This presentation provides information on Guillain-Barre syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP). It discusses their etiology, clinical presentation, diagnosis, and physiotherapy management. Both GBS and CIDP result from an autoimmune attack on peripheral nerves causing demyelination. While GBS is acute, CIDP is chronic with progressive symptoms over time. Clinical features include weakness, numbness, and sensory loss. Physiotherapy focuses on maintaining function, mobility, and recovery through various exercises depending on the patient's stage of illness. Prognosis is generally good, with around 65% of GBS patients achieving near complete recovery within a year.

1. Welcome
To My
Presentation
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2. Presentation on..2

3. Presented by..
Abid Hasan Khan
B.Sc. In Physiotherapy
Roll : 30
Session : 2015-16
Bangladesh Health Professions Institute (BHPI),
CRP-Savar, Dhaka.
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4. Supervised by..
Harun-Or-Rashid
Senior Clinical Physiotherapist &
In charge (Neurology Unit)
Physiotherapy Department,
Centre for the rehabilitation of the paralyzed (CRP)
Savar, Dhaka.
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5. Contents
 Introduction
 GBS & CIDP
 Epidemiology
 Etiology
 Is CIDP as same as Guillain-Barre syndrome?
 Clinical presentation
 Diagnosis
 Physiotherapy Management
 Prognosis
 References
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6. Introduction
Guillain-Barre syndrome (GBS) is an acute inflammatory disease of
the peripheral nerves. An autoimmune attack on the myelin results in
demyelination. Loss of myelin can occur in sensory, motor or
autonomic nerves. A chronic form of this illness may present with
progressive symptoms and result in CIDP (Chronic inflammatory
demyelinating polyneuropathy).
(Ruts et al., 2010)
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8. GBS & CIDP
Guillain Barre syndrome (GBS) may defined as post
infectious polyneuropathy occurs due to demyelination of
mostly motor neuron but sometimes sensory and autonomy
neurons. It is also known as Acute inflammatory
demyelinating polyneuropathy.
(Van Doorn et al., 2008)
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9. Continues..
On the other hand,
Chronic inflammatory demyelinating polyneuropathy
(CIDP) is the most common chronic autoimmune
neuropathy. This condition is treatable for relatively long
periods of time (months to years) in the majority of patients.
(Dalakas, 2011)
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10. Epidemiology
It has been reported that 16% of patients with CIDP have rapidly
progressive weakness within 8 weeks from onset of disease,
which is followed by a chronic course. These patients are
considered to have acute-onset CIDP (A-CIDP). On the other
hand, 8%–16% of patients with GBS have one or more
deteriorations shortly after initial improvement or stabilization
following plasma exchange or IV immunoglobulin (IVIg),
described as treatment-related fluctuations (TRF).
(Ruts et al., 2010)
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11. Etiology
 For both of the diseases, the cause is mainly unknown.
 An autoimmune process is presumed to be triggered by
various agents -
• Bacteria :
- Campylobacter Jejuni.
- Mycopalsma Pneumonia.
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12. Continues..
• Viruses :
- Cytomegalo virus (CMV)
- Epstein-Barr Virus (EBV)
- Human Immunodeficiency Virus (HIV)
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13. Is CIDP as same as Guillain-Barre
syndrome?
Chronic inflammatory demyelinating polyneuropathy (CIDP) is closely
related to Guillain-Barre syndrome (GBS). Both are nerve problems,
and both cause symptoms such as weakness and numbness. But GBS
usually comes on days or weeks after a person has an illness. CIDP
isn’t linked to illness. With GBS, once treated, most people recover
fairly quickly. CIDP, on the other hand, tends to be a longer-term
problem. In rare cases, people who don’t recover from GBS may
develop CIDP.
(Ruts et al., 2010)
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14. Clinical Presentation
Both CIDP & GBS arises between the ages of 30 and 60
years and is characterized by a progressive, symmetric,
proximal and distal muscle weakness, paresthesia, sensory
dysfunction, and impaired balance.
a) Paresthesia & numbness are frequent & early symptoms
which usually begin at toe.
(Ruts et al., 2010)
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b) Muscle weakness: Symmetrical muscle weakness usually
starts at lower limb involving the proximal muscles greater
than the distal. Weakness first noted as difficulty in walking.
It ascends progressive towards trunk musculature & arm
muscles.
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16. Continues…
c) Lower motor neuron type paralysis: The weakness can
progress to total motor paralysis. It is flaccid type &
ascending type in nature.
d) Respiratory complication: Weakness of respiratory
muscle may also occur & sometimes leads to respiratory
failure. Patient with partial respiratory failure complains of
unable to speak a complete phrase within one breath.
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17. Continues…
e) Sensory loss: Sometimes deep sensations i.e. touch,
pressure, vibration tends to be more affected than the
superficial pain, temperature and tingling sensation.
f) Pain: 50% patients experience pain which generally
maximal in the back, shoulder & buttocks.
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18. Continues…
g) Autonomic disturbance: Profuse sweating, headache,
cardiac arrhythmia, blurred vision.
h) Cranial nerve abnormality: Facial drop, dysphagia,
dysarthria.
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19. Diagnosis
 A detailed History.
 Symptoms & sign.
 Investigation :
- CSF study shows a very high protein with no or few
lymphocytes.
- EMG & nerve conduction studies (NCV) may confirm a
demyelinating neuropathy.
- Cerebrospinal fluid analysis and nerve biopsy
(Köller et al., 2011 & Van Doorn et al., 2008)
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20. Physiotherapy management
Physiotherapy management can be divided into two stages &
it depends widely on patient’s physical status - Respiratory
status, Muscles power, Joint ROM & psychological make up
of patient’s :
1) Acute progressive stage.
2) Recovery stage.
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21.  Acute progressive stage
In this stage, patient is under intensive care unit & the aim of
physiotherapy are –
 Maintain clear airway
 Prevent lung infection
 Maintain joint ROM
 Support joints in a functional position to prevent
deformity
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 Assist in prevention of pressure sore
 Maintain peripheral circulation
 Reduce joint pain
 Maintain muscle power
 Provide psychological support to the patient (if conscious) &
relatives.
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a) Maintenance of clear airways :
• Proper positioning.
• Breathing will be assisted by intermittent positive pressure
ventilation (IPPV)
• Assisted coughing.
• Manual techniques used to assist in maintaining &
clearing the airways - Vibration, Shaking & clapping.
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b) To maintain normal joint ROM :
• Passive movement.
• Quick stretching.
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25. Quick stretching
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26. Continues…
c) To support joints :
• Positioning of peripheral joints of body (foot & wrist) by
pillow.
• Resting splint.
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27. Resting splint27

28. Continues…
d) Prevention of pressure sore :
• Care & checking the skin regularly.
• Position should be changed for every two hourly.
e) Maintenance of circulation :
• Passive movements.
• Gentle but firm massage.
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29. Continues…
f) Maintain muscle power :
• Passive movement (If loss of AROM)
• Isometric exercise.
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30. Isometric exercise30

31.  Recovery stage
When the patient can maintain his own airway & ventilation
& some motor recovery is occurring, an assessment of the
patient’s problem is required to define treatment priorities :
a) Respiratory system :
• Rate, depth & pattern of breathing should noted &
maintenance of airway & ventilation capacity by BCE,
DBE & ACBT.
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b) To reduce pain :
• Gentle active assisted movement within pain free range.
• Mobilization of the joints.
c) To improve & support normal joint ROM :
• Active assisted movement.
• Splints.
• Pulley & cycling (depends on patient ability).
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33. Pulley33

34. Cycling34

35. Continues…
d) To improve muscle power :
• Strengthening exercise by using suspension therapy.
• Isotonic exercise by using variable weight.
• Progressive resistance exercise by using Thera band.
• PNF techniques.
• Hydrotherapy.
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36. Strengthening exercise by Suspension
therapy
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37. Isotonic exercise37

38. Resistance exercise by Thera band38

39. Hydrotherapy
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40. Continues…
e) To improve functional ability :
• Side change from supine to side lying & side lying to
prone lying.
• Bridging practice.
• Back strengthening exercise practice.
• Supine to sitting practice.
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41. Bridging practice41

42. Back strengthening exercise practice42

43. Continues…
f) To improve balance & coordination :
• Sitting over the edge of bed & support the proximal key &
moving the distal key points.
• Sitting on a gymnastic ball & rock it forward, backward &
sideways.
• Practice finger to nose & heel to shin coordination
exercise (when patient can perform AROM)
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• Standing practice with the support of standing frame.
• Sit to stand practice with use of standing frame.
• Standing balance practice with open eyes & close eyes.
• Ball throw practice in standing.
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45. Balance exercise
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46. Standing frame
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47. Continues…
g) To re-educate normal gait pattern :
• Before re-education of gait pattern an assessment of hip,
knee, ankle motion should be done .An orthotic device eg.
Toe pick up splint can be given in order to increase the
ankle dorsiflexion during swing phase of gait cycle.
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48. Continues…
• Walking practice in parallel bar.
• Walking practice with walking frame.
• Walking practice in even surface, rough surface & in
straight line.
• Stairing practice-ascending & descending.
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49. Toe pick up splint & walking frame49

50. Parallel bar walking
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51. Stairing practice51

52. Continues…
h) Motivation :
• Ensuring the patient about the recovery.
• Motivation & general psychological approach to life in
general.
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53. Prognosis
Recent trial data show that 30–40% of patients with CIDP are
either ‘cured’ or in ‘chronic remission’. Although these figures
are rewarding to both physicians and patients. And studies of
outcome in GBS suggest that at the end of one year from onset of
the neuropathy 65% of patients achieve an almost complete cure
so that they regain the ability to perform manual work. Of the
35% who do not, about 8% will die in the acute stage usually
from cardiac arrhythmias or pulmonary emboli.
(Dalakas, 2011 & Winer, 2001)
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54. References
 Ruts, L., Drenthen, J., Jacobs, B.C. and Van Doorn, P.A., (2010). Distinguishing
acute-onset CIDP from fluctuating Guillain-Barre syndrome: a prospective study.
Neurology, 74(21), pp.1680-1686.
 Dalakas, M.C., (2011). Advances in the diagnosis, pathogenesis and treatment of
CIDP. Nature Reviews Neurology, 7(9), p.507.
 van Doorn, P.A., Ruts, L. and Jacobs, B.C., (2008). Clinical features,
pathogenesis, and treatment of Guillain-Barré syndrome. The Lancet Neurology,
7(10), pp.939-950.
 Köller, H., Kieseier, B.C., Jander, S. and Hartung, H.P., (2005). Chronic
inflammatory demyelinating polyneuropathy. New England Journal of Medicine,
352(13), pp.1343-1356.
 Winer, J.B., (2001). Guillain Barre syndrome. Molecular Pathology, 54(6), p.381.
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