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Neurology > Demyelinating Diseases > Flashcards

Demyelinating Diseases Flashcards

1
Q

Parts of neurons

A

Cell body
Dendrites
Axons

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2
Q

Advatanges of myelinated neuron

A

Conduct impulse faster

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3
Q

Function of myelin on neurons

A

Act as insulator and help propagate signal faster

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4
Q

Most neuron are myelinated or unmyelinated “

A

Myelinated

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5
Q

2 cells responsible for myelinazation of neuron

A

Oligodendrocytes in CNS

Schwann cells in PNS

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6
Q

Do Schwann cells make multiple or just one myelin sheath

A

Just one

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7
Q

Importance of node of renvier

A

Determines rate of conduction

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8
Q

3 main connective tissue that bundle axons

A

Endoneruoem - nerve filament
Perineurium - fascicles
Épineurium -

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9
Q

Large diameter axons function

A

Light touch

Motor signal

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10
Q

Consequence of damage to myelin sheath

A

Slow nerve conduction

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11
Q

Condpsequence of demyelination of

A

Large fiber sensory dysfunction
Motor weakness
Diminished reflexes

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12
Q

What are demyelination disease

A

Acquired conditions with preferential damage to myelin

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13
Q

When do you have damage to axons

A

When there’s progression of disease as secondary damage

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14
Q

2 mechanism of demyelination

A

Damage of myelin sheath

Damage of cells that produce myelin sheath

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15
Q

What is dysmyelination

A

Formation of abnormal myelin sheath

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16
Q

classification of demyelination diseases

A

Demyelination due to inflammatory processes
Viral demyelination
Demyelination caused by acquired metabolic derangements
Hypoxic ischemic forms of demyelination
Demyelination by focal compression

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17
Q

Disease of inflammatory demyelination

A

Multiple sclerosis
Neuromyelitis optics
Acute disseminated encephalomyelitis
Acute hemorrhagic leucoencephalitis

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18
Q

Type of MS

A

Classical
acute
Concentric sclerosis

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19
Q

Commonest demyelination g disease

A

MS

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20
Q

Causes of MS

A

Polygenic defects - the higher the number of defective genes the higher severity
Environmental - high latitude zones, growing up in high prevalence areas, studies are considering EBV and HHV6

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21
Q

MS concordance rate higher in monozygotic or dizygotic twins

A

Monozygotic

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22
Q

MS more in women or men

A

Women 2x

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23
Q

Age of appearance of MS

A

15-55 yo

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24
Q

Clinical manifestation of MS

A 
Muscle weakness
Parenthèsia , focal sensory loss
Optic neuritis, diplopia 
Ataxia, vertigo
Autonomic motor abnormalities of bladder , bowel, sexual function 
Painful muscle spasms
Trigeminal neuralgia
Fatigue
Depression
Cognitive difficulties
Psychiatric disturbances 
Seizures
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25
Q

MS pathology

A

Autoimmune cell mediated process
T cell produce ifn gamma -> macrophages activation
TH17 -> IL17 with neutrophils and monocytes recruitment
Activated leucocytes Attach myelin and destroy it

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26
Q

Immune cell found in MS lesiosn

A

CD4
CD8
Macrophages

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27
Q

Possible mechanism triggering immune response in MS

A

Viral injury to CNS -> exposure of myelin antigens -> damage

Molecular mimicry of viral antigens and myelin -> immune rxn against virus going towards myelin

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28
Q

MS treatment

A

Agent that deplete B cells

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29
Q

MS morphology

A

MS plaques

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30
Q

What do you;see in macrophages at early stage of MS

A

Myelin fragments

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31
Q

Presentation of inactive plaque in MS

A

Gliosis with scar tissueu

Demyelinated axons

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32
Q

Early stage MS plaque presentation

A

Shadow plaque due to remyelination

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33
Q

Why is remyelinzation infective in advanced lesion of MS

A

Gliosis leading to barrier between myelin producing cells and axons

34
Q

What is smouldering plaque In MS

A

Lesion that expand at periphery and dies down in center

35
Q

Classical MS characteristics

A

Different size and shape of plaque , multiple, randomly distributed
Involving cortex, subcortex, cerebellar white matter, brain stem, spinal cord
Periventricular white matter

Firmer lesion than white matter -> well circumscribed , depressed, glassy grey tan, irregular shaped

36
Q

Microscopy of active plaque

A 
Perivascular infiltrates of lymphocytes and macrophages 
Lipid laden macrophages 
Myelin debris In macrophages 
Depletion of Oligodendrocytes 
Sparing of axons
37
Q

Micro of inactive plaque

A

Hypocellular
Gliotic
Reduced ddmyelinated axons
Reduced Oligodendrocytes

38
Q

PATHOphysiology MS

A
39
Q

Concentric sclerosis MS

A

Alternate bands of demyelination and myelinated white matter

Rare but rapidly progressive

40
Q

Neuromyelitis optica

A

Development of bilateral optic neuritis and acute transverse myelitis at same time or with period between them

41
Q

Call presentation of neuromyelitis optica

A

Visual loss
paraplegia
sensory loss

42
Q

Does neuromyelitis optica affect more women than men

A

Yes

43
Q

Call vary from first attack in neuromyelitis optica good

A

Poor recovery

44
Q

Neuromyelitis optica pathogenesis

A

Different from MS

Antibody dependent and complement mediated

45
Q

Associated with neuromyelitis optica

A 
Thyroiditis 
type one diabetes 
celiac disease 
SLE 
Sjogren syndrome
46
Q

Inflammatory demyelination neuropathies common or uncommon ?

A

Uncommon

47
Q

Pathogenesis o f inflammatory demyelination neuropathies

A

Immune disorder
Antibodies and Activated T lymphocyte react to antigens on peripheral nerves
Inflammatory and Marcrophage reaction that destroys myelin and axons

48
Q

How can you strongly provide evidence of inflammatory demyelination neuropathies

A

By giving plasma exchange which will improve significantly clinical presentation by removing the antibodies

49
Q

Two main inflammatory demyelinating neuropathies in pns

A

Guillard barre syndrome

Chronic inflammatory ray demyelinating disease

50
Q

What is guillain barre

A

Demyelinating peripheral neuropathy

Counterpart fo MS in peripheral nervous system

51
Q

Types of guillain barre

A

Acute inflammatory demyelination pooyneuropathy 90%
AMAN
MFS

52
Q

Guillain barre clinical presentation

A

Ascending paralysis
Paresthésia -> start in the toes and fingertips
Weakness
Areflexia
Many patients completely paralyzed and unable to breathe

53
Q

Mortality rate of guillain barre

A

5%

54
Q

Guillain barre main complications leading to death

A

die from respiratory paralysis
Cardiac arrest
Sepsis
Other complications

55
Q

Percentage of patients that recovered but have residual weakness

A

10%

56
Q

What type of illness occurs in 2/3 of patients before developing guillain barre

A

Acute flu like illness

57
Q

Other complications of guillain barre

A

Muscle atrophy
Joint weakness
Pneumonia

58
Q

Type of infection or condition involved in cases guillain

A 
Campylobacter jéjuni (20-30%) - More in AMAN 
Cytomegalovirus  ( 20-30%)
 Mycoplasma pneumoniae
Hepatitis E
Other infections 
Vaccination
59
Q

Guillain barre pathogenesis

A

Antibodies cross reaction with gangliosides
C jejuni have lipo oligosaccharides mimic carbohydrate moiety of gangliosides in human peripheral nerves
Antibodies associated with some guillain barre reflect in gangliosides inn human peripheral system

60
Q

Gangliosides that have serum antibodies found in AMAN

A

GM1a
GM1b
GD1a

61
Q

MFS gangliosides that have antibodies rxns

A

GD1b
GD3
GT1a
GQ1b

62
Q

Manifestation happening in MFS

A

Ataxia

Ophtalmoplegia

63
Q

Antibodies found in GBS following CMV

A

Anti GM2

64
Q

Where rxns in guillain barre of antibodies occur

A

Axonal membrane of Nodes of fancier

Paranodal myelin

65
Q

Morphology of GBS

A

Perivenular and Endoneural infiltration by lymphocytes, macrophages , plasma cells
Segmental demyelination of peripheral nerves ,
Demyelinating widespread but more severe at stromal side

66
Q

Always severe axonal demyelination in GBS ?

A

Variable

67
Q

Lab findings Hallmark of GBS

A

Csf protein increase

No increase in cells albuminocytological dissociation

68
Q

Mortality rate

A

2-5%

69
Q

Complications leading to death inGBS

A

Respiratory paralysis
Autonomic instability
Cardiac arrest
Related complications

70
Q

Most common chronic acquired inflammatory peripheral neuropathy

A

Chronic inflammatory demyelinating polyradiculoneuropathy

71
Q

What is Chronic inflammatory demyelinating polyradiculoneuropathy

A

Chronically progressive or relapsing symmetric sensorimotor poly neuropathy

72
Q

What makes difference between CIPD and GBS

A

8 weeks or more symptoms in Chronic inflammatory demyelinating polyradiculoneuropathy

73
Q

Chronic inflammatory demyelinating polyradiculoneuropathy presentation evolution

A

Start insidious
Slow evolution (slow progressive or slow relapsing )
Partial or complete recovery between recurrences

74
Q

Clinical presentation of Chronic inflammatory demyelinating polyradiculoneuropathy

A

Preceding infection - infrequent
Initial limb weakness - proximal and distal
Sensory symptoms - tingling, numbness of hands and feet
Motor symptoms - predominant

75
Q

Type of patients with more precipitous onset of symptoms in Chronic inflammatory demyelinating polyradiculoneuropathy

A

Children

76
Q

Manifestation in Chronic inflammatory demyelinating polyradiculoneuropathy in other form of infection

A

Gait abnormalities
Motor deficit - symmetric weakness of both proximal and distal muscle
Sign of cranial nerve involvement - facial muscle paralysis , diplopia

77
Q

Is it easy to find gangliosides involved in CIDP

A

No

78
Q

Type of complement fixing immunoglobulin found in CIPD on myelin

A

IgG

IgM

79
Q

CIPD pathogenesis

A

In blood -> APC with auto reactive T cell
Activated T cell leads to plasma cells releasing antibodies
Antibodies go to peripheral nervous system and

80
Q
A

Sural nerve biopsy

81
Q

Technique used for micros lab findings in CIDP

A

Sural nerve biopsy

82
Q

Micro of CIDP

A

Neurology (31 decks)

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