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1. selfexplanatory.2022
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Saba Parvin Haque
M.Sc. Life Sciences
(Specialization in Neurobiology)
from “Sophia College”
(Autonomous), Mumbai.

2. Guillain-Barré
Syndrome
(GBS)

3. What Is Guillain-Barré Syndrome (GBS)?
• Guillain-Barré syndrome (GBS) happens when a person’s own immune
system harms their body’s nerves. This harm causes muscle weakness and
sometimes paralysis.
• Early symptoms of GBS include weakness and tingling. People with GBS usually first feel these
symptoms in both legs. Some people then have weakness and tingling in their arms and upper body.
• The weakness can increase until people cannot use some muscles. In severe cases, people can become
paralyzed.
• Symptoms can progress over hours, days, or weeks. But most people start to recover 2 to 3 weeks after
symptoms first start. Recovery may take as little as a few weeks or as long as a few years. Most people
recover fully, but some have permanent nerve damage. Some people have died from GBS.
What are the symptoms of GBS?

4. What causes GBS?
• Diarrhea or a respiratory illness:
• Viral infections:
• Vaccination:
• GBS is rare. CDC estimates that only about 3,000 to 6,000 people
develop GBS each year in the United States.
How common is GBS?
Who is at risk for developing GBS?
• Anyone can develop GBS. However, in the United States, it is more
common in men and adults older than 50.

5. GBS
Sub-types
Acute Inflammatory Demyelinating
Polyneuropathy (AIDP)
1
Acute Motor Axonal Neuropathy
(AMAN)
2
Acute Motor-Sensory Axonal
Neuropathy (AMSAN)
3
Miller Fisher Syndrome (MFS)
4
Acute Autonomic Neuropathy
5

6. Sub-types Pathologic features Clinical features
Acute Inflammatory
Demyelinating
Polyneuropathy
(AIDP)
Immunological attack
Demyelination Polyneuropathy
Probably both humoral and
cellular immune mechanisms
Most common subtype (up to 90 percent of GBS
cases in the United States)
Progressive, symmetrical weakness; hyporeflexia
or areflexia
Remyelination
Acute Motor Axonal
Neuropathy
(AMAN)
Antibodies against gangliosides
GM1, GD1a, and GD1b in
peripheral motor nerve axons; no
demyelination
Acute motor or motor-sensory axonal neuropathy
accounts for 5 to 10 percent of GBS cases
Strongly associated with Campylobacter jejuni
infection; more common in the summer, in younger
patients, and in China or Japan
Only motor symptoms
Hyperreflexia
Acute Motor-
sensory
Axonal Neuropathy
(AMSAN)
Mechanism similar to that of
acute motor axonal neuropathy,
but with sensory axonal
degeneration
Similar to those of acute motor axonal neuropathy,
but with predominantly sensory involvement
1
2
3

7. https://images.app.goo.gl/ZKyshupR3LRsvDpD9
Acute Inflammatory
Demyelinating
Polyneuropathy (AIDP)
1
Acute Motor Axonal
Neuropathy (AMAN)
2
Acute Motor-Sensory
Axonal Neuropathy
(AMSAN)
3
Guillain-Barré Syndrome (GBS) Sub-types

8. Sub-types Pathologic features Clinical features
Miller Fisher
Syndrome
(MFS)
Demyelination
Immunoglobulin G antibodies
against gangliosides GQ1b, GD3,
and GT1a
5% of GBS cases
Ataxia
Areflexia
ophthalmoplegia
Facial, bulbar weakness occurs in
50 percent of cases
Trunk, extremity weakness occurs in
50 percent of cases
Acute Autonomic
Neuropathy
Mechanism unclear
Rarest subtype
Cardiovascular and dysrhthmias
Motor or sensory involvement is lacking
Recovery is slow, may be incomplete
4
5
How is GBS treated?
Common treatments include the following:
• Plasma exchange (a procedure that removes and replaces the liquid part of the blood)
• High-dose immunoglobulin therapy (an infusion of antibodies)

9. https://images.app.goo.gl/jQ5Yu8SeoFGBf8r5A
Miller Fisher
Syndrome (MFS)
4

10. • Abnormalities in NCS that are consistent
with demyelination are sensitive and
represent specific findings for GBS.
Signs of demyelination can include the
following:
• Nerve conduction slowing
• Prolongation of the distal latencies
• Prolongation or absence of the F-waves
• Conduction block or dispersion of responses:
Evidence frequently demonstrated at sites of
natural nerve compression.
Nerve Conduction Studies (NCS)

11. The principals of nerve conduction studies:
• NCS involve the application of a depolarising square wave electrical pulses to the skin
over a peripheral nerve producing:
• a propagated nerve action potential (NAP) recorded at a distant point over the same
nerve: and
• a compound muscle action potential (CMAP) arising from the activation of muscle
fibres in a target muscle supplied by the nerve.
• In both cases these may be recorded with surface or needle electrodes.
Nerve Conduction Studies (NCS)

12. Figure: Schematic representation of phase cancellation and temporal dispersion in demyelination. In the normal nerve, the responses are
synchronised in time and therefore summate (amplitude is higher that that of the individual components). Temporal dispersion results in
an increased duration and reduced amplitude of CMAP (compound muscle action potential).
Mallik, A. (2005). https://doi.org/10.1136/jnnp.2005.069138

13. • Guillain-Barré Syndrome | Campylobacter | CDC. (n.d.). https://www.cdc.gov/campylobacter/guillain-
barre.html
• Acute Inflammatory Demyelinating Polyradiculoneuropathy: Background, Pathophysiology, Epidemiology.
(n.d.). Retrieved October 5, 2021, from https://emedicine.medscape.com/article/1169959-overview
• Andary, M. T., MD. (2021, July 29). Guillain-Barre Syndrome: Practice Essentials, Background,
Pathophysiology. https://emedicine.medscape.com/article/315632-overview
• Nerve conduction studies in Guillain-Barré syndrome: Influence of timing and value of repeated
measurements. (2021, January 15). ScienceDirect.
https://linkinghub.elsevier.com/retrieve/pii/S0022510X2030603
• Yildirim, S., Adviye, R., Gül, H. L., & Türk Börü, Ü. (2016). Acute Motor Axonal Neuropathy (Aman) With
Motor Conduction Blocks In Childhood; Case Report. Iranian journal of child neurology, 10(1), 65–69.
• https://images.app.goo.gl/Akc9Z896KhQzu3cB8
References

14. Thank You