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Guillain-Barre Syndrome Workup

  • Author: Michael T Andary, MD, MS; Chief Editor: Milton J Klein, DO, MBA  more...
 
Updated: Feb 12, 2016
 

Approach Considerations

Guillain-Barré syndrome (GBS) is generally diagnosed on clinical grounds. Basic laboratory studies, such as complete blood counts (CBCs) and metabolic panels, are normal and of limited value in the workup. They are often ordered, however, to exclude other diagnoses and to better assess functional status and prognosis. The ordering of specific tests should be guided by the patient's history and presentation.

Electromyography (EMG) and nerve conduction studies (NCS) can be very helpful in the diagnosis. Abnormalities in NCS that are consistent with demyelination are sensitive and represent specific findings for classic GBS. Delayed distal latencies, slowed nerve conduction velocities, temporal dispersion of waveforms, conduction block, prolonged or absent F waves, and prolonged or absent H-reflexes are all findings that support demyelination. Needle EMG may be normal in acute nerve lesions, and it may take 3-4 weeks for fibrillation to develop. In the acute phase, the only needle EMG abnormality may be abnormal motor recruitment, with decreased recruitment and rapid firing motor units in weak muscles. Unfortunately, electrodiagnostic studies can be completely normal in acute GBS and a normal study does not rule GBS.[95, 96]

Frequent evaluations of pulmonary function parameters should be performed at bedside to monitor respiratory status and the need for ventilatory assistance.

Lumbar puncture for cerebrospinal fluid (CSF) studies is recommended. During the acute phase of GBS, characteristic findings on CSF analysis 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 inflammation of the nerve roots.

Imaging studies, such as magnetic resonance imaging (MRI) and 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.

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Peripheral Neuropathy Workup

A basic peripheral neuropathy workup is recommended in cases in which the diagnosis is uncertain. These studies may include the following:

  • Thyroid panel
  • Rheumatology profiles
  • Vitamin B-12
  • Folic acid
  • Hemoglobin A1C
  • Erythrocyte sedimentation rate (ESR)
  • Rapid protein reagent
  • Immunoelectrophoresis of serum protein
  • Tests for heavy metals
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Biochemical Screening

Biochemical screening includes the following studies:

  • Electrolyte levels
  • Liver function tests (LFTs)
  • Creatine phosphokinase (CPK) level
  • ESR

The following should be considered:

  • LFT results are elevated in as many as one third of patients
  • CPK and ESR may be elevated with myopathies or systemic inflammatory conditions
  • A stool culture for C jejuni and a pregnancy test are also indicated
  • The syndrome of inappropriate antidiuretic hormone (SIADH) may occur
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Serologic Studies

Serologic studies are of limited value in the diagnosis of GBS. Assays for antibodies to the following infectious agents may be considered:

  • C jejuni
  • Cytomegalovirus (CMV)
  • Epstein-Barr virus (EBV)
  • Herpes simplex virus (HSV)
  • HIV
  • Mycoplasma pneumoniae

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 autoantibodies

Serum autoantibodies 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.[97]

Specific antibodies found in association with GBS include the following:

  • Antibodies to GM1: Frequently found in the sera of patients with the acute motor axonal neuropathy (AMAN) or acute demyelinating polyradiculoneuropathy (AIDP) variants of GBS
  • Anti-GM1 antibodies: Elevated titers are closely associated antecedent C jejuni infections
  • Anti-GQ1b antibodies: 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.

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Nerve Conduction Studies

Nerve conduction studies (NCS) can be very helpful in the diagnostic workup and prognostic evaluation of patients with suspected GBS. Abnormalities in NCS that are consistent with demyelination are sensitive and represent specific findings for classic GBS.[95]

Signs of demyelination can include the following:

  • Nerve conduction slowing
  • Prolongation of the distal latencies
  • Prolongation or absence of the F-waves [1, 2]
  • Conduction block or dispersion of responses: Evidence frequently demonstrated at sites of natural nerve compression.

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).

Although NCS results classically show a picture of demyelinating neuropathy in most patients, axonal neuropathy and inexcitable results are found in certain subgroups. The inexcitable studies may represent either axonopathy or severe demyelination with distal conduction block.

Other characteristics of GBS include the following:

  • Nerve motor action potentials: May be decreased, but this is technically difficult to determine until the abnormality is severe; the extent of decreased action potentials correlates with prognosis
  • Compound muscle action potential (CMAP): Amplitude may be decreased
  • Sensory abnormalities: Exhibited by most patients, but these findings are much less marked than they are in motor nerves; sural sparing is a common finding in patients with clinical sensory deficits
  • Abnormal (delayed, small, or absent) H-reflex: May be noted

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 CMAP is observed on NCS. On needle examination, profuse and early denervation potentials (fibrillations) also support the conclusion that there has been axonal injury.

In some cases, neurophysiologic testing is normal in patients with GBS, especially in the first 1-2 weeks of the disease. This is believed to be due to the location of demyelinating lesions in proximal sites not amenable to study.[96]  For example, a retrospective, single-center study by Luigetti et al found that in 37% of patients with GBS who underwent an early nerve conduction study (ie, 4 days or less after disease onset), neurophysiologic results were normal. As a result, the investigators, whose study involved 71 patients with GBS, suggested that extensive neurophysiologic assessment should be performed in patients who are in the early phases of GBS.[98]

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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.

Forced vital capacity (FVC) is very helpful in guiding disposition and therapy.[75] Patients with an FVC of less than 15-20 mL/kg, maximum inspiratory pressure of less than 30 cm water, or a maximum expiratory pressure of less than 40 cm water generally progress to require prophylactic intubation and mechanical ventilation. Respiratory assistance should also be considered when there is a decrease in oxygen saturation (arterial partial pressure of oxygen [PO2] < 70 mm Hg).

Negative inspiratory force (NIF) is a relatively easy bedside test to measure respiratory muscle function and can easily be performed every half hour to hour in difficult cases. Normal is usually greater than 60 cm water. If the NIF is dropping or nears 20 cm water, respiratory support needs to be available.

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Lumbar Puncture

Most, but not all, patients with GBS have an elevated CSF protein level (>400 mg/L), with normal CSF cell counts. Elevated or rising protein levels on serial lumbar punctures and 10 or fewer mononuclear cells/mm3 strongly support the diagnosis.

A normal CSF protein level does not rule out GBS, however, as the level may remain normal in 10% of patients. CSF protein may not rise until 1-2 weeks after the onset of weakness.

Normal CSF cell counts may not be a feature of GBS in HIV-infected patients. CSF pleocytosis is well recognized in HIV-associated GBS.

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Magnetic Resonance Imaging

MRI is sensitive, but nonspecific, for diagnosis. However, it can reveal nerve root enhancement and may be an effective diagnostic adjunct.[99, 100]

Spinal nerve root enhancement with gadolinium is a nonspecific feature seen in inflammatory conditions and is caused by disruption of the blood-nerve barrier. Selective anterior nerve root enhancement appears to be strongly suggestive of GBS,[101] with the cauda equina nerve roots being enhanced in 83% of patients.

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Other Studies

Muscle biopsy may help to distinguish GBS from a primary myopathy in unclear cases. Many different abnormalities may be seen on electrocardiography, including second- and third-degree atrioventricular (AV) block, T-wave abnormalities, ST depression, QRS widening, and various rhythm disturbances.

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Histology

Lymphocyte and macrophage infiltration is observed on microscopic examination of peripheral nerves, with macrophage influx 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.

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Contributor Information and Disclosures
Author

Michael T Andary, MD, MS Professor, Residency Program Director, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine

Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, Association of Academic Physiatrists

Disclosure: Received honoraria from Allergan for speaking and teaching.

Coauthor(s)

Joyce L Oleszek, MD Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Colorado at Denver Health Sciences Center, The Children's Hospital of Denver

Joyce L Oleszek, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Kelly Maurelus, MD Clinical Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center

Kelly Maurelus, MD is a member of the following medical societies: American Medical Student Association/Foundation, Student National Medical Association

Disclosure: Nothing to disclose.

Rashida Y White-McCrimmon, MD Resident Physician, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center

Rashida Y White-McCrimmon, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Chief Editor

Milton J Klein, DO, MBA Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital and Ohio Valley General Hospital

Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

Angela Cha-Kim, MD Assistant Professor, Director of Spinal Cord Injury, Department of Physical Medicine and Rehabilitation, Loma Linda University Medical Center

Angela Cha-Kim, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Paraplegia Society

Disclosure: Nothing to disclose.

Heather Rachel Davids, MD Physician, Department of Anesthesiology, Interventional Pain Medicine, University of Colorado Health Sciences Center

Heather Rachel Davids, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, and Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte 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.

J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

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.

Edward A Michelson, MD Associate Professor, Program Director, Department of Emergency Medicine, University Hospital Health Systems of 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.

Andrew C Miller, MD Fellow, Department of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh Medical Center (UPMC); Attending Physician, Department of Emergency Medicine, UPMC St Margaret's Hospital

Andrew C Miller, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Aishwarya Patil, MD Physiatrist (Rehabilitation Physician), Vice Chair, Immanuel Rehabilitation Center

Aishwarya Patil, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and Association of Physicians of India

Disclosure: Nothing to disclose.

Razi M Rashid, MD, MPH Resident Physician, Department of Neurology, Northwestern University Hospital

Disclosure: Nothing to disclose.

Daniel D Scott, MD, MA Associate Professor, Department of Physical Medicine and Rehabilitation, University of Colorado School of Medicine; Attending Physician, Department of Physical Medicine and Rehabilitation, Denver Veterans Affairs Medical Center, Eastern Colorado Health Care System

Daniel D Scott, MD, MA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, National Multiple Sclerosis Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

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.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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