College aantekeningen

Lecture Notes - Clinical Immunology - Multiple Sclerosis

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Clinical Immunology

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Vrije Universiteit Amsterdam (VU)

Clinical aspects of multiple sclerosis (including treatment approaches), the animal models for MS, pathology of MS, theoretical concepts of MS

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multiple sclerosis
clinical immunology
vu amsterdam optional course

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CLINICAL IMMUNOLOGY

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1. College aantekeningen - Lecture notes - clinical immunology - multiple sclerosis
2. College aantekeningen - Lecture notes - clinical immunology - hiv & cancer
3. College aantekeningen - Lecture notes - clinical immunology - ibd & celiac disease
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CLINICAL IMMUNOLOGY
Topic 1: Multiple Sclerosis
LECTURE 1: OVERVIEW OF MS CLINICAL ASPECTS Monday, 28/10/2019
Affects 2-3 million individuals globally  1:1000 in the Netherlands diagnosed with MS; affects women more
than men (2-3 : 1), disease of the young (20-40 yo)

CNS disease in the spinal cord; primary
pathology: INFLAMMATORY
DEMYELINATION of axonal myelin 
disrupted axonal function due to
demyelinating lesions, detectable in MRI

Secondary pathological process: NON-
INFLAMMATORY DEGENERATION  not so
visible in MRI; seen as atrophic lesions only if
it’s severe enough

Degeneration in MS: chronic demyelination of axons + gliosis of astrocytes + chronic activation of microglia
MRI localizations to look for MS lesions:
a. Periventricular
b. Juxtacortical – cortical (below or in the cerebral cortex)
c. Infratentorial (cerebellum & brainstem)
d. Spinal cord

Causes of MS:
a. Familial  e.g. in monozygotic twins, 30% chance to develop MS among them, 2-5% increased risk if a
first-degree relative is affected
b. Environmental  further away from equator, lower vit D status affect the risk of MS; viruses (EBV),
smoking (also associated with worse MS outcome), early obesity (e.g. since childhood)
c. Genes  HLA region on chromosome 6 (also associated with many other autoimmune diseases, in
addition to MS); allelic variants in HLA-DRA locus is identified as risk factors for MS development –
more variants = more likely to develop MS

Symptoms of MS:
a. Optic neuritis (70% of all cases complains of having this; if one
has optic neuritis, there’s 50% chance to have MS diagnosis
later, thus require thorough MRI scan)  decreased acuity,
central blurry-ness, loss of colour discrimination, retroorbital
pain
Eye movements disorder  diplopia (d/t brainstem MS
lesion, usually in younger patients)
b. Lhermitte’s sign (if lesion in spinal cord)  flexing the neck
(extend the spinal cord) causes the “electrical transmission”
down the back; MS suspicion if Lhermitte (+) in young patients,
Ddx for Lhermitte (+):
c. Motor symptoms (d/t demyelinating lesions down the motor
tract)  loss of strength
d. Bladder-sexual dysfunction (one of the most common) 
incontinence, sexual dysfunction
e. Psychological function disorders  attention deficit, memory
loss, disturbed language functions, unable to multitask/slower
functioning
f. Fatigue (most common – albeit invisible): high impact, but
cause is unknown

, CLINICAL IMMUNOLOGY
Topic 1: Multiple Sclerosis
Symptoms arise due to inflammation within CNS  semi-acute attack; origin: optic nerve, brain stem, spinal
cord. Mostly comes to the clinic with exacerbation of neurological symptoms  keep on increasing over a few
weeks, then stagnates (complete/incomplete remission) before it comes up again

MS courses:
a. RRMS (relapsing remitting MS – most
common)  inflammatory
predominance; unpredictable accidents
b. SPMS (secondary progressive MS) 
degenerative predominance
c. PPMS (primary progressive MS) 
typically older, male patients

How to diagnose MS:
Dx criteria: McDonald criteria (see below)

Monitored over 1 year

Diagnosis of MS has to be
reassured, both clinically &
radiologically, before
communicating to the patient 
report this as CIS/clinically
isolated syndrome (symptoms +
w/o radiological evidence) or
RIS/radiological isolated
syndrome (radio + w/o
symptoms)

, CLINICAL IMMUNOLOGY
Topic 1: Multiple Sclerosis
Presence of oligoclonal bands in CSF  if
oligoclonal bands concentration is high,
it is indicative for MS tx
Oligoclonal band: proteins that present
when there is inflammatory lesion of
CNS, when coupled with demyelinating
lesion evidence in MRI and/or MS
symptoms = MS

Other cases that allows presence of
oligoclonal band in CSF: … (?)

Has to make sure of both “dissemination in space & time”
a. Dissemination in space  demyelinating lesions visible in 2 out of 4 localizations in MRI
b. Dissemination in time  >1x relapse OR new lesions on follow-up MRI, contrast-enhancing lesion +
non-enhancing lesions at the same time
Contrast-enhancing lesion: active lesion/newly formed
Non-contrast-enhancing lesion: older lesion, but we don’t know how old

Tx aimed at RIS/CIS has to be weighed carefully
 harm vs. benefit, although the risk of MS
development in those with RIS/CIS history is
very high

Diagnosis of PPMS has different Dx criteria:
a. Progression (+)
b. 2/3 the criteria above (time OR space OR
oligoclonal band)

MS follow up:
a. Clinical: frequency depending on
severity
b. Radiological (after 3 months)
c. Biochemical (biomarkers: neuro filament
light  elevated when axon is broken
down, increased in serum & CSF)

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