Gbs Clinical

8/2/2019 Gbs Clinical

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Journey To Healthby Andy GriffithManteo, North Carolina

Cindi had had frequent and major attacks of sore throat all of her life. So,shortly after our marriage we returned to Los Angeles and went to see a throatspecialist, Dr. Robert Feder. He determined her sore throats were coming from

her tonsils, and scheduled an operation. Early the next morning we drove overto Cedars-Sinai Medical Center and Dr. Feder took out her tonsils. While shewas recuperating, I got a bad case of the flu. Not exactly a honeymoon of therich and famous.

My illness was strange. As I got better, the symptoms of influenza were

replaced by pain--terrible, searing pain that ricocheted through my entire body.Cindi and I joked about our invalid status and settled in that Saturday to watchthe Kentucky Derby on television.

But after the race, when I stood up and took a few steps, I pitched headlonginto a nightmare. I was overcome by pain so encompassing that I couldn't feel

my feet. I had no control over them, and fell to the floor in agony.


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We couldn't reach any of our doctors that weekend. Yet I was sodesperate for relief from the pain that I took some of the codeineprescribed for Cindi for her throat. It barely made a difference.

On Monday my doctor met us at a local hospital. There a roomful ofdoctors attempted to find out what was wrong. For four days theyhadn't a clue. Finally they did a spinal tap. When the results came in,one mystery was solved. I had Guillain-Barre syndrome, a rare form ofnerve inflammation. It's thought to be caused by an allergic reaction toa viral infection, such as the flu. The nerves become inflamed andbegin to send erroneous and scrambled messages to the brain. In somepeople it causes little pain but extensive paralysis; in cases such asmine, it causes little paralysis but intense pain.

There are no drugs or surgery to treat Guillain-Barre--so the doctor sentme home. "There is nothing we can do," he said. "You've got to ride itout. I'll prescribe some pain medication, but use as little as possible.Come back in a week."


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Introduction

Guillain-Barr syndrome (GBS) is an acute,

frequently severe, and fulminant

polyradiculoneuropathy that is autoimmune in nature.

collection of clinical syndromes that manifests as anacute inflammatory polyradiculoneuropathy with

resultant weakness and diminished reflexes.


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It occurs year-round at a rate of about one case per

million per month, or ~3500 cases per year in the

United States and Canada.

Males are at 1.5-fold higher risk for GBS than females,in western countries adults are more frequently

affected than children.

With poliomyelitis under control in developed

countries, GBS is now the most important cause of

acute flaccid paralysis


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History

The French physician Jean Landry first described

the disorder in 1859.

In 1916, Georges Guillain, Jean Alexandre Barr,

and Andr Strohl diagnosed two soldiers with the

illness and described the key diagnostic abnormality

of increased spinal fluid protein production, but

normal cell count.


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Epidemiology

Worldwide, the annual incidence is about 0.6

4occurrences per 100,000 people.

Men are one and a half times more likely to beaffected than women.

The incidence increases with age; there areapproximately 1 cases per 100,000 people aged below30 years and about 4 cases per 100,000 in those olderthan 75 years.

The incidence of GBS during pregnancy is 1.7 casesper 100,000 of the population.

Congenital and neonatal GuillainBarr syndromehave also been reported


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GBS is also known as

acute idiopathic polyradiculoneuritis,

acute idiopathic polyneuritis,

French polio,

Landry's ascending paralysis and

Landry Guillain Barr syndrome.


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Related anatomy and physiology


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PathophysiologyGuillain-Barr is the result of a cell-mediated immune

attack on peripheral nerve myelin proteins.The best-accepted theory is that an infectious organism

contains an amino acid that mimics the peripheral nerve

myelin protein.

The immune system cannot distinguish between the twoproteins and attacks and destroys peripheral nerve myelin.

the ganglioside GM1b, is the most likely target of the

immune attack.

With the autoimmune attack there is an influx of

macrophages and other immune-mediated agents that

attack myelin, cause inflammation and destruction, and

leave the axon unable to support nerve conduction.


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Research InputCampylobacter jejuni infection in Guillain-Barr syndrome:A prospective case control study in a tertiary care hospital

A Sharma1, V Lal1, M Modi1, C Vaishnavi2, S Prabhakar1

Background: This study was carried out to determine therelationship between C. jejuni infection and GBS in an Indian

setting.

Materials and Methods: This prospective study was carried out ona cohort of 50 patients with GBS who were treated in a tertiary

care hospital in India. Based on electrophysiological findings thepatients were divided into various subtypes. Serology for C.jejuni (Immunoglogulin G, IgG and Immunoglogulin, IgM) usingELISA was done both in patients and 40 age, sex andgeographically matched controls.


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Conclusions

Preceding C. jejuni infection is common among GBS

patients and is often associated with the axonal variety

of GBS. Axonal variety of GBS generally presents in a

younger age group as compared to AIDP.


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SIGNS & SYMPTOMS

Areflexic motor paralysis with or without sensorydisturbance.

Bulbar weakness

Pain

Deep tendon reflexes attenuate or disappear

Cutaneous sensory deficits

Bladder dysfunction


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subtypes

1.Acute inflammatory demyelinatingpolyradiculoneuropathyAIDP

2.Acute motor axonal neuropathyAMAN 3.Acute motor and sensory axonal

neuropathyAMSAN

MFS 4.Miller fisher syndrome


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Gbs Clinical

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