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Neuro Boards > Demyelinating Diseases > Flashcards

Demyelinating Diseases Flashcards

1
Q

Multiple Sclerosis

A

chronic inflammatoy disorder characterized by progressive neurological decline that manifests in different clinical phenotypes

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2
Q

MS risk factors

A

gender (female)
family history
geograpahical latitude
low vitamin D levels

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3
Q

Chronic MS symptoms

A

fatigue exacerbated by heat (Uhthoff’s phenomenon) that improves with cooler temperatures
sleep disturbances, depression, euphoria, urinary retention, paroxysmal spasms, and cognitive decline

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4
Q

treatment for paroxysmal spasms in MS

A

carbamazepine

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5
Q

neuropsych testing in MS

A

deficits in long term memory (most common), verbal fluency, as well as speed and working memory

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6
Q

epilepsy and MS

A

rare complication, seen in only 2-5%

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7
Q

MS symptoms

A

broad spectrum of acute focal neurological symptoms, including but not limited to focal sensory or motor deficits, monocular visual loss, diplopia, and gait disturbance

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8
Q

MS diagnostic criteria

A

2017 McDonald Criteria

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9
Q

2017 McDonald Criteria

A

diagnosis based on patients that have evidence of demyelination with dissemination in space and time
can be based on clinical changes (relapse), feature son imaging, and CSF findings

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10
Q

Dissemination in Space (DIS)

A

development of lesions in two distinct anatomical locations indicating a multifocal disease process

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11
Q

Dissemination in Time (DIT)

A

appearance of new CNS lesions on imaging over time, or lesions of different appearance (bright vs dark) indicating new and old
oligoclonal bands in CSF now considered indication of DIT as well

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12
Q

remitting-relapsing MS (RRMS)

A

clearly defined attacks with neurologic recovery (complete or incomplete) between them

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13
Q

secondary progressive MS (SPMS)

A

seen in patients who initially had RRMS but now experiencing a gradual worsening regardless of occasional attacks
early aggressive treatment may delay this progression

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14
Q

primary progressive MS (PPMS)

A

progressive decline of neurological function without clearly defined attacks over the course of at least 1 year

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15
Q

Clinically Isolated Syndrome (CIS)

A

defined as a monophasic demyelinating episode in someone who otherwise has no clinical history of demyelinating disease

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16
Q

CIS treatment

A

initiation of a disease-modifying therapy (DMT) after CIS can delay time to a definitive diagnosis of MS

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17
Q

radiologically isolated syndrome (RIS)

A

diagnosed in a patient with an MRI that is consistent with MS but they have no clinical history of transient focal neurological deficits
when diagnosed, patients have a 33% chance of having a clinical demyelinating attack over the following two years
risk of MS is higher of oligoclonal bands are present in CSF

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18
Q

typical findings in CSF in MS

A

elevated protein
elevated CSF IgG index
oligocloncal bands in CSF that do not present in the serum
possibly slight elevation of WBC count (lymphocytic preodminant)

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19
Q

typical finding in MRI in MS

A

demyelinating lesions related to MS are ovoid, >3mm in diameter, and are typically located in particular regions: periventricular (Dawson’s fingers), juxtacortical, cortical, or spinal cord
acute: contrast enhance due to damage to blood brain barrier
chronic: hyperintense on T2/FLAIR sequences

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20
Q

typical demyelinating attacks

A

optic neuritis
transverse myelitis

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21
Q

optic neuritis presentation

A

presents with monocular decreased visual acuity, loss of color vision, and an afferent pupillary defect (APD) due to demyelinating lesion of the optic nerve
often painful with extraocular movements
children more likely to present with headache and bilateral symptoms
can be initial presentation of MS or NMO

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22
Q

optic neuritis funduscopic exam

A

swollen optic disc

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23
Q

optical coherence tomography (OCT) in optic neuritis

A

thinning of the retinal nerve fiber layer weeks to months after an acute attack

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24
Q

visual evoked potentials (VEPs) in optic neuritis

A

prolonged P100 latency, even in patients with distant histories of ON with no residual visual deficits

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25
Q

optic neuritis in DIT/DIS

A

not considered an event of dissemination in time/space

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26
Q

transverse myelitis presentation

A

presents with myelopathic findings (weakness, hyperreflexia, sensory symptoms, and occasionally bowel/bladder dysfunction)
Lhermitte’s sign - electric shock sensation down the neck/spine with neck flexion or extension may also be present

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27
Q

MRI in transverse myelitis

A

T2/FLAIR hyperintense lesion involving the spine +/- contrast enhancement based on the lesion’s acuity

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28
Q

Transverse myelitis as demyelinating presentation

A

can be initial presentation, however it is also important to exclude infectious, rheumatologic, postvaccination/postinfectious, and nutritional mimics of demyelinating disease

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29
Q

treatment if transverse myelitis related to inflammatory or idiopathic

A

once other etiologies ruled out, initiation of steroids

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30
Q

MS on gross anatomy

A

grey plaques within white matter representing loss of myelinated tissue

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31
Q

microscopic analysis of MS lesions

A

can gauge the chronicity of demyelinating plaque

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32
Q

active plaques microscopic analysis

A

destruction of oligodendroglia while sparing neurons and their axons, inflammatory infiltrates of the parenchyma and in the perivascular space, as well as macrophages containing myelin debris

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33
Q

recovery phase microscopic analysis

A

recruited oligodendrocyte precursor cells remyelinate active plaques leading to reduced myelin density and thin myelin sheaths
- almost half of chronic MS plaques will show some degree of remyelination
- remyelinated plaques are known as “shadow plaques”

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34
Q

chronic inactive plaques in microscopic analysis

A

sharply demarcated hypocellular plaques with myelin loss and glial scar formation via astrocytes

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35
Q

stain for myelin

A

luxol fast blue (LFb)

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36
Q

acute treatment in MS first line

A

high dose steroid therapy: IV methylprednisolone (1gm per day for 3-5 days) +/- prednisone taper
- oral steroids have been shown to have equal benefit and can be used first line, but typically not recommended for acute optic neuritis given risk of recurrence in either eye seen in the optic neuritis treatment trial (ONTT)

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37
Q

acute treatment in MS second line

A

if IV steroids fail to improve symptoms, providers can try plasma exchange (PLEX)
- has more established data for acute MS exacerbation treatment than dose IVIG

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38
Q

acute treatment in MS DMTs

A

not recommended as the sole treatment for acute MS exacerbations

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39
Q

disease-modifying therapies: forms

A

oral
injectables
infusions

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40
Q

Oral DMTs

A

dimethyl fumarate
diroximel fumarate
fingolimod
siponimod
ozanimod
ponesimod
teriflunomide
cladribine

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41
Q

injectable DMTs

A

interferons
glatiramer acetate
ofatumumab

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42
Q

infusion DMTs

A

mitoxantrone
alemtuzumab
natalizumab
ocrelizumab

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43
Q

dimethyl fumarate: efficacy

A

moderate to high

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44
Q

dimethyl fumarate: mechanism of action

A

reduces toxic oxidative stress through activation of the nuclear 1 factor (erythroid-derived 2)-like 2 (Nrf2) antioxidant response pathway
may also suppress pro-inflammatory cytokines

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45
Q

dimethyl fumarate: side effects

A

flushing (most common), nausea, diarrhea, and leukopenia

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46
Q

treatment for dimethyl fumarate flushing

A

aspirin by inhibiting the prostaglandin pathway

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47
Q

dimethyl fumarate: monitoring

A

interval complete blood counts and liver function testing should be done to monitor for medication-related complications

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48
Q

diroximel fumarate

A

approved for relapsing-remitting MS
fewer GI side effects
same MOA

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49
Q

fingolimod efficacy

A

moderate to high efficacy

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50
Q

fingolimod: mechanism of action

A

sequesters lymphocytes in lymph nodes, thereby reducing the number of lymphocytes in peripheral circulation and the central nervous system
performed by downregulating sphingosine-1-phopsphate receptors (S1PR) expressed on lymphocytes in secondary lymphoid tissue

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51
Q

fingolimod similar MOA to:

A

siponimod, ozanimod, ponesimod

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52
Q

fingolimod mnemonic

A

FINGolimod using its long FINGers to sequester lymphocytes, via sFINGosine-1-phosphate receptor downregulation on lymphoid tissue

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53
Q

fingolimod: side effects

A

first dose bradycardia, AV block, QT prolongation due to activation of S1PRs on atrial myocytes
macular edema

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54
Q

fingolimod: monitoring

A

EKG monitoring and observation required during first dose
frequent ophthalmologic examinations

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55
Q

fingolimod: rare fatal side effects

A

infections: cryptococcus meningitis, disseminated varicella-zoster, herpes simplex encephalitis, and PML

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56
Q

fingolimod: sudden cessation risk

A

severe rebounding of disease

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57
Q

siponimod: approved for

A

relapsing-remitting MS

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58
Q

siponimod: mechanism of action

A

downregulates sphingosine-1-phosphate receptors (S1PR) expressed on lymphocytes in secondary lymphoid tissue, like fingolimod

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59
Q

siponimod: side effects

A

macular edema
bradycardia - risk reduced by slow daily titration of medication, c/i in known bradycardic patients

60
Q

siponimod monitoring

A

CYP2C9 and funduscopic testing required prior to initiation due to significant variability in metabolism and macular edema, respectively
- certain CYP2C9 variants require greatly reduced dose while some patients with homozygous variants should not receive the drug at all

61
Q

teriflunomide efficacy

A

mild effectiveness

62
Q

teriflunomide mechanism of action

A

reduces T- and B-cell activation, proliferation, and function by inhibiting pyrimidine synthesis for DNA replication by blocking dihydroorotate dehydrogenase

63
Q

teriflunomide side effects

A

leukopenia, alopecia, GI symptoms
hepatotoxicity
category X for pregnancy due to teratogenicity

64
Q

teriflunomide mnemonic

A

TERIflunomide is TERRIble for baby development

65
Q

cladribine mechanism of action

A

purine antimetabolite

66
Q

cladibrine side effects

A

leukopenia, malignancy, teratogenicity

67
Q

interferons effectiveness

A

mild effectiveness

68
Q

interferons mechanism of action

A

nonselective immunomodulation

69
Q

interferons side effects

A

myalgias, flu-like symptoms, injection site reactions

70
Q

interferons risk

A

decreased effectiveness over time due to formation of neutralizing antibodies with prolonged use

71
Q

glatiramer acetate effectiveness

A

moderate effectiveness

72
Q

glatiramer acetate mechanism of action

A

selective immunomodulation

73
Q

glatiramer acetate side effects

A

tends to be better tolerated than interferons
lipoatrophy at injection sites
no risk for the formation of neutralizing antibodies, unlike beta-interferons or natalizumab

74
Q

ofatumumab mechanism of action

A

monoclonal antibody to CD20 B-cells

75
Q

ofatumumab effectiveness

A

proven to be more effective than teriflunomide in randomized drug trials

76
Q

ofatumumab side effects

A

injection site irritation, upper respiratory infections, headache

77
Q

ofatumumab screening

A

hepatitis B and low immunoglobulins should be done prior to initiating therapy

78
Q

mitoxantrone mechanism of action

A

type II topoisomerase inhibitor

79
Q

mitoxantrone approved for

A

secondary progressive MS

80
Q

mitoxantrone side effects

A

dose-related cardiotoxicity
alopecia, menstrual irregularity, amenorrhea, and leukopenia
category D for pregnancy

81
Q

mitoxantrone monitoring

A

pretreatment cardiac output screening is advised, and monitoring should occur with the first treatment

82
Q

alemtuzumab mechanism of action

A

monoclonal antibody targeting of the CD-52 receptor on activated T- and B-lymphocytes, leading to cytotoxic and complement-mediated depletion

83
Q

alemtuzumab side effects

A

lymphopenia and autoimmune-related syndromes including thyroid disease (30-40%), thrombocytopenia (1%), and anti-glomerular basement membrane-related nephropathy

84
Q

natalizumab effectiveness

A

highly effective

85
Q

natalizumab mechanism of action

A

monoclonal antibody targeting of alpha 4-integrin which is expressed on activated T-lymphocytes, which blocks the transmigration of T-cells across the blood-brain barrier

86
Q

natalizumab side effects

A

progressive multifocal leukoencephalopathy (PML)

87
Q

natalizumab risk of PML

A

usually fatal opportunistic infection of CNS within oligodendrocytes due to reactivation of latent JC polyomavirus infection
risks include: positive anti-JC virus antibodies before initiating therapy, prior use of immunosuppressive therapy, and more than 24 months of natalizumab therapy

88
Q

natalizumab monitoring

A

JCV titers checked before starting therapy
JC viral positive patients can still undergo treatment, however the risk for PML increases when the duration of therapy is greater than 2 years

89
Q

natalizumab treatment for PML

A

discontinuation of natalizumab
PLEX used to accelerate drug clearance
restoration of immune function may result in immune reconstitution inflammatory syndrome (IRIS)

90
Q

natalizumab sudden cessation

A

without transition to another therapy can lead to worsening of symptoms

91
Q

ocrelizumab approved for

A

primary progressive and relapsing-remitting MS

92
Q

ocrelizumab mechanism of action

A

binds CD20 B-cells leading to cell-mediated cytotoxicity

93
Q

ocrelizumab side effects

A

increased risk of infection

94
Q

dalfampridine mechanism of action

A

inhibition of voltage-dependent potassium channels causes improved nerve conduction

95
Q

dalfampridine treatment associated with

A

improvements in strength, ambulation, and endurance

96
Q

dalfampridine monitoring/contraindications

A

renally cleared, so patients with CKD are at risk for toxic blood levels, so should be avoided in ESRD
contraindicated in patients with epilepsy

97
Q

rebounding demyelinating disease

A

seen with the cessation of fingolimod or natalizumab when no substitute medication is initiated
often presents within a few months of discontinuation
symptoms include fulminant encephalopathy and focal neurological deficits
treatment includes high dose steroids and/or PLEX

98
Q

tumefactive MS

A

presents with a large >2cm demyelinating lesion with incomplete ring enhancement, mass effect, minimal surrounding edema, and low cerebral blood volume
- may be difficult to differentiate from brain tumor, ADEM, or abscess
- tumors often more significant surrounding edema and higher cerebral blood volume than TMS
- biopsy sometimes required to confirm the diagnosis

99
Q

tumefactive MS pathology

A

foamy microphages containing phagocytosed myelin debris

100
Q

marburg variant disease (acute/fulminant MS)

A

fulminant form of MS with large tumefactive lesions, associated with high mortality rate
relatively unresponsive to therapy but high dose steroids and PLEX may help

101
Q

marburg variant disease pathology

A

more macrophage infiltrates and necrosis than typical MS

102
Q

Balo’s concentric MS

A

imaging will show concentric alternating bands of preserved myelination with alternating areas of demyelination
also described as “onion bulbs” when seen pathologically

103
Q

Schilder’s disease

A

seen primarily in childhood
lesions will be large in size, contrast-enhancing, and usually involve the centrum semiovale

104
Q

pregnancy with MS

A

generally safe
- children born from parents with MS have a 3-5% risk of developing MS themselves
relapse rates decrease over duration of pregnancy and increase postpartum
pregnancy and breastfeeding have no effect on overall disease progression

105
Q

pregnancy with MS: ok meds

A

glatiramer acetate and interferon beta are felt to be safest options for pregnancy
high dose corticosteroids can be used for acute relapses during pregnancy and are not teratogenic

106
Q

pregnancy with MS: avoid meds

A

DMTs should be discontinued or avoided if possible during pregnency, especially if patient is taking teriflunomide or motixantrone

107
Q

MS mimics

A

infectious
inflammatory
other demyelinating disease
other

108
Q

MS mimics: infection

A

HIV
Lyme
Neurosyphilis
Bartonella infection
PML
Whipple’s disease

109
Q

MS mimics: inflammatory disease

A

Sjogren’s syndrome
Systemic lupus erythematosus (SLE)
Sarcoidosis (intramedullary lesions are most often found in the cervical cord)
Behcet’s disease
CNS vasculitis (primary or secondary)
Susac’s syndrome

110
Q

MS mimics: other demyelinating disease

A

ADEM
NMO
Leukodystrophies

111
Q

MS mimics: other

A

CADASIL
B12 deficiency

112
Q

neuromyelitis optica spectrum disorder (NMOSD)

A

inflammatory CNS disorder distinct from MS
most commonly associated with antibodies to aquaporin-4 (APQ4)

113
Q

NMO core clinical characteristics

A

optic neuritis (longitudinal/chiasmal lesion)
longitudinally extensive transverse myelitis (LETM) is defined by a single lesion involving 3 or more vertebral segments
brainstem/diencephalic lesions
area postrema syndrome

114
Q

NMO diagnosed based on what criteria

A

2015 Wingerchuk criteria

115
Q

what to check when NMO suspected

A

antibodies to aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG)

116
Q

AQP4

A

water channel localized in the CNS at the endfeet of astrocytes

117
Q

MOG

A

found on oligodendrocytes

118
Q

NMO CSF findings

A

oligoclonal bands often absent

119
Q

NMO pathologic findings

A

perivenous infiltration of lymphocytes, inflammation, and demyelination

120
Q

NMO Treatment: acute

A

high dose steroids, then PLEX or IVIG if symptoms are steroid-resistant

121
Q

NMO treatment: long term

A

IVIG
immunosuppressants (azathioprine, mycophenolate)
monoclonal antibodies (if anti-AQP4 antibody positive)

122
Q

monoclonal antibodies in NMO treatment

A

inebilizumab
satralizumab
eculizumab

123
Q

inebilizumab mechanism of action

A

CD19-directed antibody

124
Q

satralizumab mechanism of action

A

interleukin-6 (IL-6) receptor antagonist

125
Q

eculizumab mechanism of action

A

complement-binding monoclonal antibody

126
Q

acute disseminated encephalomyelitis (ADEM)

A

aka postinfectious encephalomyelitis
monophasic autoimmune illness that presents abruptly with headaches, fever, and widespread CNS demyelination and occurs primarily in children and young adults

127
Q

ADEM resolution

A

symptoms usually resolve within a week without residual neurologic deficits
children more likely to make a complete recovery than adults

128
Q

ADEM onset

A

7-14 days after environmental exposure
most commonly occurs after viral URI but can occur after immunizations as well

129
Q

MRI in ADEM

A

multiple bilateral hyperintense T2-weighted lesions with poor margins and variable enhancement

130
Q

hyperacute variant of ADEM

A

acute hemorrhagic leukoencephalitis (Hurst’s disease)
unlike traditional ADEM will show hemorrhagic lesions radiologically
pathology: perivenous infiltration of lymphocytes, inflammation, and demyelination

131
Q

ADEM vs MS/NMO

A

acute demyelinating lesions for MS are perivascular
acute demyelinating lesions for ADEM are perivenular

132
Q

progressive multifocal leukoencephalopathy (PML)

A

usually fatal infection of oligodendrocytes caused by reactivation of latent JC polyomavirus

133
Q

PML presentation

A

subacute progressions of encephalopathy, focal motor deficits, ataxia, diplopia, and/or hemianopia

134
Q

PML: CNS infection

A

established via hematogenous dissemination of the latent virus in the kidneys which then crosses the blood-brain barrier

135
Q

PML: who is at risk

A

patients with impaired immune systems: HIV, leukemia, and those on immunosuppresive agents (chemotherapy/monoclonal antibodies)

136
Q

JCV positive patients risks

A

natalizumab is high risk of causing PML when treatment is greater than 2 years
if on immunosuppressive medications at time of diagnosis should have medications discontinued and then consider PLEX to remove drug from circulation

137
Q

HIV-related PML

A

started on HAART therapy
restoration of immune function may result in immune reconstitution inflammatory syndrome (IRIS),

138
Q

immune reconstitution inflammatory syndrome (IRIS)

A

presents with worsening neurologic symptoms and contrast enhancing cerebral edema
IRIS occurs 3-6 weeks after treatment for PML and should be treated with high-dose IV steroids followed by an oral slow taper regimen

139
Q

PML: imaging

A

non-enhancing FLAIR lesions preferentially involving the white matter without mass effect

140
Q

PML: pathology

A

demyelination, bizarre astrocytes, and enlarged oligodendroglial nuclei with intranuclear inclusions
immunohistochemistry staining for the JC virus is considered the gold standard for diagnosis

141
Q

PML monitoring

A

JC virus PCR titers can also be used for diagnostic purposes and should be performed before biopsy if clinical suspicion is high

142
Q

central pontine myelinolysis

A

aka osmotic demyelination syndrome due to rapid correction of hyponatremia leading to demyelination of the base of the pons
extrapontine demyelinating lesions are infrequent but when present they are seen at cortical gray-white matter junctions

143
Q

central pontine myelinolysis seen in

A

alcoholics, end-stage renal disease, chronically malnourished patients, and patients undergoing hepatic transplant

144
Q

central pontine myelinolysis presentation

A

acutely with AMS, hypotension, and hypoventilation with progression to pseudobulbar palsy and quadriparesis
severe cases can progress to a locked in syndrome
no available therapies, but many patients improve over time

145
Q

what can be used for both ulcerative colitis and MS?

A

ozanimod

Neuro Boards (15 decks)

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