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3P: Neuro > Multiple Sclerosis > Flashcards

Multiple Sclerosis Flashcards

1
Q

MS definitions and presentations

A
  • autoimmune de-myelination liaisons of CNS white matter (not PNS matter)
  • lesions (plaques) are multi focal (2 or more)
  • localization: any level of the CNS
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2
Q

Complaints of MS

A

Wide range of deficits on initial or recurring attacks

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3
Q

Temporal profile of MS

A
  • onset can be acute, but typically subacute or insidious

- course: typically episodic or cyclic, relapse-remitting, can become chronic and progressive

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4
Q

Diagnosis of MS

A

Starts with history and neuro exam evidence for 2+ lesions in CNS

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5
Q

OD significance of MS

A
  • MS is often preceded by transient episode of optic neuritis (visual loss)
  • MS often involves visual, pupillary, or oculomotor deficits
  • importance of recognizing that seemingly in-related deficits could be MS
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6
Q

Pathogensis of MS

A

-small breaches of BBB (possibly triggered by microglia) or blood CSF barrier (in choroid plexus) allow lymphocytes into CNS, followed by an AI attack involving damage to oligodendrocyte

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7
Q

Original hypothesis on specific mechanism of MS

A
  • Ab against Myelin Basic Protein

- T cells release cytokines toxic to oligodendrocyte

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8
Q

Secondary tissue changes in MS

A
  • following oligodendrocyte damage/death, macrophages attack debris and myelin sheath.
  • astrocytes form glial scar around zone of damage
  • axons can survive in non-myleinated state, or there can be axonal damage as well
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9
Q

Distribution of MS

A

Multi-focal

-evidence for 2 or more focal lesions in the CNS

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10
Q

Temporal profile of MS

A
  1. 2 or more attacks separated by > 1m apart or

2. Chonric and progressive lasting at least 6 months

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11
Q

Complaints in MS

A
  • visual, cognitive, psychiatric, motor, sensory, pain
  • visual system: visual loss localizing from optic disc to visual cortex
  • mental status: cognitive impairments, psychiatric symptoms
  • cranial nerves: motor, sensory deficits, vertigo, pupillary dysregulation
  • motor systems: weakness, fatigue, impaired coordination/balance
  • sensory systems: generally sensory loss, also parenthesia/pain
  • autonomic dysfunction: bladder, bowel, sexual
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12
Q

Common presentations of MS with optometric significance

A
  • history of optic neuritis episode
  • pupillary constriction of dilation deficits, horners syndrome
  • EOMS: nerve palsies, conjugate gaze palsy, internuclear ophthalmoplegia
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13
Q

Common precursor to MS

A

Optic neuritis

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14
Q

____ of patients with optic neuritis later develop MS

A

50%

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15
Q

Inflammatory de-myelination of the optic nerves

A

Optic neuritis

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16
Q

Etiology of optic neuritis

A
  1. Inflammatory process triggered during or after resolution of viral infection
  2. Pro inflammatory chemical exposure
  3. Vitamin B12 deficiency
17
Q

Onset of optic neuritis

A

Typically 30-45 years, but can be later

18
Q

Gender and optic neuritis

A

2x more likely in females

19
Q

Visual loss due to optic neuritis

A

Usually monocular vision loss, central scotoma, reduced acuity around scotoma, impaired color detection, can be complete monocular vision loss

20
Q

OD exam for optic neuritis

A

Depends on whether inflammation extends to optic disc or is limited to retro-bulbar segment of optic nerve. Thus, optic disc can be swollen and inflamed or normal. Prior episodes can lead to optic disc pallor

21
Q

Exacerbating or precipitating factors for optic neuritis

A 
Infection
Heat or over heating (VF deficits especially sensitive) 
Dehydration 
Sleep deprivation
Anemia 
Dietary factors
22
Q

Heat induced transient vision loss

A

Uthoff phenomenon

Transiently induced by hot bath

23
Q

Temporal profile of optic neuritis

A
  1. Cyclic/episodic, relapse-remitting

2. Chronic and progressive, aka “primary progressive MS”

24
Q

Less severe outcomes of MS

A

If 1st attack had an acute onset, few types of symptoms/signs, predicts rapid/complete remission. More likely to follow relapse-remitting course. Caveat to “less severe” prediction: relapse-remitting patient’s can potentially develop secondary progression MS where plaques become permanent lesion sites

25
Q

More severe outcomes of MS

A

If 1st attack was more gradual (subacute or insidious), multiple functional systems affected, spinal cord involvement, more at risk for primary progressive MS

26
Q

Epidemiology of MS

A
  • 1:1000
  • 2x more in females
  • 20-40y
  • more common in caucasians, especially in higher latitude regions
  • genetic risk: siblings 2.6% risk, more in twins
  • mutations in IL-2 and IL-7 possibly
27
Q

Diagnostic criteria for MS

A
  • MRI evidence or 2 or more plaques in white matter
  • Evoked potential findings: reduced conduction velocity
  • CSF analysis by electrophoresis: “oligoclonal bands”
28
Q

MRI of 2 or more white matter plaques in MS

A
  • plaques can be supratentorial, infratentorial, or in spinal cord
  • often appear as fingers extending from periventricular zones
  • MRI with contrast (gadolinium) can highlight plaques
  • plaques can heal or can stabilize and become permanents lesions
29
Q

Evoked potentials for MS

A

Reduced conduction velocity (increased latency)

-visual, auditory, or somatosensory evoked potentials

30
Q

CSF analysis by electrophoresis in MS

A

Oligoclonal bands

  • increased protein, increased IgG, normal or increased lymphocytes
  • elevated lymphocytes: up to 50 cells per ul
  • oligoclonal bands refers abnormal bands at specific molecular weights
  • bands-large amounts of same immunoglobulin (IgG) being produced
  • 85% sensitivity for MS
  • 92% specificity for MS
31
Q

Short term treatment for MS

A

For acute attack (Rapid onset)

  • glucocorticoids: methylprednisone or prednisone
  • rapid and potent immunosuppressive strategy
32
Q

Long term treatment for MS: 1st line

A

Interferon 1-beta

  • increases suppressor T cells systemically
  • decreases lymphocytes invasion of CNS across barriers
  • decreases inflammatory cytokines from T cells
  • decreases antigen presentation mechanisms
33
Q

Long term treatment for MS: 2nd line

A

Being developed

  • off-label use of chemotherapies to reduce lymphocyte proliferation
  • targeting enzymes in lymphocytes to reduce proliferation, invasion, inflamamtion
  • monoclonal Ab to neutralize lymphocyte-mediated inflammation
  • Ab of mature oligodendrocyte from glial stem cells, increasing oligodendrocytes
34
Q

Differential Dx in MS

A

Overlap among MS and other neuoimmunological and demyelinating diseases

  • neuromyelitis optica
  • acute disseminated encephalmyelitis (ADEM)
  • progressive multifocal leukoencephaolopathy
35
Q

Neuromyelitis optica as a DiffDx for MS

A

AI disease involving Ab against aquaporin-4. Lesion localization is specifically combination of optic nerve and spinal cords. Multi focal and stable

36
Q

Acute dissemination encephalomyelitis (ADEM) as DiffDx for MS

A

AI mechanism triggered by recent infection or VAx, attacks against gray matter as well as whit matter, rapid onset of neuro signs, initally focal or multifocal signs then diffuse localization/ distribution. Can be stable or remission

37
Q

Progressive multifocal leukoencephalopathy as diffdx for MS

A

Viral infection of the CNS that evidently most affects oligodendrocytes. Chronic progressive course of white matter damage/lesions

3P: Neuro (11 decks)

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