Multiple Sclerosis Flashcards

1
Q

What is MS? What is the underlying pathophysiology?

A

Chronic progressive AI condition of the CNS

Inflammation and infiltration of immune cells leading to damage to the myeline surrounding CNS neurones (oligodendrocytes provide the myleine for CNS)
Damage to myeline affects the electrical signalling leading to functional deficit
Re-myelination can occur in early disease meaning the symptoms resolve
Later disease stages means re-myelination is not possible and the symptoms become more permenant

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2
Q

What is the characteristic about the presentation of MS over time?

A

Symptoms change due to the lesions being disseminated in time and space
I.e. lesions vary in location over time

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3
Q

What are the causes of MS?

A
Multiple genes i.e. HLA DBR1*1501
EBV
Low vitamin D
Smoking 
Obesity
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4
Q

What is the typical time course of symptoms presenatation in MS?

A

Progess over more than 24hrs

Symptoms last days-weeks at 1st presentation

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5
Q

How and what might someone with MS present with?

A

Optic neuritis
-most common presentation

Eye movement abnormalities
-diplopia due to CN6 lesion
I.e. CN6 palsy presents with: internuclear opthalmoplegia and conjugated lateral gaze disorder

Focal weakness

  • Bell’s palsy
  • Horners syndrome
  • limb paralysis
  • incontinence

Foal sensory symptoms

  • trigeminal neuralgia
  • numbness
  • parasthesia
  • Lhermitte’s sign

Sensory ataxia
-loss of proprioceptoive sense

Cerebellar ataxia
-cerebellar lesion

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6
Q

What is Lhermitte’s sign and why does it occur in MS?

A

Electric shock sensation down spine and limbs when flexing neck

Due to stretching of demyelinated dorsal column

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7
Q

What is internuclear opthalmoplegia and why does it occur?

A

Uncoordinated eye movement meaning that when moving eyes laterally one eye will remain fixed in position due to inability to adduct

Damage to interneurone connecting the cranial nerve nuclei for CN6 + CN3, which leads to problems with coordination
(Extra= interneurone called medial longitudinal fasciculus)

Opthalmoplegia
-problems with muscles around the eyes

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8
Q

What is conjugate lateral gaze disorder?

A

Disordered movement of the eyes when looking laterally which occurs in 6th nerve palsy

Eye on side of lesion not able to abduct
Eg if left eye affected and asked patient to look laterally to left, the right eye (uneffected) will adduct towards the left but the left eye will remain forwards due the muscle responsible for moving it laterally not being able to function

This is what occurs secondary to internuclear opthalmoplegia

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9
Q

What are the differrent classifications of disease pattern for MS?

A

Clinicaly isolated syndrome

  • 1st episode of demyelination and neurological signs
  • cannot diagnose MS from one episode as does not fit the criteria that the disease is disseminated in time and space

Relapsing-remitting

  • most common pattern
  • episodes of disease followed by recovery
  • classified based on whether disease is active or worsening

Secondary progressive

  • relapsing and remitting which is now progessed to worsening symptoms of with incomplete remission
  • classified based on whether active +/- progressing

Primary
-worseing of disease and neurological symptoms from point of diagnosis without initial relapses or remissions

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10
Q

How is MS diagnosed?

A

Symptoms suggesting the lesion is changing location over time
Dissemination in time and space
MRI support
Relapsing symptoms
Progressive over 1 year period for primary progressive
Exlcusion of other causes of symptoms

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11
Q

What investigations can be done when MS is suspected?

A

Visual evoked potentials (VEPs) and somatosensory evoked potentials (SSEPs) can highlight delay in conduction due to demyelination

Lumbar puncture
-Oligoclonal bands= antibodies characteristic of inflammatory process of MS

Optical coherance tomography (OCT)

Biomarkers I.e. light chains

NMO IgG
-helps to differentiate NMO (neuromyelitits optica) which can have similar presentation to MS

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12
Q

What pathophysiological changes are associated with early and late disease? How might the character of the diseae change?

A

Early:

  • inflammation and demyelination
  • relapses

Late:

  • atrophy, axonal loss and increasing tissue destruction
  • progressive disability i.e. increase in disability changes with gradual decrease in axonal loss

NOTE: atrophy is present throughout the disease but only reaches disability threshold in later stages of disease

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13
Q

What is optic neuritis and why is it associated with MS?
What are the key presenting features of optic neuritis?
What are the other possible causes?
How is it treated?

A

Demyelination of the optic nerve and associated inflammation

  • Central scotoma= enlarged blind spot i.e. can be described as enlarging black cloud = ACUTE LOSS/REDUCTION OF VISION in one eye
  • Pain on eye movement
  • impaired colour vision

Steroids= should recover w/i 2-6 weeks

-relative afferent pupillary defect (RAPD)= test for with swinging light test i.e. parodxymal dilation in response to light

Other causes:

  • sarcoidosis
  • SLE
  • diabetes
  • syphilis
  • measles
  • mumps
  • lyme disease
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14
Q

What are the 2 types of management for MS?

A

Symptomatic management:
-controls sensory disturbances, spasticity, sphincter dysfunction, fatigue and depression

Disease modifying drugs + biological therapy
-aims to induce long-term remission
Eg= Beta-interferons, MAbs, inflammatory cytokines

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15
Q

What are examples of symptomatic treatments for MS?

A

Exercise= maintain activity + strength

Neuropathic pain
-amitriptyline or Gabapentine

Depression
-antidepressants i.e. SSRIs

Urge incontinence
-anticholinergic i.e. Tolterodine or Oxybutynin

Spasticity
-baclofen/gabapentin/ physiotherapy

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16
Q

How do you treat MS relapses?

A

Steroids:
-methylprednisolone 500mg daily for 5 days

NOTE: relapses are due to inflammation so makes sense to treat with steroids to reduce inflammation