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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
MS pathology
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
26
Immune cell found in MS lesiosn
CD4 CD8 Macrophages
27
Possible mechanism triggering immune response in MS
Viral injury to CNS -> exposure of myelin antigens -> damage Molecular mimicry of viral antigens and myelin -> immune rxn against virus going towards myelin
28
MS treatment
Agent that deplete B cells
29
MS morphology
MS plaques
30
What do you;see in macrophages at early stage of MS
Myelin fragments
31
Presentation of inactive plaque in MS
Gliosis with scar tissueu | Demyelinated axons
32
Early stage MS plaque presentation
Shadow plaque due to remyelination
33
Why is remyelinzation infective in advanced lesion of MS
Gliosis leading to barrier between myelin producing cells and axons
34
What is smouldering plaque In MS
Lesion that expand at periphery and dies down in center
35
Classical MS characteristics
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
Microscopy of active plaque
``` Perivascular infiltrates of lymphocytes and macrophages Lipid laden macrophages Myelin debris In macrophages Depletion of Oligodendrocytes Sparing of axons ```
37
Micro of inactive plaque
Hypocellular Gliotic Reduced ddmyelinated axons Reduced Oligodendrocytes
38
PATHOphysiology MS
39
Concentric sclerosis MS
Alternate bands of demyelination and myelinated white matter | Rare but rapidly progressive
40
Neuromyelitis optica
Development of bilateral optic neuritis and acute transverse myelitis at same time or with period between them
41
Call presentation of neuromyelitis optica
Visual loss paraplegia sensory loss
42
Does neuromyelitis optica affect more women than men
Yes
43
Call vary from first attack in neuromyelitis optica good
Poor recovery
44
Neuromyelitis optica pathogenesis
Different from MS | Antibody dependent and complement mediated
45
Associated with neuromyelitis optica
``` Thyroiditis type one diabetes celiac disease SLE Sjogren syndrome ```
46
Inflammatory demyelination neuropathies common or uncommon ?
Uncommon
47
Pathogenesis o f inflammatory demyelination neuropathies
Immune disorder Antibodies and Activated T lymphocyte react to antigens on peripheral nerves Inflammatory and Marcrophage reaction that destroys myelin and axons
48
How can you strongly provide evidence of inflammatory demyelination neuropathies
By giving plasma exchange which will improve significantly clinical presentation by removing the antibodies
49
Two main inflammatory demyelinating neuropathies in pns
Guillard barre syndrome | Chronic inflammatory ray demyelinating disease
50
What is guillain barre
Demyelinating peripheral neuropathy | Counterpart fo MS in peripheral nervous system
51
Types of guillain barre
Acute inflammatory demyelination pooyneuropathy 90% AMAN MFS
52
Guillain barre clinical presentation
Ascending paralysis Paresthésia -> start in the toes and fingertips Weakness Areflexia Many patients completely paralyzed and unable to breathe
53
Mortality rate of guillain barre
5%
54
Guillain barre main complications leading to death
die from respiratory paralysis Cardiac arrest Sepsis Other complications
55
Percentage of patients that recovered but have residual weakness
10%
56
What type of illness occurs in 2/3 of patients before developing guillain barre
Acute flu like illness
57
Other complications of guillain barre
Muscle atrophy Joint weakness Pneumonia
58
Type of infection or condition involved in cases guillain
``` Campylobacter jéjuni (20-30%) - More in AMAN Cytomegalovirus ( 20-30%) Mycoplasma pneumoniae Hepatitis E Other infections Vaccination ```
59
Guillain barre pathogenesis
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
Gangliosides that have serum antibodies found in AMAN
GM1a GM1b GD1a
61
MFS gangliosides that have antibodies rxns
GD1b GD3 GT1a GQ1b
62
Manifestation happening in MFS
Ataxia | Ophtalmoplegia
63
Antibodies found in GBS following CMV
Anti GM2
64
Where rxns in guillain barre of antibodies occur
Axonal membrane of Nodes of fancier | Paranodal myelin
65
Morphology of GBS
Perivenular and Endoneural infiltration by lymphocytes, macrophages , plasma cells Segmental demyelination of peripheral nerves , Demyelinating widespread but more severe at stromal side
66
Always severe axonal demyelination in GBS ?
Variable
67
Lab findings Hallmark of GBS
Csf protein increase | No increase in cells albuminocytological dissociation
68
Mortality rate
2-5%
69
Complications leading to death inGBS
Respiratory paralysis Autonomic instability Cardiac arrest Related complications
70
Most common chronic acquired inflammatory peripheral neuropathy
Chronic inflammatory demyelinating polyradiculoneuropathy
71
What is Chronic inflammatory demyelinating polyradiculoneuropathy
Chronically progressive or relapsing symmetric sensorimotor poly neuropathy
72
What makes difference between CIPD and GBS
8 weeks or more symptoms in Chronic inflammatory demyelinating polyradiculoneuropathy
73
Chronic inflammatory demyelinating polyradiculoneuropathy presentation evolution
Start insidious Slow evolution (slow progressive or slow relapsing ) Partial or complete recovery between recurrences
74
Clinical presentation of Chronic inflammatory demyelinating polyradiculoneuropathy
Preceding infection - infrequent Initial limb weakness - proximal and distal Sensory symptoms - tingling, numbness of hands and feet Motor symptoms - predominant
75
Type of patients with more precipitous onset of symptoms in Chronic inflammatory demyelinating polyradiculoneuropathy
Children
76
Manifestation in Chronic inflammatory demyelinating polyradiculoneuropathy in other form of infection
Gait abnormalities Motor deficit - symmetric weakness of both proximal and distal muscle Sign of cranial nerve involvement - facial muscle paralysis , diplopia
77
Is it easy to find gangliosides involved in CIDP
No
78
Type of complement fixing immunoglobulin found in CIPD on myelin
IgG | IgM
79
CIPD pathogenesis
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
Sural nerve biopsy
81
Technique used for micros lab findings in CIDP
Sural nerve biopsy
82
Micro of CIDP

Neurology (31 decks)

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