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“Through my illness I learned rejection. I was written off. That was the moment I thought, okay, game on. No prisoners. Everybody's going down.”

Lance Armstrong (1971–)


On completion of this chapter, the student/practitioner will be able to:

  • Discuss possible etiologies of Guillain-Barré Syndrome (GBS).

  • Discuss the clinical presentation and variations of GBS.

  • Develop an evaluative algorithm for individuals with GBS.

  • Discuss treatment options for individuals with GBS.

Key Terms

  • Guillain-Barré Syndrome

  • Inflammatory demyelinating polyradiculopathy


Guillain-Barré syndrome (GBS) is a relatively common acute form of peripheral neuropathy in which the body's immune system suddenly and rapidly attacks the peripheral nervous system. More specifically, the pathology is an inflammatory demyelinating polyradiculopathy, a consequence of inflammation of peripheral nerves and spinal nerve roots. GBS most commonly affects the myelin sheaths, but in severe cases, the axons are also damaged.1 The exact mechanism by which the immune system is attacked is unclear; however, the pathology of GBS is understood, and effective treatment methods are available.

GBS is an autoimmune disease that typically is preceded by an acute bacterial or viral infection. Although the exact cause is unknown, GBS has been shown to be preceded frequently by a respiratory infection or stomach virus. In rare cases, GBS may manifest in a patient after receiving certain vaccinations. GBS can be identified by various degrees of ascending weakness, sensory abnormalities, diminished or absent reflexes, and autonomic dysfunction, all of which occur symmetrically and evolve rapidly. GBS often emanates in the legs, and the associated pain, weakness, and paresthesia can spread quickly to the arms and face depending on the severity of the disease in a particular patient. On average, the disease achieves its most severe neurological state (i.e., its nadir) within 8 days; however, the nadir must occur during a period of less than 4 weeks to satisfy the diagnostic criteria of acute GBS.2 In the event that symptoms continue to progress beyond a 4-week period, the diagnostic focus shifts from acute GBS to a more chronic form of inflammatory neuropathy known as chronic inflammatory demyelinating polyneuropathy (CIDP). GBS requires hospitalization for early recognition and treatment.

The diagnosis of GBS is clinically based; however, the diagnosis is typically supported by laboratory and electrophysiological testing to rule out more esoteric neuropathies. Specific criteria have been established for the diagnosis of GBS.3 It is a syndrome divided into several subtypes. Consideration of motor, sensory, cranial nerve, and autonomic involvement is important in differentiating between other neurological diagnoses and the following GBS subtypes2,3:

  • Acute inflammatory demyelinating polyradiculoneuropathy

    • Most common—85% of cases

    • Characterized by primary demyelination of sensory and motor nerves

  • Acute axonal motor neuropathy and acute axonal motor and sensory neuropathy

    • 5% to 10% of cases

    • Axonal degeneration with motor ...

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