Clinical Science Of Guillain Barre

Syndrome
( Source : McCance, Robbin, https://www.omim.org/entry/139393,
https://ghr.nlm.nih.gov/condition/guillain-barre-syndrome )

ETIOLOGY:

GBS is considered to be an autoimmune disease triggered by a preceding bacterial or

viral infection. Approximately two thirds of cases are preceded by an acute, influenza-
like illness from which the affected individual has recovered by the time the neuropathy
becomes symptomatic. Infections with Campylobacter jejuni (Food Poisoning),
cytomegalovirus (CMV infections present as upper respiratory tract infections,
pneumonias, and nonspecific, flulike illnesses) , Epstein-Barr virus, and Mycoplasma
pneumoniae, or prior vaccination, have significant epidemiologic associations with
Guillain-Barré syndrome.
DIAGNOSIS :

HISTORY TAKING PHYSICAL EXAMINATION LAB EXAMINATION

Nerve conduction
Weakness in the limbs Vital Signs : velocities are slowed
(Starts from lower limbs to - Tachycardia / because of multifocal
upper limb) Bradycardia destruction of myelin
(Worsening) - Hypertension / segments in many
( Motor disturbance ) Hypotension axons within a nerve.

Paresthesias Neurological Exam : A lumbar puncture is

(tingling, burning, shocklike
sensations, particularly in the
limbs)
Pain
(throbbing and aching,
particularly in the lower back,
buttocks, and legs)
Numbness.
(Sensory disturbance)
Palpitation
( Autonomic Disturbance)
History of Infection
(3-6 Prior Infection)
- Motor Function :
Decreased Muscle
Strength
- Sensory Function :
Hypoesthesia
- Physiological Reflex :
Deep tendon reflexes
disappear
performed
in patients suspected
of having GBS;
Cerebrospinal
fluid (CSF) protein
levels are elevated due
to inflammation
and altered
permeability of the
micro circulation within
the
spinal roots as they
traverse the
subarachnoid space.
Inflammatory cells, on
the other hand, remain
confined to
 the roots, therefore,
there is little or no

GENETIC FACTOR :

Some studies show that normal variations in certain genes may be associated with an
increased risk of developing Guillain-Barré syndrome; however, more research is
necessary to identify and confirm associated genes. Many of the genes that may
increase the risk of Guillain-Barré syndrome are involved in the immune system, and
their roles in fighting infection may contribute to the development of the condition
Almost all cases of Guillain-Barré syndrome are sporadic, which means they occur in
people with no history of the condition in their family. A few families with more than one
affected family member have been described; however, the condition does not have a
clear pattern of inheritance. Multiple genetic and environmental factors likely play a part
in determining the risk of developing this condition. As a result, inheriting a genetic
variation linked with Guillain-Barré syndrome does not mean that a person will develop
the condition.
Pandey and Vedeler (2003) genotyped 83 patients and 196 healthy controls in Norway
for immunoglobulin KM genes (genetic markers of the constant region of kappa
immunoglobulin chains; 147200) by PCR-RFLP. The frequency of KM3 homozygotes
was significantly increased in the patients compared with controls. Conversely, the
frequency of KM1/KM3 heterozygotes was significantly decreased in patients compared
with controls. The results suggested that KM genes may be relevant to the etiology of
Guillain-Barre syndrome.