1. Guillain–Barré syndrome
By: Dacy Gaston, RN, BSN

2. What is it?
Guillain-Barre syndrome is a serious disorder that occurs when the body's defense (immune) system mistakenly attacks part of the nervous system. This leads to nerve inflammation that causes muscle weakness and other symptoms (Grossman & Port, 2014)

3. Who Discovered it?
Octave Landry is credited with the first reported case of what later came to be known as GBS. In 1859, Landry described a neurologic condition characterized by ascending motor paralysis with poor prognosis that he referred to as "ascending paralysis” AKA “Landry’s paralysis” (Afifi, 1994)
Figure 1. Octave Landry. Adapted from Wikipedia, retrieved from

4. Who Discovered it?
Later Guillain Barré syndrome was coined by the French physicians Jean- Alexandre Barré, Georges Guillain and Andre Strohl in the early 1900s following tests on soldiers returning from World War 1. Many cases of an identical condition had been described over the preceding 80 years but these neurologists identified one of the characterizing features of the disease – the increased concentration of protein in the spinal fluid without evidence of inflammation (Afifi, 1994) No one knows why Strohl wasn’t included in the naming of the disease….
Figure 2. Guillain, Barre, Strohl. Adapted from

5. Pathway to disease
Upper Respiratory infection or gastrointestinal infection often precedes the onset of GBS.
All forms of Guillain–Barré syndrome are autoimmune diseases, due to an immune response to foreign antigens.
Ascending paralysis ensues as the disease progresses.
The end result of this autoimmune process is an attack on the peripheral nerves and damage to myelin, the fatty insulating layer of the nerve, and a nerve- conduction block leading to muscle paralysis that may be accompanied by sensory or autonomic disturbances.
Guillain–Barré, unlike disorders such as multiple sclerosis (MS) and Lou Gehrig's disease (ALS), is a purely peripheral nerve disorder and does not in general cause nerve damage to the brain or spinal cord (Caple, 2013)
Can mimic these diseases so do a proper patient history and work up.

6. Signs and Symptoms
The disorder is characterized by symmetrical weakness that usually affects the lower limbs first, and rapidly progresses in an ascending fashion. Patients generally notice weakness in their legs.
Numbness and tingling may or may not be present.
As the disease progresses the arms and facial muscles become affected.
Bulbar weakness
Oropharyngeal dysphagia-drooling, difficulty swallowing or difficulty maintaining an open airway.
Facial weakness
Repertory distress may require ventilation.
Sensory loss, proprioception and areflexia are important factors of GBS.
In severe cases of GBS, loss of autonomic function is common, manifesting as wide fluctuations in blood pressure, orthostatic hypotension, and sinus tachycardia among other cardiac arrhythmias (Caple, 2013)

7. Scary Stuff (Well, kinda scary):
Can happen really fast!!!
Post infection the disease can progress within days to cause severe symptoms.
Sometimes hospitalization is required if the inflammation moves to the nerves that are in the diaphragm and breathing is being affected.
Don’t worry though TOOOOO much,
Only about 1.65%-1.79% per 100,000 people a year are affected
And only 3% of those percentages is fatal
Recurrence rate is only about 3% (Caple, 2013)

8. Risk Factors Men > Women Infectious agents such as:
Campylobacter jejuni enteritis --- most associated (Koga, 2006)
Epstein-Barr Virus
Cytomegalovirus
Mycoplasma
HIV
Influenza
Systemic illness : i.e. Hodgkin's lymphoma, SLE
Vaccinations
(Caple, 2013)

9. Interesting Fact:
Following the 1976 H1N1 Vaccine, there was an increase in the reported incidences of GBS. Studies showed that there was a link, although small, associated with that particular vaccine and Guillain- Barre Syndrome.
In response to the 2009 H1N1 scare, there was obviously a curiosity in the link and a study was done to show that there was still a small, but measurable risk, with the pH1N1 vaccine and developing GBS (Wise, et.al, 2012)
BUT!!!!!--- the benefits far outweigh the risks of not getting the vaccine, so therefore was deemed not a significant risk factor to not getting vaccinated.

10. Diagnostic and Testing
The diagnosis of GBS depends on findings such as rapid development of muscle paralysis, areflexia, absence of fever, and a likely inciting event. Cerebrospinal fluid analysis (through a lumbar spinal puncture) and electrodiagnostic tests of nerves and muscles (such as nerve conduction studies) are common tests ordered in the diagnosis of GBS
CSF characteristic findings include albumino-cytological dissociation. As opposed to infectious causes, this is an elevated protein level (100–1000 mg/dl), without an accompanying increased cell count (absence of pleocytosis). A sustained increased white blood cell count may indicate an alternative diagnosis such as infection.
EMG and nerve conduction studies may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. F waves and H-reflexes may be prolonged or absent. Needle EMG is frequently normal in acute cases. Reduced, neuropathic recruitment in weak muscles can be seen. Fibrillations will be seen on needle EMG if some axonal injury occurs after three to four weeks. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing (Grossman & Port, 2014)

11. Treatment
Supportive care is the cornerstone of successful management in the acute patient. Of greatest concern is respiratory failure due to paralysis of the diaphragm. Intubation may be needed when evidence of impending failure of the muscles of breathing is present 
Subsequent treatment consists of attempting to reduce the body's attack on the nervous system, either by plasmapheresis, filtering antibodies out of the blood stream, or by administering intravenous immunoglobulins (IVIg), to neutralize harmful antibodies and inflammation causing disease. These two treatments are equally effective and a combination of the two is not significantly better than either alone (Grossman & Port, 2014)

12. Patient Teaching Post Infection
Manage psychosocial aspects of GBS (anxiety, education)
Full recovery may take up to two years with strict adherence to rehab regimen.
Support groups may be beneficial.
(Caple, 2013)

13. A picture is worth a thousand words….
IN CONCLUSION………
A picture is worth a thousand words….

15. Questions!
1) A 28 year old male comes to you complaining of profound weakness and numbness in his feet that he said has “seemed to get worse and moving up his legs” he just got over a really bad stomach flu a few days ago. You may suspect
A) B12 deficiency
B) Bad sushi from downtown Savannah
C) Guillian Barre symptoms
D) The feeling you get right before you take a patho test.

16. Questions
2) Guillain Barre symptoms can be life threatening if not treated promptly and correctly?
A) True
B) False

17. Questions
3) Guillain Barre Syndrome is a demyelination of the myelin in:
A) The Central Nervous System
B) The Peripheral Nervous System

18. Questions:
4) Which medications are used to treat Guillain Barre Syndrome? Check all that apply
A) Doxycycine
B) IvIg
C) Plasmapheresis
D) Supportive therapy

19. Questions: 5) Who is your favorite South University professor?
A) Dr. Seus
B) Dr. Gupta
C) Dr. Mokoko
D) Dr. House

21. References:
Afifi, A. (1994) The Landry-Guillain-Barre-Strohl Syndrome 1859 to 1992 a historical perspective. Journal of Family and Community Medicine, 1(1),
Caple, C. (2013). Guillain-Barre Syndrome. Retrieved from
Grossman, S., Porth, C. (2014). Disorders of Motor Function: Guillain-Barre Syndrome. Porth’s Pathophysiology: Concepts of Altered Health States (p. 467). Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Koga, M., Gilbert, M., Takahashi, M., Li, J., Koike, S., Hirate, K., Nobuhiro, Y. (2006). Comprehensive analysis of bacterial risk factors for the development of Guillain-Barre syndrome after campylobacter jejuni enteritis. The Journal of Infectious Diseases, 193,
Wise, M., Viray, M., Sejvar, J., Lewis, P., Baughman, A., Connor, W., Giambrone, R., Hale, C., Hogan, B., Meek, J., Murphree, R., Oh, J., Reingold, A., Tellman, N., Conner, S., Singleton, J., Lu, P., DeStefano, F., Fridkin, S., Vellozzi, C., Morgan, O. (2012) Guillain-Barre syndrome during the H1N1 influenza vaccination campaign: population based surveillance among 45 million americans. American Journal of Epidemiology, 175(11),