GUILLAIN – BARRE - SYNDROME

It is an acute inflammatory demyelinating polyneuropathy

characterized by progressive muscle weakness and
areflexia

INCIDENCE:
• 2 per 1,00,000 populations per year
• Male>female
• All ages- increases with age
• 1 – 3 weeks after viral or other infections or
immunization
 AETIOLOGY

GIT infection
Campylobacter jejuni (26-41%)
Cytomegalovirus (10-22%) Respiratory tract
infection Mycoplasma pneumoniae Ebstein-Barr
virus (10%) Vaccines
Rabies
Avian-flu influenza
Guillain-Barré syndrome has been reported to follow
vaccinations
epidural anesthesia
thrombolytic agents
 PATHOGENESIS

• In Guillain-Barré syndrome, the myelin sheath surrounding

the axon is lost.
• Demyelination is a common response of neural tissue to many
agents and conditions, including physical trauma, hypoxemia,
toxic chemicals, vascular insufficiency, and immunological
reactions.
• Loss of the myelin sheath in Guillain-Barré syndrome makes
nerve impulse transmission is aborted.
• Peripheral nerve demyelination in Guillain-Barré syndrome is
believed to be immunologically mediated(autoimmune
disorder)
• Humoral factors and cell-mediated immune phenomena have
been implicated in the damage of myelin and/or the myelin-
producing Schwann cells
 TYPES

o ACUTE INFLAMMATORY
DEMYELINATING POLYNEUROPATHY(AIDP)- autoimmune
response directed against Schwann cell membranes.
o MILLER FISHER SYNDROME (MFS)- Anti-GQ1b antibodies
are present in 90% of cases.
o ACUTE MOTOR AXONAL NEUROPATHY (AMAN) also
known as Chinese paralytic syndrome- Anti-GD3 antibodies
are found more frequently in AMAN.
o ACUTE MOTOR, SENSORY AXONAL NEUROPATHY(AMSAN)
associated with a high mortality rate, owing to cardiovascular
involvement, and associated dysrhythmias.
 CLINICAL MANIFESTATION

o The syndrome may develop rapidly over the course

of hours or days, or may take up to 3 to 4 weeks to
develop.
o Most patients demonstrate the greatest weakness
in the first weeks of the disorder.
o Patients are at their weakest point by the third
week of the illness.
o In the beginning, a flaccid, ascending paralysis
develops quickly.
o The patient may first notice weakness in the
lower extremities that may quickly extend to
include weakness and abnormal sensations in
the arms.
o Deep tendon reflexes are usually lost, even in
the earliest stages.
o The trunk and cranial nerves may become
involved.
o Respiratory muscles can become affected,
resulting in respiratory compromise.
 DIAGNOSIS

o The history of the onset of symptoms can be

revealing because symptoms of Guillain-Barré
syndrome usually begin with weakness or
paresthesias of the lower extremities and
ascend in a symmetrical pattern.
o A lumbar puncture may be performed and reveal
increased protein.
o Also, nerve conduction studies record
impulse transmission along the nerve fiber.
 CLINICAL FEATURES

 Pain – back pain(initial)

 Paresthesia – feet then hands (glove and stocking pattern)
 Weakness- ascending, symmetrical, flaccid
 Areflexia
 Respiratory and bulbar involvement
 Facial weakness
 Papilloedema (CSF protein elevates)
 Autonomic involvement: tachycardia, fluctuating BP, retention
of urine
 TREATMENT

o The main medical management for Guillain-

Barré syndrome include
– Plasmapheresis
– Administration of intravenous immune
globulin
o The first therapy proven to benefit patients with
Guillain-Barré syndrome is plasmapheresis.
This procedure mechanically removes humoral
factors.
o Plasma exchange is recommended for patients
who
– Are unable to walk unaided
– Demonstrate worsening vital capacities
– Require mechanical ventilation
– Have significant bulbar weakness
o Intravenous immunoglobulin (IVIG) is also useful
in managing Guillain-Barré syndrome.
 assessment

History
On observation
On examination
Reflexes
Tone
Muscle power
Sensory assessment
Chest assessment
Musculoskeletal assessment
Bladder and bowel
Balance
Gait
Functional assessment
 Physiotherapy
management
Principles:
Maintenance of airway and ventilatory capacity
Maintenance and improve joint range
Strengthen and re-educate normal muscle function
Re-education of sensory awareness
Restoration of normal function
Restoration of maximal independence
Motivation
 Acute stage:

Maintain a clear airway

Prevention of lung infections
To maintain normal jt. ROM
Support of joints
Prevention of pressure sores
Maintanance of circulation
Psychological support
 Recovery stage:

Passive active assissted active

Strengthening exs
Sensory re-education
Balance training
Gait training
Bladder control training
Independence of self care
Foot wear modification
THANK YOU
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