GBS, also known as Guillain-Barre syndrome, is an acute immune-mediated polyneuropathy that results in demyelination of peripheral nerves. It typically presents with ascending paralysis, though some patients experience descending paralysis or a Miller-Fisher variant characterized by ophthalmoplegia. Physiotherapy management aims to prevent complications through techniques like chest physiotherapy, range of motion exercises, positioning, and addressing pain and weakness. Treatment includes supportive care, plasmapheresis, IVIG, and focusing on recovery of motor and sensory function.
3. DEFINITION
GBS is defined as acute or sub-acute symmetrical
predominantly motor neuropathy involving one or more
peripheral nerves.
Frequently it may involve the facial and other cranial nerves,
does not have any etiology, reaches a peak of disability by
09 weeks.
It has a mesophasic course and ends up usually with
recovery.
4. AETIOLOGY
Although there is no definite etiology of GBS , there are
certain factors which have been found to predispose the
occurrence of GBS.
Age : common between 15-25 years of age.
Sex : common in females.
Viral infection : V.Zoster, Mumps & Cytomegalovirus. It is
also associated with Mycoplasm & Campylobactor
infections.
Post immunization : immunization with both live or dead
vaccines or anti-toxins.
5. Post trauma
Immunodeficiency
Drugs : prolonged use of anti-depressant drugs like
Zimetidine or Gold therapy which are neuro-toxins
and found to cause GBS.
Auto-immune : due to the presence of an antigen
CD positive T cells.
Surgery : after 4-5 weeks of a major surgery patient
may show signs of GBS which can be attached to
the following reasons :-
Release of neural antigens that provokes auto
immune response
due to surgical stress
because of blood transfusion
Explanation – both antibody and cell mediated
6. reactions to peripheral nerve myelin are involved.
Some patients produce antibodies to myelin,
glycoproteins or gangliosides. Other develop a ‘ T
cell ‘ mediate.
- Segmental demyelination results with secondary
axonal changes and damage.
- Peri-vascular infiltration with lymphocytes occurs
within the peripheral nerves and nerve roots.
- Lymphocytes & macrophages release cytotoxic
substances ( cytokines) which damage myelin
sheath.
- When axonal damage and nerve death occurs then
the recovery is prolonged.
7. PATHOLOGY
Disease progress and affect the spinal roots and nerve process
It primarily involves schwann cells
Resulting segmental demyelination
If axon remains, initial impulse can be conducted with reduced velocity
Then axons are degenerated and complete conduction block occurs
There is associate peri-vascular lymphocytic inflammatory exudates of PNS
and other symptoms like heart, lungs, kidney problems
8. CLINICAL FEATURES
Patient have a clear history of upper respiratory tract
infection
1-3 weeks prior to neuropathy also with gastrointestinal
infections
Three types according to clinical features are :
1. Ascending paralysis
2. Descending paralysis
3. Miller-fisher variant
Syndromes begin with myalgia, paraesthesia of lower limb
followed by weakness.
9. ASCENDING PARALYSIS
Lower limb weakness
Ascends to involve pelvic girdle muscles
Abdominals and thoracic muscles involvement
Upper limb involvement
10. ON EXAMINATION OF ASCENDING TYPE
- Symmetrical weakness of muscles
- Loss of muscle tone
- Flaccidity
- Reduced DTR
- Frequently involvement of 7th cranial nerve leading to
bilateral facial weakness.
- Occulomotor cranial nerve involvement leading to ptosis
- In severe cases dysphagia, dysarthria and diplopia
occurs
- Paralysis progress about 10 days then remain
unchanged.
- Recovery phase takes place in about 6 months to 2
years.
12. ON EXAMINATION OF DESCENDING TYPE :
- pharyngeal muscles involvement
MILLER – FISHER VARIANT
- Opthalmoplegia
- Areflexia
- Ataxia
- This symptoms are commonly seen in this type of variant
without any significant limb weakness.
13. COMPLICATIONS OF GBS
1. Respiratory impairments – respiratory failures.
2. Autonomic instability – retention of urine and orthostatic
hypotension.
3. Bulbar palsy.
4. Secondary infections – respiratory tract, urinary tract,
gastrointestinal tract.
5. Prolonged immobilization leading to pressure sores,
DVT, heterotrophic ossification, myositis ossificans.
6. Fluid and electrolyte imbalance
7. Pupil edema
14. DIAGNOSIS
NCV test :
- Prolonged latency period
- Reduced amplitude
- Slow frequency
- But when carried out early in the illness may
present normal values.
- Inference : findings of multifocal demyelination soon
develops with slowing motor conduction with
conduction block and prolonged distal latency.
15. Ancillary investigation :
Performed to identify any precipitating infections i.e. viral or
bacterial studies
Electrolytes are checked for inappropriate secretions of
anti-diuretics hormone
CSF studies :
- Cell count normal
- Protein count elevated
- Ultrasound of the abdomen
DIFFERENTIAL DIAGNOSIS
Poliomyelitis : secondary functions involvement but in GBS
there is symmetrical involvement.
Myositis ossificance.
Myasthenia gravis : decrease in reflex, occular involvement
16. MEDICAL TREATMENT
PREVENTION OF COMPLICATION
- Pressure sores : frequent change in the position, Alfa bed
(water + air) bed.
- DVT : limb elevation, effleurage distal to proximal, stroking,
low molecular weight heparin injection, ankle toe exercises.
- Respiratory complication : ventilator support, breathing
exercises.
- Reduction of urine: catheterization
- Plasmapheresis: change in plasma level in the blood needs
exchange of 200-250 ml of plasma per kg body weight.
- Intravenous immunoglobulin therapy : 0.45 / kg for 5 days.
17. PT MANAGEMENT IN GBS
CAUSES FOR DISABILTIY IN GBS
1. Primary cause
- Muscle weakness
- Loss or impairment of sensory input from joints, muscles, spine,
skin
- Pain
- Respiratory insufficiency
2. Secondary cause :
- Disease and neurogenic wasting
- Muscle fatigue
- Cardio – respiratory deconditioning
- Contractures
- Poor sleep
- confusion
18. AIMS OF PT MANAGEMENT
1. Maintain clear airways
2. Prevent lungs infections
3. Maintain ROM
4. Support joints in a functional position to minimize
damage or deformity
5. Assist in prevention of pressure sores
6. Maintain peripheral circulation
7. Provide psychological support
19. INTERVENTIONS
ACUTE PHASE :
- Poor respiratory function – chest care , postural drainage,
suction
- Joints and soft tissue pain – passive and accessory
movements, careful functionality, desensitization with
rubbing, vibrating, heat and ice.
- Progressive weakness – assisted and passive movement
positioning.
- Autonomic dysfunction – awareness of postural
hypotension and cardiac arrhythmias, time reassurance.
20. SUB-ACUTE PHASE :
- Pressure sores – regular positioning, passive movements
- Neuropraxia – awareness positioning
- Sensory loss – encouraging patient to observe limbs
when moved and to concentrate in the movements
performed
- Low confidence – reassurance , encouragement and
introduction of exercises of patients who have recovered.
- Disorientation – constant input of time and place,
discussion of news and topics of interest.
21. RECOVERY PHASE :
- Weakness – strengthening exercises and functional
activities
- Joint and soft tissue pain – ice, heat , vibration, ultrasound
- Tendency to fatigue – short sessions with frequent rests
- Lack of postural sensation – joint approximation, weight
bearing activities, sensory input, balance reduction, and
compensatory use of eyes
- Autonomic dysfunction – tilt table
- Tremors – reassure that it will improve when muscles gain
strength
- Emotional factors – reassurance, understanding and
encouragement
- Incomplete recovery – provision of assistive aids ex.
Calipers, home exercises and periodic assessments.