eMedicine Specialties > Physical Medicine and Rehabilitation > Peripheral Neuropathy
Guillain-Barre Syndrome: Differential Diagnoses & Workup
Updated: Sep 15, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Differential Diagnoses
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
Laboratory 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.21
- 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.22
- 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.
More on Guillain-Barre Syndrome |
| Overview: Guillain-Barre Syndrome |
Differential Diagnoses & Workup: Guillain-Barre Syndrome |
| Treatment & Medication: Guillain-Barre Syndrome |
| Follow-up: Guillain-Barre Syndrome |
| References |
| Further Reading |
| « Previous Page | Next Page » |
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Further Reading
Related eMedicine topics:
Campylobacter Infections [Infectious Diseases]
Campylobacter Infections [Pediatrics: General Medicine]
Cytomegalovirus
Cytomegalovirus Infection
Guillain-Barré Syndrome [Emergency Medicine]
Guillain-Barre Syndrome in Childhood
Intravenous Immunoglobulin
Clinical guidelines:
EFNS guidelines for the use of intravenous immunoglobulin in treatment of neurological diseases. European Federation of Neurological Societies - Medical Specialty Society. 2008 Sep. 16 pages. NGC:006937
Practice parameter: immunotherapy for Guillain-Barre syndrome: report of the Quality Standards Subcommittee of the American Academy of Neurology. American Academy of Neurology - Medical Specialty Society. 2003 Sep 23. 5 pages. NGC:003155
Clinical trials:
The Changes of Cytokines in Guillain Barré Syndrome: the Correlation With Clinical Manifestations and Skin Innervation
Keywords
Guillain-Barré syndrome, Guillain-Barre syndrome, Guillain-Barre, demyelination, Campylobacter jejuni, demyelinating neuropathy, polyradiculoneuropathy, GBS, C jejuni, acute inflammatory demyelinating polyradiculoneuropathy, Landry-Guillain-Barre syndrome, Landry-Guillain-Barre-Strohl syndrome, acute demyelinating neuropathy, infectious polyneuritis, acute polyradiculoneuritis, axonal Guillain-Barre syndrome, acute motor axonal neuropathy, acute motor-sensory axonal neuropathy, Miller-Fisher syndrome, pharyngeal-cervical-brachial GBS
Differential Diagnoses & Workup: Guillain-Barre Syndrome