weakness. They are frequently ascending in nature and are more pronounced in a distal distribution.
  • Sensory symptoms are usually mild. In most cases, objective findings of sensory loss tend to be minimal and variable.
  • On nerve conduction studies (NCS), 58-76% of patients exhibit sensory abnormalities.
• Cranial nerve involvement
• • Cranial nerve involvement is observed in 45-75% of patients with GBS. Common complaints may include the following:
  • • Facial droop
    • Diplopias
    • Dysarthria
    • Dysphagia
  • Facial and oropharyngeal weakness usually appears after the trunk and limbs are affected.
• Pain
• • In a prospective, longitudinal study of pain in patients with GBS, 89% of patients reported pain that was attributable to GBS at some time during their illness. On initial presentation, almost 50% of patients described the pain as severe and distressing.
  • The mechanism of pain is uncertain and may be a product of several factors. Pain can result from direct nerve injury or from the paralysis and prolonged immobilization.
  • Most patients complain of back and leg pain, often described as aching or throbbing in nature. The mechanism of pain is thought to be inflamed nerve roots. Dysesthetic symptoms are observed in approximately 50% of patients during the course of their illness. Dysesthesias frequently are described as burning, tingling, or shocklike sensations and are often more prevalent in the lower extremities than in the upper extremities. Dysesthesias may persist indefinitely in 5-10% of patients. Other pain syndromes in GBS include the following:
  • • Myalgic complaints, with cramping and local muscle tenderness
    • Visceral pain
    • Pain associated with conditions of immobility (eg, pressure nerve palsies, decubitus ulcers)
  • The intensity of pain on admission correlates poorly with neurologic disability on admission and with the end outcome.
• Autonomic changes
• • Autonomic nervous system involvement with dysfunction in the sympathetic and parasympathetic systems can be observed in patients with GBS.
  • Autonomic changes can include the following:
  • • Tachycardia
    • Bradycardia
    • Facial flushing
    • Paroxysmal hypertension
    • Orthostatic hypotension
    • Anhidrosis and/or diaphoresis
  • Urinary retention and paralytic ileus also can be observed. Bowel and bladder dysfunction rarely presents as an early symptom or persists for a significant period of time.
  • Dysautonomia is more frequent in patients with severe weakness and respiratory failure.
  • Autonomic changes rarely persist in a patient with GBS.
• Respiratory involvement
• • Upon presentation, 40% of patients have respiratory or oropharyngeal weakness.
  • Typical complaints include the following:
  • • Dyspnea on exertion
    • Shortness of breath
    • Difficulty swallowing
    • Slurred speech
  • Ventilatory failure with required respiratory support is observed in up to one third of patients at some time during the course of their disease.

Physical

• Vital signs
• • Cardiac arrhythmias, including tachycardias and bradycardias, can be observed as a result of autonomic nervous system involvement.
• Tachypnea may be a sign of ongoing dyspnea and progressive respiratory failure.
• Blood pressure lability is another common feature with alterations between hypertension and hypotension.
• Cranial nerves
• • Facial weakness (cranial nerve VII) is observed most frequently, followed by symptoms associated with cranial nerves VI, III, XII, V, IX, and X. Involvement of facial, oropharyngeal, and ocular muscles results in facial droop, dysphagia, dysarthria, and findings associated with disorders of the eye.
  • Ophthalmoparesis may be observed in up to 25% of patients with GBS. Limitation of eye movement most commonly results from a symmetric palsy associated with cranial nerve VI. Ptosis from cranial nerve III (oculomotor) palsy also is often associated with limited eye movements. Pupillary abnormalities, especially those accompanying ophthalmoparesis, are relatively common as well.
• Motor examination
• • Lower extremity weakness usually begins first and ascends symmetrically and progressively over the first several days.
  • Upper extremity, trunk, facial, and oropharyngeal weakness is observed to a variable extent.
  • Marked asymmetric weakness calls the diagnosis of GBS into question.
• Sensory examination
• • Despite frequent complaints of paresthesias, objective sensory changes are minimal.
  • A well-demarcated sensory level should not be observed in patients with GBS; such a finding calls the diagnosis of GBS into question.
• Reflex changes
• • Reflexes are absent or hyporeflexic early in the disease course and represent a major clinical finding on examination of the patient with GBS.
  • Pathologic reflexes, such as the Babinski sign, are absent.
  • Hypotonia can be observed with significant weakness.

Causes

GBS is considered to be a postinfectious, immune-mediated disease targeting peripheral nerves. Up to two thirds of patients report an antecedent illness prior to the onset of neurologic symptoms.^{32, 69} Respiratory infections are most frequently reported, followed by gastrointestinal infections.

In several studies, Campylobacter jejuni was the most commonly isolated pathogen. Serology studies in a Dutch GBS trial identified 32% of patients as having had a recent C jejuni infection, while studies in northern China documented infection rates as high as 60%.^{29, 62} Gastrointestinal and upper respiratory tract symptoms can be observed with C jejuni infections. C jejuni infections can also have a subclinical course, resulting in patients with no reported infectious symptoms prior to development of GBS. Patients who develop GBS following an antecedent C jejuni infection often have a more severe course, with rapid progression and a prolonged, incomplete recovery. A strong clinical association has been noted between C jejuni infections and the pure motor and axonal forms of GBS.

The virulence of C jejuni is thought to be based on the presence of specific antigens in its capsule that are shared with nerves. Immune responses directed against capsular lipopolysaccharides produce antibodies that cross-react with myelin to cause demyelination. C jejuni infections demonstrate significant association with antibodies against gangliosides GM1 and GD1b. Although GM1 antibodies can be found with demyelinating GBS, GM1 antibodies are more common in the axonal and inexcitable groups. Even in the subgroup of patients with GM1 antibodies, however, the clinical manifestations vary. Host susceptibility is probably one determinant in the development of GBS after infectious illness.⁶²

Cytomegalovirus (CMV) infections are the second most commonly found infections preceding GBS; they account for the most common viral triggers of GBS. The aforementioned Dutch GBS study found CMV to be present in 13% of patients.⁶⁴ CMV infections present as upper respiratory tract infections, pneumonias, and nonspecific, flulike illnesses. GBS patients with preceding CMV infections often have prominent involvement of the sensory and cranial nerves. CMV infections are significantly associated with antibodies against the ganglioside GM2.

Other significant, although less frequently identified, infectious agents in GBS patients include Epstein-Barr virus (EBV), Mycoplasma pneumoniae, and Varicella-Zoster virus. An association between GBS and human immunodeficiency virus (HIV) also is well recognized. Infections with Haemophilus influenzae, para-influenza virus type 1, influenza A virus, influenza B virus, adenovirus, and herpes simplex virus have been demonstrated in patients with GBS, although not more frequently than they have in controls.⁶⁷

Various events, such as surgery, trauma, and pregnancy, have been reported as possible triggers of GBS, but these associations remain mostly anecdotal in the medical literature. Vaccinations also have been linked to GBS, by temporal association. In most cases, however, no definite causal relation has been established between vaccines and GBS (with the exception of rabies vaccine prepared from infected brain tissue and the aforementioned swine flu vaccine, which was administered in 1976). Subsequent surveys have found no significantly increased incidence of GBS after vaccination programs.⁶⁷

See also the following related eMedicine topics:
Campylobacter Infections [Infectious Diseases]
Campylobacter Infections [Pediatrics: General Medicine]
Cytomegalovirus
Cytomegalovirus Infection

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to Be Considered

Toxic neuropathies (eg, arsenic, thallium, organophosphates, lead)
Multifocal motor neuropathy
Critical illness polyneuropathy
Vasculitic neuropathies
Diphtheritic polyneuritis
Acute myasthenia gravis
Tick paralysis
Paralytic shellfish poisoning
Porphyria polyneuropathy
Chronic inflammatory demyelinating polyneuropathy
Acute myelopathy (for example, from compression, transverse myelitis, vascular injury)
Periodic paralysis
Paraneoplastic neuropathy
Relapsing inflammatory polyneuropathy
Neoplastic meningitis 
Conversion disorder/hysterical paralysis

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• CSF studies
• • During the acute phase of GBS, characteristic findings include albuminocytologic dissociation, which is an elevation in CSF protein (>0.55 g/L) without an elevation in white blood cells.
  • The increase in CSF protein is thought to reflect the widespread inflammatory disease of the nerve roots.
• Basic laboratory studies, such as complete blood counts and metabolic panels, are of limited value in the diagnosis of GBS. They are often ordered, however, to exclude other infectious or metabolic causes of the weakness.
• A basic peripheral neuropathy workup is recommended in cases in which the diagnosis is uncertain. These studies may include thyroid panel, rheumatology profiles, vitamin B-12, folic acid, hemoglobin A1C, erythrocyte sedimentation rate (ESR), rapid protein reagent, and immunoelectrophoresis of serum protein, as well as tests for heavy metals. The ordering of specific tests should be guided by the patient's history and presentation.
• Serologic studies are of limited value in the diagnosis of GBS.
• • An increase in titers for infectious agents, such as CMV, EBV, or Mycoplasma, may help in establishing etiology for epidemiologic purposes.
  • HIV has been reported to precede GBS, and serology should be tested in high-risk patients to establish possible infection with this agent.
• Serum auto-antibodies are not measured routinely in the workup of GBS, but results may be helpful in patients with a questionable diagnosis or a variant of GBS.
• • Antibodies to glycolipids are observed in the sera of 60-70% of patients with GBS during the acute phase, with gangliosides being the major target antigens.³⁵
  • Antibodies to GM1 frequently are frequently found in the sera of patients with the motor axonal neuropathy or AIDP variants of GBS. Antecedent C jejuni infections are closely associated with elevated titers of anti-GM1 antibodies.
  • Anti-GQ1b antibodies are found in patients with GBS with ophthalmoplegia, including patients with the Miller-Fisher variant.
  • Other antibodies to different major and minor gangliosides also have been found in GBS patients.

Imaging Studies

• Magnetic resonance imaging (MRI)
• • Although nonspecific, MRI can reveal nerve root enhancement.
  • Imaging studies, such as MRI or computed tomography (CT) scanning of the spine, may be more helpful in excluding other diagnoses, such as mechanical causes of myelopathy, than in assisting in the diagnosis of GBS.

Other Tests

• EMG
• • EMG studies can be very helpful in the diagnostic workup of patients with suspected GBS. Abnormalities in NCS that are consistent with demyelination are sensitive and represent specific findings for classic GBS.²
  • Although NCS results classically show a picture of demyelinating neuropathy in most patients, other electrophysiologic subgroups include axonal and inexcitable groups. The inexcitable studies may represent either axonopathy or severe demyelination with distal conduction block.
  • Although most patients exhibit sensory abnormalities on NCS, these findings are much less marked than they are in motor nerves.
  • On NCS, demyelination is characterized by nerve conduction slowing, prolongation of the distal latencies, prolongation of the F-waves, conduction block, and/or temporal dispersion. Changes on NCS should be present in at least 2 nerves in regions that are not typical for those associated with compressive mononeuropathies (preferentially in anatomically distinct areas, such as an arm and a leg or a limb and the face).
  • The needle examination is of limited value in GBS. Reduced motor unit recruitment and absent denervation help to support the suggestion of a demyelinating mechanism, although the same changes can be observed in early axonal damage with pending wallerian degeneration. In severe cases, denervation changes may be observed later in the disease course.
  • In the axonal variant of the disease, absent or markedly reduced distal compound muscle action potentials (CMAP) are observed on NCS. On needle examination, profuse and early denervation potentials also support the conclusion that there has been axonal injury.
• Pulmonary function tests
• • Maximal inspiratory pressures and vital capacities are measurements of neuromuscular respiratory function and predict diaphragmatic strength. Maximal expiratory pressures also reflect abdominal muscle strength. Frequent evaluations of these parameters should be performed at bedside to monitor respiratory status and the need for ventilatory assistance.
  • Respiratory assistance should be considered when the expiratory vital capacity decreases to <18 mL/kg or there is a decrease in oxygen saturation (arterial PO₂ < 70 mm Hg).

Procedures

• Lumbar puncture for CSF studies is recommended.

Histologic Findings

Lymphocyte and macrophage infiltration is observed on microscopic examination of peripheral nerves. Macrophage influx is believed to be responsible for the multifocal demyelination seen in GBS. A variable degree of wallerian degeneration also can be observed with severe inflammatory changes. Cellular infiltrates are scattered throughout the cranial nerves, nerve roots, dorsal root ganglions, and peripheral nerves.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Rehabilitation Program

Physical Therapy

Estimates suggest that approximately 40% of patients who are hospitalized with GBS require inpatient rehabilitation. Unfortunately, no long-term rehabilitation outcome studies have been conducted, and treatment is often based on experiences with other neurologic conditions. The goals of the therapy programs are to reduce functional deficits and to target impairments and disabilities resulting from GBS.

Early in the acute phase of the disease course, patients may not be able to fully participate in an active therapy program. At that stage, patients benefit from daily range of motion (ROM) exercises and proper positioning to prevent muscle shortening and joint contractures. Addressing upright tolerance and endurance also may be a significant issue during the early part of rehabilitation. Active muscle strengthening can then be slowly introduced and may include isometric, isotonic, isokinetic, or progressive resistive exercises. Mobility skills, such as bed mobility, transfers, and ambulation, are targeted functions. Patients should be monitored for hemodynamic instability and cardiac arrhythmias, especially upon initiation of the rehabilitation program. The intensity of the exercise program also should be monitored, because overworking the muscles may, paradoxically, lead to increased weakness.

Occupational Therapy

Occupational therapy professionals should be involved early in the rehabilitation program to promote upper body strengthening, ROM, and activities that aid functional self-care. Both restorative and compensatory strategies can be used to promote functional improvements. Energy conservation techniques and work simplification also may be helpful, especially if the patient demonstrates poor strength and endurance.

Speech Therapy

Speech therapy is aimed at promoting speech and safe swallowing skills for patients who have significant oropharyngeal weakness with resultant dysphagia and dysarthria. In ventilator-dependent patients, alternative communication strategies also may need to be implemented. Once weaned from the ventilator, patients with tracheostomies can learn voicing strategies and can eventually be weaned from the tracheostomy tube. Cognitive screening also can be performed conjointly with neuropsychology to assess for deficits, since cognitive problems have been reported in some patients with GBS, especially after they have had an extended stay in the intensive care unit (ICU).

Recreational Therapy

Participation in recreational therapy assists in the patient's adjustment to disability and improves integration into the community. Recreational activities, either new or adapted, can be used to promote the growth, development, and independence of a long-term hospital patient.

Medical Issues/Complications

Good supportive care is critical in the treatment of patients with GBS.³¹ Because most deaths related to GBS are associated with complications of ventilatory failure and autonomic dysfunction, many patients with GBS need to be monitored closely in ICUs by physicians experienced in acute neuromuscular paralysis and its accompanying complications. Competent intensive care includes the following features:

• Respiratory therapy
• Cardiac monitoring
• Safe nutritional supplementation
• Monitoring for infectious complications, such as pneumonia, urinary tract infections, and septicemia

Approximately one third of patients with GBS require ventilatory support. Monitoring for respiratory failure, bulbar weakness, and difficulties with swallowing help to anticipate complications. Proper positioning of the patient to optimize lung expansion and secretion management for airway clearance is required to minimize respiratory complications. Serial assessment of ventilatory status is needed, including measurements of vital capacity and pulse oximetric monitoring. Respiratory assistance should be considered when the expiratory vital capacity decreases to less than 18 mL/kg or when a decrease in oxygen saturation is noted (arterial PO₂ <70 mm Hg).

Close monitoring of heart rate, blood pressure, and cardiac arrhythmias allows early detection of life-threatening situations. Critically ill patients require continuous telemetry and close medical supervision in an ICU setting. Antihypertensives and vaso-active drugs should be used with caution in patients with autonomic instability.

Enteral or parenteral feedings are required for patients on mechanical ventilation to ensure that adequate caloric needs are met when the metabolic demand is high. Even patients who are off the ventilator may require nutritional support if dysphagia is severe. Precautions against dysphagia and dietary manipulations should be used to prevent aspiration and subsequent pneumonias in patients at risk.

The prevention of secondary complications of immobility, such as deep venous thrombosis (DVT), pressure sores, and contractures, also is required. This preventative action entails careful positioning, frequent postural changes, and daily ROM to prevent the latter 2 complications. Subcutaneous heparin and thromboguards are often used in the treatment of immobile patients to prevent lower extremity DVTs and secondary pulmonary embolisms (PE). Pain management with analgesics and adjunct medications also may be needed. Modalities such as transcutaneous electrical nerve stimulation (TENS) and heat may prove beneficial in the management of myalgia. Desensitization techniques can be used to improve the patient's tolerance for activities.

Although bowel and bladder dysfunction is generally transitory, management of these functions is needed to prevent other complications. Initial management should be directed toward safe evacuation and the prevention of overdistension. Monitoring for secondary infections, such as a urinary tract infection, also is an area of concern.

Hospitalized patients with GBS may experience mental status changes, including hallucinations, delusions, vivid dreams, and sleep abnormalities. These occurrences are thought to be associated with autonomic dysfunction and are more frequent in patients with severe symptoms. Such problems resolve as the patient recovers.

Surgical Intervention

Tracheotomy may be required in a patient with prolonged respiratory failure, especially if mechanical ventilation is required for more than 2 weeks. Percutaneous feeding tubes also may be needed, in order to meet the nutritional needs of patients with prolonged, severe dysphagia. A central venous line needs to be placed for patients undergoing plasmapheresis.

Consultations

• Consultation with a neurologist can be helpful in the initial diagnosis, workup, and treatment of patients admitted to the medical floor with GBS.
• Critical care specialists may be required for patients in the ICU to help manage respiratory failure and multiple medical complications.
• Consultation with a pulmonologist may be needed to perform workup and to manage respiratory issues, such as acute respiratory distress syndrome (ARDS), pneumonia, and respiratory failure.
• Consultation with a cardiologist may be required if significant cardiovascular complications, such as labile blood pressure and cardiac arrhythmias, arise from the associated autonomic dysfunction.
• Consultation with a surgeon may be required for the placement of tracheostomies, enteral feeding tubes, and central lines.
• Physical medicine and rehabilitation specialists should evaluate patients for impairments and disabilities arising from the disease and should help to determine the most appropriate setting for and intensity of rehabilitation care.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Immunomodulatory therapy, such as plasmapheresis or the administration of IVIGs, is frequently used in GBS patients.¹⁶ The efficacy of plasmapheresis and IVIGs appears to be about equal in shortening the average duration of disease.^{23, 52, 61, 65} Combined treatment has not been shown to produce a further, statistically significant reduction in disability. The decision to use immunomodulatory therapy is based on the disease's severity and rate of progression, as well as on the length of time between the condition's first symptom and its presentation. Risks, such as thrombotic events associated with IVIGs, should be taken into consideration.^{10, 50} Patients with severe, rapidly progressive disease are most likely to benefit from treatment, with improvements occurring in the rate of functional recovery.

Drug Category: Immunomodulatory agents

These medications are used to improve the clinical and immunologic aspects of GBS. They may decrease auto-antibody production and increase the solubilization and removal of immune complexes.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• GBS treatment requires careful and intensive care to monitor for such complications as respiratory difficulties and autonomic dysfunction. Approximately one third of patients require admission to an ICU, primarily because of respiratory failure. After medical stabilization, patients can be treated on a general medical/neurologic floor, but continued vigilance remains important in preventing respiratory, cardiovascular, and other medical complications. Continued care also is needed to minimize problems related to immobility, neurogenic bowel and bladder, and pain. Early involvement of allied health staff is recommended.

Further Outpatient Care

• Although follow-up studies generally have assessed patients 6-12 months after onset, some studies have reported continued improvements in strength even beyond 2 years. With prolonged recovery possible, GBS patients with continued neurologic deficits may benefit from ongoing physical therapy and conditioning programs.
• Numerous papers have addressed the issue of persistent fatigue after recovery from GBS.^{20, 31} Studies have suggested that a large percentage of patients continue to have fatigue-related problems, subsequently limiting their function at home, work, and during leisure activities. Treatment suggestions range from gentle exercise to the prescription of medications traditionally used to stimulate initiation.²¹ The effectiveness of various interventions continues to be studied.
• GBS can produce long-lasting changes in the psychosocial status of patients and their families.^{5, 6, 7} Changes in work and leisure activities can be observed in just over one third of these patients, and psychosocial functional health status can be impaired even years after the GBS event. Interestingly, psychosocial performance does not seem to correlate with the severity of residual physical function. Poor conditioning and easy fatigability may be contributory factors. Therefore, providing long-term attention and support for this population group is important.

Inpatient/Outpatient Medications

• Immunomodulatory medications have been used to hasten recovery. In well-controlled clinical trials, the efficacy of IVIGs in GBS patients has been shown to equal that of plasma exchange.^{23, 52, 61, 65} IVIG treatment is easier to implement and potentially safer than plasma exchange, and the use of IVIGs versus plasma exchange may be a choice of availability and convenience. Attempts have been made to employ oral and IV steroids in the treatment of GBS, but they have not been found to have a clinical benefit; these drugs are not currently employed in GBS treatment.
• Hemodynamic changes related to autonomic dysfunction are usually transitory, and patients rarely require long-term medications to treat blood pressure or cardiac problems.
• Pain medications may be required in the inpatient and outpatient settings. A tiered pharmacologic approach that starts with nonsteroidal anti-inflammatory drugs or acetaminophen, with narcotic agents added as needed, is usually recommended. Most patients do not require narcotic analgesics after the first couple of months of illness. Adjunct medications for pain, such as tricyclic antidepressants and certain anticonvulsants, also may be beneficial for dysesthetic-type pains.
• Anticoagulants, such as heparin or low–molecular weight heparin, are recommended to prevent thromboembolic disease in the sedentary patient.

Transfer

• Patients may require transfer to the ICU if serious respiratory or cardiac problems occur. Upon medical and neurologic stabilization, patients may need to be transferred to an inpatient rehabilitation unit if functional impairments persist.

Deterrence

• C jejuni is the most common cause of bacterial gastro-enteritis in industrialized countries and is also the organism that is most frequently identified in association with GBS. Preventive measures to control C jejuni infections, such as vaccinations, may be the best means to prevent GBS.

Complications

• A small percentage (~10%) of patients have an acute relapse after initial improvement or stabilization after treatment. Some patients also demonstrate treatment fluctuations during their clinical course. Although the procedures are controversial, there is no convincing evidence that IVIG treatment or plasma exchange has a significant effect on the rate of treatment failure or of acute relapse.⁵⁶ The risk of relapse does appear to be higher in patients in whom there has been a later onset of treatment, a more protracted disease course, and more associated medical conditions. Additional plasma exchange or IVIG treatments often result in further improvement.⁶⁰

Prognosis

• Although most patients with GBS make good recovery, 2-12% of them die from complications related to GBS, and a significant percentage of survivors have persistent motor sequelae. Estimates indicate that 75-85% of patients experience good recovery, 15-20% have moderate residual deficits, and 1-10% are left severely disabled. Although the exact prevalence is uncertain, up to 25,000-50,000 persons in the United States may have long-term functional deficits from GBS.
• Older age, poor upper extremity (UE) muscle strength, the need for mechanical ventilation, Medical Research Council (MRC) scores of less than 40, and preceding gastrointestinal infections have been found to have an adverse effect on outcomes associated with GBS.⁶⁸ A rapidly progressing onset of weakness also has been associated with less favorable outcomes in many studies, although in other reports, delayed time to peak disability has been shown to be an independent predictor of poor outcome at 1 year.

  Low mean CMAP amplitudes of less than 20% of the lower limit of normal or the presence of inexcitable nerves on initial electrophysiologic studies are other predictors of poorer functional outcomes. Persistence of a low mean CMAP on later testing (>1 mo after onset) results in an even higher sensitivity and specificity of testing than does the initial test after onset. The sex of the patient, the presence of underlying pulmonary disease, or manifestation of dysautonomia has no prognostic significance.

• The speed of recovery varies. Recovery often takes place within a few weeks or months; however, if axonal degeneration has occurred, recovery can be expected to progress slowly over many months, because regeneration may require 6-18 months. In general, slower and less complete recovery is observed in older patients.

Patient Education

• Patients with GBS and their families should be educated on the illness, the disease process, and the anticipated course. GBS is a life event with a potentially long-lasting influence on patients' physical and psychosocial well-being.^{5, 6, 7} Family education and training also is recommended to prevent complications during the early stages of the disease and to assist in the recovery of function during the rehabilitation stages.
• For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see eMedicine's patient education article Guillain-Barré Syndrome.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Patients who are diagnosed with GBS should be admitted to a hospital for close monitoring until it has been determined that the course of the disease has reached a plateau or undergone reversal. Although the weakness may initially be mild and nondisabling, symptoms can progress rapidly over just a few days. Continued progression may result in a neuromuscular emergency with profound paralysis, respiratory insufficiency, and/or autonomic dysfunction with cardiovascular complications. Early recognition and treatment of GBS also may be important in the long-term prognosis, especially in the patient with poor clinical prognostic signs, such as older age, a rapidly progressing course, and antecedent diarrhea.⁶³

Special Concerns

• Immunotherapy for children with GBS has not been rigorously studied with randomized, well-controlled studies. Despite this fact, immunotherapy is standardly used in the pediatric patient with GBS.¹
• Immunotherapy for pregnant women has not been studied, and safety for use during pregnancy has not been established.
• Older age is a risk factor for a less favorable prognosis. Recovery is often slower and less complete in elderly patients. In addition, mortality rates in elderly persons with GBS are higher than in younger patients with the condition.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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Article Last Updated: Nov 14, 2008