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Dunedin RACP Study Course > MS > Flashcards

MS Flashcards

1
Q

Common PO therapies MS

A

Fingolimod,
Teriflunomide,
Dimethyl Fumuarate,
Cladribine

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2
Q

Clinical Features MS

A

– sensory, motor, cerebellar, cognitive

– optic neuritis

– internuclear ophthalmoplegia

– acute partial myelopathy

– partial/almost complete resolution of deficits with MS

– Lhermitte’s & Uhthoff’s symptoms

– Exercise induced symptoms

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3
Q

Smoking and MS

A

Increased relapse rate in smokers

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4
Q

Mimickers of MS

A

Neuromyelitis Optica Spectrum Disorder (NMOSD) - Separate disease
- NMO antibodies to aquaporin 4

Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD)
- separate disease

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5
Q

Classic MRI findings in MS

A

Characteristic sites
– periventricular, corpus callosum, centrum semiovale
– radiating out from corpus callosum = Dawson’s fingers
– brainstem, cerebellum

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6
Q

Test in MS

A
  • Magnetic Resonance Imaging
  • Evoked Potentials (EPs) - good to find lesions you can’t see clinically or on MRI
    – VEP = visual EP (optic neuritis – subclinical disease)
    – SEP = somatosensory (limbs)
    – BAER = brainstem EP = auditory pathways.
  • Central Motor Conduction Time (CMCT)
    – motor pathways = corticospinal tracts to limbs
    – MEPs = Motor Evoked Potentials
  • Lumbar puncture - CSF
    – basic CSF studies normal, maybe a few lymphocytes.
    Oligoclonal bands +ve in CSF but NOT in serum, Increased CSF IgG synthesis.
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7
Q

Other Ddx for MS

A

– NMOSD & MOGAD

– Inflammatory diseases
* SLE, Sjogren’s, PAN, Behcet’s, ADEM etc

– Infectious diseases
* HIV, HTLV 1, PML, Lyme disease, Syphilis

– Granulomatous disease
* Sarcoidosis, Wegener’s granulomatosis

– Diseases of Myelin
* Adrenoleukodystrophy, Metachromatic Leucodystrophy

– Miscellaneous
* Spinocerebellar ataxia, vitamin B12 deficiency, ACM, mitochondrial cytopathy, vascular disease, CADASIL, Susac’s syndrome etc etc

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8
Q

Pregnancy and MS

A

– Relapse rate reduced during pregnancy, especially in 3rd trimester.

– Increase in relapse rate in 6 months after delivery

– No increase in sustained neurological disability due to pregnancy

– No increase in
* stillbirths, ectopic pregnancy, etc

  • Discontinuation of DMTS before attempting a planned pregnancy is usually recommended
  • Caution in using Gonadotropin-releasing hormone (GnRH) protocols for IVF in women with MS as this may significantly increase the MS relapse rate
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9
Q

MS Poorer Prognostic Factors

A
  • Demographics
    – Male
    – Older than 40 years at onset of disease
  • Relapse Characteristics
    – Frequent relapses early in disease course
    – Multifocal relapses
    – More severe relapses
    – Shorter inter-attack interval
    – Poorer recovery from relapses
  • Disease Course
    – Rapid accrual of disability
    – Progressive rather than relapsing remitting course from onset
  • MRI Features at onset predicting poorer prognosis
    – High T2 lesion load
    – >2 GAD enhancing lesions
    – >T1 hypointense lesions (“Black Holes”)
    – Early atrophy
    – Infratentorial as opposed to supratentorial lesions
  • MRI Features during Treatment predicting poorer prognosis
    – New T2 lesions
    – >1 GAD enhancing lesion
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10
Q

MS treatment acute exacerbations

A

PO/ IV steroids

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11
Q

Natalizumab brand/ MOA

A

Tysabri (alpha 4 integrin antagonist)

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12
Q

monoclonals in MS

A

Alemtuzumab, Rituximab, Ocrelizumab

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13
Q

Sx of PML

A

Progressive multifocal leucoencephalopathy

  • Rapidly progressive demyelination in brain
  • Dementia, motor dysfunction, visual loss
  • Previously mortality 30-50% in 3 months if untreated & late Dx
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14
Q

Patients who get PML

A

immunocompromised
- AIDS,
- transplant Pt,
- Immune system altering drugs eg , MS Pt on DMTs

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15
Q

Alemtuzumab MOA

A

Humanised monoclonal Ab binds CD52 (on B cells)

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16
Q

AE Alemtuzumab

A

– 2-3% ITP ( may be fatal)

– 20-30 % autoimmune thyroid disease at 5 years

– DON’T give live vaccines after Alemtuzumab Rx

– Listeria meningitis & cryptosporidial infections (rarely)

– Immune mediated conditions including hepatitis and haemophagocytic lymphohistiocytosis, bleeding in lungs, MI, stroke, arterial dissection and severe neutropaenia

16
Q

Ocrelizumab MOA

A

Humanized anti CD20 monoclonal antibody

  • Depletes B lymphocytes
17
Q

Fingolimod MOA

A
  • Decreases ability of lymphocytes to enter CNS by preventing the egress of lymphocytes from lymphatic tissues.
18
Q

Fingolimod AE

A
  • Potential serious cardiac side effects.
  • 1 st dose monitoring for bradycardia. Heart block.
  • OCT monitoring for macula edema (?1% Pts)
  • Need to have antibodies or to immunise patients against Varicella Zoster before Rx
  • > 15 PML cases reported so far
19
Q

Teriflunomide MOA

A

Inhibits pyrimidine synthesis (dihydroorotate dehydrogenase inhibitor)

20
Q

AE Teriflunamide

A
  • Hypertension
  • LFT & FBS abnormal
  • Alopecia, diarrhea

– X categorisation regarding pregnancy

– Prolonged half-life due to enterohepatic circulation

– Cholestyramine or activated charcoal can hasten elimination

21
Q

Dimethyl Fumarate MOA

A

Mechanism of action in MS is unclear.

22
Q

Dimethyl Fumarate AE

A

– Flushing -30%

– Self limited GI side effects -30%

  • Lymphocytes decrease by = 20-30% (possibly more)
    – Monitoring required
    – Discontinue if lymphocytes <0.5 for 6 months
23
Q

Pathophys NMO Disorder

A

Astrocytopathy – Aquaporin 4 Abs in high concentrations in foot processes of astrocytes along endothelial lining of blood brain barrier

Pathology is ?? complement mediated destruction of astrocytes with secondary demyelination

24
Q

demographics NMO Disorder

A

90% patients are women.

Disproportionately affects non-Caucasians.

25
Q

NMOD clinically vs MS and with Ix

A
  • Optic Nerve disease important (often more severe than ON in MS)
  • Spinal Cord disease important (often more severe than myelitis in MS)
  • May be significant pleocytosis on CSF. Usually no OCBs (maybe transientlypresent during a relapse).

Doesn’t respond to interferon or other MS treatments

NO decrease in chance of relapse during pregnancy (cf MS)

NMOSD has a worse prognosis than MS

– 50% walking problems at 5 years

26
Q

MOGAD

A

Myelin Oligodendrocyte Glycoprotein Associated Disease

– MS mimicker (screen ?MS patients for this & for NMOSD).
– Important to differentiate from RRMS

– ADEM presentation in children

– Opticospinal (NMO type) presentation in adolescents & adults

– Maybe monophasic or recurrent disease course

27
Q

Pathophys MOGAD

A

– Oligodendrocyte directed pathology = Oligodendrocytopathy

28
Q

MS and vaccinations

A
29
Q

Basic INO presentation

A

– complex eye movement disorder
* loss or slowed aDduction
* horizontal nystagmus of aBducting eye
* lesion in MLF on side of decreased Adduction
* if bilateral is usually coupled with vertical nystagmus on upward gaze.

– maybe bilateral or unilateral

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