Guillain barre

syndrome
 Definition
• It is an acute inflammatory demyelinating
polyneuropathy (AIDP), a disorder affecting
the peripheral nervous system characterized
by progressive symmetrical muscle weakness
and areflexia affecting more than one
peripheral nerves
• The syndrome was named after the French
physicians Guillain, Barré and Strohl, who
were the first to describe a disease affecting
French soldiers (motor weakness, areflexia
and CSF abnormalities) in 1916.
• The exact cause is unknown.
• The underlying mechanism involves
an autoimmune disorder in which the
body's immune system mistakenly attacks the
peripheral nerves and damages their myelin
insulation.
• Usually this immune dysfunction is triggered by
an infection or, less commonly, surgery
or vaccination.
• It is usually triggered by an acute infectious
process
• A mild respiratory or gastrointestinal
infection precedes the neuropathic symptoms
by 1 to 3 weeks (sometimes longer) in about
60 percent of cases. (within a month)
• Onset : Acute or Subacute
• Reaches its peak of disability within 4-5 days
and has monophasic course and usually ends
with recovery
 Synonyms
• AIDP (Acute Inflammatory Demyelinating
Polyneuropathy)

• AIP (Acute Infective Polyneuropathy)

• LGBSS (Landry Guillain Barre Strohl Syndrome)

• AIP (Acute Idiopathic Polyneuropathy)

 Infections that may trigger GBS
• Often it is after an infection of the lungs or
stomach and intestines.
• Infections that may trigger GBS include:
– Campylobacter jejuni : which can cause a type of
food poisoning.
– Mycoplasma which can cause pneumonia.
– Cytomegalovirus (CMV) which can cause fever,
chills, sore throat, swollen glands, body aches, and
fatigue.
• Varicella-zoster virus : which can cause
chickenpox 
• Influenza virus and potentially influenza vaccine
 Predisposing factors
• Although there is no specific etiology of GBS
there are certain factors which have been found
to predispose GBS
• Age : 15-25 years
• Sex : Common in males
• Infection :
• Vaccination : Rabis, Typhoid, Tetanus Or Influenza
• Surgery
• Trauma
• Drugs: Prolonged use of antidepressant drugs
• Idiopathic
• Incidence : 0.4 to 1.7 per 100000
• Male > Females
• With the marked decline in the incidence of
polio, Guillain-Barré syndrome is now the
most common cause of acute flaccid paralysis
in healthy people
 Pathophysiology
1. Lymphocytes migrate through the
endoneurial vessels. At this stage no nerve
damage has occurred. (myelin and axon
intact)
2. More lymphocytes extrudes and
macrophages appear. The first effect on the
nerve is breakdown of myelin, the axon
being spared (segmental demyelination).
3. The lesion is more intense, there is polymorphonuclear
leukocytes as well as lymphocytes.
• There is interruption of the axon in addition to myelin
sheath damage.
• Denervation atrophy of muscle
• Nerve cell body central chromatolysis.
• If the axonal damage is distal, the nerve cell body will
survive, and regeneration and clinical recovery is likely.
4. Axonal interruption has occurred proximally, nerve cell
body may die and undergo dissolution. In this situation,
there is no regeneration, only the possibility of collateral
reinnervation of muscle from surviving motor fibers.
 Clinical Features
• Progression :
– The motor paralysis spreads within 30mins to 4 weeks
after infection. (within a month)

– Takes 4 to 5 days for weakness to reach its peak after onset

– After that it remains plateau for 15-20 days

– Then recovery occurs within 4-6 months.

– Rare case recovery extend upto 2 years

• The clinical course of GBS is divided into three phases:
I. The initial phase begins when the first definitive
symptom develops; it takes 4 to 5 days to reach peak
II. The plateau phase lasts several days to two weeks.
III. The recovery phase is believed to coincide with
remyelination and axonal process regrowth. This
phase extends over four to six months; patients with
severe disease may take up to two years to recover,
and recovery may not be complete.
 Motor :
• LMN type of weakness
• GBS characterized by a rapidly evolving,
relatively symmetrical ascending LMN type
weakness or flaccid paralysis (Affects LE first
 to arms)
• The proximal parts are more severly involved
then distal
• But weakness starts from distal parts
• Approximately 80-90%of patient with GBS
become non ambulatory during the illness
• Landry’s ascending paralysis
• “Rubbery Legs”
• Maximal weakness generally develops within
12–14 days of the onset
• Later the trunk, intercostal, neck, and cranial
muscles may be affected
• Paralysis or weakness of the intercostal and
diaphragm  lead to an inability to cough and
to decreased vital capacity, tidal volume, and
oxygen saturation.
• Ventilatory failure with required respiratory
support is observed in up to one third of
patients at some time during the course of
their disease
• Cranial nerve :, III, V, VI, VII, IX, X, and XII
• Facial, Bulbar weakness (oropharyngeal
dysphagia, which includes difficult swallowing,
drooling, and/or trouble maintaining an open
airway)and Extra occular muscles weakness
• Tendon reflexes are usually diminished or
absent (hyporeflexia or areflexia)
 Sensory
• Sensory symptoms in the toes and fingers are the
earliest symptoms
• 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.
 Myalgia
• Due to release of substance called cytokinins.
That will damage the muscle by irritating nerve
terminals
• Pain/muscle aching typically associated with
vigorous exercise.
• Pain was usually symmetrical and most frequently
in the large-bulk muscles such as the gluteals,
quadriceps, and hamstrings and less often in the
lower leg and upper-extremity muscles.
 ANS
• Unexplained ANS symptoms are noted in
approximately 50% of patients.
– Cardiac dysrhythmias (sinus tachycardia and less
often bradycardia)
– Low cardiac output
– Fluctuations in blood pressure
– Orthostatic hypotension
– Facial flushing
– Loss of sweating, or episodic profuse sweating
– Retention or overflow incontinence
 Investigation
• CSF : Elevation of CSF protein concentration
Normal cell count
• EMG : Reduction in the amplitude of MUAP and reduced
recruitment
• NCV :
– Slowed conduction velocity
– Prolonged distal latencies
– Conduction block in motor nerves
• F WAVE : prolonged or absent
• H-reflex : delayed, or more often absent
 Diagnostic Criteria
• Acute Onset
• Symmetrical involvement
• Predominantly proximal weakness
• More than one limb involved (usually b/l UL
AND LL)
• Areflexia
• Orthostatic hypotension
• Almost complete recovery
Required features
• Progressive weakness in both arms and legs
• Areflexia (or hyporeflexia).
Features supportive of diagnosis
• Progression of symptoms over days to 4 weeks (acute onset)
• Relative symmetry
• Mild sensory signs or symptoms
• Cranial nerve involvement, especially bilateral facial
weakness
• Complete recovery
• Autonomic dysfunction
• Typical CSF
• EMG/nerve conduction studies (characteristic signs of a
demyelinating process in the peripheral nerves)
 Clinical Sub types of GBS
• AIDP : Acute inflammatory demyelinating
polyneuropathy
– Sensory symptom, motor weakness, ANS disturbances and
cranial nerve involvement
– Adults more affected
– Electro diagnosis : demyelinating
• AMAN : Acute motor axonal neuropathy
– Muscle weakness without sensory symptom, CN involvement
uncommon
– Children and adult
– Electro diagnosis : axonal (normal sensory action potential)
• AMSAN : Acute motor sensory axonal neuropathy
– Uncommon form
– Sensory symptoms in addition to AMAN
– Mostly adults
– Electrodiagnosis : Axonal and reduced or absent SNAP
• Miller fisher syndrome :
– Areflexia, opthalmoplegia and ataxia but usually no
limb weakness
– Uncommon
– Adults and children
– Electrodiagnosis : Demyelinating
 Differential Diagnosis
• Acute spinal cord disease : Extensor plantar
responses, sensory level, prominent sphincter
involvement, and the cellular spinal fluid
• Myopathy : Absence of sensory symptoms,
preserved reflexes, normal spinal-fluid protein
and raised serum creatine kinase levels
• Poliomyelities : Fever and symptoms of
meningities, Pure motor, Asymmetric
 Medical Intervention
• Immunotherapy
– Plasma exchange or plasmapheresis
– Intravenous Immunoglobulins (IVIg)
• Corticosteroids
• Ventilatory Support
 Prognosis
• 10 % of patients may die in the acute phase of
the disease
• If respiratory failure doesn't occur: recovery is
excellent
• 60 % make a full recovery
• 40 % show some permanent residual symptoms
and signs, usually weakness of distal leg muscles,
absent ankle jerks, or distal sensory loss
 Assesment
• Demographic Details
• History :
– Patterns and sequence of symptom onset
– Recent infection, illness. Injury, prior episodes of sensorimotor
problem
• Observation :
– Attitude of limbs
– Deformity
– Wasting
– Atrophic changes
– Ventilator Assistance : vital parameters
• SENSORY SYSTEM
– Identify pattern of sensory loss or changes (use
body chart)
– Identify specific type of sensory change (e.g.,
paresthesia, anesthesia, hyperesthesias) use body
chart
– Identify pain type and location (use body chart)
what makes it better & worse
• MOTOR FUNCTION
– Reflexes (DTR and superficial reflexes)
– MMT (testing should be as muscle specific as
possible rather than assessing muscle groups
grade 1-5)
– Cranial nerve examination
– ROM
– Balance : Equilibrium reactions sitting and
standing (if testable)
• AUTONOMIC SYSTEM
– Blood prssure resting and immediately after activity (prone.
sitting, standing)
– Heart rate resting and immediately after activity,
– Body temperature stability
– Bowel and bladder control
– Sweat function : Galvanic skin resistance test, ninhydrin sweat
test
• FUNCTIONAL ASSESMENT : Current and prior functional
status (ADL, including bowel and bladder function,
ambulation)
• Guillain-Barré syndrome disability scale, adapted
from Hughes et al. (1978)
• 0  A healthy state 
• 1   Minor symptoms and capable of running 
• 2   Able to walk 10 m or more without assistance
but unable to run 
• 3   Able to walk 10 m across an open space with
help 
• 4   Bedridden or chair bound 
• 5   Requiring assisted ventilation for at least part of
the day 
• 6  Dead 
PT MANAGEMENT
• PT management is given according to the
stage of the disease :

– Acute stage

– Recovery Stage (Subacute Stage)

 Acute Stage
• Aims :
1. Maintain clear airway and prevent resp. infection
2. Manage Dysphagia
3. Maintain ROM
4. Prevent deformity and contractures
5. Prevent pressure sores
6. Maintain circulation
7. Maintain muscle properties
8. Relieve pain
9. Postural hypotension management
10. Psycological support
 1. Maintain clear airway and prevent resp.
infection
Respiratory management :
• In acute stage pt continuously need respiratory assistance
(ventilator) : IPPV via tracheostomy tube then pt must be
continuously seen by therapist.
• Maintain clear airway
– If no lung infection is there : Continuous change in position 2hrly
– Postural Drainage : 3hrly
– Periodic suctioning
– Percussion, Vibration, Shaking, manual mobilisation with ambu bag
– Chest PNF techniques
• Nebulisation
• If patient is weaned from ventilator :
– Deep breathing exercise
– Diaphragmatic exercise
– Incentive spirometer
– Coughing techniques (self assisted and manually
assisted coughing techniques)
 2. Dysphagia Management

• Treatment is focused on positioning, head control, and

oralmotor coordination (e.g., sucking an ice cube,
Stimulating the gag response, facilitating swallowing with
pressure on neck and thyroid notch timed with in term to
swallow)
• A conscious swallowing technique is introduced with thick
liquids and progressed to thinner liquids after the patient's
oromotor coordination response is enough to control
movement of fluids
• Any crumbly foods should be avoided (cakes, cookies, chips)
• Patient should not attempt to talk or be
interrupted during eating and swallowing is
comfortable and consistent.
• Feeding training should occur during frequent
short sessions to prevent fatigue,
3. Maintain ROM at all Joints :
• Passive ROM (5rep  3times/Day)
• Slow, Gradual and prolonged Stretching
• Proper Positining
• Continuous passive motion (CPM)
• More emphasize on distal joints because they are
last to recover
• Facilitation techniques such as skin stroking,
brushing, vibration, icing and tapping may be used
in conjunction with the muscle reeducation process.
4. Prevent deformity and contracture :
– Light splintage and pillow to keep the joint in
neutral position
– AFO
– Mild stretching
5. Prevention and treatment of
pressure sore :
– Changing position regularly-every 2hrly
– Gentle massage over pressure prone areas
– Keep skin dry and soft
– Air bed, Water bed : Give more even distribution
of the weight
– If pressure sore has developed :
• Ice cube application
• LASER
• UVR
6. Maintain Circulation
– ATM and PROM
– Effleurage massage
– Stockings and compressive bandages
7. To maintain muscle properties :
– IDC
– Functional electrical stimulation
– Soft tissue massage
8. Pain Management:
– Relaxed passive movements
– Proper positioning
– TENS
– Cryotherapy
9. Prevention of postural hypotension :
– Get the patient into erect position very gradually
using tilt table
– Vitals should be examined (HR, BP,RR)
– Elastocrepe bandage and compression bandage
– Abdominal corset along with tilt table usage
10. Psychological support :
– Motivate the patient
– Tell about the treatment and significance of the
treatment
 Sub Acute stage/Recovery
Stage
• Reassessment is necessary to define treatment
strategies
• Aim :
1. Strengthening weak muscles
2. Sensory reeducation
3. Functional reeducation
4. Increase balance and coordination
5. Gait training
6. Respiratory and cardio vascular conditioning
1. Progressive program of active exercise :
– Strength returns in descending pattern
– The most important point to remember while designing
exercise programme is that exercise will not hasten or
improve the regeneration rate during rehabilitation process
– The major goal is to maintain patients body into optimal
state
• Don’t over burst
• Pace recovery process
– Prevent muscle fatigue
• Frequent rest period
• Short period of non fatiguating functional activity
• Initially low repetition and high frequency
• Strengthening :
– Exercise must be planned based on the MMT grade of
individual muscles
– < Grade 1 :
• Facilitation technique-stroking, brushing, icing, vibration,
tapping
• Quick Stretching
• IG stimulation,
• Passive ROM
– Grade 1:
• Facilitation techniques,
• Faradic Stimulation,
• Suspension exercise,
• Hydrotherapy,
• PNF
 Grade 2 :
• Active assisted exercise  Active exercise using
reeducation board, suspension therapy,
Overhead Slings
Grade 3 :
– Resisted exercise – manual, Dumbell,
therabands, spring, pulley weights,
Hydrotherapy, PRE
Grade 4-5 : Continue all above exercise
– Circuit training
– Endurance Training : Cycling, swimming
2. Sensory Reeducation :
– Roods approach
– Sensory stimulation by various materials ,
textures, shapes, weights
3. Functional Reeducation :
– Incorporate improvement of the muscle strength
into various activities of daily living
– Transition to Quadripud, kneeling, sitting,
standing, mobility and gait training
– If very slow and gradual improvement
functional electrical stimulation or orthosis can be
used to perform functional task
– Orthosis : AFO, KAFO, Thumb Splint
4. Balance Training :
– Physio Ball and wobble board
– Displacing CoG and Bos

5. Gait Training :
– Started in parallel bar  walking unsupported on
even surface  uneven surface
– Sensory reeducation
• Refrences:
– Adams and victor’s PRINCIPLE OF NEUROLOGY : 8th
edition
– Neurological rehabilitation : DARCY A. UMPHRED
5th edition
– Physiotherapy in neuro conditions : Glady Samuel
Raj