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Year 4 Neurology and Special Senses > Neuro: MS > Flashcards

Neuro: MS Flashcards

1
Q

What is multiple sclerosis?

A

Chronic and progressive condition that involves demylination of the myelinated neurones in the central nervous system.
his is caused by an inflammatory process inolving the acitvation of immune cells against the myelin.

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2
Q

Which patients are typicall effected by MS

A

Women under 50

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3
Q

When might women specifically see an improvement in MS symptoms?

A

During pregnancy and the post partum period

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4
Q

What is myelin?

A

Myelin covers the axons of neurones in the central nervous system.
This myelin helps the electrical impulse move faster along the axon.
Myelin is provided by cells that wrap themselves around the axons.

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5
Q

Which cells provide myelin?

A

Schwann cells - PNS

Oligodendrocytes - CNS

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6
Q

Which system does MS effect and therefore which cells?

A

CNS - the oligodendrocytes

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7
Q

Pathophysiology of MS

A

There is inflammation around myelin and infiltration of immune cells that cause damage to the myelin. This affects the way electrical signals travel along the nerve leading to the symptoms of multiple sclerosis.

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8
Q

What is the pathophysiology behind MS remission?

A

In early disease, re-myelination can occur and symptoms can resolve. In the later stages of the disease, re-myelination is incomplete and symptoms gradually become more permanent.

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9
Q

What happens during an MS ‘‘attack’’?

A

Lesions of demyelination occuring throughout the CNS

Specific lesions may cause symptoms (ie. optic neuritis) whilst others do not

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10
Q

Characteristic feature of MS lesions?

A

Variation in location over time, meaning that different nerves are affected and symptoms change over time
- ‘disseminated in time and space’

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11
Q

Factors that may influence the cause of dyemilination in MS?

A 
Multiple genes
EBV
Low vitamin D
Smoking
Obesity
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12
Q

Over what time period do MS symptoms usually progress?

A

More than 24 hours

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13
Q

Signs and symptoms in MS?

A

Optic neuritis
Eye movement abnormalities
Focal weakness (bells palsy, horners syndrome, limb paralysis, incontinence)
Focal sensory symptoms (trigeminal neuralgia, numbness, paaesthesia, Lhermitte’s sign)
Ataxia (sensory, cerbellar)

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14
Q

Lesions in the sixth cranial nerve may cause which two disorders?

A

Internuclear ophtalmoplegia - unilateral lesions

Conjugate lateral gaze disorder - bilateral lesions

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15
Q

What is internuclear opthalmoplegia?

A

Unilateral lesions in the sixth nerve causes a condition called internuclear ophthalmoplegia.

Internuclear refers to the nerve fibres that connect between the cranial nerve nuclei that control eye movements (3rd, 4th and 6th cranial nerve nuclei).

The internuclear nerve fibres are responsible for coordinating the eye movements to ensure the eyes move together.

Ophthalmoplegia means a problem with the muscles around the eye.

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16
Q

What is conjugate lateral gaze disorder?

A

Lesions in the sixth cranial nerve cause a conjugate lateral gaze disorder.

Conjugate means connected. Lateral gaze is where both eyes move together to look laterally to the left or right. It is disordered in a sixth cranial nerve palsy.

When looking laterally in the direction of the affected eye, the affected eye will not be able to abduct. For example, in a lesion affecting the left eye, when looking to the left, the right eye will adduct (move towards the nose) and the left eye will remain in the middle as the muscle responsible for making it move laterally is not functioning.

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17
Q

What is Lhermitte’s sign?

A

An electrical shock sensation that travels down the spinal and into the limbs when flexing the neck

It indicates disease in the cervical spinal cord in the dorsal column.

It is caused by stretching the demyelinated dorsal column.

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18
Q

What is ataxia?

A

Discoordinated movement

19
Q

What ins sensory ataxia?

A

Sensory ataxia is the result of loss of the proprioceptive sense, which is the ability to sense the position of the joint (e.g. is the joint flexed or extended).

This results in a positive Romberg’s test and can cause pseudoathetosis.

20
Q

What is cerebellar ataxia?

A

Cerebellar ataxia is the result of problems with the cerebellum coordinating movement. This suggests cerebellar lesions.

21
Q

What are the possible disease patterns in multiple sclerosis?

A

Clinically isolated syndrome
Relapsing-remitting
Secondary progressive
Primary progressive

22
Q

What is clinically isolated syndrome in terms of MS?

A

First episode of demyelination and neurological signs and symptoms
Not diagnostic of MS as lesions have not ben disseminated in time and spcae
These patients may never have another episode or develop MS
Pts with lesions seen on MRI are more likely to go on and develop MS

23
Q

What is relapsing-remiting MS?

A

Most common pattern at initial diagnosis
Characterised by episodes of disease and neurological symptoms followed by recovery
Different areas, episodes
Can be further classified as active, not active, worsening and nor worsening

24
Q

What is ‘active MS’?

A

New symptoms are developing or new lesions are appearing on MRI

25
Q

What is ‘not active’ MS?

A

No new symptoms or MRI lesions are developing

26
Q

What is worsening MS?

A

Overall worsening of disease over time (regardless of relapses)

27
Q

What is not progressing MS?

A

No worsening of disease over time

28
Q

What is secondary progressive MS?

A

Secondary progressive MS is where there was relapsing-remitting disease at first, but now there is a progressive worsening of symptoms with incomplete remissions.

Symptoms become more and more permanent.

Secondary progressive MS can be further classified based on whether the disease is active and/or progressing.

29
Q

What is primary progressive MS?

A

Primary progressive MS is where there is a worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions. This can be further classified in a similar way to secondary progressive based on whether it is active and/or progressing.

30
Q

How is MS diagnosed?

A

Diagnosis is made by a neurologist based on the clinical picture and symptoms suggesting lesions that change location over time.

Symptoms have to be progressive over a period of 1 year to diagnose primary progressive MS.

Other causes for the symptoms need to be excluded.

Supportive investigations:
MRI scans can demonstrate typical lesions
Lumbar puncture can detect ‘‘oligoclonal bands’’ in the cerborospinal fluid (CSF)

31
Q

How does optic neuritis present and what are the key features?

A

Unilateral reduced vision developing over hours to days:

  • Central scotoma - this is an enlarged blind spot
  • Pain of eye movement
  • Impaired colour vision
  • Relative afferent pupillary defect
32
Q

Causes of optic neuritis?

A 
MS
Sarcoidosis
SLE
Diabetes
Syphilis
Measles
Mumps
Lyme disease
33
Q

How should optic neuritis?

A

Patients presenting with acute loss of vision should be seen urgently by an ophthalmologist for assessment.

It is treated with steroids and recovery takes 2-6 weeks. Around 50% of patients with a single episode of optic neuritis will go on to develop MS over the next 15 years.

Changes on an MRI scan help to predict which patients will go on to develop MS.

34
Q

How is MS managed?

A

MDT: physio, neurologists, CNS, OT
Disease modifying drugs
Relapse management - steroids
Symptomatic treatments:

Spacisity: baclofen, gabaPentin, physio
Neuropathic pain: amitriptyline, gabapentin
Depression: SSRIs, CBT, TCA
Incontinence: oxybutynin,, indwelling catheter, pelvic floor exercises, percutaneous tibial nerve stimulation
Fatigue: CBT, CVS exercise, management of other symptoms to improve sleep
Paroxysmal symtpoms: carbamazepine, gabapentin, levetiracetam, amitriptyline

35
Q

Treatment of MS - disease modifying drugs?

A

Aim of treatment is to induce remission with no evidence of disease activity

Target various mechanisms: interlukins, inflammatory cytokines and various immune cells

36
Q

Treating relapses of MS?

A

Methyprednisolone:
500mg orally daily for 5 days or 1g IV daily for 3-5 days where oral treatment has failed previously or where relapses are severe

37
Q

Symptomatic treatments of MS?

A

Exercise to maintain activity and strength
Neuropathic pain - amitriptyline or gabapentin
Depression - SSRIs, CBT
Urge incontinence - oxybutynin (caution as my worse cognitive impairment)
Spacisity: baclofen, gabapentin and physiotherapy

38
Q

Management of trigeminal neuralgia?

A 
Baclofen (Lioresal)
Carbamazepine (Tegretol) - FIRST LINE
Gabapentin (Neurontin)
Lamotrigine (Lamictal)
Oxcarbazepine (Trileptal)
Pregabalin (Lyrica)
39
Q

DMTs that may be used to manage relapsing remmiting MS?

A

First-line injectables such as beta-interferon and glatiramer
New oral agents such as dimethyl fumarate, teriflunomide and fingolimod
Biologics such as natalizumab and alemtuzumab.

40
Q

Pregnancy in MS?

A

Risk of relapse increases 6 months post partum due to hormonal changes
Many DMTs not compatible with pregnancy/breastfeeding and may require a washout periord
Some DMTs safter than others
DMTs should not be delayed due to family planning as this could lead to irreversable disability later in life

41
Q

MS clinical modes of presentation?

A
  1. Optic neuritis
  2. Double vision
  3. Sensory disturbance in face or limbs
  4. Weakness due to upper motor neurone involvement
  5. Impaired balance or clumsiness of the limbs
  6. Neuropathic pain (e.g. trigeminal neuralgia)
  7. Bladder symptoms
  8. Cognitive impairment (although this usually occurs late)
42
Q

McDonald criteria for diagnosing MS.

A
  1. Lesions consistent with an inflammatory process
  2. No alternative diagnosis
  3. Multiple lesions in time and space (Relapsing remitting MS)
  4. Progressive neurological deterioration for 1 year (Primary progressive MS)
43
Q

Investigations to consider in ?MS

A
  1. MRI of brain or spinal cord - will demonstrate demyelination plaques
  2. Immunoelectrophoresis of CSF - will show oligoclonal bands of IgG

Year 4 Neurology and Special Senses (24 decks)

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