Guillain Barre Syndrome


Article Author:
Thy Nguyen


Article Editor:
Roger Taylor


Editors In Chief:
Allison Castro


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
10/27/2018 12:31:36 PM

Introduction

Guillain-Barre syndrome (GBS) is the most common cause of acute, flaccid, neuromuscular paralysis in the United States. Guillain-Barre syndrome was first discovered more than a century ago. Advances in the past century include investigating the immune-mediated pathophysiology of the disease, recognizing the spectrum of presentations, advancing diagnostic modalities, prognostic models, and performing randomized trials of treatments to improve outcome. Given the morbidity that can occur without treatment, all physicians should have a knowledge of this rare disease.[1][2][3][4]

Etiology

The Guillain-Barre syndrome (GBS) and its variants are considered post-infectious, immune-mediated neuropathies. Evidence from animal models suggests a key role of molecular mimicry. In Campylobacter jejuni gastrointestinal infections, a lipooligosaccharide present in the outer membrane of the bacteria is similar to gangliosides that are components of the peripheral nerves.[5] Therefore, an immune response triggered to fight infection can lead to a cross-reaction on host nerves.

Many infections have been linked with GBS. The most common are gastrointestinal or respiratory illnesses. Up to 70% of patients have reported an antecedent illness in the 1 to 6 weeks before the presentation of GBS.[6] During the Zika virus outbreak, many GBS cases were described.[7] Case reports detail many other possible etiologies linked to GBS including medications and surgeries. (Evidence level III)

In 1976, flu vaccination against the influenza A/H1N1 antigen led to a well-documented, increased incidence of cases of GBS; however, further surveillance data of flu vaccinations in subsequent years have described only one additional case of GBS for every 1 million vaccines. Subsequent studies estimate that developing GBS after a flu infection is up to 7 times more likely than developing GBS after a vaccination.[8][9][10][11][12] (Evidence level IV)

Epidemiology

Although rare, with an incidence of 0.4 to 2 per 100,000, Guillain-Barre syndrome (GBS) has major effects on the health care system. The cost of medical care for a patient with GBS has been estimated at up to $318,966. Overall, the cost of treating patients with GBS has been estimated at $1.7 billion dollars per year. Males are affected at a slightly higher incidence than females. Each year, it is estimated 100,000 patients worldwide would contract GBS.[13][14] (Evidence level III)

Pathophysiology

Antecedent infections are reported in up to 70% of patients with Guillain-Barre Syndrome (GBS).[15] Therefore, molecular mimicry plays a substantial role in our understanding of GBS, particularly the axonal variant. The lipooligosaccharide of Campylobacter jejuni is similar to the gangliosides of peripheral nerve membranes.[5] Passive immunization of rabbits with these ganglioside-like lipooligosaccharides have led to similar clinical syndromes of flaccid tetraplegia, similar to the acute motor axonal neuropathy variant of GBS.[16][17] Ganglioside antibodies have been shown to have different peripheral nerve targets. Anti-GD1a antibodies bind to paranadol myelin, nodes of Ranvier, and neuromuscular junction.[18][19]  GM1 and GQ1B antibodies bind to a peripheral nerve or neuromuscular junction.[20][21] These different peripheral nerve targets may play a role in the heterogeneity of the clinical presentation of GBS. Additionally, complement cascade is activated and plays a key role in the disease’s pathogenesis.[22]

Certain gangliosides are more likely to be associated with specific presentations. For example, Miller-Fisher syndrome is associated with the anti-GQ1B antibody.[23] The axonal motor neuropathy form may be associated with anti-GM1 antibodies.[24] The pharyngeal-cervical-brachial variant of GBS may be associated with anti-GT1A antibodies.[25] However, besides Miller-Fisher syndrome’s association with anti-GQ1B antibodies, sensitivity and specificity of all antibodies for specific subtypes are low-to-moderate yield for clinical utility.

Given that not all patients test positive for anti-ganglioside antibodies, further research is needed to elucidate the roles of anti-ganglioside antibodies in GBS, as causal or epiphenomenon. Less is known about the pathophysiology behind the acute inflammatory demyelinating polyneuropathy variant (AIDP) of GBS, despite the fact that it is considered the most common variant in the United States.

History and Physical

Guillain-Barre syndrome (GBS) patients describe a fulminant course of symptoms that usually include ascending weakness and non-length dependent sensory symptoms. By definition, the nadir is usually reached within 4 weeks. Symmetric involvement is a key feature of GBS.[6] GBS is usually considered monophasic; therefore, a relapsing or remitting course at presentation would be considered atypical.[26] Additionally, a prior GBS event (recurrent GBS) is also unusual, occurring in < 10% of all patients.[27] If the patient reports progression beyond 8 weeks, other diagnoses should be considered.

GBS often presents (up to 70% of patients) within 1 to 6 weeks of antecedent illness.[28] Other antecedent events that have been linked with GBS include vaccinations (specifically a 1976 strain of swine flu vaccine), surgery, trauma, or other infections. [28][11] 

Classically, patients with GBS will have a pattern of proximal and distal weakness, which is flaccid and often profound if hospitalized. Significant neck flexion weakness may be present and can portend need for intubation. Areflexia or hyporeflexia is usually present. (Rare cases without hypo/areflexia have been described, mostly in the AMAN variant of GBS).[29] Besides the flaccid weakness and areflexia, patients experience non-length-dependent sensory symptoms; therefore, unlike more common chronic neuropathies such as diabetic neuropathy, patients may report dysesthesias in the hands followed by the feet. Patients can develop facial diplegia due to the involvement of both facial cranial nerves. They can also develop dysphagia due to the involvement of the glossopharyngeal, vagus, and hypoglossal cranial nerves.[6] Autonomic nerves can lead to significant morbidity; therefore, most physicians recommend monitoring in an intermediate or intensive care unit for cardiac arrhythmias or blood pressure lability. Dysautonomia is a primary etiology of the morbidity and mortality attributable to GBS. Additionally, the involvement of the lower cranial nerves (glossopharyngeal, vagus, and hypoglossal nerves) or involvement of the nerves to the muscles of respiration may lead to the need for artificial ventilation. Respiratory failure can occur in up to 30% of patients, usually leading to a prolonged hospitalization and recovery.[30]

Besides the classic GBS presentation described above, many variants of GBS have been described. There is a variant with pure motor involvement called "AMAN (acute motor axonal neuropathy)" that is more common in Asian countries.[31] Rarely,  these patients can have normal reflexes.[29] There is also a regional variant involving primarily the pharyngeal, neck, and upper extremity muscles called the "pharyngeal-cervical-brachial" variant).[32] Some variants can involve the central nervous system, termed "Bickerstaff Encephalitis."[33] There is also a variant that presents with paraparesis.[34] Arguably, the most famous variant is the Miller Fisher syndrome.[35][36] This is classically described as a triad of ophthalmoplegia, areflexia, and ataxia; however, other cranial nerves besides the oculomotor nerves have been reported in this variant.[36]

Evaluation

Guillain-Barre syndrome (GBS) is considered a clinical diagnosis; therefore, a diagnosis can be made with confidence at the bedside in most cases. For atypical cases or unusual subtypes, ancillary testing can be useful.[26]

Electromyography and nerve conduction studies may be helpful in distinguishing GBS from its mimics. Nerve conduction studies (NCS) utilize technology to help distinguish between demyelinating and axonal forms of neuropathy. Needle electromyography may help to determine the acuity of a patient’s symptoms. In some cases, these studies may be helpful in evaluating for other considerations in the differential diagnosis such as neuromuscular junction disorders or diabetic neuropathy. Classically, electrodiagnostic studies should be undertaken at 10 to 14 days after symptom onset due to the time for Wallerian degeneration of sensory and motor nerve fibers; however, there have been many studies that reveal that early, nonspecific findings may be helpful in diagnosing GBS as early as 3 to 7 days after symptom onset.[37][38] 

The more common early electrodiagnostic findings in GBS include absent or prolonged H-reflexes and/or F-wave latencies.[39][38] The sural sparing pattern is considered specific for GBS as compared to other polyneuropathies.[40] This pattern would show an intact sural sensory response with abnormal upper extremity sensory responses. Other findings would depend on the variant of GBS. Acute inflammatory demyelinating polyneuropathy would be more likely to have partial motor conduction block, temporal dispersion, slow conduction velocities, prolonged/absent F-wave latencies, and prolonged distal latencies.[41][31] AMAN would usually show a pattern of low, compound muscle action potential amplitudes or even inexcitable motor nerves; however, partial motor conduction block or complete conduction block can be seen in AMAN nerve conduction study (NCS). This phenomenon is explained by “reversible conduction failure.”[42] Complement is deposited in nodes of Ranvier and paranodal regions on peripheral nerves. Subsequently, the nerves can undergo Wallerian degeneration leading to significant and prolonged axonal damage or can reverse, deemed conduction failure.[43][22] This phenomenon explains the relatively rapid recovery of some severely weak patients with AMAN. Sensory nerves would be spared both clinically and electrodiagnostically in AMAN. Acute motor and sensory axonal neuropathy (AMSAN) would show low amplitude motor and sensory potentials. Miller Fisher syndrome is more often described with reduced or absent sensory nerve action potentials.[44] 

Cerebrospinal fluid (CSF) shows a classic pattern of albuminocytologic dissociation. This term means that spinal fluid shows a normal amount of white blood cells and an elevated CSF protein level.[4][26] However, this pattern is only present in 80% of patients at 2 weeks following symptom onset. Therefore, the absence of this classic finding does not exclude the diagnosis. If the white blood cell count is elevated, this should prompt consideration of other infectious GBS mimics, such as HIV seroconversion.[6] 

A number of ganglioside antibodies have been associated with GBS. Antibodies include anti-GM1, anti-GD1A, anti-GT1A, and anti-GQ1B. These range in sensitivity from up to 60% (anti-GM1 antibodies in acute motor axonal neuropathy) to up to more than 90% (anti-GQ1B antibodies in Miller Fisher syndrome). However, these laboratory studies usually require some time to obtain results and, therefore, may not be as helpful in decision making at the time of a patient admission.[45][46][47]

Imaging studies such as magnetic resonance imaging (MRI) spine may show enhancement of the nerve roots, indicating a breakdown of the blood-nerve barrier due to inflammation in GBS. However, MRI utility in GBS is most useful to rule out other etiologies of quadriparesis or facial diplegia such as transverse myelitis or intracranial disease.[48][49]

A negative inspiratory force (NIF) should be performed on patients with suspected GBS.  Serial NIFs should be followed in patients with high risk of respiratory compromise.  Patients that are unable to perform a NIF of -20 to -30 cm H2O should be considered at a very high risk.  

Treatment / Management

In randomized controlled trials, there are two treatment options currently considered the standard of care in Guillain-Barre syndrome (GBS). These include either intravenous immunoglobulin (IVIG) or plasma exchange. IVIG is thought to act by its immune modulating action; however, the exact mechanism remains to be elucidated. IVIG is given 2 grams/kilogram divided over 5 days. (Evidence level I)[50]) Plasma exchange is thought to act by removing pathogenic antibodies, humoral mediators, and complement proteins involved in the pathogenesis of GBS. Similar to IVIG, its exact mechanism of action in the treatment of GBS has not been proven. Plasma exchange is generally given as a volume of exchange over five sessions. Plasma exchange and IVIG have been shown to be equally efficacious. (Evidence level I)[51] The effect is present if either treatment is given within 4 weeks, but the stronger effect may be present if treatment is administered within two weeks. (Evidence level II)[52][53][54][52] Surprisingly, corticosteroids (both oral prednisone and intravenous methylprednisolone) have not shown benefit over placebo or in combination with IVIG and plasma exchange over either modality alone. Overall, treatment is generally considered to shorten the course of recovery of GBS. Treated patients in one study achieved independent ambulation 32 days faster than untreated patients. (Evidence level I)[55][56][53][51][57][58]

 Overall, most patients with GBS do well, with up to 85% of patients achieving independent ambulation with recovery; however, there is a significant proportion of patients (20%) with morbidity. (Evidence level III) Further studies of plasma exchange followed by IVIG and IVIG concurrent with steroids have not shown significant improvement. (Evidence level I)[59][60] An ongoing trial of 2 courses of IVIG should have results within the next year. (Evidence level III) [61] There are also ongoing trials of complement inhibitors in patients with refractory GBS. (Evidence level II)[62][63][64]

Differential Diagnosis

Following the eradication of poliovirus, Guillain-Barre syndrome (GBS) is the most common cause of acute or subacute, flaccid neuromuscular weakness worldwide; however, other disorders may mimic GBS. If the flaccid weakness occurs in a critically ill patient with multiorgan involvement, critical illness neuropathy and myopathy should be considered. Other etiologies which may mimic GBS include tick paralysis. There would be an initial presentation of neuromuscular junction disorder, acute intermittent porphyria, HIV infection, spinal cord disorders, toxic neuropathies and even infections (such as West Nile virus or rabies). Some atypical clinical features should lead providers to consider other diagnoses. These include early bowel and bladder involvement, asymmetric features, and hyperreflexia or normal reflexes.

Distinguishing GBS from its mimics would require a thoughtful evaluation of history, clinical presentation, and ancillary data. Regarding the clinical presentation, the presence of dilated pupils may be more suggestive of tick paralysis or botulism. Ancillary testing such as electromyography and nerve conduction studies may distinguish GBS from critical illness neuropathy/myopathy along with history and clinical context. Cerebrospinal fluid testing showing pleocytosis rather than the classic albuminocytologic dissociation may lead to further consideration of infectious etiologies such as HIV or West Nile Virus infection.

Prognosis

After the acute phase of illness, Guillain-Barre syndrome (GBS) patients tend to do well. More than 80% achieve independent ambulation after 6 months.[30] Mortality during the acute phase of the illness is less than 5%.[65] However, there is a subset of patients, less than 20%, who continue to have significant disability despite receiving the standard of care for GBS. Studies are underway to try to identify these patients early. Early identification of poor prognostic factors could lead to trials of further treatment specific to this subgroup. In a cohort of Dutch patients, a  prognostic tool, Erasmus GBS Outcome score, utilizes the patient’s physical examination, age, and presence of diarrhea to predict the patient’s ability to walk in the near future.[66] Patients with a significant likelihood of residual disability would be most amenable to further therapeutic trials.

Studies to assess whether plasma exchange followed by IVIG would have an additional benefit were not significant.[60] Additionally, a number of studies regarding the addition of corticosteroids to IVIG were also not significant; however, there may have been a benefit in patients with worse prognostic factors (such as age and GBS disability score).[59] According to a small case series, two courses of IVIG has been suggested as a possible intervention.[67] There may be some limitations of IVIG use based on adverse effects, however.[68] Currently, there is an ongoing randomized controlled trial of 2 courses of IVIG with patients with refractory GBS.[61] Additionally, there is much interest in the key role of complement activation in the pathogenesis of GBS; therefore, a randomized controlled trial of eculizumab in patients with GBS is being studied.[63]

Other clinical features have been shown to predict the need for ventilation during the illness. These include fulminant course (onset to admission < 7 days), bulbar weakness, and neck flexion weakness. These predictive factors would suggest triage to an intensive care unit rather than a stepdown unit.[69]

Following recovery, patients may continue to contend with residual fatigue, pain, and paresthesias for up to several years. (Evidence level III)[70][71]

Complications

The most feared complications are respiratory compromise and bulbar palsies.

Consultations

  • Neurology
  • Pulmonology/Intensive Care
  • +/- Infectious Disease
  • +/- Immunology

Enhancing Healthcare Team Outcomes

The care of the patient with Guillain-Barre syndrome (GBS) requires all members of the healthcare team. Nurses are integral in recognizing and preventing complications, including decubitus ulcers, dysautonomia, and infection prevention. Pharmacists should be well-versed in the adverse effects that may occur with the administration of treatments for GBS, such as IVIG. Respiratory therapists can assist with preventing atelectasis and aspiration pneumonia. Physical and occupational therapists are crucial as the patient begins to regain function and strength. Following recovery, patients often may find it helpful to enlist in support groups available through the GBS foundation.


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Guillain Barre Syndrome - Questions

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Several weeks after an upper respiratory tract infection, a 52-year-old man develops weakness of his lower extremity muscles, decreased reflexes, and paresthesias. A lumbar puncture only shows a mild increase in protein. Which of the following is most likely?



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A patient is admitted to the hospital after an URTI infection. She complains of lethargy and an inability to eat for a few days. She appears dehydrated and ill. She denies smoking or the use of any medications. Two days later, she complains of being unable to move her legs and complains of painful needle like feelings in both legs. Her ankle reflexes are absent. She has no other sensory or motor defects. Over the next few days, her weakness ascends up to the hips, and she is now bed ridden. What is the most likely diagnosis?



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What is the most common finding in a patient with Guillain-Barre syndrome?



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For which group is the influenza vaccination not indicated?



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Which of the following disorders presents with ascending paralysis?



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Which of the following is the best treatment for a patient with Guillain Barre Syndrome?



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What percent of patients with Guillain Barre Syndrome will present with a prior upper respiratory tract infection (URTI)?



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Which of the following features in CSF finding is NOT typical of a patient with Guillain Barre syndrome?



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Which of the following findings is least likely in Guillain-Barre syndrome?



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A patient presents with a rapidly progressive weakness of both her legs and the weakness is moving up the trunk. She also has absent reflexes but no sensory change. Select the most likely diagnosis.



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A patient with Guillain-Barre syndrome is least likely to have which clinical finding?



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A 17-year-old male has recovered from an upper respiratory infection but develops progressive weakness of both legs and then his arms. He has no loss of sensation or loss of bowel or bladder control. After 8 days he requires mechanical ventilation. What would CSF analysis show?



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A patient recovering from a viral infection notices significant weakness in the legs which is ascending.There is associated severe pain in the muscles. Exam reveals a loss of position sense and no reflexes. What is the diagnosis?



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A patient is recovering from mild flu-like symptoms when she notices a rubbery feeling in her legs with difficulty walking. There is a deep aching pain in the leg muscles and altered sensation when she touches her legs. The next morning she is having trouble swallowing and breathing and rushed to the hospital where she in admitted to the ICU and intubated for respiratory support. What is the likely diagnosis?



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Which of the following statements about the causes of Guillain-Barre syndrome is true?



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A 77 year old who has been hospitalized for Guillain-Barre syndrome develops a cardiac arrhythmia and subsequently dies. Cardiac arrhythmia ranks as what number cause of death in the elderly with this condition?



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Which of the following treatments is not effective in treating Guillain-Barre syndrome?



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Which statement about Guillain-Barre syndrome is FALSE?



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Which of the following diseases is characterized by ascending paralysis?



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Which of the following is the best management of Guillain-Barre syndrome?



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An adult develops ascending weakness and is suspected to have Guillain-Barre syndrome. He becomes short of breath. Select the criterion that is not an indication for intubation and mechanical ventilation.



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An 8-year-old girl living in Chicago in February has developed clumsiness, progressive weakness, and loss of facial expression. Ataxia of upper and lower extremities is present, bilateral facial weakness is noted, and there are decreased deep tendon reflexes. Select the correct statement.



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What is the most common acquired paralysis in a previously healthy child?



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What percent of Guillain Barre syndrome cases report pain in extremities?



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What percent of Guillain Barre syndrome cases do not present with antecedent infection?



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A patient presents with ascending paralysis after a short period of diarrhea. Which of the following investigations would most likely yield a positive result in this patient?



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Which of the following cerebrospinal fluid (CSF) analysis results suggest Guillain- Barre syndrome?



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All of the following clinical findings are suggestive of Guillain Barre syndrome except:



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Which of the following treatment modalities is not indicated in patients with acute Guillain-Barre syndrome?



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Which of the following statements regarding Guillain-Barre syndrome (GBS) is not true?



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An OT is treating a patient with Guillain-Barre syndrome who has only fair strength in the upper extremities. How should the therapist start?



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A newly admitted patient with Guillain-Barre syndrome is to be evaluated by OT. Which of the following is most important when assessing upper extremity function?



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What should be the initial OT intervention for a patient with Guillain-Barre syndrome paralysis causing complete paralysis?



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Which of the following is true about Guillain-Barre syndrome?



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Which of the following is not true about Guillain-Barre syndrome?



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A patient has Guillain-Barre syndrome. What findings would be expected?



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Which of the following would not be seen with Guillain-Barre syndrome?



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What is the defect associated with Guillain-Barre syndrome?



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Which of the following least applies to Guillain Barre Syndrome?



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Which of the following is the most likely to be the precipitating factor in the onset of Guillain Barre Syndrome?



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Which of the following is the term used to describe the damage to the nerves in Guillain Barre syndrome?



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Which of the following is most typical of the paralysis associated with Guillain Barre Syndrome?



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Which of the following is the most atypical symptom of Guillain-Barre syndrome?



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Which of the following is a sudden onset symptom of Guillain Barre Syndrome requiring immediate or emergent care?



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Which of the following is true of Guillain-Barre syndrome?



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Which of the following is not treatment for Guillain Barre Syndrome?



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A patient with recent gastrointestinal illness now has the complaint of weakness and numbness in the lower extremities, with exam findings of absent deep tendon reflexes in both legs with symmetric weakness in both legs and his facial muscles; his most likely diagnosis:



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Which is true regarding Guillain Barre syndrome?



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An 11 year old female has had a URI that has resolved. 10 days later she has bilateral leg weakness that progresses to involve the trunk. Exam shows absent deep tendon reflexes and marked lower extremity and trunk weakness but no atrophy. Lumbar puncture shows CSF with elevation of protein but no white blood cells. Select the most likely diagnosis.



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A patient presents with complaints of bilateral lower extremity weakness that started yesterday. Today, the whole body feels weak, but there is no pain. The vital signs are normal. Which of the following questions is most appropriate?



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What structure is affected in Guillain-Barre syndrome?



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What type of arterial blood gas can be seen in a patient with Guillain-Barre syndrome?



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What antibody may be seen in patients with Guillain-Barre syndrome?



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Which of the following statements about Guillain-Barre Syndrome is correct?



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Which of the following is not associated with an axonal polyneuropathy?



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Which of the following conditions is treated with parenteral immunoglobulin to confer passive immunity?



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You are caring for a patient with Guillain-Barre syndrome. Which of the following are expected findings? Select all that apply.



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A 17-year-old patient presents to the emergency department with worsening numbness, tingling, and weakness that started a few days ago in her feet and now involves both lower extremities. She reports that she had an upper respiratory infection a 2 weeks ago that resolved without treatment. Which of the following is likely to develop? Select all that apply.



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You are caring for a patient with Guillain-Barre syndrome. Which of the following is correct? Select all that apply.



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A 58-year-old presents with symmetrical muscle weakness that started in the legs and progressed upwards to the arms. A diagnosis of Guillain-Barre syndrome is made. Signs and symptoms of Guillain-Barre syndrome may include which of the following? Select all that apply.



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A 40-year-old is transferred to the critical care unit with a diagnosis of Guillain-Barre syndrome. Which of the following can be a precipitating cause? Select all that apply.



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A 50-year-old male is seen the emergency department with rapidly progressing muscle weakness that started in his legs. His spouse reports a recent upper respiratory infection. The patient is admitted to the critical care unit for further monitoring of suspected Guillain-Barre syndrome that is rapidly worsening. Which nursing considerations will guide his plan of care? Select all that apply.



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Guillain Barre Syndrome - References

References

Lehmann HC,Hughes RA,Kieseier BC,Hartung HP, Recent developments and future directions in Guillain-Barré syndrome. Journal of the peripheral nervous system : JPNS. 2012 Dec     [PubMed]
Govoni V,Granieri E, Epidemiology of the Guillain-Barré syndrome. Current opinion in neurology. 2001 Oct     [PubMed]
Frenzen PD, Economic cost of Guillain-Barré syndrome in the United States. Neurology. 2008 Jul 1     [PubMed]
Yuki N,Hartung HP, Guillain-Barré syndrome. The New England journal of medicine. 2012 Jun 14     [PubMed]
Koga M,Yuki N,Hirata K, Antecedent symptoms in Guillain-Barré syndrome: an important indicator for clinical and serological subgroups. Acta neurologica Scandinavica. 2001 May     [PubMed]
Schonberger LB,Bregman DJ,Sullivan-Bolyai JZ,Keenlyside RA,Ziegler DW,Retailliau HF,Eddins DL,Bryan JA, Guillain-Barre syndrome following vaccination in the National Influenza Immunization Program, United States, 1976--1977. American journal of epidemiology. 1979 Aug     [PubMed]
Asbury AK,Cornblath DR, Assessment of current diagnostic criteria for Guillain-Barré syndrome. Annals of neurology. 1990     [PubMed]
Ishii J,Yuki N,Kawamoto M,Yoshimura H,Kusunoki S,Kohara N, Recurrent Guillain-Barré syndrome, Miller Fisher syndrome and Bickerstaff brainstem encephalitis. Journal of the neurological sciences. 2016 May 15     [PubMed]
Ho TW,Mishu B,Li CY,Gao CY,Cornblath DR,Griffin JW,Asbury AK,Blaser MJ,McKhann GM, Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies. Brain : a journal of neurology. 1995 Jun     [PubMed]
Sheikh KA,Zhang G, An update on pathobiologic roles of anti-glycan antibodies in Guillain-Barré syndrome. F1000 biology reports. 2010 Mar 25     [PubMed]
Willison HJ,Yuki N, Peripheral neuropathies and anti-glycolipid antibodies. Brain : a journal of neurology. 2002 Dec     [PubMed]
Fokke C,van den Berg B,Drenthen J,Walgaard C,van Doorn PA,Jacobs BC, Diagnosis of Guillain-Barré syndrome and validation of Brighton criteria. Brain : a journal of neurology. 2014 Jan     [PubMed]
Al-Shekhlee A,Hachwi RN,Preston DC,Katirji B, New criteria for early electrodiagnosis of acute inflammatory demyelinating polyneuropathy. Muscle     [PubMed]
Chanson JB,Echaniz-Laguna A, Early electrodiagnostic abnormalities in acute inflammatory demyelinating polyneuropathy: a retrospective study of 58 patients. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2014 Sep     [PubMed]
Appropriate number of plasma exchanges in Guillain-Barré syndrome. The French Cooperative Group on Plasma Exchange in Guillain-Barré Syndrome. Annals of neurology. 1997 Mar     [PubMed]
Alshekhlee A,Hussain Z,Sultan B,Katirji B, Guillain-Barré syndrome: incidence and mortality rates in US hospitals. Neurology. 2008 Apr 29     [PubMed]
van Doorn PA, Diagnosis, treatment and prognosis of Guillain-Barré syndrome (GBS). Presse medicale (Paris, France : 1983). 2013 Jun     [PubMed]
Misawa S,Kuwabara S,Sato Y,Yamaguchi N,Nagashima K,Katayama K,Sekiguchi Y,Iwai Y,Amino H,Suichi T,Yokota T,Nishida Y,Kanouchi T,Kohara N,Kawamoto M,Ishii J,Kuwahara M,Suzuki H,Hirata K,Kokubun N,Masuda R,Kaneko J,Yabe I,Sasaki H,Kaida KI,Takazaki H,Suzuki N,Suzuki S,Nodera H,Matsui N,Tsuji S,Koike H,Yamasaki R,Kusunoki S, Safety and efficacy of eculizumab in Guillain-Barré syndrome: a multicentre, double-blind, randomised phase 2 trial. The Lancet. Neurology. 2018 Jun     [PubMed]
Yamaguchi N,Misawa S,Sato Y,Nagashima K,Katayama K,Sekiguchi Y,Iwai Y,Amino H,Suichi T,Yokota T,Nishida Y,Kohara N,Hirata K,Nishiyama K,Yabe I,Kaida KI,Suzuki N,Nodera H,Tsuji S,Koike H,Kira JI,Hanaoka H,Kusunoki S,Kuwabara S, A Prospective, Multicenter, Randomized Phase II Study to Evaluate the Efficacy and Safety of Eculizumab in Patients with Guillain-Barré Syndrome (GBS): Protocol of Japanese Eculizumab Trial for GBS (JET-GBS). JMIR research protocols. 2016 Nov 7     [PubMed]
Guillain G,Barré JA,Strohl A, [Radiculoneuritis syndrome with hyperalbuminosis of cerebrospinal fluid without cellular reaction. Notes on clinical features and graphs of tendon reflexes. 1916]. Annales de medecine interne. 1999 Jan     [PubMed]
Yuki N,Taki T,Inagaki F,Kasama T,Takahashi M,Saito K,Handa S,Miyatake T, A bacterium lipopolysaccharide that elicits Guillain-Barré syndrome has a GM1 ganglioside-like structure. The Journal of experimental medicine. 1993 Nov 1     [PubMed]
CAMPBELL AM, The aetiology of polyneuritis. Proceedings of the Royal Society of Medicine. 1958 Mar     [PubMed]
Cao-Lormeau VM,Blake A,Mons S,Lastere S,Roche C,Vanhomwegen J,Dub T,Baudouin L,Teissier A,Larre P,Vial AL,Decam C,Choumet V,Halstead SK,Willison HJ,Musset L,Manuguerra JC,Despres P,Fournier E,Mallet HP,Musso D,Fontanet A,Neil J,Ghawché F, Guillain-Barré Syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study. Lancet (London, England). 2016 Apr 9     [PubMed]
Willison HJ,Jacobs BC,van Doorn PA, Guillain-Barré syndrome. Lancet (London, England). 2016 Aug 13     [PubMed]
Gregson NA,Jones D,Thomas PK,Willison HJ, Acute motor neuropathy with antibodies to GM1 ganglioside. Journal of neurology. 1991 Dec     [PubMed]
O'Leary CP,Veitch J,Durward WF,Thomas AM,Rees JH,Willison HJ, Acute oropharyngeal palsy is associated with antibodies to GQ1b and GT1a gangliosides. Journal of neurology, neurosurgery, and psychiatry. 1996 Dec     [PubMed]
Chiba A,Kusunoki S,Shimizu T,Kanazawa I, Serum IgG antibody to ganglioside GQ1b is a possible marker of Miller Fisher syndrome. Annals of neurology. 1992 Jun     [PubMed]
Yikilmaz A,Doganay S,Gumus H,Per H,Kumandas S,Coskun A, Magnetic resonance imaging of childhood Guillain-Barre syndrome. Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery. 2010 Aug     [PubMed]
Zuccoli G,Panigrahy A,Bailey A,Fitz C, Redefining the Guillain-Barré spectrum in children: neuroimaging findings of cranial nerve involvement. AJNR. American journal of neuroradiology. 2011 Apr     [PubMed]
Ortiz-Salas P,Velez-Van-Meerbeke A,Galvis-Gomez CA,Rodriguez Q JH, Human Immunoglobulin Versus Plasmapheresis in Guillain-Barre Syndrome and Myasthenia Gravis: A Meta-Analysis. Journal of clinical neuromuscular disease. 2016 Sep     [PubMed]
Hughes RA, Plasma exchange versus intravenous immunoglobulin for Guillain-Barré syndrome. Therapeutic apheresis : official journal of the International Society for Apheresis and the Japanese Society for Apheresis. 1997 May     [PubMed]
Hughes RA,Brassington R,Gunn AA,van Doorn PA, Corticosteroids for Guillain-Barré syndrome. The Cochrane database of systematic reviews. 2016 Oct 24     [PubMed]
Plasmapheresis and acute Guillain-Barré syndrome. The Guillain-Barré syndrome Study Group. Neurology. 1985 Aug     [PubMed]
van der Meché FG,Schmitz PI, A randomized trial comparing intravenous immune globulin and plasma exchange in Guillain-Barré syndrome. Dutch Guillain-Barré Study Group. The New England journal of medicine. 1992 Apr 23     [PubMed]
Hughes RA,Swan AV,van Doorn PA, Intravenous immunoglobulin for Guillain-Barré syndrome. The Cochrane database of systematic reviews. 2014 Sep 19     [PubMed]
Sejvar JJ,Baughman AL,Wise M,Morgan OW, Population incidence of Guillain-Barré syndrome: a systematic review and meta-analysis. Neuroepidemiology. 2011     [PubMed]
Jacobs BC,Rothbarth PH,van der Meché FG,Herbrink P,Schmitz PI,de Klerk MA,van Doorn PA, The spectrum of antecedent infections in Guillain-Barré syndrome: a case-control study. Neurology. 1998 Oct     [PubMed]
Lasky T,Terracciano GJ,Magder L,Koski CL,Ballesteros M,Nash D,Clark S,Haber P,Stolley PD,Schonberger LB,Chen RT, The Guillain-Barré syndrome and the 1992-1993 and 1993-1994 influenza vaccines. The New England journal of medicine. 1998 Dec 17     [PubMed]
Susuki K,Nishimoto Y,Yamada M,Baba M,Ueda S,Hirata K,Yuki N, Acute motor axonal neuropathy rabbit model: immune attack on nerve root axons. Annals of neurology. 2003 Sep     [PubMed]
Yuki N,Yamada M,Koga M,Odaka M,Susuki K,Tagawa Y,Ueda S,Kasama T,Ohnishi A,Hayashi S,Takahashi H,Kamijo M,Hirata K, Animal model of axonal Guillain-Barré syndrome induced by sensitization with GM1 ganglioside. Annals of neurology. 2001 Jun     [PubMed]
Willison HJ,O'Hanlon G,Paterson G,O'Leary CP,Veitch J,Wilson G,Roberts M,Tang T,Vincent A, Mechanisms of action of anti-GM1 and anti-GQ1b ganglioside antibodies in Guillain-Barré syndrome. The Journal of infectious diseases. 1997 Dec     [PubMed]
Greenshields KN,Halstead SK,Zitman FM,Rinaldi S,Brennan KM,O'Leary C,Chamberlain LH,Easton A,Roxburgh J,Pediani J,Furukawa K,Furukawa K,Goodyear CS,Plomp JJ,Willison HJ, The neuropathic potential of anti-GM1 autoantibodies is regulated by the local glycolipid environment in mice. The Journal of clinical investigation. 2009 Mar     [PubMed]
Chiba A,Kusunoki S,Obata H,Machinami R,Kanazawa I, Serum anti-GQ1b IgG antibody is associated with ophthalmoplegia in Miller Fisher syndrome and Guillain-Barré syndrome: clinical and immunohistochemical studies. Neurology. 1993 Oct     [PubMed]
Goodfellow JA,Bowes T,Sheikh K,Odaka M,Halstead SK,Humphreys PD,Wagner ER,Yuki N,Furukawa K,Furukawa K,Plomp JJ,Willison HJ, Overexpression of GD1a ganglioside sensitizes motor nerve terminals to anti-GD1a antibody-mediated injury in a model of acute motor axonal neuropathy. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2005 Feb 16     [PubMed]
Susuki K,Rasband MN,Tohyama K,Koibuchi K,Okamoto S,Funakoshi K,Hirata K,Baba H,Yuki N, Anti-GM1 antibodies cause complement-mediated disruption of sodium channel clusters in peripheral motor nerve fibers. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2007 Apr 11     [PubMed]
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