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JL Neurology > Week 4 > Flashcards

Week 4 Flashcards

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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
What is rhodopsin (for rods) made from?
Retinal vitamin A derivative + opsin (GPCR)
26
What does light convert 11-cis-retinal to?
All-trans-retinal (activated form)
27
What activates transfucin leading to molecular cascade that decreases cGMP, leading to closure of sodium channels and hyperpolarisatio?
All-trans-retinal
28
Is there more glutamate in the dark or light?
In the dark
29
What photoreceptors are for dim light?
Rods - more convergence
30
Where in the retina are rods found?
Peripheral retina
31
Where in the retina are ocnes fround?
Central retina - fovea
32
Do rods have higher visual acuity than cones?
No they have low visual acuity
33
Are bipolar cells (OFF pathway) more positive in light or dark?
Dark - more glutamate
34
Are bipolar cells (ON pathway) more positive in light or dark?
Light
35
What cells in signal transmission (vision) produce APs?
Ganglion cells
36
In relation to vision what does lateral inhibition imporve?
Stimulus localisation
37
What modifies the receptive fields of ganglion cells to have a center-surround organisation?
Lateral inhibition
38
What does center-surround organisation/lateral inhibtion serve to do?
Emphasise areas of difference (contrast) i.e,. sharpens boundary between objecys of different luminance
39
Nerve fibres from what half of each retina cross over at optic chiasm?
Nasal half
40
What are motor end plates?
The synapses formed between motor neurons and muscle are called the motor end plate
41
Who is lkely to be affected by the presynaptic disorder botulism?
IV drug users - black tar heroin
42
What symptoms does botulism give?
Rapid onset weakness without sensory loss
43
What involves antibodies to presynaptic calcium channels leading to less vesicle release. Strong association with underlying small cell carcinoma?
Lambert Eaten Myasthenic Syndrome
44
Name a post synaptic disorder?
Myasthenia Gravis
45
What is the most common disorder of neuromuscular junction?
Myasthenia grais
46
What condition is related to antibodies to acetyl choline receptors (AChR)?
Myasthenia gravis
47
In Myasthenia Gravis what happens to the number of ACh receptors and endplate folds?
Reduced number and flattening of endplate folds
48
What do 75% of myasthenia gravis patients also have?
Hyperplasia of thymus or thymoma
49
What are some clnical features of myasthenia gravis?
Weakness fluctuating - worse through day Extraocular weakness, facial and bulbar weakness limb weakness typically proximal
50
How do you treat myasthenia gravis?
Acetylcholinesterase inhibitor - pyridostigmine | Thymectomy
51
What is the actin myosin ratio in smooth muscle?
10 : 1
52
What is a fasciculation?
Visible, fast, fine spontaneous twitch
53
What precipitates fasciculations?
Stress, caffeine and fatigue
54
What is usually a sign of disease in the motor neurone, not the muscle?
Fasciculations
55
What is myotonia?
Failure of muscle relaxation after use - chloride channel
56
What infalmmatory condition is symmetrical, progressive proximal weakness, raised CK and responds to steroids?
Polymyositis
57
Heliotrope rash on face and up to 50% have underlying malignancy>?
Dermatomyositis
58
Give a degenerative muscle disease?
Inclusion body myositis
59
Slowly progressive weakness in 6th decade of life with characteristic thumb sparing?
Inclusion body myositis
60
What is the commonest muscular dystrophy?
Myotonic dystrophy
61
What heritance is myotonic dystrophy?
Autosomal dominant
62
Myotonia, weakness, cataracts, ptosis, frontal balding, cardiac defects Trinucleotide repeat disorder with anticipation
Myotonic dystrihyt
63
Myalgia, muscle weakness and myoglobinuria?
Rhabdomyolysis
64
Gie two complications of rhabdomyolysis?
Acute renal failure | DIC
65
What are the two peaks of incidence for myasthenia gravis?
Females in 3rd decade | Males in 6th/7th decade
66
Name an untreatable and rapidly progressing neurodegenerative condition?
Motor neuron disease
67
Name some symptoms of MND?
Muscle weakness | speech, swallo and breathing
68
What condition shows upper and/or lower motor neurone signs without sensory problems
MND
69
What does MND lead to?
Focal onset, continuous spread and finally generalised paresis
70
How long is average MND survival time?
3 years
71
90% sporadic, 10% familial?
MND
72
wHAT IS THE 70% site of onset for MND?
Extremities
73
What motor neuron is more affected in MND?
Lower motor neurone 90%
74
Is the bulbar variant of MND more common in women or men?
Women (60-80 years)
75
How is MND diagnosed?
Diagnosis of exclusion
76
What kind of ementia is asociated with MND?
Fronto temporal
77
Are these signs upper or lower motor neuron - spasticity, babinski sign?
UMN
78
Name some bulbar UMN signs?
1. Exaggerated snout reflex 2. Clonic jaw jerk 3. Emotional lability 4. Forced yawning
79
Name some cervical and lumbar region UMN sings?
1. Clonic deep tendon reflexes 2. Wasted limb 3. Hoffman reflex 4. Hyperreflexia
80
Upper or lower MN dysfunction - severe weakness, fasciculations, muscle cramps, muscle hypotonicity, muscle atrophy, hyporeflexia?
Lower
81
upper or lower MN dysfunction - pseudobulbar affect, moderate weakness, spasticity, hyperreflexia, extensor plantar reflexes?
Upper

JL Neurology (12 decks)

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