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Intro to Demyelinating Disorders Flashcards

1
Q

What cells are shown below?

A

insert diagram

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2
Q

What are glial cells?

A

neural tissue cells that do not propagate an action potential but support and protect neurons

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3
Q

When does myelination begin?

A
  • third trimester
  • increases rapidly at birth
  • continues throughout life
  • oligodendrocyte = neuroepithelial
    origin from neural tube
  • schwann cell = neural crest origin
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4
Q

Myelin is

A

a membranous cytoplasmic projection (lamellipodum) of an oligodendrocyte or a schwann cell that surrounds a neuronal axon forming the protective sheath

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5
Q

Schwann cell

A

insert diagram

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6
Q

Myelination in the CNS vs PNS

A
  • CNS: one oligodendrocyte can
    myelinate up to 50 axons
  • PNS: one schwann cell myelinates one
    axon
  • PNS: myelin sheaths are thicker in
    diameter
  • CNS: axon >0.2 micrometers to be
    myelinated
  • PNS: 1-2 micrometers to be myelinated
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7
Q

Oligodendrocyte and Schwann cell origin

A

insert diagram

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8
Q

Which fibers are myelinated earlier in development? Sensory or Motor fibers?

A

Sensory fibers

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9
Q

Myelination in the CNS can be intrinsic or adaptive.

A
  • intrinsic = early on during birth and
    early childhood
  • adaptive = as neuronal network forms
  • dwindles with age
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10
Q

What promotes the proliferation of oligodendrocytes?

A

Astrocytes

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11
Q

In the PNS how is myelination initiated?

A

proteins expressed on axon surface interact with glial cell receptors and promote the differentiation of progenitor cells to mature myelinating schwann cells

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12
Q

What is the main component of the myelin sheath?

A

primarily plasma membrane so
Lipid

like cholesterol

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13
Q

How is adaptive myelination initiated?

A

proteins expressed on axon surface interact with receptors on glial cells and promote the differentiation of progenitor cells to mature myelinating cells

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14
Q

Myelin Sheath

A

insert diagram

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15
Q

The juxtaparanodal area of the axon is rich in

A

K+ voltage gated ion channels

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16
Q

What is the bare area of the axon called?

A

Node/nodal area

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17
Q

Schmidt-Lanterman incisures are found

A

between the internodal lamellae formed by schwann cells in the pns

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18
Q

Nodes of Ranvier:
- are
- contain

A
  • gap between two adjacenet myelin
    sheaths across an axon is called the
    node of Ranvier
  • nodes of ranvier contain clusters of
    voltage gated sodium channels
  • electrical current generated ollowing
    depolarisation travels across the
    insulated internode segment, with little
    change to the next node causing
    depolarisation
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19
Q

Label the diagram below

A

insert node of ranvier diagram

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20
Q

Saltatory Conduction:
- is
- advantages

A
  • action potentials leap from node to node,
    increasing conduction velocity
  • reduces loss of electrical current across axon
  • unmyelinated = 0.5-2m/s, myelinated = 70-
    100 m/s
  • increased efficiency of electrical
    transmission as less ion channels are
    needed (only ones at nodes) -> saves energy
    for cell
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21
Q

Saltatory Conduction:

A

insert diagram

22
Q

Demyelinating Diseases:

A

damage to the myelin sheath

23
Q

Dysmyelinating Disease:

A

abnormal formation of the myelin sheath

24
Q

Demyelinating Diseases: Pathological Effects:

A
  • reduced conduction velocity
  • reduced distance in propagation of signal
    across an axon
  • both efferent and afferent neurons can be
    affected as well as higher functions, such as
    cognition
25
Pathology of Demyelinating Diseases: Causes:
- brain injury or ischaemia - toxins/chemicals - metabolic - neurodegenerative - infection - autoimmune effects (myelin sheath proteins are antigenic)
26
Demyelinating Diseases: Symptoms:
- visual impairment - cognitive changes - speech impairment - balance problems - incoordination - sensory loss - weakness - incontinence - pain - fatigue
27
Multiple Sclerosis: - is - incidence - causes
- autoimmune demyelinating disease - most common demyelinating disease with 1 in 1000 incidence - increased incidence in females - genetic susceptibility and environmental triggers
28
Multiple Sclerosis: Subtypes (3):
- relapsing-remitting = episodes of relapse followed by remission, in the majority of cases without complete repair - primary progressive = no periods of improvement or relapse - secondary progressive = with relapse- remission phase followed by progressive disease years later with no remission phase
29
Multiple Sclerosis: What leads to ongoing symptoms, accumulation of neurologic deficits and disability?
failure of remyelination
30
Multiple Sclerosis: Clinical Features:
- earliest presentation generally visual impairment due to optic nerve affected - not all cases of optic neuritis develop MS - ataxia - nystagmus - sensory and motor impairment of trunk and limbs - loss of bladder control
31
Multiple Sclerosis: Treatment:
- steroids - disease modifying treatments - aim to control immune response to decrease the rate and severity of replace episodes - social prescribers
32
Multiple Sclerosis: Pathophysiology:
- T helper and B cells involved - secrete cytokines that recruit macrophages and other leucocytes that destroy myelin - leading to the formation of white matter lesions called plaques - plaques can be active; containing macrophages, broken down myelin and lymphocytes - inactive plaques = resolved inflammation, astrocyte proliferation and no myelin-gliosis that can lead to the formation of a glial scar
33
Multiple Sclerosis:
insert images
34
As age increases, remyelination is
less efficient
35
Autoimmune Demyelinating Diseases:
- demyelination due to immune function can follow viral infections, even mild ones - caused by cross reactivity between myelin proteins and immune cells/antibodies - the resulting diseases are acute and monophasic
36
Acute Disseminated Encephalomyelitis (ADEM):
- autoimmune demyelinating disease following viral infection - non-localised symptoms (headache, lethargy, coma) - rapid progression with either complete recovery or fatality in a minority of cases
37
Neuromyelitis optica:
optic nerve and spinal cord affected by autoimmune demyelination
38
Gullian-Barre Syndrome:
- autoimmune demyelinating disease of the PNS
39
Guillain-Barre Syndrome: Presentation:
- often following infection like diarrhoeal illness (campylobacter), upper respiratory tract infection, COVID, hep E - progressive weakness over 2-4 weeks, reaches nadir by 4-6 weeks - affects arms/legs/facial muscles/speech/swallowing/breathing - may affect autonomic nervous system - varying degrees of severity - recovery thereafter (may not be complete)
40
Gullian-Barre Syndrome is a monophasic illness. True or False?
True
41
Guillain-Barre Syndrome: Treatment:
- plasma exchange - IV immunoglobulins
42
Guillain-Barre Syndrome: Subtypes:
- acute demyelinating polyradiculoneuropathy (AIDP): europe, north ameria - acute motor axonal neuropathy (AMAN): asia
43
Dysmyelinating Diseases: Leukodystrophies: - are, cause, nature
- inherited diseases that emerge at a young age and are progressive
44
Krabbe Disease:
- dysmyelinating leukodystrophy - autosomal recessive - causes by build up of cytotoxic metabolic compound which inhibits myelin sheath formation - appears between 3-6 months of age, survival beyond 2 years is rare - loss of myelination in both CNS and PNS; loss of oligodendrocytes
45
Metachromatic Leukodystrophy:
- dysmyelinating leukodystrophy - autosomal recessive - affects macrophages
46
Adrenoleukodystrophy:
- dysmyelinating leukodystrophy - x linked recessive - young males affects - 10 years of life max
47
Charcot-Marie-Tooth Disease:
- hereditary heterogenous (dominant) disease - dysmyelinating leukodystrophy in some subtypes - mutations in different proteins linked - progressive disease that usually presents between 0-20 years of age - CMT1 are subtypes caused by demyelination when the mutation is autosomal dominant - CMT4 when autosomal recessive which is the most rare and severe - CMT2 subtypes affect neuronal axons
48
Remyelination: CNS:
- regenerative process - axon regeneration is limited in CNS but remyelination occurs - remyelination relies on oligodendrocytes and the differentiation of oligodendrocyte precursor cells (OPCs) - success of remyelination depends on the location of a lesion, presence of OPCs, degree of inflammation and the presence of gliosis
49
Remyelination does occur in MS patients however is negatively affected by
disease progression
50
Remyelination: PNS:
- schwann cells can proliferate and remyelinate axons - depends on the presence of progenitor cells and successful differentiation - in comparison with CNS, schwann cells create a positive growth environment that promotes both axon growth and remyelination in the event of injury

NSB (50 decks)

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