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GBS: GoodBye Symptoms via Physical Therapy Interventions

GBS: GoodBye Symptoms via Physical Therapy Interventions
Jennifaye V. Brown, PhD, PT, NCS
January 31, 2017
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History

Guillain-Barré Syndrome was first addressed in 1859 in a published report by Jean Baptiste Octave Landry de Thezillat. As the subject of his report, there were ten individuals with ascending paralysis (i.e., starting from the distal or the periphery part of the body and coming up to and towards the neck). In 1876, the syndrome was otherwise known as Landry’s Ascending Paralysis.

Around the time of World War I, three French physicians collaborated and delineated how the course of the disease presented itself. These three physicians were: Jean-Alexander Barre, Georges Charles Guillain, and Andre Strohl. They looked at components of the disease process that dealt with abnormal reflexes, and the peripheral nervous system. In 1916, further findings were published, but Strohl's contributions were not acknowledged. In 1927, Barre and Guillain refined the classic paper, and thereafter, it has been known as Guillain-Barré Syndrome. In 1976, GBS as we know it began to receive more attention due to an outbreak of these component symptoms and signs after the Swine Flu vaccine was given.

Guillain-Barré: Definition and Etiology

At first, Guillain-Barré was known as Landry's Ascending Paralysis. Ascending means that the impairments start distally at the fingers and the toes, and move towards the trunk. Common terminology now for GBS is acute inflammatory demyelinating polyneuropathy (AIDP).

Acute = a short, but sudden onset

Inflammatory = the body's immune systems malfunctions

Demyelinating = the myelin sheath of neurons is damaged

Polyneuropathy = many nerves have a pathological problem; damage to peripheral nerves

Syndrome vs. Disease

Why is GBS referred to as a syndrome, rather than a disease? The reason is because it is not clear that there is a specific disease-causing agent involved. A syndrome is a medical condition characterized by a collection of symptoms and signs. We have a tendency to use the word disease as a catch-all term; however, there truly is not a specific disease-causing agent that results in Guillain-Barré. A symptom is what the patient feels; a sign is what the healthcare professional can observe or measure.

What is GBS?

GBS is an autoimmune disease of the nervous system and an immune mediated dysfunction of the peripheral nervous system. It includes two basic parts, the peripheral nerves, and nerve root demyelination. The blood vessels go through an inflammatory process at the cellular level. The attack of myelin on the axon can occur in motor or sensory nerves.

Etiology

What it the etiology of GBS? Half (50%) of the time, it results from a microbial infection, such as cytomegalovirus (CMV), which is a virus related to chicken pox and mononucleosis. It is usually silent, with no signs or symptoms. You can get cytomegalovirus from urine, saliva, breast milk, and sex organ transplants. You see it often in Epstein-Barr, which is a part of the herpes virus family. Commonly known as the kissing sickness, mononucleosis can be contracted from saliva. With Epstein-Barr syndrome, you usually have fatigue, fever, an inflamed throat, and an enlarged spleen.

Viruses are much smaller than bacteria. The reason why we have such a problem with viruses is they can't survive without a host. Viruses are reproduced by attacking cells and turning normal cells into malignant cells. In contrast, bacteria are complex single cells with a rigid wall but a thin membrane, and it reproduces on its own. It's very harmless. We all have good bacteria and bad bacteria in our bodies. Good bacteria can aid digestion and fight cancer cells. In humans, less than 1% of bacteria will cause diseases that are harmful.

Overall, when we look at microbial infections, the viral etiologies are the biggest culprit in causing Guillain-Barré. Most people contract Guillain-Barré after having the flu or food poisoning, usually caused by Campylobacter jejuni. Another cause is diarrhea. Somewhere related to the flu, but in its own separate entity and etiology for Guillain-Barré Syndrome, is respiratory illness.

The problem is that infection will change the nature of neurons in the peripheral nervous system. What the infection does is it causes the immune system to treat the neurons as foreign cells. Or, the immune system is less discriminating towards the neurons, and can't differentiate between neurons. That's the key factor in how the infection creates problems in the immune system. The infection causes the immune system to go haywire; the immune system reacts by turning on neurons in the body and treating them like a foreign object like they do not belong.

In the beginning, I stated that currently GBS is known as acute inflammatory demyelinating polyneuropathy (AIDP). This has now become a classic category. In fact, 75 to 80% of the cases fall into this classic category. The immune system attacks the myelin, and therefore there is secondary axonal degeneration.


jennifaye v brown

Jennifaye V. Brown, PhD, PT, NCS

Jennifaye V. Brown, PT, PhD, NCS has a BA-Psychology (Emory University), a MS- Physical Therapy (University of Miami-FL) and a PhD-Exercise Science (University of South Carolina).  Dr. Brown has 27 years of clinical experience focused in neurorehabilitation across the continuum of care and has presented numerous continuing education courses on adult neurologic assessment and treatment intervention for acquired brain injury.  Dr. Brown’s special interests and extensive clinical background include gait analysis and training.  Her approach to effective gait analysis and treatment is to know the lesion site, understand neuroanatomical functions and along with past medical history, environmental, psychosocial and cultural factors, determine prognosis and devise realistic goals reflective of the client and caregiver’s lived experiences.  She is the creative force behind the Stroke Gait Center, which is a collaborative effort to partner with healthcare professionals to fabricate AFOs (specializing in accommodating ladies’ footwear) utilizing 3D printing based on a full spectrum gait-related physical therapy evaluation. Her current research agenda explores the perceptions and opinions of individuals with stroke regarding their experiences with AFO fabrication, modification and maintenance. As an Advanced Credentialed Clinical Instructor by the Clinical Instructor Education Board and a three 10-year term board certified neurologic clinical specialist by the American Board of Physical Therapy Specialties (ABPTS) of the APTA, Dr. Brown has taught at PT and PTA programs in Georgia and South Carolina (SC). She is a member of the APTA, Neurology Section of the APTA, SC Chapter of the APTA, American Heart Association/American Stroke Association, Aerobics & Fitness Association of America, and the Neuro-Developmental Treatment Association.  Dr. Brown is currently an Assistant Clinical Professor at Ohio University in the Physical Therapy Program.



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