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Year 3 - Neurology (DP) > Focal Deficits > Flashcards

Focal Deficits Flashcards

1
Q

What is the F:M ratio of MS?

A

3:1

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2
Q

What are the four types of clinical course for MS?

A

Relapsing remitting
Progressive relapsing
Primary progressive
Secondary progressive

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3
Q

What is the pattern of pyramidal dysfunction in MS?

A 
Increased tone
Spasticity
Weakness:
- Extensors of upper limbs
- Flexors of lower limbs
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4
Q

How does optic neuritis present?

A

Painful visual loss over 1-2 weeks

RAPD

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5
Q

How does cerebellar dysfunction present in MS?

A 
Ataxia
Intention tremor
Nystagmus
Past-pointing
Pendular reflexes
Dysdiadokinesis
Dysarthria
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6
Q

Why is there diplopia in MS?

A

CN vi palsy

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7
Q

What causes internuclear ophthalmoplegia in MS?

A

Injury/Dysfunction of medial longitudinal fasciculus

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8
Q

What are the signs/symptoms of MS?

A 
Distortion of binocular vision
Failure of adduction:
- Diplopia
Nystagmus in adducting eye
Lag
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9
Q

How can fatigue in MS be treated?

A

Amantadine
Modafinil (if sleepy)
Hyperbaric oxygen

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10
Q

What causes lower urinary tract dysfunction in MS?

A

Increased tone at bladder neck
Detrusor hyperactivity
Detrusor syphincteric dysenergia

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11
Q

What criteria is used to diagnose MS?

A

McDonald criteria

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12
Q

What CSF finding is highly indicative of MS?

A

Oligoclonal bands (Ig) present in CSF but not serum

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13
Q

How is a mild exacerbation of MS treated?

A

Symptomatic treatment

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14
Q

How is a moderate exacerbation of MS treated?

A

Oral steroids

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15
Q

How is a severe exacerbation of MS treated?

A

Admission

IV steroids

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16
Q

How is pyramidal dysfunction treated conservatively in MS?

A

Physiotherapy

OT

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17
Q

How can spasticity be treated in MS?

A

Oral medication (Baclofen, Tizanidine)
Botox
Intrathecal baclofen/phenol

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18
Q

How can sensory symptoms be treated in MS?

A 
Gabapentin
Amitriptyline
TENS
Acupuncture
Lidocaine infusion
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19
Q

How can lower urinary tract dysfunction be treated in MS?

A

Bladder drills
Anticholinergics (Oxybutynin)
Desmopressin
Catheterisation

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20
Q

What are the first line therapies for MS?

A 
Interferon beta (Avonex, Rebif, Betaseron, Extavia)
Glitiramer Acetate (Copaxone)
Tecfedira
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21
Q

What are the second line therapies for MS?

A

Monoclonal antibodies:
- Tysabri (Natalizumab)
- Lemtrade
Fingolimad

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22
Q

What is the third line therapy for MS?

A

Mitoxantrone

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23
Q

What drug is first line in relapsing remitting MS?

A

Tecfedira

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24
Q

What type of drug is Fingolimad?

A

Sphingosine 1-phosphate modulator

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25
Q

When are Tysabri and Lemtrada useful?

A

Rapidly evolving severe relapsing remitting MS

Despite use of an Interferon beta

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26
Q

How does Tysabri work?

A
  1. Leucocyte migration
  2. Leucocyte priming and activation in tissues
  3. Modulation of leucocyte apoptosis
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27
Q

What is Tysabri associated with? Why?

A

Progressive Multifocal Leucoencephalopathy:

- Due to JC virus

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28
Q

When is Mitoxantrone used?

A

Relapsing progressive MS

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29
Q

How is Mitoxantrone delivered?

A

12 infusions over 2 years

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30
Q

What organ is Mitoxantrone toxic to?

A

Heart

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31
Q

What do the following define:

  • A brief episode of neuro dysfunction
  • Due to focal brain/retinal ischaemia
  • Clinical symptoms lasting <1 hour
  • Without evidence of acute infarction
A

TIA

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32
Q

What is the Rosier Score?

A 
Has there been loss of consciousness/syncope?
- Yes = -1 point
- No = 0 points
Has there been seizure activity?
- Yes = -1 point
- No = 0 points
Is there a new acute onset (1 point for each):
- Asymmetrical facial weakness
- Asymmetrical arm weakness
- Asymmetrical leg weakness
- Speech disturbance
- Visual field defect
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33
Q

What does a Rosier score of >0 mean?

A

Stroke likely

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34
Q

How is the size of stroke classified?

A

Oxford Classification

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35
Q

Apart from the left side of the body, what else does the right side of the brain control?

A

Creativity
Music
Spatial orientation
Artistic awareness

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36
Q

Apart from the right side of the body, what else does the left side of the brain control?

A

Spoken language
Reasoning
Number skills
Written language

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37
Q

What do non-dominant hemisphere (usually right sided) cortical events tend to affect?

A

Spatial awareness resulting in neglect

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38
Q

What is Type 1 small vessel disease?

A

Arteriosclerotic:

  • Fibrinoid necrosis
  • Lipohyalinosis
  • Microatheroma and microaneurysms
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39
Q

What is Type 2 small vessel disease?

A

Sporadic and Hereditary cerebrl amyloid angiopathy

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40
Q

What is Type 3 small vessel disease?

A

Genetic small vessel disease:

- eg. Cerebral Autosomal-Dominant Arteriopathy with Cerebral Infarcts and Leucoencephalopathy (CADASIL)

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41
Q

What is Type 4 small vessel disease?

A

Inflammatory and immunologically related:

  • EGPA
  • GPA
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42
Q

What is Type 5 small vessel disease?

A

Venous collagenosis

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43
Q

What is Type 6 small vessel disease?

A

Other:

- eg. Post-radiation angiopathy

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44
Q

How much more likely is a patient with AF to have a stroke?

A

5x

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45
Q

What sort of primary intracerebral haemorrhage does hypertension often lead to?

A

Deep

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46
Q

What sort of primary intracerebral haemorrhage does amyloid angiopathy often lead to?

A

Lobar

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47
Q

What typically causes a secondary intracerebral haemorrhage?

A

AVM
Aneurysm
Tumour

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48
Q

What is the drug of choice in Tayside for thrombolysis in stroke? What does do we give?

A

Alteplase

0.9mg/kg IV (max 90mg)

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49
Q

When can medical thrombolysis be used in CVA?

A

When they present within 4.5 hours of symptoms onest AND in who an intracerebral haemorrhage has been excluded

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50
Q

What are some indications for imaging immediately at presentation in a stroke?

A

Indications for thrombolysis/anticoagulation
On anticoagulation therapy
Known bleeding tendency
Reduced consciousness (GCS <13)
Unexplained progressive/fluctuating symptoms
Papilloedema/Fever/Neck stiffness
Severe headache at onset

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51
Q

After what time period is a CT not sensitive for blood?

A

~1 week

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52
Q

What is the initial antiplatelet therapy following a stroke? How long does this last?

A 
300mg aspirin (+/- 75mg clopidogrel)
2 weeks
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53
Q

What anticoagulant therapy is preferred to prevent a stroke?

A

Rivaroxaban
OR
Dabigatran

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54
Q

What BP do we aim for to prevent strokes?

A

<140/90

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55
Q

How do we manage cholesterol in stroke prevention?

A

80mg Atorvastatin if rasied
OR
20mg if not raised

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56
Q

What other condition is important to control to prevent strokes?

A

Diabetes

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57
Q

What lifestyle factor results in a huge contribution to chance of stroke?

A

Smoking

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58
Q

What are the features of a rapid assessment in the TIA clinic?

A

History
Carotid imaging
ECG
Blood tests

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59
Q

If a TIA is diagnosed, what treatment can be commenced?

A

Aspirin 300mg

Carotid endarterectomy

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60
Q

What is the ABCD2 of stroke risk following a TIA?

A 
Age >60 years = 1 point
Blood pressure >= 140/90 = 1 point
Clinical features
- Unilateral weakness = 2 points
- Speech disturbance ONLY = 1 point
- Other = 0 points
Duration:
- >=1 hours = 2 points
- 10-59 minutes = 1 point
- <10 minutes = 0 points
Diabetes = 1 point
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61
Q

In terms of the ABCD2 score, what score indicates a high risk for stroke?

A

> =4

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62
Q

What are the general features of Motor Neurone Disease?

A

Muscle weakness and wasting
Upper +/or lower motor signs
NO sensory signs
Focal onset and continuous spread

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63
Q

Where is the most common site of onset of Motor Neurone Disease?

A

Extremities (Upper > Lower)

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64
Q

Are UMN or LMN more commonly affected initially?

A

LMN

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65
Q

Is bulbar onset in Motor Neurone Disease more common in men or women?

A

Women

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66
Q

Primary bulbar onset in Motor Neurone Disease is seen in how many patients?

A

25%

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67
Q

What is the average age of onset of the bulbar variant of Motor Neurone Disease?

A

60-80 years

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68
Q

What are the signs and symptoms of Motor Neurone Disease?

A

Prominent tongue fasciculations
Weak palate
Dysarthria
Dysphagia

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69
Q

The bulbar variant of Motor Neurone Disease involves the LMN degeneration of what cranial nervea?

A

ix
x
xii

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70
Q

What results in the pseudobulbar variant of Motor Neurone Disease?

A

Damage to UMN in corticobulbar tract

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71
Q

What are the signs and symptoms of pseudobulbar palsy?

A

Similar to bulbar palsy

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72
Q

What causes progressive muscular dystrophy?

A

LMN degeneration

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73
Q

What are the signs and symptoms of progressive muscular dystrophy?

A

Wasting, weakness and fasciculations:

  • Usually asymmetric
  • Starts in a hand/foot and spreads
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74
Q

What motor neurones is Primary Lateral Sclerosis confined to?

A

UMN

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75
Q

What are the signs/symptoms of Primary Lateral Sclerosis?

A

Slowly progressive:

  • Tetraparesis (usually starts in legs)
  • Pseudobulbar palsy
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76
Q

What are the UMN signs in ALS?

A

Hyperreflexia and Babinski sign
Increased tone
Pyramidal weakness
Spasticity

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77
Q

What are the LMN signs in ALS?

A

Progressive focal weakness and wasting
Cramps
Fasciculations

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78
Q

What are the criteria of EMG findings that help diagnose motor neurone disease?

A

El-Escorial criteria

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79
Q

What algorithm can aid the use of EMG findings of chronic neurogenic changes in motor neurone disease?

A

Awaji algorithm

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80
Q

What is the most common neuropathogenetic cause of ALS and FTD?

A

TDP-43 (TARDBP)

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81
Q

What are the common misdiagnoses of motor neurone disease?

A

Carpal tunnel
Stroke
Neuropathy

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82
Q

What are some motor neurone disease mimics that may give false positive results on investigation?

A

Multifocal Motor Neuropathy
Kennedy’s Disease
Inclusion Body Myopathy
Cervical Spondylotic radiculomyelopathy

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83
Q

What are the following signs of:

  • Exaggerated snout reflex
  • Clonic jaw jerk
  • Emotional lability
  • Forced jawing
A

Bulbar UMN lesion

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84
Q

What are some signs/symptoms of cervical and lumbar UMN lesions?

A

Clonic deep tendon reflexes
Preserved reflex in weak/wasted muscles
Hoffman reflex
Hyperreflexia

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85
Q

What reflex is lost in UMN lesions?

A

Superficial abdominal reflexes

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86
Q

What is the commonest intronic hexanucleotide repeat expansion in motor neurone disease?

A

C9ORF72

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87
Q

What is the most common extra-axial brain tumour? Where does it arise from?

A

Meningioma

Arises from meningeal mesenchymal cells

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88
Q

What are some other examples of extra-axial brain tumours?

A

Pituitary adenomas
Craniopharyngiomas
Choroid plexus papillomas
Acoustic neuromas

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89
Q

How common are primary brain tumours in children?

A

The 2nd most common cancers in kids

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90
Q

How do brain tumours tend to present?

A

Progressive neurological deficit
Usually motor weakness
Seizures

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91
Q

When is a headache worse in the context of a brain tumour?

A

In the morning (wakes them up)
Coughing
Leaning forward

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92
Q

What can cause the headache in brain tumours?

A 
Increased ICP
Invasion/Compression of:
- Dura
- Blood vessels
- Periosteum
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93
Q

What can headaches in brain tumours be secondary to?

A

Diplopia (CNs iii, iv, vi ; INO)

Difficulty focusing

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94
Q

What percentage of neuroepithial tissue tumours are caused by astrocytes? What percentage of these are high grade?

A

60%

66.6%

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95
Q

What are the WHO Grade i Astrocyric tumours?

A

Pilocytic
Pleomorphic
Xanthastrocytoma
Subependymal giant cell

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96
Q

What is a WHO Grade ii Astrocyric tumour?

A

Low grade astrocytoma

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97
Q

What is a WHO Grade iii Astrocyric tumour?

A

Anaplastic astrocytoma

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98
Q

What is a WHO Grade iv Astrocyric tumour?

A

Glioblastoma multiforme

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99
Q

What is the WHO Astrocytic tumour grading based on?

A

Pathological findings:

  • Endothelial proliferation
  • Cellular pleomorphism
  • Mitoses
  • Necrosis (Glioblastoma multiforme)
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100
Q

What are the only truly benign astrocytic tumours?

A

Grade i astrocytomas

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101
Q

What populations are Grade i astrocytomas most common in?

A

Children and young adults

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102
Q

Where do pilocytic astrocytomas tend to affect?

A

Optic nerve
Hypothalamic gliomas
Cerebellum
Brainstem

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103
Q

How is a pilocytic astrocytoma treated?

A

Surgery (curative)

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104
Q

What are the three types of Grade ii “low grade” astrocytomas?

A

Fibrillary
Gemistocytic
Protoplasmic

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105
Q

What histological features do low grade astrocytomas show?

A

Hypercellularity
Pleomorphism
Vascular proliferation
Necrosis

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106
Q

Where are low-grade astrocytomas most common?

A

Temporal lobe
Posterior frontal lobe
Anterior parietal lobe

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107
Q

How do low-grade astrocytomas tend to present?

A

Seizures

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108
Q

What is the treatment for Grade ii astrocytomas?

A

Surgery +/-

  • Serial imaging
  • Radiation
  • Chemo
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109
Q

How do we decide whether to do adjuvant therapies in Grade ii astrocytomas?

A

Molecular profile (The following have better prognosis):

  • IDH-1
  • 1p19q
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110
Q

What is brachytherapy?

A

Placement of radioactive isoptopes directly into tissue

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111
Q

When is brachytherapy appropriate?

A

Tumour <4cm
Performance status >=70%
No subependymal spread

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112
Q

What are glioblastomas?

A

Grade ii astrocytomas

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113
Q

Why is surgery carried out on Grade ii astrocytomas?

A

Seizure control
Prevent/Treat herniation
Treat CSF obstruction

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114
Q

What defines a large Grade ii astrocytoma?

A

Diameter >6cm

Crossing midline

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115
Q

What WHO grades are malignant astrocytomas?

A

iii and iv

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116
Q

What is the median survival for anaplastic astrocytomas (Grade iii)?

A

2 years

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117
Q

What is the most common primary astrocytoma?

A

Glioblastoma multiforme

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118
Q

What is the median survival for Glioblastoma multiformes?

A

12-14 months

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119
Q

How does a Glioblastoma multiforme spread?

A

White matter tracking

CSF pathways

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120
Q

What are some causes of multiple glioblastomas?

A

NF
Tuberous sclerosis
Von Hippel-Lindau
PML

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121
Q

What is the Stupp protocol for treatment of malignant astrocytomas?

A

Surgery + Radiotherapy + Temozolomide

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122
Q

What is the PCV chemotherapy regime?

A

Procarbazine
CCNU
Vincristine

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123
Q

What does radiotherapy have a clear role in in terms of brain tumours?

A

Treating malignant tumours post-surgery

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124
Q

What are side effects of radiotherapy for brain tumours?

A

IQ drop by 10 points
Skin and hair changes
Fatigue

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125
Q

Where are oligodendrial tumours most common?

A

Frontal lobes

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126
Q

In what age range are oligodendrial tumours most common?

A

25-45 years

Smaller peak in kids 6-12 years

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127
Q

How do olidodendrial tumours present?

A

Seizures

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128
Q

How is the affinity for the cerebral cortex in oligodendrial tumours displayed?

A

In the transcortical penetration - Infiltration into:

  • Subarachnoid space
  • Leptomeninges
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129
Q

How do oligodendrial tumours appear macroscopically?

A

Solid

Greyish-pink

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130
Q

How can oligodendrial tumours be differentiated by astrocytomas?

A

Calcification (usually peripheral)
Cysts
Peritumoural haemorrhage

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131
Q

What makes up a neoplastic collision-type tumours?

A

Oligodendrial and astrocytic cells

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132
Q

What can neoplastic collision-type tumours arise from?

A

Common precursor - O2A cells

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133
Q

What is the treatment for chemosensitive oligodendrial tumours?

A

Procarbazine
Lomustine
Vincristine

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134
Q

What effect can radiotherapy have in oligodendrial tumours?

A

Reduces seizures

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135
Q

What is the median survival for low grade oligodendrial tumours?

A

10yrs

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136
Q

What is the M:F ration for meningiomas?

A

2:3

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137
Q

Breast cancer and meningioma?

A

NF ii = 22q

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138
Q

What subgroup of meningioma do the following describe:

  • Carpet/Sheet-like lesion
  • Infiltrates dura and sometimes bone
A

Meningioma en plaque

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139
Q

How can we reduce the recurrence of Meningioma en plaque?

A

Remove involved bone

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140
Q

Where are the most common meningioma locations?

A

Parasagittal
Convexity
Sphenoid
Intraventricular

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141
Q

What are the symptoms of a meningioma?

A

Headaches
Skull base -> CN neuropathies
Regional anatomical disturbance

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142
Q

What percentage of meningiomas are histologically benign?

A

90%

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143
Q

What are the classic types meningiomas?

A

Meningotheliomatous
Fibrous
Transitional

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144
Q

What are the other three groups of meningiomas?

A

Angioblastic
Atypical
Malignant

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145
Q

What are the two types of grade ii aggressive meningiomas?

A

Clear cell

Choroid

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146
Q

What are the two types of grade iii aggressive meningiomas?

A

Rhabdoid

Papillary

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147
Q

How do meningiomas appear on CT?

A

Homogenous and densely enhancing
Oedema
Hyperostosis/Skull ‘blistering’

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148
Q

How do meningiomas appear on MRI?

A

Dural tail

Patency of dural sinuses

149
Q

When is angiography indicated in meningioma?

A

If embolisation is planned

150
Q

How do meningiomas appear on angiography?

A

Hypervascular:

  • Arterial phase
  • Well into venous phase
  • Slow washout
151
Q

What vessels are meningiomas commonly supplied by?

A

Dural arteries

152
Q

What is the five year survival for meningiomas?

A

90%

153
Q

What condition are vestibular schwannomas associated with?

A

NF ii

154
Q

What are the symptoms of an acoustic neuroma?

A

Hearing loss
Tinnitus
Dysequilibrium

155
Q

What can larger acoustic neuromas affect?

A

CNs v, vii and viii
Brainstem
Hydrocephalus

156
Q

What is the medical management of an acoustic neuroma?

A

Periodic neuro exam
Hearing aid
Periodic MRI

157
Q

When is gamma knife surgery useful in acoustic neuromas?

A

If <3cm

If surgery is high risk

158
Q

What negative effects can occur after surgery for an acoustic neuroma?

A

CN vii palsy
Corneal reflex
Nystagmus
Abnormal eye movements

159
Q

What is grade 1 of facial nerve function?

A

Normal symmetric function in all areas

160
Q

Incomplete eye closure on maximal effort and spasm suggests what grade of facial nerve function?

A

Grade iv

161
Q

Incomplete eye closure, slight mouth corner movement and spasms absent suggest what grade of facial nerve function?

A

Grade v

162
Q

When there is no facial movement and loss of tone, what grade of facial nerve function is that?

A

Grade vi

163
Q

What is the peak incidence for germ cell tumours?

A

10-12 years

164
Q

Are germ cell tumours more common in men or women?

A

Men

165
Q

How do germ cell tumours appear on CT?

A

Iso- or hyperdense

166
Q

How can germ cell tumours metastasize?

A

Via CSF

167
Q

What are the most common CNS germ cell tumours?

A

Germinomas

168
Q

What CNS germ cell tumours are radiosensitive?

A

Germinomas

169
Q

How are germ cell tumours treated?

A

Radiotherapy if >3 years

Cis-platin (1st line if <3 years)

170
Q

What can radiotherapy cause if the patient is younger than 3 years?

A

Excess hypothalamic and cognitive dysfunction

171
Q

What tumours is alpha-fetoprotein present in?

A

Yolk sac tumours

Teratomas

172
Q

What tumours is hCG present in?

A

Choriocarinoma

Germinoma

173
Q

What cells produce alpha-fetoprotein?

A

Yolk sac endoderm

Embryonic intestinal epithelium

174
Q

What cells produce hCG?

A

Syncytiotrophoblasts

175
Q

What tumours produce placental alkaline phosphatase?

A

Germinoma
(Choriocarcinoma)
(Yolk sac tumours)

176
Q

What cells produce placental alkaline phosphatase?

A

Primordial germ cells

Syncytiotrophoblasts

177
Q

What can a patient be loaded with before surgery for a brain tumours?

A

Phenytoin OR

Keppra

178
Q

What cover can be provided pre-op for brain tumours?

A

Dexamethasone with lansoprazole

179
Q

How are post-surgical seizures treated?

A

Phenytoin OR

Lorazepam

180
Q

Why is diazepam not used to treat post-op seizures?

A

Stays in fat
Leaks out later:
- Patient stops breathing

181
Q

When is dexamethasone stopped upon discharge after brain tumour removal?

A

If benign tumour

182
Q

What is the maintenance dose of dexamethasone upon discharge?

A

2mg od

183
Q

What are headache red flags?

A 
New onset in >55 year olds
Known/Previous malignancy
Immunosuppressed
Early morning headache
Exacerbation by valsava (increases ICP)
184
Q

What is the one year prevalence of migraine?

A

10-15%

185
Q

What is the M:F ratio for migraines?

A

1:2/5

186
Q

What is the usual amount of migraines a sufferer has per month?

A

1

187
Q

What percentage of migraines are associated with an aura?

A

20%

188
Q

What is the IHS criteria for diagnosis of migraine without aura?

A 
1. At least 5 attacks lasting 4-72 hours each
AND
2. Two of:
- Moderate to severe
- Unilateral
- Throbbing pain
- Worst on movement
AND
3. One of:
- Autonomic features
- Photophobia
- Phonophobia
189
Q

What do stress triggers release in the brain that is linked to migraines?

A

Serotonin

190
Q

What happens to vasculature in migraines?

A

Constrict and dilate

191
Q

Why is there pain in migraines?

A

Chemicals (including substance P) irritate nerves and blood vessels

192
Q

What is the neurophysiology of migraine with aura?

A
  1. Cortical spreading depolarisation/depression
  2. Trigeminal vascular system activation resulting in cranial blood vessel dilatation
  3. Release of:
    - Substance P
    - Neurokinin A
    - CGRP
193
Q

Where are the migraine centres?

A

Dorsal raphe nucleus

Locus coeruleus

194
Q

What is the most common manifestation of an aura?

A

Visual

195
Q

How long do auras tend to last in migraines?

A

20-60 minutes

196
Q

When does the headache follow the aura?

A

<1 hour later

197
Q

What are the visual aura patterns in an aura?

A

Central scotomata
Central fortification
Hemianopia

198
Q

What can trigger a migraine with aura?

A 
Sleep
Diet
Stress
Hormones
Physical effort
199
Q

What NSAID doses act as an abortive measure for migraines?

A

Aspirin 900mg
Naproxen 250mg
Ibuprofen 400mg
(All +/- anti-emetic)

200
Q

What percentage of patients who take an NSAID to relieve a migraine have some reduction in pain at 2 hours?

A

60%

201
Q

What percentage of migraine patients have complete relief from NSAIDs?

A

25%

202
Q

How do triptans work?

A

5-HT agonists:

  • 5-HT1B
  • 5-HT1-
203
Q

How can triptans be administered?

A

PO
Sublingual
S/C

204
Q

When are triptans administered?

A

At start of headache

205
Q

What triptans are available are what is their relative efficacy?

A

Rizatriptan = Eletriptan > Sumatriptan

206
Q

What triptans can provide sustained relief?

A

Frovatriptan

207
Q

When should migraine prophylaxis be considered?

A

> 3 attacks per month OR

Very severe

208
Q

How long must a prophylactic drug for migraine be trialled?

A

Minimum of 4 months

209
Q

What beta blocker can be used as migraine prophylaxis? What dose is given?

A

Propanolol

80-240mg daily

210
Q

When is a beta-blocker contraindicated in migraine prophylaxis?

A

Asthma
Peripheral vascular disease
Heart failure

211
Q

What carbonic anhydrase inhibitor (NA/GABA) can be used in migraine prophylaxis? What dose is given?

A

Topiramate

25-100mg

212
Q

What are the adverse effects of carbonic anhydrase inhibitors?

A

Weight loss
Paraesthesia
Impaired concentration
Enzyme inducer

213
Q

What dose of amitriptyline can be used in migraines?

A

25mg

214
Q

What are the side effects of amitriptyline?

A

Dry mouth
Postural hypotension
Sedation

215
Q

What other drugs can be used for migraine prophylaxis?

A

Gabapentin
Pizotifen
Sodium valproate

216
Q

When would imaging be considered in migraines?

A

Late onset >55 years
Known malignancy
Acephalgic migraine (ie no headache)

217
Q

What are trigeminal autonomic cephalagias characterised by?

A

Unilateral trigeminal distribution pain

218
Q

What are trigeminal autonomic cephalagias associated with?

A

Ipsilateral cranial autonomic features:

  • Ptosis
  • Miosis
  • Nasal stuffiness
  • Nausea and vomiting
  • Tearing
  • Eye lid oedema
219
Q

If autonomic features are present in a trigeminal autonomic cephalagia, what investigations are indicated?

A

MRI brain

MR angiography

220
Q

What are the common populations for cluster headaches?

A

30-40 year olds

Men (M:F is 5:1)

221
Q

When are cluster headaches common?

A 
Striking circadian (around sleep)
Seasonal variation
222
Q

How long do cluster headaches last?

A

45-90 mins average

Range of 20 mins to 3 hours

223
Q

How frequent are cluster headaches?

A

1-8/day

224
Q

How long can bouts of cluster headaches last?

A

A few weeks to months

225
Q

How is a cluster headache treated?

A

High flow oxygen for 20 mins
S/C sumatriptan 6mg
Steroids (reduce course over 2 weeks)

226
Q

What drug can be used for cluster headache prophylaxis?

A

Verapamil

227
Q

In what populations is paroxysmal hemicrania common in?

A

50-60 year olds

Female > Male (M:F is 1:2)

228
Q

How long does a paroxysmal hemicrania last?

A

10-30 minutes

Range of 2 mins to 45 hours

229
Q

How frequent do paroxysmal hemicrania attacks last?

A

1-40/day

230
Q

How is paroxysmal hemicrania treated?

A

Indomethicin (absolute response)

231
Q

How can cluster headaches and paroxysmal hemicrania be distinguished?

A

Cluster headaches last longer and are less frequent

232
Q

What is SUNCT?

A

Short-lived Unilateral Neuralgiform headache with Conjunctival injection and Tearing

233
Q

How is SUNCT treated?

A

Lamotrigine

Gabapentin

234
Q

In what populations is trigeminal neuralgia common?

A

> 60 year olds

Women > Men

235
Q

How is trigeminal neuralgia triggered?

A

Touch

236
Q

What divisions of the trigeminal nerve are most commonly affected in trigeminal neuralgia?

A

V2 and V3

237
Q

What sort of pain is present in trigeminal neuralgia?

A

Severe, unilateral, stabbing

238
Q

How long does an attack of trigeminal neuralgia last?

A

1-90 seconds

239
Q

How frequent are trigeminal neuralgia attacks?

A

10-100/day

240
Q

How long can bouts of trigeminal neuralgia last before remission?

A

Few weeks to months

241
Q

What sort of pain is felt in cluster headaches and paryoxysmal hemicrania?

A

Severe, unilateral boring

242
Q

What sort of pain is felt in SUNCT?

A

Severe, unilateral, stabbing

243
Q

What is the M:F ratio in SUNCT?

A

2:1

244
Q

How long do attacks of SUNCT last?

A

15-120 seconds

245
Q

How frequent are attacks of SUNCT?

A

1/day - 30/hour

246
Q

What can trigger a cluster headache?

A

Alcohol

247
Q

What can trigger paroxysmal hemicrania?

A

Mechanical

248
Q

What can trigger SUNCT?

A

Cutaneous triggers

249
Q

What is the first line medical treatment for trigeminal neuralgia?

A

Carbamazepine

250
Q

What other drugs can be used to treat trigeminal neuralgia?

A

Gabapentin
Phenytoin
Baclofen

251
Q

What surgical treatments are available for trigeminal neuralgia?

A

Ablation

Decompression

252
Q

What is the main curare toxin?

A

D-tubocurarine

253
Q

How do curares cause NMJ dysfunction?

A

Occupies the same position as Ach on the receptor

Does not open ion channel

254
Q

How can curare toxicity result in morbidity and mortality?

A

No muscle contraction

No respiration

255
Q

Via what methods of administration is curare toxic?

A

IM

IV

256
Q

How long does it take for curares to have effect?

A

1-15 minutes

257
Q

Where are Clostridium botulinum found?

A

Soil

258
Q

How can IVDUs get botulism?

A

Black tar heroin

259
Q

How does botulinum toxin affect the NMJ?

A
  1. Cleaves presynaptic proteins involved in vesicle formation
  2. Blocks vesicle docking with presynaptic membrane
260
Q

How does botulism present?

A

Rapid onset weakness (No sensory loss)

261
Q

What is Lambert-Eaton Myaesthenia Syndrome?

A

Autoantibodies to presynaptic calcium channels (reducing vesicle release)

262
Q

How does Lambert-Eaton Myaesthenia Syndrome present?

A

Progressive weakness starting in the proximal limbs (legs affected worse than the arms):
- Difficulty climbing stairs and standing up from sitting

263
Q

What is Lambert-Eaton Myaesthenia Syndrome associated with?

A

Small-cell lung cancer (paraneoplastic syndrome)

264
Q

What is Myaesthenia Gravis?

A

Antibodies against postsynaptic Ach receptors

265
Q

What is the pathophysiology of Myaesthenia Gravis?

A

Reduced number of Ach receptors and endplate flattening

266
Q

When does Myaesthenia Gravis become symptomatic?

A

When Ach receptors reduced to 30% of normal

267
Q

In what percentage of Myaesthenia Gravis patients are Ach antibodies present?

A

80-90%

268
Q

75% of patients with Myaesthenia Gravis also have what?

A

Hyperplasia of the thymus OR

Thyoma

269
Q

What do the antibodies in Myaesthenia Gravis do?

A

Block Ach binding

Trigger inflammation damaging folds of postsynaptic membrane

270
Q

What are the two peaks of incidence in Myaesthenia Gravis?

A

Females in 3rd decade

Males in 6th/7th decades

271
Q

What is the M:F ratio in Myaesthenia Gravis?

A

2:3

272
Q

What are the clinical features of Myaesthenia Gravis?

A

Weakness gets worse throughout day
Extraocular weakness
Facial and bulbar weakness
Limb weakness is usually proximal

273
Q

What medical treatment can be used in Myaesthenia Gravis?

A

Pyridostigmine (Acetylcholinesterase inhibitor)

274
Q

Emergency treatment of Myaesthenia Gravis?

A

Plasma exchange OR

IV Ig

275
Q

What cause morbidity in Myaesthenia Gravis?

A

Respiratory failure

Aspiration pneumonia

276
Q

What is each muscle fibre surrounded by?

A

Endomysium

277
Q

What is each muscle fascicle surrounded by?

A

Perimysium

278
Q

What are a large number of fascicles surrounded by?

A

Epimysium

279
Q

What is the actin:myosin ratio in smooth muscles?

A

10:1

280
Q

What can precipitate fasciculations in a healthy muscle?

A

Stress
Caffeine
Fatigue

281
Q

When do pathological fasciculations occur?

A

Denervated muscle which becomes hyperexcitable

282
Q

What is myotonia and what channel affects it?

A

Failure of muscle relaxation

Chloride channel

283
Q

What are some signs/symptoms in muscle disease?

A

Myalgia
Muscle weakness
Wasting
Hyporeflexia

284
Q

What are inflammatory causes of muscle disease?

A

Dermatomyositis

Polymyositis

285
Q

What are congenital causes of muscle disease?

A

Congenital myaesthenic syndromes

Congenital myopathies

286
Q

What are inherited causes of muscle disease?

A

Muscular dystrophies
Dystrophinopathies
Limb girdle muscular dystrophies
Myotonic dystrophy

287
Q

Symmetrical, progressive, proximal weakness over weeks to months
Raised CK which responds to steroids

A

Polymyositis

288
Q

Symmetrical, progressive, proximal weakness over weeks to months
Raised CK which responds to steroids
‘Heliotrope’ rash on face
Up to 50% have underlying malignancy

A

Dermatomyositis

289
Q

Slowly progressive weakness
6th decade
Thumb sparing
Poor steroid response

A

Inclusion body myositis

290
Q

What is the mode of inheritance of myotonic dystrophy?

A

Autosomal dominant

291
Q

What are the features of myotonic dystrophy?

A 
Myotonia
Weakness (hands/feet/face/neck at first)
Cataracts
Ptosis
Frontal balding
Cardiac defects
292
Q

What causes myotonic dystrophy?

A

Trinucleotide repeat disorder with anticipation

293
Q

What causes BMD?

A

Mutations in dystrophin gene

294
Q

What causes DMD?

A

Mutations in dystrophin gene

295
Q

What is the mode if inheritance of DMD and BMD?

A

X-linked recessive

296
Q

What is a viral cause of myopathy?

A

Coxsackie

297
Q

What cause of infectious myopathy can arise from uncooked pork?

A

Cistercercosis

298
Q

What other infectious causes are there of myopathy?

A

Trypanosomiasis

Borrelia

299
Q

What drugs can cause a nectrosing myopathy?

A

Statins (HMG Co-A reductase inhibitors)
Fibrates
Nicotinic acid

300
Q

What steroids cause corticosteroid myopathies?

A

Fluorinated:

  • Dexamethasone
  • Triamcinolone
301
Q

What drugs can cause lysosomal storage myopathies?

A

Hydroxychloroquine

Amiodarone

302
Q

What drugs can cause antimicrotubular myopathies?

A

Colchicine

Vincristine

303
Q

What drugs can cause hypokalaemic myopathy?

A

Diuretics

Oral contraceptives

304
Q

What drugs can cause inflammatory myopathies?

A

D-penicillamine

Interferon-alpha

305
Q

What is rhabdomyolysis?

A

Damage to skeletal muscle causing leakage of toxic intracellular contents into plasma

306
Q

What can cause rhabdomyolysis?

A

Crush injuries
Toxins
Post-convulsions

307
Q

What is the triad of symptoms in rhabdomyolysis?

A

Myalgia
Muscle weakness
Myoglobinuria

308
Q

What are complications of rhabdomyolysis?

A

Acute renal failure

DIC

309
Q

Why is 99.9% of sound reflected?

A

High impedence of cochlear fluid

310
Q

How many dB of sound is lost from air?

A

30 dB

311
Q

How does the middle ear overcome sound loss from the air?

A

Increase the sound pressure (+34dB)

312
Q

What are the three mechanisms for impedence matching?

A
  1. Area ratio of eardrum to stapes is 20:1 (+26dB)
  2. Lever action of ossicles is 1.3:1 (+2dB)
  3. Buckling of eardrum gives 2x pressure increase (+6dB)
313
Q

What separates the scala vestibuli from the scala media?

A

Reissner’s membrane

314
Q

What separates the scala media from the scala tympani?

A

Basilar membrane

315
Q

Where do the scala tympani and scala vestibuli connect?

A

Helicotrema

316
Q

What fluid is in the scala tympani and scala vestibuli?

A

Perilymph

317
Q

What does the scala tympani meet?

A

Oval window

318
Q

What does the scala vestibuli meet?

A

Round window

319
Q

What does pressure at the oval window cause at the round window?

A

Complimentary motion

320
Q

What is the structure of the basilar membrane?

A

Thick and taut near base

Thin and floppy near apex

321
Q

Where are hair cells located?

A

Between:

  • Basilar membrane
  • Reticular lamina
322
Q

Where do the tips of hair cells lie?

A

In the tectorial membrane

323
Q

Where are the cell bodies of hair cells?

A

In the spiral ganglion

324
Q

What happens when hair cells are forced towards the kinocilium?

A

TRPA1 channels open
Potassium enters
Depolarisation

325
Q

What is the function of inner hair cells?

A

Main source of afferent CN viii signals

326
Q

How many afferent fibres are there per hair cell?

A

~10

327
Q

How many outer hair cells does one inner hair cell supply with its afferent signals?

A

Many

328
Q

What is the function of outer hair cells?

A

Primarily receive efferent inputs
Control stiffness
Amplify membrane vibration

329
Q

What motor protein is present in the membrane of outer hair cells and what can it change?

A

Prestin

Changes length of the cell

330
Q

What do outer hair cells respond to?

A

A receptor potential

A change in length

331
Q

What effect does furosemide have on outer hair cells?

A

Inactivates the membrane motor

332
Q

What happens when there is a length change of an outer hair cell?

A
  1. Increase movement of basilar membrane
  2. Increased bending of inner hair cells
  3. Transduction
333
Q

What is the concentration gradient of potassium in the endolymph?

A

Inwards to the cell (4-5mV EqK)

334
Q

What is the endolymph potential?

A

80mV

335
Q

What is the Volley principle?

A

All neurones innervating a single hair cell code frequency together

336
Q

What is the pathway from the cochlear to the auditory cortex?

A

Cochlea
Cochlear nucleus (medulla)
Superior olive (pons)
Inferior colliculus (caudal midbrain)
Medial geniculate body (rostral midbrain)
Auditory cortex (sup. temporal gyrus in temporal lobe)

337
Q

What are the three cochlear nuclei?

A

Dorsal cochlear nucleus
Posteroventral cochlear nucleus
ANteroventral cochlear nucleus

338
Q

What do the three cochlear nuclei span?

A

Pontomedullary junction

339
Q

What signal arrives at the left superior olive first?

A

The signal from the ipsilateral ear

340
Q

What part of the vestibular system is responsible for sensing head angular acceleration?

A

Semicircular canals

341
Q

When is the sensation of head angular acceleration useful?

A

During head rotation

342
Q

What parts of the vestibular system are responsible for sensing head linear acceleration?

A

Saccule

Utricle

343
Q

When is the sensation of head linear acceleration useful?

A

Translational motion

Gravity (extension head tilt)

344
Q

What are the semicircular canals filled with

A

Endolymph

345
Q

What part of the semicircular canals contains clusters of hair cells?

A

Crista

346
Q

What part of the semicircular canals is a bulge containing cristae?

A

Ampulla

347
Q

Where do the cilia in the semicircular canals project?

A

Into the gelatinous cupula

348
Q

Where do the hair cells lie in the otolith organs?

A

Macula

349
Q

What divides the hair cells in the otolith organs into two populations with opposing polarities?

A

Striola

350
Q

What is the function of the vestibulo-ocular reflex?

A

Keeps eyes still as the head moves in space

351
Q

What is the function of the vestibulo-colic reflex?

A

Keeps the head still in space

Keeps head level when walking

352
Q

What is the function of the vestibular-spinal reflex?

A

Adjusts posture for rapid changes in posture

353
Q

What antibiotics can cause vestibular dysfunction?

A

Aminoglycoside:

  • Gentamicin
  • Streptomicin
354
Q

How does alcohol affect the vestibular system?

A 
Enters blood and capula
Floats in endolymph
Capula bends a little more
Hair cells bend (as if rotating)
Sensation of spinning
355
Q

What is the resting potential of photoreceptors?

A

-20mV

356
Q

What happens to the membrane potential upon light exposure?

A

Hyperpolarisation:

  • PNa is reduced so Na Channels close
  • PK > PNa
  • Vm approaches EK so hyperpolarisation
357
Q

What makes up rhodopsin?

A

Retinal (vit. A) and opsin (GPCR)

358
Q

What happens to rhodopsin when exposed to light?

A

Changed into:

  • All-trans-retinal AND
  • Opsin
359
Q

What enzyme turns all-trans-retinal to 11-cis-retinal?

A

Isomerase

360
Q

What is the other name for Vitamin A?

A

All-trans-retinol

361
Q

What does all-trans-retinal activate? What does it do?

A

Transducin:

  • Decreases cGMP
  • Closure of cGMP-gated sodium channels
  • Hyperpolariation (due to decreased sodium entry)
362
Q

What neurotransmitter is more abundant in the dark?

A

Glutamate

363
Q

If the space between photoreceptors is decreased, what effect does this have on visual acuity?

A

Increases acuity

364
Q

What do ON-centre bipolar/ganglion cells detect?

A

Increases in luminance

365
Q

What do OFF-centre bipolar/ganglion cells detect?

A

Decreases in luminance

366
Q

What layer do magnocellular LGN neurones project to?

A

Layer IVc-alpha

367
Q

What layer do parvocellular LGN neurones project to?

A

Layer IVc-beta

368
Q

What layer do koniocellular LGN neurones project to?

A

Synapse in layers II and III (bypass IV):

- Blobs visible by cytochrome oxidase staining

369
Q

Where are the most binocular neurones found in striate cortex?

A

Layer iii

Year 3 - Neurology (DP) (5 decks)

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