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4th Year > CCC - GP Neuro > Flashcards

CCC - GP Neuro Flashcards

1
Q

Who gets MS?

A

Females, 30yrs old, White

20% have affected relative

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2
Q

What is the pathophysiology of MS?

A

Demyelination of neurones

Affects movement and sensation

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3
Q

What are the patterns of MS?

A 
Relapsing-remitting
Secondary progressive (follows relapsing-remitting)

As disease gets more advanced remissions are less frequent and have less remyelination

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4
Q

How does MS present? (4)

A

Optic neuritis = vision loss progressing over few days
Transverse myelitis = tight band around level of inflammation or shock-like sensations travelling down spine induced by neck flexion
Cerebellar symptoms = balance issues, ataxia
Brainstem syndromes = ataxia, nystagmus, dysphagia etc

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5
Q

When would you diagnose MS?

A

After two isolated attacks

Dx is by neurologist

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6
Q

What tests may be helpful in MS?

A

MRI
LP
MOG and MBP antibodies

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7
Q

Why might an MRI be useful in MS?

A

Sensitive for plaque detection

Can exclude other causes

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8
Q

Why might an LP be useful?

A

Oligoclonal bands of IgG in CSF but not serum may suggest CBS infection

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9
Q

Why might MOG and MBP antibodies be useful?

A

In those with MS-like lesion, can predict conversion to definitive MS

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10
Q

What are the disease-modifying therapies available for MS?

A

INF-beta = reduces relapse by 30%

Monoclonal Ab eg. Natalizab = reduces relapses and lesions on MRI

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11
Q

What is the treatment of a relapse of MS?

A

Methylprednisolone 1g OD 3 days
Used max 2x per year
Does not affect progression

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12
Q

How many develop secondary progressive MS from R-R MS?

A

50% after 10yrs

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13
Q

What is Motor Neurone Disease?

A

Degeneration of anterior horn cells of the spinal cord and motor cranial nuclei

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14
Q

Which motor neurones does MND affect?

A

Upper and lower

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15
Q

What are the 3 types of MND?

A

Amyotrophic lateral sclerosis 50%
Progressive muscular atrophy 25%
Progressive bulbar palsy 25%

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16
Q

What is Amyotrophic lateral sclerosis?

A

Combined LMN wasting and UMN hyperreflexia

17
Q

What is Progressive muscular atrophy?

A

Anterior horn cell lesions
Affect distal before proximal muscles
Better prognosis that ALS

18
Q

What is Progressive bulbar palsy?

A

Loss of function of brainstem motor nuclei (LMN) -> tongue weakness, chewing/swallowing difficulties, facial weakness

19
Q

How does NMD present?

A

Weakness
Stiffness
Cramping
Generally focal onset with mixed UMN/LMN features

20
Q

What is different about Primary lateral sclerosis?

A

Has either pure UMN or pure LMN features

21
Q

What does MND never affect?

A

Eye movements

22
Q

What is the management of MND?

A

Riluzole - may prolong life by 2-4 months

Treats secretions with Buscopan and cramps with diazepam/baclofen

23
Q

What is the prognosis of MND?

A

Death within 3-5yrs from ventilatory failure

24
Q

What are the features of Parkinson’s? (6)

A 
Pill-rolling tremor
Lead-pipe or cog-wheel rigidity
Difficulty initiating movement
Slow movements
Shuffling gait
Micrographia
25
Q

What is the mean onset of Parkinson’s?

A

65yrs

26
Q

What is the pathophysiology of Parkinson’s?

A

Degeneration of dopaminergic neurons in substantia nigra -> decreased striatal dopamine

27
Q

What is required for a Parkinson’s diagnosis?

A

Bradykinesia + 2+ of:

  • Rigidity
  • Resting tremor
  • Postural instability
28
Q

What investigations may be useful in Parkinson’s?

A

CT/MRI - to exclude other diagnoses

29
Q

What is the first line management of Parkinson’s?

A

Levodopa

Effects diminish over time

30
Q

What two ‘effects’ are relevant to Levodopa?

A

On-off effect

End-of-dose effect

31
Q

What is the on-off effect of Levodopa?

A

Fluctuations between periods of exaggerated involuntary movements and periods of immobility

32
Q

What is the end-of-dose effect of Levodopa?

A

Duration of benefit is reduced after each dose

33
Q

What are other examples of potential Parkinson’s drugs?

A

MAOIs eg. selegiline
Amatadine
Tolcapone (inhibits dopamine breakdown)

4th Year (15 decks)

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