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RB Y3 1.2 Neurology > Multiple Sclerosis > Flashcards

Multiple Sclerosis Flashcards

1
Q

what is MS

A

autoimmune inflammatory disorder characterized by demyelination of the CNS

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2
Q

how are plaques distributed in the CNS?

A

widely throughout the CNS - non-anatomical locations

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3
Q

describe the plaques

A

well circumscribed, firm, grey lesions

they vary greatly in size and location etc

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4
Q

where is a common location for plaques

A

cerebral white matter, around lateral ventricles

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5
Q

outline the pathophysiology

A
  • T cells from the periphery enter the CNS through a defective BBB and mount an immune attack on the oligodendrocytes - inflammatory reaction
  • this results in demyelination of neurons with relative preservation of axons
  • the immune attacks will typically happen in bouts, before the body stops teh attack
  • early on in disease the oligodendrocytes heal (=relapsing and remitting features),but over time the oligodendrocytes die and axons beign to be damaged(= chronic disease progression)
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6
Q

how do astrocytes respond to injury

A
  • with reactive astrogliosis - astrocytes undergo changes: cell hypertrophy, proliferation, cell body swell etc
  • this forms a glial scar
  • which further inhibits remyelination and axonal regeneration - disease further progresses
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7
Q

aetiology of MS

A

not fully known - combination of genetic and environmental factors

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8
Q

most common age and sex

A

female, 3rd and 4th decade

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9
Q

geographically, where are you at greater risk

A

countries further away from the equator (asscoiated with low levels of sunlight and vitamin D)

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10
Q

is there a familial component?

what genes are involved

A

it is 30x more common in 1st degree relatives

multiple genes, including HLA genes

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11
Q

which specific HLA gene is implicated

A

HLA DRB1

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12
Q

what role do viruses play in the aetiology of MS, and which virus is it linked to in particular

A
  • viral infections can precipitate MS relapses in someone and can also trigger MS development in a genetically susceptible individual
  • EBV
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13
Q

what other environmental factor is MS development linked with?

A

lack of sunlight exposure and low vitamin D levels

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14
Q

outline the disease course

A
  • highly variable
  • Most patients initially present a relapsing-remitting clinical course. Relapses can be induced, e.g. by stress, and early on show complete recovery.
  • After 10-15 years of the disease, the pattern becomes progressive with less recovery, during which time clinical symptoms slowly deteriorate.
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15
Q

what is the most common type of MS

A

RRMS

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16
Q

RRMS

  • how do attacks and recovery last
  • how many relapses a year
A
  • attacks (relapses) usually occur over a few days and recovery takes a few weeks - partial or complete
  • usually pts have around 1 relapse a year
  • if relapses dont recover fully, disability can accumulate over time
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17
Q

benign MS

A

in RRMS, patients go without relapses for a few years - benign MS

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18
Q

compare the pathological ativity of RRMS and PPMS

A

RRMS shows the most inflammatory activity. PPMS is thought to be a primarily degenerative process and shows less inflammation

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19
Q

2y progressive MS

A

75% of RRMS patients will develop this around 35 years after disease onset - damage is not recovered from fully and disability accumulates

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20
Q

PPMS

A

this is a less common type, a primarily progressive disease, gradually worsening of disability without any relapse or regression

this tends to present later in life

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21
Q

what are some poor prognostic signs

A

older age, motor signs at onset, many relapses early on, lots of MRI lesions, axonal loss

22
Q

outline the criteria for diagnosis

A
  • At least 2 episodes suggestive of demyelination, there must be dissemination in time and place (attack >1hr, >30days between)
  • Unattributable to other cause
23
Q

when is the McDonald criteria used

A

mainly for research purposes, rarely in clinical practice

24
Q

what is the classical presentation

A

temporary visual loss/optic neuritis or sensory symptoms

presentation is often monosymptomatic

25
Q

what are the classical ophalmic features

A
  • optic neuritis (unilateral, pain on moving eye, red desaturation)
  • graying/blurring of vision
26
Q

sensory symptoms

A
  • pain
  • paresthesia
  • patch of wetness/burning
  • DCML loss
  • numbness
  • trigeminal neuralgia/neuropathy
  • L’hermitte sign
27
Q

what is l’hermitte sign

A

electrical shock on neck flexion

28
Q

what is a classical motor sign

A

muscle cramping and weakness

foot dragging/slapping after long periods of walking, resolves with rest

29
Q

what is teh Uthoff phenomenon

A

symptoms worsen due to increase in temperature eg after exercise or hot shower

30
Q

urinary problems

A
  • LUT dysfunction: bladder hyperreflexia causing urge incontinence: frequency, nocturia, urgency, retention
31
Q

why are UTIs more common

A

stagnant urine due to urinary retention

32
Q

primary and secondary causes of fatigue

A

primary due to demyelination

secondary due to poor sleep hygiene, depression, restless legs, urinary frequency etc

33
Q

name some differentials

A
  • Myelopathy due to cervical spondylosis
  • Fibromyalgia – vague symptoms, generalised weakness and non-specific fatigue
  • Sleep disorders
  • Vasculitis
  • Granulomatous disorder
  • Vascular disease
  • Structural lesion
  • Infection
  • Metabolic disorder
34
Q

first line assessment

A

MRI brain and spinal cord

  • hyperintensities in the periventricular white matter - multiple scattered plaques
35
Q

drawbacks of MRI

A

sensitive but not specific

may be susceptible to over interpretation in the absence of clincal correlation

36
Q

LP results

A

oligoclonal bands on CSF electrophoresis in 90% cases

note, these are not specific to MS

37
Q

why dowe do blood tests and what blood tests do we do

A

to exclude alternate diagnoses/concomitant illnesses

  • PV, FBC, CRP, TSH
  • Renal liver bone profile
  • Auto antibody screen
  • Borellia, HIV, syphilis serology
  • B12 and folate
38
Q

lifestyle modifications

A

most patients benefit from regular exercise programme

good sleep hygiene to try to challenge fatigue

39
Q

management of an acute relapse

A

a short course of steroids will help speed recovery, but not influence long term outcome

  • oral prednisolone or IV methylprednisolone for more severe cases
40
Q

management of weakness and spasticity

A
  • physiotherapy
  • gabapentin (anti convulsant)
  • baclofen
41
Q

what does botulinum toxin do

A

causes flaccid paralysis

42
Q

management of sensory symptoms

A
  • Anti-convulsant e.g. gabapentin
  • Anti-depressant e.g. amitriptyline
  • Tens machine – pain relief using a mild electrical current
  • Acupuncture
  • Lignocaine infusion (anaesthetic)
43
Q

mangement of LUT dysfunction

A
  • bladder training
  • anti-muscarinics eg oxybutynin, tolertodine - improve frequency and urgency
  • desmopressin (decrease urine production)
  • catheter
44
Q

how do anti muscarinics help bladder problems

A
  • Normal bladder voiding involves stimulation of the muscarinic receptors on the detrusor muscle by ACh (detrusor muscle has parasympathetic innervation). ACh is still released during involuntary contractions. Blocking muscarinic receptors also affect efferent control on detrusor contraction but improve afferent regulation.
45
Q

what is the purpose of DMARDs

A

they reduce relapses, development of new MRI lesions and accumulation of disability

46
Q

how are DMARDs administered

A

SC or IM injection - can be self administered

47
Q

are DMARDs well tolerated

A

generally, apart from flu like side effects and injection site irritation

48
Q

first line DMARDs

A
  • Interferon Beta – Avonex, Rebif, Betaseron, Extavia
  • Glitiramer Acetate (Copaxone)
  • Tecfedira (oral)
49
Q

when are 2nd line DMARDs used - monoclonal Ab and Fingolimod

A

very aggressive MS - although they have high efficacy in preventing relapses and reducing disability accumulation they may have the potential to cause serious adverse side effects

50
Q

2nd line DMARDs

A
  • Monoclonal antibody – Tysabri, Lemtrada, Zymbrata
  • Fingolimod
51
Q

first line management of neuropathic pain

A

gabapentin

52
Q

management of fatigue

A

amantidine

modafinil if excessive day time sleepiness

RB Y3 1.2 Neurology (23 decks)

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