Guillain-Barré syndrome (GBS) can be described as a collection of clinical syndromes that manifests as an acute inflammatory polyradiculoneuropathy with resultant weakness and diminished reflexes. Although the classic description of GBS is that of a demyelinating neuropathy with ascending weakness, many clinical variants have been well documented in the medical literature.

1. Guillain-Barre Syndrome
Presented by: Shubham Singh

2. Topic to be covered
❑ Gross structure of peripheral nerve.
❑ Brief description of peripheral polyneuropathy.
❑ Introduction to GBS (Guillain-Barre Syndrome).
❑ Epidemiology.
❑ Etiology of GBS.
❑ Pathophysiology of.
❑ Clinical presentation.
❑ Making diagnosis.
❑ Treatment.
❑ Prognosis.
❑ Modern approach.

3. Peripheral Nervous System
Sympathetic
Somatic nervous
system
Autonomic nervous
system
Para-
sympathetic
Afferent
Efferent
❖ composed of fibres from both somatic and visceral (autonomic) nervous system,
together with their associated ganglion containing nerve cell bodies and
supportive connective tissues.
Gross Structure of Peripheral Nerve

4. Structure of a nerve

5. Interrupted nerve signal

6. Polyneuropathy : collective term for a syndrome which includes
all inflammatory and degenerative diseases involving the peripheral
nervous system.
❖ includes primary degenerative diseases which begins in nerve
parenchyma.
❖ Initiated by toxic, metabolic or vascular causes.
❖ the main presenting feature include widespread sensory and motor
disturbance of the peripheral nerves.
Polyneuropathy

7. Polyneuropathy
Acute Ascending
Polyneuropathy
Sub-acute Sensorimoter
Polyneuropathy
Chronic sensorimotor
Polyneuropathy
❖ Depending upon nature and involvement of pathways commonly occurring
polyneuropathy
- GBS
- prophyria
- diphtheria
symmetrical asymmetrical acquired genetic
- carcinoma
- amyloid
- diabetic
neuropathy
- polyarteritis
nodosa
- arsenical
- lead
- thalidomide
neuropathy
- peroneal muscular
atrophy
- hypertrophic
intestinal neuritis

8. ❖ stands for ‘GUILLAIN-BARRE SYNDROME’
❖ also known as ‘GUILLAIN-BARRE LANDRY SYNDROME’
❖ A classic LMN disorder
❖ It is reactive, self limited, auto immune disease presents with acute
generalized weakness.
❖ GBS is a polyneuropathy resulting from acute demyelination of PNS
& cranial nerves(MFS).
❖ It may be axonal, demyelinating or mixed.
Introduction to GBS
Represents group of demyelinating
inflammatory poly neuropathies

9. Myelinated and demyelinated nerve.

10. GBS
AIDP MFS
Acute Inflammatory
Demyelinating
Polyneuropathy
- most common
- accounts for 70-80%
- Autoimmune disorder,
antibody mediated Is
triggered by antecedent
viral or bacterial infection
- Inflammatory
demyelination may be
accompanied by axonal
nerve loss
- Remyelination occurs
after the immune reaction
stops
AMSAN
AMAN
Acute Motor
Axonal
Neuropathy
Acute Motor and
Sensory Axonal
Neuropathy
Miller Fisher
Syndrome
-Demyelination and
inflammation of
cranial nerve III and
VI, spinal ganglia,
and peripheral
nerves
- cardinal feature
ophthalmoplegia,
ataxia, areflexia
- Sensory loss
unusual, but
proprioception may
be impaired.
Classification of GBS
AMAN & AMSAN are axonal
types where axons themselves
are damaged by immune
response
APAN
Acute Panautonom
neuropathy
-Sympathetic,
parasympathetic
nervous systems
are involved.
- Cardiovascular
involvement is
common (postural
hypotension,
tachycardia,
hypertension,
dysrhythmias).
- Blurry vision, dry
eyes.

11. Change in axon and myelin in various forms of GBS
Normal motor neuron AIDP AMAN & AMSAN

12. rapid deteriotion of vision
abnormal muscle coordination, paralysis of the eye muscles.
cardinal feature: ophthalmoplegia, ataxia, areflexia
Clinical presentation in MFS

13. Epidemiology
❖ Found worldwide with ratio of 1-2 in a lakh i.e. 1:100000.
❖ Affects both sexes but men being more affected (1.5 times) than
women.
❖ Young or middle aged adult 20-50 years are being more affected.
❖ Most people reach the greatest stage of weakness within the first
two weeks after symptoms appear
❖ By the third week 90 percent of affected individuals are at their
weakest.
❖ 70% of people with GBS eventually experience full recovery.

14. Survey report by NCBI of reported case of GBS

15. Etiology
❖ Neither contagious nor inherited, it is idiopathic.
❖ Researchers believed to be an autoimmune disease while others believe that
it is due to hypersensitivity or allergy to unknown viruses or allergens.
❖ In about half of all cases the onset of syndrome follows viral or bacterial
infections:
▪ Campylobacteriosis
▪ GIT Infections
▪ Viral hepatitis
▪ Porphyria
❖ GBS and its variants are considered post infectious immune mediated
neuropathies ex. Epstein Barr virus.
❖ In around 50% of cases the onset of symptom is preceded by a mild gastro-
intestinal or respiratory infections.

16. Etiology of polyneuropathies
❖ Infective condition:
local infection of peripheral nerve. e.g. virus (herpes zooster), and bacteria
(leprosy).
Infection with organisms e.g. diphtheria, tetanus, botulism
❖ Post-infective polyneuropathy: GBS
❖ Toxic substances
heavy metals: mercury, lead, arsenic,
organic chemicals: aniline, cyanide
drugs: thalidomide, isoniazid.
❖ Deficiency, metabolic & blood disorders
alcoholism, porphyria, leukemias, diabetes mellitus
❖ Trauma: compression/stretching,

17. Pathophysiology of GBS
❖ The disease process affects the spinal roots and nerve processes primarily
involving the Schwan cell this results in segmental demyelination, which results
in reduced conduction velocity.
❖ Both sensory and motor nerve conduction velocities are reduced.
❖ In some patients axonal demyelination may occur that results in complete
conduction block.
❖ Sometimes autonomic functions affected usually cardiac muscles which may
leads to sinus arrhythmia and variable blood pressure.
❖ Visual impairment is rare, though papilloedema is occasionally seen.
❖ An associated perivascular lymphocytic inflammatory exudate of the peripheral
nervous system and other organs (such as heart, lung, kidney) are seen.

18. Spinal roots and nerve
processes
reduced conduction
velocity
Schwann cell
Segmental demyelination
involving
Both sensory
and motor
nerve
conduction
velocities are
reduced
Results in
weakness
Disease
affects
complete conduction
block
paralysis

19. Cross reaction of antibodies

20. Normal and disturbed transmission.

21. Clinical presentation
❖ Characterized by sensation such as tingling in the feet or hands or even
pain (specially in children), often starting in the legs or back.
❖ Symmetrical weakness of muscles i.e. weakness on both sides of the
body in the next few weeks.
❖ Some patients experience paresthesia in toes & legs others have
symptom only one side of the body(rare).
❖ Variation of symptom is seen: some may include mild difficulty in
walking, requiring crutches the others may have complete paralysis of
arms and legs and respiratory involvement.
❖ Muscle wasting, hypotonia and partial or complete loss of the associated
deep tendon reflex.

22. ❖ An individual with GBS presents with:
sensory symptoms(pricking sensations in the hands and feet)
followed by motor, both follows pattern distal to proximal.
coordination problems and unsteadiness
diminished reflexes followed by areflexia(DTR in the legs such as knee
jerks are usually lost, reflexes may also be absent in the arms)
difficulty with eye muscles and vision
difficulty swallowing, speaking, or chewing
pain that can be severe, particularly at night
abnormal heart beat/rate or blood pressure
problems with digestion and/or bladder control.
❖ These symptoms can increase in intensity over a period of time.

23. Distal limbs involvement
Abnormal sensations such as tingling,
pain and numbness
Diminished or absent deep tendon reflexes
Increased cerebrospinal fluid protein without elevated cell
count
Abnormal nerve conduction velocity findings
Sometimes, a recent viral infection or diarrhea
Recent onset,
within days
to at most
four weeks symmetrical weakness

24. A 12 years old child presenting with GBS

25. Making diagnosis
❖ difficult to diagnose GBS in its earliest stages
❖ diagnosis is purely clinical and involves
Spinal tap
Diagnostic criteria
NCV
Electromyogram
change in the cerebrospinal,
fluid contains more protein
than usual but very few
immune cells
slow signal conduction

26. Differential Diagnosis
❖ Intracranial or spinal cord abnormalities
brain stem encephalitis
cord compression
❖ Anterior Horn cell abnormalities
poliomyelitis
❖ Spinal nerve root abnormalities
Compression
Inflammation
❖ Peripheral nerve abnormalities
CIDP
porphyria
❖ Neuro muscular junction abnormalities
myasthenia gravis
❖ Muscular abnormalities
Polymyositis
dermatomyositis

27. Treatment
- Drugs: Analgesics for muscle and joint pain
Muscle relaxants for spasm
Tricyclic antidepressant and anti convulsant
for painful sensation
Corticosteroid
- : plasmapheresis & high dose immunoglobin
therapy (IVIg)
Medical management Physiotherapy management
- physical therapy
- splintage
- mobilization
- re-education
Acute care
Rehabilative Care

28. Principles of Physiotherapy Management
❖ maintenance of airway and ventilatory capacity.
❖ maintain and improve joint range.
❖ strengthening and re-educate normal muscle function.
❖ re-education of sensory awareness and motor function.
❖ restoration of normal function.
❖ motivation and psychological support
Physiotherapy Management

29. Physiotherapy Management
Acute (progressive stage)
❖ maintenance of clear airway and prevention of lung infractions(chest
physiotherapy, postural drainage)
❖ support of joint and maintenance of normal joint movement
❖ maintenance of circulation.
❖ prevention of pressure sores.
❖ relief of pain (using TENS)
❖ psychological support
Acute progressive Stage Recovery stage

30. Recovery stage/ rehabilative care
❖ respiratory system: rate, depth, pattern of breathing, vital capacity and
chest expansion.
❖ strength(Isometric, isotonic, isokinetic exercises) and endurance
training(by changing duration and intensity).
❖ functional training
❖ balance and proprioception training(PNF techniques)
❖ motivation and general psychological approach

33. Prognosis
❖ Approximately 85 percent of patients with GBS achieve a full and functional
recovery within six to 12 months*
❖ Recovery is maximal by 18 months past onset. However, some patients
have persistent minor weakness, areflexia, and paresthesia*
❖ Approximately 7 to 15 percent of patients have permanent neurologic
sequelae including bilateral footdrop, intrinsic hand muscle wasting and
sensory ataxia.
❖ The mortality rate is less than 5 percent*
❖ Causes of death include adult respiratory distress syndrome, sepsis,
pulmonary emboli, and cardiac arrest.

34. ❖ Several factors during the acute phase of illness predict subsequent
poor recovery. These factors include
age older than 60 years
severe, rapidly progressive disease
prolonged mechanical ventilation for more than one month
preexisting pulmonary disease predict a poor outcome.
❖ In general, a poor long-term prognosis is directly related to the severity
of the acute episode and delay in onset of specific treatment.

35. Modern Approach and Methodology
1.
National Institute of Neurological Disorders and Stroke (NINDS), the component of
the National Institutes of Health (NIH)
mouse model
- with an altered autoimmune
regulator gene that generates autoimmunity against the peripheral nervous system
(PNS).
- certain proteins or peptides in viruses and bacteria may be the same as those found
in myelin, and the production of antibodies to neutralize the invading viruses or
bacteria could trigger the attack on the myelin sheath.
2.
Indian Institute of Sciences (IISc) Bang lore, with the advancement in artificial
Intelligence and development of non invasive electrode technology

36. Shubham Singh
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