Guillain-Barré Syndrome

I. Anatomical and Physiological Background

 Peripheral nervous system consists of the cranial and spinal nerves and their
associated ganglia.
 In the peripheral nervous system, the cranial and spinal nerves, which consist of
bundles of nerve fibers or axons, conduct information to and from the central
nervous system. Although the nerves are surrounded by fibrous sheaths as they
run to different parts of the body, they are relatively unprotected and are
commonly damaged by trauma.
 Cranial nerves and their ganglia = 12 pairs that exit the skull through the
foramina
 Spinal nerves and their ganglia = 31 pairs that exit the vertebral column through
the intervertebral foramina (8 Cervical, 12 Thoracic, 5 Lumbar, 5 Sacral, 1
Coccygeal)
 Each spinal nerve is connected to the spinal cord by two roots: the anterior root
and the posterior root. The anterior root consists of bundles of nerve fibers
carrying nerve impulses away from the central nervous system. Such nerve
fibers are called efferent fibers. Those efferent fibers that go to skeletal muscles
and cause them to contract are called motor fibers. Their cells of origin lie in the
anterior gray horn of the spinal cord.
 The posterior root consists of bundles of nerve fibers, called afferent fibers, that
carry nervous impulses to the central nervous system. Because these fibers are
concerned with conveying information about sensations of touch, pain,
 temperature, and vibration, they are called sensory fibers. The cell bodies of
these nerve fibers are situated in a swelling on the posterior root called the
posterior root ganglion.
 The spinal nerve roots pass from the spinal cord to the level of their respective
intervertebral foramina, where they unite to form a spinal nerve. Here, the motor
and sensory fibers become mixed together; thus, a spinal nerve is made up of a
mixture of motor and sensory fibers.
 The anterior rami join one another at the root of the limbs to form complicated
nerve plexuses. The cervical and brachial plexuses are found at the root of the
upper limbs, and the lumbar and sacral plexuses are found at the root of the
lower limbs.
 Axon is the common terminal point for synaptic communication. Can either be
myelinated or unmyelinated. The loss of myelin is associated with delayed or
blocked conduction in the demyelinated axons.
 In PNS: many neurons are myelinated. Myelin forms when a Schwann cell wraps
its membrane around an axon up to 100 times. The myelin is then compacted
when the extracellular portions of a membrane protein called protein zero (P0)
lock to the extracellular portions of P0 in the opposing membrane.
 Nodes of Ranvier have unmyelinated portions of the PNS axons; periodic 1-μm
constrictions that are about 1 mm apart.
 CNS has most neurons are myelinated (White matter) and the cells that form the
myelin are called Oligodendrocytes. Oligodendrocytes emit multiple processes
that form myelin on many neighboring axons
 Myelin Sheaths - formed by oligodendroglia in the CNS differs chemically and
immunologically from that formed by Schwann cells peripherally it covers the
nerve accelerate axonal transmission of neural impulses.
Reference:
Snell’s Clinical Neuroanatomy 7th Ed.

II. Definition
 Is a progressive, symmetrical weakness of the limbs, with hyporeflexia
or areflexia, with or without sensory abnormalities.
 GBS is the most common cause of rapidly evolving motor paresis and paralysis
and sensory deficits. Individuals affected with GBS typically reach maximal
weakness within 2 to 3 weeks, but spend weeks to months recovering.
 The most common form of GBS is also known as acute inflammatory
demyelinating polyradiculoneuropathy.
 References:
Goodman's Pathology Implications for the Physical Therapist 4th Ed.
Braddom's Physical Medicine and Rehabilitation 5th Ed.

III. Etiology
 Acute infection in one study preceded onset of GBS.
 Bacterial (Campylobacter jejuni) and viral (Haemophilus inflenzae, Epstein-Barr
virus, and cytomegalovirus) infections, surgery, and vaccinations have been
associated with the development of GBS. Acute infection in one study preceded
onset of GBS. In one study, 90% of persons with GBS had illnesses (e.g.,
respiratory or gastrointestinal) during the preceding 30 days.
Reference:
Goodman's Pathology Implications for the Physical Therapist 4th Ed.

IV. Epidemiology
 The most common cause of acute neuromuscular paralysis in the Western world,
with an annual incidence of 1 to 2 per 100,000.
 Although GBS occurs at all ages, peaks in frequency can be seen in young
adults and in the fifth through the eighth decades. Occurrence is slightly greater
for men than women and for whites more than blacks.
  The most common is the acute demyelinating polyradiculoneuropathy (AIDP)
affecting both motor and sensory nerves. This type accounts for 95% of all cases
of GBS in Europe and North America.
 Purely axonal forms are rare ( <5%). They can occur as an acute motor axonal
neuropathy (AMAN) or acute motor and sensory axonal neuropathy (AMSAN).
 The axonal forms of GBS are more common in Asia and South America, making
up 30% of the cases in those populations.
References:
Goodman's Pathology Implications for the Physical Therapist 4th Ed.
Braddom's Physical Medicine and Rehabilitation 5th Ed.

V. Pathophysiology

Bacterial Infection Viral Infections Respiratory or

Surgery &
(Campylobacter (Haemophilus inflenzae, Epstein- Gastrointestinal illnesses
vaccinations
jejuni) Barr virus, Cytomegalovirus) during the preceding 30 days

GUILLAIN-
BARRE
SYNDROME
Aqua Gentle
therapy massage

AROME or
Hot packs
AAROME

Splinting Tilt table

Proper bed Deep breathing Functional and Neuromuscular Gait training

positioning & coughing weight training Facilitation using assistive
and turning exercises exercises Techniques Devices

References:
Goodman's Pathology Implications for the Physical Therapist 4th Ed.
Braddom's Physical Medicine and Rehabilitation 5th Ed.
VI. Clinical Manifestation
 Characterized by a rapidly ascending symmetric motor weakness and distal
sensory impairments.
 The first neurologic symptom is often paresthesia in the toes.
 This is followed within hours or days by weakness distally in the legs. Weakness
spreads to involve arms, trunk, and facial muscles. Flaccid paralysis is
accompanied by absence of DTRs.
 Occasionally, sensory and motor symptoms begin in the hands and arms instead
of the feet and legs. Palatal and facial muscles become involved in about half of
all cases; even the muscles of mastication may be affected, but nerves to
extraocular muscles typically are not involved.
 Presents with progressive onset of limb weakness both proximally and distally
that is typically symmetrical, with strength nadir in 2 to 4 weeks.
 Reflexes are typically lost early in the disease; although reflexes can be retained
or even brisk with axonal forms.
 Sensory loss is variable.
 The cranial nerves can be affected, with facial palsy and bulbar weakness.
 Muscles of respiration are frequently affected with decline of vital capacity and
ventilatory
support is required in 25% of cases.
 The autonomic system can be affected, causing tachycardia, hypertension, and
cardiac arrhythmias.
 Pain can be a significant complaint and might even precede onset of clinical
weakness. In the acute stages the pain is often described as deep and aching,
affecting the back, buttocks, and posterior thighs.
 Later neuropathic pain can be described with degeneration and regeneration of
sensory nerves.
 Fatigue is a common complaint, even after good neurologic recovery from GBS.
 Sensory symptoms such as distal hyperesthesias, paresthesias (tingling,
burning), numbness, and decreased vibratory or position sense are common.
The sensory disturbances often have a stocking-and-glove pattern rather than
the dermatomal distribution of loss.
References:
Goodman's Pathology Implications for the Physical Therapist 4th Ed.
Braddom's Physical Medicine and Rehabilitation 5th Ed.
Umphred’s Neurological Rehabilitation, 6th Ed.

VII. Sequelae
 Neuropathic pain
 Autonomic changes
 Distal weakness in the extremities

Reference:
Goodman’s Pathology Implications for the Physical Therapist, 4th Ed.
VIII. Prognosis
 The primary methods of managing GBS have helped to improve mortality rates, which
can exceed 5%.
 Factors that predict a poor outcome include onset at an older age, a protracted time
before recovery begins, and the need for artificial respiration.
 A recent analysis of prognostic predictors in GBS concluded a younger age, absence of
preceding diarrhea, lower levels of disability and admission, longer interval between
symptoms and admission, and absence of ventilator support need all being favorable
factors.
 Although most persons recover, up to 20% can have remaining neurologic deficits.
 After 1 year, 67% of clients have complete recovery, but 20% remain with significant
disability.
 Even after 2 years, 8% have not recovered.
 Prognosis of GBS is typically good, especially given the often-marked initial degree of
weakness.
 Persistent disability, however, occurs in 20% of patients who will remain non-ambulatory
or require an assistive device to walk at 6 months.
 Poor outcome is associated with advanced age, male gender, axonal involvement,
antecedent diarrhea, and CMV infection.
 Relapse is rare, at a rate of 3% to 5%.

References:
Goodman's Pathology Implications for the Physical Therapist 4th Ed.
Braddom's Physical Medicine and Rehabilitation 5th Ed.

IX. Medical Assessment

 To aid in diagnosis, a lumbar puncture can be performed to withdraw cerebrospinal fluid.
 Electrophysiologic tests will reveal slowed NCVs the entire length of the nerve when
demyelination is present, as well as fibrillation potentials when axonal degeneration
occurs.
 To determine the extent of demyelination of the more proximal nerve roots, an F-wave
electrophysiologic test may be performed.
 Lumbar puncture is routinely performed in the workup of patients presenting with rapidly
progressive weakness.
 Electrodiagnostic testing is the most useful confirmatory test for GBS and can
differentiate between the more common demyelinating form (AIDP) and axonal forms,
AMAN, and AMSAN.
 Needle examination typically shows decreased firing of motor units on maximal
contraction.

References:
Goodman's Pathology Implications for the Physical Therapist 4th Ed.
Braddom's Physical Medicine and Rehabilitation 5th Ed.
 X. Medical Treatment
 Plasmapheresis, a technique (also called plasma exchange) that removes plasma from
circulation and filters it to remove or dilute circulating antibodies, significantly improves
the impairments in GBS. Typically, the client will have four to six exchanges of 500 mL
per treatment over the period of a week.
 Plasmapheresis is instituted when respiratory function drops precipitously (to 1.0-1.5 L),
and the person is placed on a respirator.
 High-dose intravenous (IV) administration of immunoglobulin (Ig; a protein the immune
system normally uses to attack foreign organisms) has been found safe and effective in
the treatment of GBS. The therapeutic dose is 0.4 g/kg/day for 5 days.
 Plasma exchange administered five times over the course of 2 weeks is beneficial when
started within 4 weeks of onset of weakness but is most effective within the first 2 weeks.
 IVIG has been shown to be as effective as plasma exchange and is usually the preferred
treatment because of greater convenience and availability. It is administered at 0.4 g/kg
daily for 5 consecutive days.

References:
Goodman's Pathology Implications for the Physical Therapist 4th Ed.
Braddom's Physical Medicine and Rehabilitation 5th Ed.

XI. PT Assessment
 ROM
 MMT
 Pulse oximetry
 Auscultation of breath sounds
 Assessment of balance
 Assessment of ambulatory status
References:
Goodman's Pathology Implications for the Physical Therapist 4th Ed.
Braddom's Physical Medicine and Rehabilitation 5th Ed.

XII. PT Treatment
 Aqua therapy
 Hot packs
 Gentle massage
 Gentle stretching
 Active or active-assistive range of motion exercises
 Neuromuscular facilitation techniques
 Use of assistive devices
 Deep breathing and coughing exercise
 Proper bed positioning and turning
 Splinting
 Tilt table
 Functional and weight-training exercises
 Gait training

References:
Goodman's Pathology Implications for the Physical Therapist 4th Ed.
Braddom's Physical Medicine and Rehabilitation 5th Ed.

Prepared by:
DELROSARIO DINSON
DIMANDAL EARL ERICK.