Multiple Sclerosis Flashcards

1
Q

What is the epidemiology of MS?

A
  • Chronic cell-mediated autoimmune disorder characterised by demyelination of CNS
  • 3:1 women
  • Common age of onset 20-40yrs
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2
Q

What are the types of MS?

A
  1. Relapsing-remitting: most common, acute attacks (e.g. 1-2 months) followed by remission
  2. Secondary progressive: relapsing-remitting who have deteriorated and developed neurological signs and symptoms between relapses, gait and bladder disorders generally seen
  3. Primary progressive: progressive deterioration from onset, more common in older people
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3
Q

When can you diagnose MS?

A

If >/=2 relapses and either; objective clinical evidence of >/=2 lesions or objective clinical evidence of one lesion together with reasonable historical evidence of previous relapse.

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4
Q

What are the visual symptoms of MS?

A
  • Optic neuritis - pain on eye movement, blurring of vision, red colour saturation
  • Hemianopia, diplopia
  • Uthoff’s phenomenon (worsening of vision after rise in body temp)
  • Intranuclear ophthalmoplegia (INO) (lesion in medial longitudinal fasiculus, results in impaired abduction of ipsilateral eye, contralateral eye abducts but with nystagmus)
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5
Q

What sensory symptoms are there in MS?

A
  • Pins/needles
  • Numbness
  • Trigeminal neuralgia
  • Decreased vibration sense
  • Lhermitte’s syndrome (paraethesia in limbs on neck flexion)
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6
Q

What symptoms are there in MS?

A
  • Spastic weakness - most common in legs
  • Cerebellar ataxia + tremor
  • Urinary incontinence
  • Sexual dysfunction
  • Intellectual deterioration
  • Swallowing disorders
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7
Q

What are the investigations for MS?

A
  • MRI: high signal T2 lesions, periventricular plaques, Dawson fingers (hyper intense lesions to the corpus callosum)
  • CSF: oligoclonal bands (+ not in serum), increased intrathecal synthesis of IgG
  • Visual evoked potentials: delayed but well preserved waveform
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8
Q

What is the management for acute relapse of MS?

A

High dose steroids e.g. PO or IV methyl prednisolone
- Inpatient: IV methyl prednisolone 1g IV daily for 3 days - given in morning as can cause sleep disturbance
- Outpatient: PO methyl prednisolone 500mg for 5 days
Check for infection before commencing steroids.

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9
Q

Where is the lesion to cause loss of vision in one eye?

A

Anterior to the optic chias, therefore in the right optic nerve, retina or eye itself (if blind in right eye). A lesion at or behind the chias that causes visual impairment would affect both eyes.

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10
Q

What is a relative afferent pupillary defect (RAPD)?

A

Sign of optic neuropathy (damage to CNII). Can be detected by swinging light test.
In an eye affected by optic neuropathy the pupil paradoxically dilates when light is shone into that eye as the direct stimulus (light via ipsilateral damaged optic nerve) is weaker than the indirect stimulus (light via intact contra lateral optic nerve).

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11
Q

What does vertigo and nausea show?

A
  1. Vestibular pathology: vertigo is principle symptom. Patients may describe spinning or feeling world around them is moving, often associated with nausea. Vertigo can be made worse by head movement in vestibular pathology (also maybe hearing loss +/- tinnitus)
  2. Cerebellar lesion: patient may be aware their voice has changed (staccato dysarthria), poor coordination in arms, unsteadiness whilst walking, ask if one side of body feels worse than the other, in unilateral Cerebellar lesions patient will have ataxia in ipsilateral arm and leg
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12
Q

What symptoms would sensory ataxia show?

A
  • History of sensory disturbance (numbness, pins + needles etc) in limbs or trunk
  • Balance is worse in dark or if they are not looking at their feet
  • May find they fall over when close their eyes e.g. when washing face at sink/in shower
  • Lesion in spinal cord: Lhermitte’s phenomenon (tingling sensations upon flexion and extension of the neck) or tight band-like sensation around torso
  • Bladder urgency and frequency of micturition
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13
Q

What are the side effects of steroids?

A
  • GI irritation (PPI given alongside)
  • Common to experience some agitation, restlessness and insomnia
  • Steroid psychosis (rare)
  • Hyperglycaemia (with prolonged steroid use)
  • Avascular necrosis of femoral head
  • Hypertension
  • Osteoporosis
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14
Q

What is the action of baclofen?

A
  • Used to treat spasticity - common in MS and other CNS disorders. It can be uncomfortable as well as limiting movement.
  • Baclofen is effective in treating it but the main drawback is the doses needed to successfully reduce more severe spasticity can be very sedative
  • Alternatives are tizanidine or dantrolene
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15
Q

What is neuropathic pain?

A

Described as burning or stabbing and is often accompanied by other symptoms such as paradoxical numbness, paraesthesia, hyperpathia (increased sensitivity to painful stimuli) and allodynia (when a non painful stimuli is painful).

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16
Q

What is the mechanism of oxybutinin?

A

Anticholinergic drug that can reduce urinary frequency and urgency in patients with neuropathic bladder (in MS). Can cause incomplete bladder emptying which results in pool of residual urine and makes bladder prone to UTIs. Before prescribed do a post micturition bladder scan.

17
Q

What are the treatments for neuropathic pain?

A
  • Gabapentin/pregabalin
  • TCAs e.g. amitriptyline
  • In face related to trigeminal nerve can use carbamazepine or oxcarbazepine
  • SNRI duloxetine
  • Capsaicin cream
  • Lidocaine patches
18
Q

What are the brain stem symptoms of MS?

A
  • Vertigo
  • Slurred speech
  • Ataxia
  • Incoordination
  • 3rd/4th/6th nuclei - double vision
19
Q

What are common sites of demyelination in MS on an MRI?

A
  • Corpus callosum
  • Optic nerve
  • Cerebellum
  • Brainstem
  • Spinal cord
  • Periventricular, juxtacortical
20
Q

What would be the results of an LP in MS?

A
  • CSF cell count: WCC <50x10^6ml
  • CSF protein: <1g/ml
  • CSF/serum glucose ratio: >0.4
  • Oligoclonal bands in CSF
21
Q

What are the evoked potentials results in MS?

A
  • Visual evoked potentials: delayed in demyelination in anterior visual pathways
  • Somatosensory evoked potentials: assess the posterior column of spinal cord, brainstem and cerebral cortex - delayed in damage to one of these structures
22
Q

What is the disease modifying therapy options for MS?

A
  • Dimethyl fumarate for mild/moderate relapsing-remitting MS
  • Monoclonal antibodies alemtuzumab and natalizumab for relapsing-remitting MS
  • Interferon beta and glatiramer recommended
23
Q

What symptom control medication can be used for MS?

A
  • Spasticity: baclofen or gabapen, tizanidine or dantrolene are 2nd line
  • Tremor: botulinum toxin
  • Urgency/frequency: if post micturition residual urine >100ml, teach intermittent self catheterisation, if <100ml try tolterodine
  • Fatigue: amantadine, CBT, exercise
24
Q

What are the SEs of alemtuzumab and natalizumab?

A
  • Alemtuzumab: development of autoimmune diseases e.g. thyroid, good pastures
  • Natalizumab: development of progressive multi focal leukoencephalopathy caused by SC virus - oedema and necrosis of brain
25
Q

What are the locations and symptoms of lesions?

A
  • Lumbar spine: lumbar nerve root/cauda equina syndrome
  • Brainstem: cranial nerve or Cerebellar symptoms/signs
  • Cervical spine: upper limb symptoms/signs included
  • Thoracic spine: signs in legs, sensory level at costal margin
26
Q

What is Devic’s syndrome?

A

MS variant with transverse myelitis (loss of motor, sensory, autonomic, reflex and sphincter function below level of the lesion), optic atrophy and anti-aquaporin 4 antibodies

27
Q

What is Charles Bonnet syndrome?

A

Decreased acuity/temporary blindness +/- complex visual hallucinations of faces, animals, plants, trees

28
Q

What is the pulfrich effect?

A

Unequal eye latencies, causing disorientation in traffic as straight trajectories seem curved and distances are misjudged on looking sideways.