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I&I WC1 > Peripheral Nervous System > Flashcards

Peripheral Nervous System Flashcards

1
Q

What are non-myelinated neurons important for?

A

Regulating smooth muscles

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2
Q

How long can a peripheral nerve become?

A

Up to 1 meter

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3
Q

Differences between CNS and PNS

A
  • Damage recovery (easier in PNS)
  • CNS: Oligodendrocytes always myelinate more than one axon vs PVS: Schwann cell myelinate one axon
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4
Q

What is the function of the nodes on Ranvier?

A

Allow for ions to diffuse in and out of the neuron, propagating the electrical signal down the axon.

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5
Q

Describe the structural makeup of the nodes of Ranvier

A

These are the gaps formed between the myelin sheath where the axons are left uncovered. Accumulation of several ion channels also there.

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6
Q

How are peripheral nerves protected?

A

By the blood-nerve barrier, which consists of tight-junctions and supportive cells

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7
Q

What does this barrier prevent?

A

The transfer of substances from the plasma to the nerve fibers

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8
Q

Is this barrier absolute?

A

No, it is leaky at nerve roots, ganglion cells and nerve terminals

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9
Q

Characteristics of the blood-nerve barrier (3)

A
  • Formed by tight-junctions endothelial cells
  • Leaky at nerve roots, ganglion cells and nerve terminals
  • Passage of activated T-cells, macrophages and immunoglobulin
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10
Q

Characteristics antigen-presentation in the PNS (2)

A
  • Class II inducible on Schwann cells and endothelial cells
  • Endoneurial macrophages – critical for Wallerian degeneration
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11
Q

What is wallerian degeneration?

A

Degeneration of the part of an axon that is severed from the neuron cell body after injury –> leading to its fragmentation into smaller pieces

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12
Q

Why are peripheral nerves highly vulnerable?

A
  • Largest cells in human body
  • Require intact cell surface for normal electrophysiology
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13
Q

Two categories of immune-mediated peripheral neuropathies

A
  • Peripheral nerve specific
  • Not peripheral nerve specific
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14
Q

Two categories of peripheral nerve specific immune-mediated neuropathies

A
  • Acute
  • Chronic
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15
Q

Which disease is an acute peripheral nerve specific immune-mediated neuropathy?

A

Guillain-Barré syndrome

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16
Q

Name diseases that are chronic peripheral nerve specific immune-mediated neuropathies (3)

A
  • Chronic inflammatory demyelinating polyneurpathy (CIDP)
  • Multifocal motor neuropathy (MMN)
  • Paraprotein-related neuropathy (MAG)
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17
Q

Diseases ‘not peripheral nerve specific’ immune-mediated neuropathies (2)

A
  • Critical illness neuropathy/myopathy
  • Systemic autoimmune diseases/vasculitis
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18
Q

What are the neurological deficits in GBS? (4)

A
  • Muscle paralysis
  • Sensory deficits
  • Autonomic dysfunction
  • Areflexia
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19
Q

What are the symptoms of muscle paralysis in GBS?

A
  • Arms and legs
  • Eye movements, facial muscles, swallowing, speech
  • Respiratory insufficiency
20
Q

What are the symptoms of sensory deficits in GBS?

A
  • Pain, tingling
  • Numbness, absent pain and touch sense
  • Absent position sense (ataxia)
21
Q

What are the symptoms of autonomic deficits in GBS?

A
  • Tension fluctuations and cardiac arrhythmia
22
Q

Two categories of diagnostic criteria for GBS

A
  • Clinical features
  • Additional examinations
23
Q

What are the clinical features to look out for when considering GBS?

A
  • Rapidly progressive (<4 weeks)
  • Symmetrical paresis of arms and legs
  • Reduced or absent reflexes
24
Q

What are the additional examinations you can perform when considering GBS?

A
  • Blood
  • Cerebrospinal fluid
  • Electrophysiology
25
Q

Sequence of events in GBS

A
  • Progression
  • Plateau phase
  • Recovery phase
  • Disability
26
Q

What are the two histological classifications of GBS?

A
  • Demyelination
  • Axonal degeneration
27
Q

How is demyelinating GBS called disease wise?

A

Acute inflammatory demyelinating polyneuropathy (AIDP)

28
Q

How is axonal degenerating GBS called disease wise?

A

Acute motor axonal neuropathy (AMAN)

29
Q

How can macrophages attack the myelin? (3)

A
  • Phagocytosis of myelin debris and myelin sheaths
  • Pro-inflammatory cytokines
  • Antigen-presentation of myelin derived antigens to T cells
30
Q

How does axonal degeneration work?

A

It disconnects myelin from the axon (NOT COMPLETE YET)

31
Q

How does complement activation work in GBS?

A

Antibodies are directed against glycolipids/gangliosides, which are present in membranes of all of your cells BUT highly enriched in the nerve system. Antibody::antigen complex activate complement.

32
Q

Where does compliment activation occur during GBS?

A

Along Schwann cell surfaces

33
Q

Describe the concept of molecular mimicry in GBS

A

Generation of an immune response against the infectious agent generates anti-ganglioside antibodies that cross-react with glycolipids present in peripheral nerves and nerve roots.

34
Q

Which antibodies are associated with GBS?

A

IgM, IgG1

35
Q

Which ganglioside is often attacked?

A

GM1

36
Q

Where is GM1 present?

A
  • Myelin
  • Axolemma
  • Paranodes
  • Nodes of Ranvier (peripheral motor nerves)
37
Q

What are the three categories of treatments in GBS?

A
  • Specific treatment
  • Supportive treatment
  • Rehabilitation
38
Q

What are the options for specific GBS treatment?

A
  • Plasma exchange or plasma pheresis
  • Intravenous immunoglobulins
39
Q

What are the options for supportive GBS treatment?

A
  • Artificial respiration
  • Prevention and treatment of complications (infections, pain)
  • Physiotherapy
40
Q

Why is GBS not a typical classic auto-immune disease? (5)

A
  • No predominance in females
  • No association with other auto-immune diseases
  • No relapsing-remitting or chronic disease course
  • No association with specific HLA haplotypes
  • No improvement after corticosteroids
41
Q

Why is GBS a typical post-infectious disease?

A
  • 2/3 of patients have symptoms of a recent respiratory or GI-infection
  • Antibodies to glycolipids in serum are detected in 50-60% of the cases
  • Association type of infection and clinical features
  • Association type of infection and prognosis
  • > 95% has a monophasic disease course?
42
Q

What is the most common clinical and electrophysiological phenotype of GBS related to a preceding C.jejuni infection?

A

Pure motor clinical variant and the acute motor axonal neuropathy

43
Q

Which infections are associated with GBS?

A
  • C.jejuni
  • CMV
  • EBV
  • Mycoplasma pneumoniae
  • HEV
44
Q

Which infections commonly precede sensory motor GBS? What is their electrophysiological phenotype?

A

M. pneumoniae, CMV and EBV. Demyelinating (AIDP)

45
Q

True or False: “Clinical outcome is better if you had a preceding C.jejuni infection than if you had a preceding M.pneumoniae infection.”

A

False. You actually have a worse outcome

46
Q

What kind of data can you use to investigate an association between infections and GBS?

A
  • Epidemiological data
  • Case-control study
47
Q

What do you look for in a case-control study to study an association between Zika infection and GBS?

A
  • Zika virus positive cases vs Zika virus negative cases –> compare %GBS cases
  • GBS cases vs control cases –> compare % Zika virus positives

I&I WC1 (25 decks)

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