Guillain-Barr

Syndrome
a rare and serious condition of the peripheral
nervous system. It occurs when the body's
immune system attacks part of the nervous
system.

ETIOLOGY

GBS is common to all races and ages;

mild increase in frequency in patients
between ages 30-50; GBS is less
common in infants or the elderly.
GBS has a yearly incidence of 0.6-1.9
cases/100,000 population.
Prior infection is well established as a
precipitating event in the
development of GBS. GBS preceded
by an acute illness, 1-4 weeks before,
in about 75% of cases.

ETIOLOGY
GBS may rarely develop within a
day or two, or after 4-6 weeks, of
an acute illness.
Most antecedent illnesses
associated with GBS affect the
upper respiratory or GI
tracts.
Cytomegalovirus (CMV) is the
most common viral antecedent
infection with serologic evidence

ETIOLOGY

Epstein Barr (EBV) infection may

precede GBS in about 10% of cases;
preceding clinical signs include
mononucleosis, hepatitis, or pharyngitis.
GBS may occur with HIV
seroconversion.
Camplylobacter jejuni (C. jejuni) is,
overall, the most common antecedent
infection and has been reported in up to
32% of cases.
GBS may possibly occur after surgery,
trauma, and in the post-partum

PATHOGENESIS
Guillain-Barr syndrome is an
autoimmune disorder that
affects the nerves.
In Guillain-Barr syndrome, the
immune response damages
peripheral nerves, which are the
nerves that connect the central
nervous system (the brain and
spinal cord) to the limbs and
organs.

PATHOGENESIS
Specifically, the immune
response affects a particular part
of peripheral nerves called
axons, which are the extensions
of nerve cells (neurons) that
transmit nerve impulses.
Guillain-Barr syndrome can
affect the neurons that control
muscle movement (motor
neurons);

PATHOGENESIS
The neurons that transmit
sensory signals such as pain,
temperature, and touch (sensory
neurons); or both.
As a result, affected individuals
can experience muscle weakness
or lose the ability to feel certain
sensations.

TYPES
Acute Inflammatory
Demyelinating
Polyradiculoneuropathy
(AIDP)
In AIDP, the immune response
damages myelin, which is the
covering that protects axons and
promotes the efficient
transmission of nerve impulses.

TYPES
Acute motor axonal
neuropathy (AMAN)
The axons of motor neurons are
damaged.
Acute motor-sensory axonal
neuropathy (AMSAN).
The axons of motor and sensory
neurons are also damaged.

TYPES

Because of sensory nerve

damage, affected individuals can
lose the ability to sense the
position of their limbs and can
have abnormal or absent reflexes
(areflexia).

TYPES
Miller Fisher Syndrome
Involves cranial nerves, which
extend from the brain to various
areas of the head and neck.
Miller Fisher syndrome is
characterized by three features:
weakness or paralysis of the
muscles that move the eyes
(ophthalmoplegia), problems
with balance and coordination

CLINICAL
MANIFESTATIONS

Muscle weakness or paralysis. The

weakness often begins in the legs and
spreads to the arms, torso, and face and
is commonly accompanied by
numbness, tingling, or pain.
Dysphagia and Dyspnea.
Occasionally, the nerves that control
involuntary functions of the body such
as blood pressure and heart rate are
affected, which can lead to fluctuating
blood pressure or an abnormal

DIFFERENTIAL
DIAGNOSIS
History taking
Standard blood tests
Cerebrospinal fluid examination
Electromyography may be
helpful to establish the diagnosis.

NEUROLOGIC
EXAMINATION
Facial weakness (cranial nerve
VII) is observed most frequently,
followed by symptoms
associated with cranial nerves VI,
III, XII, V, IX, and X.
Upper extremity, trunk, facial,
and oropharyngeal weakness is
observed to a variable extent.
Reflexes are absent or reduced
early in the disease course.

TREATMENT
Plasma Exchange (PE) or
Plasmapheresis
a process in which some of the
patient's blood is removed, the
liquid part separated, and the
blood cells returned to the body,
has been used for severe cases.

TREATMENT
Intravenous Immunoglobulin
(IVIg)
healthy immunoglobulin is taken
from blood donors and given to
intravenously (directly into a
vein). The healthy antibodies
block and destroy the harmful
antibodies that are attacking the
nerves. IVIg is given usually
every day for five days. Each

MANAGEMENT
Supportive Care: ICU monitoring & basic
medical management
Maintaining Respiratory Function:
Monitoring for changes in vital capacity and
negative inspiratory force
Mechanical ventilation is required if the vital
capacity falls, making spontaneous breathing
impossible and tissue oxygenation
inadequate.
Suctioning may be needed to maintain a
clear airway.

MANAGEMENT
For autonomic dysfunction:
Assessment of BP and HR
frequently.
Sustained hypertension managed
by ACE inhibitor or beta blocking
agent.
Postural hypotension treated
with fluid bolus or positioning.
Urinary difficulties may require
intermittent catheterization.

MANAGEMENT
For nosocomial infections:
Antibiotic therapy should be
reserved.
For Deep Vein Thrombosis:
Range-of-motion exercises,
position changes, anticoagulation,
the use of anti-embolism stockings
or sequential compression boots,
and adequate hydration decrease

MANAGEMENT
Nutritional Support:
Administer IV fluids and
parenteral nutrition as a
supplement and monitor for the
return of bowel sounds.
Nasogastric tube needed in
patients who are intubated or
have significant oropharyngeal
weakness.

PROGNOSIS

Results of studies on recovery rates

differ, but most indicate that 60% to 75%
of patients recover completely.
Residual deficits of varying degree occur
in 20% to 25% of patients. Residual
deficits are most likely in patients with
rapid disease progression, those who
require mechanical ventilation, and those
60 years of age or older.
Death occurs in 5% of cases, resulting
from respiratory failure, autonomic