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JL Neurology > Week 4 > Flashcards

Week 4 Flashcards

1
Q

When do patients with MS typically present first?

A

30s and 40s

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2
Q

What demyelinating disorder is optic neuritis associated with?

A

MS

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3
Q

Give three features of pyramidal dysfunction in patients with MS?

A
  1. Increased tone
  2. Spasticity
  3. Weakness
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4
Q

Name some sensory symptoms in MS?

A
  1. Pain
  2. Paraesthesia
  3. Dorsal column loss - proprioception and vibration
  4. Numbness
  5. Trigeminal neuralgia
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5
Q

What dysfunction is present with ataxia, intention tremor, nystagmus, past pointing, pendular reflexes, dysdiadokinesis and dysarthria?

A

Cerebellar dysfunction

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6
Q

Give two features of brainstem dysfunction in MS?

A
  1. Diplopia

2. Facial weakness

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7
Q 
Medial longitudinal fasciculus
Distortion of binocular vision
Failure of adduction- diplopia
Nystagmus in abducting eye
Lag
A

Internuclear ophthalmoplegia - MS

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8
Q

What is used to treat fatigue in MS?

A

Amantadine
Modafinil if sleepy
Hyperbaric oxygen

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9
Q

Give three investigations for possible MS?

A
  1. MRI
  2. CSF
  3. Neurophysiology
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10
Q

How is a mild acute exacerbation of MS treated?

A

Symtpomatic treatment

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11
Q

How is a moderate acute exacerbation of MS treated?

A

Oral steroids

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12
Q

How is a severe acute exacerbation of MS treated?

A

Admit and IV steroids

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13
Q

Give four ways to treat spasticity in MS?

A
  1. pHYSIOTHERAPY
  2. Oral baclofen and tizanidine
  3. Botulinum toxin
  4. Intrathecal baclofen/phenol
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14
Q

Give two drugs for treating sensory symptoms in MS?

A
  1. Gabapentin

2. Amitriptyline

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15
Q

Give four ways to treat lower urinary tract dysfunction in MS?

A
  1. Bladder drill
  2. Anti cholinergics oxybutynin
  3. Desmopressin
  4. Catheterisation
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16
Q

List three first line disease modifying therapies for MS?

A
  1. Interferon Beta - avonex, rebif
  2. Glitiramer Acetate (copaxone)
  3. Tecfedira
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17
Q

List two second line therapies for MS?`

A
  1. Monoclonal antibody

2. Fingolimod

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18
Q

Name a third line therapy for MS?

A

Mitoxantrone

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19
Q

What drug is first line, oral agent in relapsing remitting MS?

A

Tecfidera

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20
Q

List the three cells involved in direct pathway for signal transmission in the retina?

A

Photoreceptors
Bipolar cells
Ganglion cells

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21
Q

What cells in teh retina receive input from photoreceptors and project to other photoreceptors and biopolar cells?

A

Horizontal cells

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22
Q

What cells in the retina receive input from bipolar cells and project to ganglion cells, biopolar cells and other amacrine cells?

A

Amacrine cells

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23
Q

What is the role of photoreceptors?

A

Transduction

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24
Q

In relation to the dark current - when is the cGMP sodium channel open/

A

In the dark and closes in the light

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25
Q

What is rhodopsin (for rods) made from?

A

Retinal vitamin A derivative + opsin (GPCR)

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26
Q

What does light convert 11-cis-retinal to?

A

All-trans-retinal (activated form)

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27
Q

What activates transfucin leading to molecular cascade that decreases cGMP, leading to closure of sodium channels and hyperpolarisatio?

A

All-trans-retinal

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28
Q

Is there more glutamate in the dark or light?

A

In the dark

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29
Q

What photoreceptors are for dim light?

A

Rods - more convergence

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30
Q

Where in the retina are rods found?

A

Peripheral retina

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31
Q

Where in the retina are ocnes fround?

A

Central retina - fovea

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32
Q

Do rods have higher visual acuity than cones?

A

No they have low visual acuity

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33
Q

Are bipolar cells (OFF pathway) more positive in light or dark?

A

Dark - more glutamate

34
Q

Are bipolar cells (ON pathway) more positive in light or dark?

35
Q

What cells in signal transmission (vision) produce APs?

A

Ganglion cells

36
Q

In relation to vision what does lateral inhibition imporve?

A

Stimulus localisation

37
Q

What modifies the receptive fields of ganglion cells to have a center-surround organisation?

A

Lateral inhibition

38
Q

What does center-surround organisation/lateral inhibtion serve to do?

A

Emphasise areas of difference (contrast) i.e,. sharpens boundary between objecys of different luminance

39
Q

Nerve fibres from what half of each retina cross over at optic chiasm?

A

Nasal half

40
Q

What are motor end plates?

A

The synapses formed between motor neurons and muscle are called the motor end plate

41
Q

Who is lkely to be affected by the presynaptic disorder botulism?

A

IV drug users - black tar heroin

42
Q

What symptoms does botulism give?

A

Rapid onset weakness without sensory loss

43
Q

What involves antibodies to presynaptic calcium channels leading to less vesicle release. Strong association with underlying small cell carcinoma?

A

Lambert Eaten Myasthenic Syndrome

44
Q

Name a post synaptic disorder?

A

Myasthenia Gravis

45
Q

What is the most common disorder of neuromuscular junction?

A

Myasthenia grais

46
Q

What condition is related to antibodies to acetyl choline receptors (AChR)?

A

Myasthenia gravis

47
Q

In Myasthenia Gravis what happens to the number of ACh receptors and endplate folds?

A

Reduced number and flattening of endplate folds

48
Q

What do 75% of myasthenia gravis patients also have?

A

Hyperplasia of thymus or thymoma

49
Q

What are some clnical features of myasthenia gravis?

A

Weakness fluctuating - worse through day
Extraocular weakness, facial and bulbar weakness
limb weakness typically proximal

50
Q

How do you treat myasthenia gravis?

A

Acetylcholinesterase inhibitor - pyridostigmine

Thymectomy

51
Q

What is the actin myosin ratio in smooth muscle?

52
Q

What is a fasciculation?

A

Visible, fast, fine spontaneous twitch

53
Q

What precipitates fasciculations?

A

Stress, caffeine and fatigue

54
Q

What is usually a sign of disease in the motor neurone, not the muscle?

A

Fasciculations

55
Q

What is myotonia?

A

Failure of muscle relaxation after use - chloride channel

56
Q

What infalmmatory condition is symmetrical, progressive proximal weakness, raised CK and responds to steroids?

A

Polymyositis

57
Q

Heliotrope rash on face and up to 50% have underlying malignancy>?

A

Dermatomyositis

58
Q

Give a degenerative muscle disease?

A

Inclusion body myositis

59
Q

Slowly progressive weakness in 6th decade of life with characteristic thumb sparing?

A

Inclusion body myositis

60
Q

What is the commonest muscular dystrophy?

A

Myotonic dystrophy

61
Q

What heritance is myotonic dystrophy?

A

Autosomal dominant

62
Q

Myotonia, weakness, cataracts, ptosis, frontal balding, cardiac defects
Trinucleotide repeat disorder with anticipation

A

Myotonic dystrihyt

63
Q

Myalgia, muscle weakness and myoglobinuria?

A

Rhabdomyolysis

64
Q

Gie two complications of rhabdomyolysis?

A

Acute renal failure

DIC

65
Q

What are the two peaks of incidence for myasthenia gravis?

A

Females in 3rd decade

Males in 6th/7th decade

66
Q

Name an untreatable and rapidly progressing neurodegenerative condition?

A

Motor neuron disease

67
Q

Name some symptoms of MND?

A

Muscle weakness

speech, swallo and breathing

68
Q

What condition shows upper and/or lower motor neurone signs without sensory problems

69
Q

What does MND lead to?

A

Focal onset, continuous spread and finally generalised paresis

70
Q

How long is average MND survival time?

71
Q

90% sporadic, 10% familial?

72
Q

wHAT IS THE 70% site of onset for MND?

A

Extremities

73
Q

What motor neuron is more affected in MND?

A

Lower motor neurone 90%

74
Q

Is the bulbar variant of MND more common in women or men?

A

Women (60-80 years)

75
Q

How is MND diagnosed?

A

Diagnosis of exclusion

76
Q

What kind of ementia is asociated with MND?

A

Fronto temporal

77
Q

Are these signs upper or lower motor neuron - spasticity, babinski sign?

78
Q

Name some bulbar UMN signs?

A
  1. Exaggerated snout reflex
  2. Clonic jaw jerk
  3. Emotional lability
  4. Forced yawning
79
Q

Name some cervical and lumbar region UMN sings?

A
  1. Clonic deep tendon reflexes
  2. Wasted limb
  3. Hoffman reflex
  4. Hyperreflexia
80
Q

Upper or lower MN dysfunction - severe weakness, fasciculations, muscle cramps, muscle hypotonicity, muscle atrophy, hyporeflexia?

81
Q

upper or lower MN dysfunction - pseudobulbar affect, moderate weakness, spasticity, hyperreflexia, extensor plantar reflexes?

JL Neurology (12 decks)

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