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How Guillain-Barre Syndrome Affects Function

Vol. 16 •Issue 3 • Page 58
Pathology Report

How Guillain-Barré Syndrome Affects Function

There was a picture of the patient on the hospital wall, taken just a few weeks earlier. Standing with his family at the beach, he appeared dripping wet, perhaps from a swim in the ocean. It was hard to believe that the man in the picture could be the same one in the hospital bed, the one with the ventilator rhythmically breathing for him.

Named for two French neurologists who first described it, Guillain-Barré Syndrome, or GBS, is a rapidly progressive form of polyneuropathy. The time from onset to the period of maximum impairment can be four weeks or less.

Typically, it begins with distal paresthesias. Following that, distal weakness in the lower extremities appears, later ascending to the arms and face. This weakness, which is relatively symmetrical and results in flaccid paralysis, is always more pronounced than the sensory changes. Many cases of GBS are mild. However, severe cases may find the motor cranial nerves and trunk muscles involved. Nearly one third of all patients will require mechanical ventilation.


Since GBS often occurs during or after an infection, it is postulated that it is an immune-mediated disorder. Essentially, the body is attacking its peripheral nerves. Certain viral and bacterial infections, as well as surgery and immunizations, have been implicated as possible triggers.

The annual incidence of GBS is approximately 1 person per 50,000. There is a slightly greater occurrence in men than women, and it is more common with increasing age.


Although not all of the details are known regarding the pathogenesis of GBS, it appears that circulating antibodies bind to the myelin of the Schwann cell in the peripheral nervous system. Fibers of the autonomic nervous system, which are also myelinated, may not be spared. Macrophages, responding to the inflammatory signals, demyelinate the nerve, beginning at the nodes of Ranvier. As the macrophages work, chemicals such as free oxygen radicals and proteases are released. This can lead to a more extensive injury than demyelination alone, as these substances can damage the axon. Eventually, a repair process begins. Schwann cells divide and remyelinate the nerves. Approximately 80-90 percent of people will have a full recovery thanks to this regenerative process.

The National Institute of Neurologic and Communicative Disorders and Stroke has developed criteria to aid in the diagnosis of GBS. These include progressive weakness in more than one extremity and loss of deep tendon reflexes, both of which must be present. Additional diagnostic procedures include withdrawing cerebrospinal fluid to look for an elevated albumin level, and a nerve conduction velocity test to check for slowing and a decreased amplitude.

Clinical Manifestations

Besides the sensory loss, absence of deep tendon reflexes and ascending flaccid paralysis, autonomic changes also might be present. These could include tachycardia, arrhythmias and hypotension. In up to 10 percent of cases, a recurrent form of GBS occurs. This can lead to confusion with chronic immune demyelinating polyneuropathy, or CIDP, which usually progresses over a period of months, as opposed to GBS, the acute form, which progresses over a period of weeks.

About half of the cases result in the progression stopping after two weeks. In up to 90 percent of the cases, the progression stops by four weeks. Once the progression stops, a static phase appears, lasting two to four weeks. Recovery then begins in a proximal to distal fashion. It may take months or even years for recovery, and roughly 10-20 percent of patients may be left with residual neurological deficits.


A severe case of GBS represents a medical emergency. Should respiratory paralysis develop, the patient will require mechanical assistance to breathe. Physical therapy starts early on with range-of-motion exercises to maintain joint mobility, being careful to stay within the patient's pain tolerance. Goodman et al, in Pathology: Implications for the Physical Therapist, recommend neuromuscular facilitation techniques be integrated into active and resistive exercises as the paralysis decreases and function returns.


Communicating with the patient who has GBS and is on a ventilator may be challenging. Besides muscle weakness preventing him from being able to write, or to mouth words, he might also be receiving medication to prevent him from fighting the vent, medication that might further impede his ability to respond. The therapist should remember that even though the patient is not responding, he might still be listening.

Some patients on the vent might be able to communicate via blinking their eyes or mouthing words. Adaptive devices, such as specially modified call buttons to contact the nurse, might be appropriate to augment the patient's communication.

Less than 5 percent of patients with GBS die. The vast majority are admitted to the hospital with the disease and, through a team effort involving the hospital staff, as well as the patient and often family members, will eventually return home. They may require a wheelchair or scooter (hopefully for just a short time), and possibly some home modifications. For many, however, that turn of events from healthy individual to paralysis will eventually become just a bad memory as they regain their strength, and like my patient, pick up where they suddenly left off.


Goodman, C., Boissonault, W., & Fuller, K. (1998). Pathology: Implications for the Physical Therapist. 2nd edition. Philadelphia: W.B. Saunders.

Porth, C. (2002). Pathophysiology. 6th edition. Philadelphia: Lippincott.

For more information, contact the Guillain Barr Syndrome Foundation International, a nonprofit organization, through its Website,

Bob Feldman teaches physical therapy at Widener University, Chester, PA.


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