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1 - MSRA > Neurology > Flashcards

Neurology Flashcards

1
Q

Receptive aphasia aka..

A

Wernicke’s aphasia

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2
Q

Area of lesion in Wernicke’s (receptive) aphasia

A

Superior temporal gyrus

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3
Q

Blood supply to superior temporal gyrus

A

Inferior division of left MCA

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4
Q

Presentation of Wernicke’s aphasia

A

Sentences that make no sense, word substitution, and neologisms, but speech remains fluent - ‘word salad’

Comprehesion is impaired

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5
Q

Expressive aphasia aka…

A

Broca’s aphasia

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6
Q

Area of lesion in Broca’s aphasia

A

Inferior frontal gyrus

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7
Q

Blood supply to inferior frontal gyrus

A

Superior division of left MCA

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8
Q

Presentation of Broca’s aphasia

A

Speech non-fluent, laboured, halting
Repetition is impaired

Comprehension normal

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9
Q

Area of lesion in conduction aphasia

A

Arcuate fasiculus (connection between Wernicke’s and Broca’s area)

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10
Q

Presentation of conduction aphasia

A

Speech fluent but repetition poor, aware of errors

Comprehension normal

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11
Q

Location of lesion in global aphasia

A

Large lesion affecting all 3 areas (superior temporal gyrus, inferior frontal gyrus, arcuate fasiculus)

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12
Q

When should anti-epileptics be started following first seizure

A
  • Neurological deficit
  • Brain imaging shows structural abnormality
  • EEG shows unequivocal epileptic activity
  • Patient or their family/carers considers risk of having further seizure unacceptable
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13
Q

First line treatment generalised tonic-clonic seizures

A

Men - sodium valproate
Females - lamotrigine or levetiracetam

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14
Q

First line treatment focal seizures

A

Lamotrigine or levetiracetam

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15
Q

Second line treatment focal seizures

A

Carbamazepine, oxcarbazepine, zonisamide

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16
Q

First line treatment absence seizures

A

Ethosuximide

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17
Q

Second line treatment absence seizures

A

Male - sodium valproate
Female - lamotrigine or levetiracetam

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18
Q

Effect of carbamazepine in absence seizures

A

May exacerbate

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19
Q

First line treatment myoclonic seizures

A

Male - sodium valproate
Females - levetiracetam

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20
Q

First line treatment tonic or atonic seizures

A

Male - sodium valproate
Female - lamotrigine

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21
Q

CN I aka

A

Olfactory nerve

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22
Q

CN I function

A

Smell

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23
Q

CN II aka

A

Optic nerve

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24
Q

CN II function

A

Sight

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25
Q

CN III aka

A

Oculomotor nerve

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26
Q

CN III function

A
  • Eye movement - medial rectus, inferior oblique, superior rectus, inferior rectus
  • Pupil constriction
  • Accommodation
  • Eyelid opening
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27
Q

CN III palsy presentation

A
  • Ptosis
  • ‘Down and out’ eye
  • Dilated, fixed pupil
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28
Q

CN IV aka

A

Trochlear

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29
Q

CN IV function

A

Eye movement - superior oblique

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30
Q

CN IV palsy presentation

A

Defective downward gaze → vertical diplopia

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31
Q

CN V aka

A

Trigeminal

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32
Q

CN V function

A
  • Facial sensation
  • Mastication
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33
Q

CN V lesion presentation

A
  • Trigeminal neuralgia
  • Loss of corneal reflex (afferent)
  • Loss of facial sensation
  • Paralysis of mastication muscles
  • Deviation of jaw to weak side
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34
Q

CN VI aka

A

Abducens

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35
Q

CN VI function

A

Eye movement - lateral rectus

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36
Q

CN VI palsy presentation

A

Palsy results in defective abduction to horizontal diplopia

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37
Q

CN VII aka

A

Facial nerve

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38
Q

CN VII function

A
  • Facial movement
  • Taste to anterior 2/3 of tongue)
  • Lacrimation
  • Salivation
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39
Q

CN VII lesion presentation

A
  • Flaccid paralysis of upper and lower face
  • Loss of corneal reflex (efferent)
  • Loss of taste
  • Hyperacusis
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40
Q

CN VIII aka

A

Vestibulocochlear

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41
Q

CN VIII function

A
  • Hearing
  • Balance
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42
Q

CN VIII lesion presentation

A
  • Hearing loss
  • Vertigo
  • Nystagmus
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43
Q

CN IX aka

A

Glossopharyngeal

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44
Q

CN IX function

A
  • Taste to posterior 1/3 of tongue
  • Salivation
  • Swallowing
  • Mediates input from carotid body and sinus
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45
Q

CN IX lesion presentation

A
  • Hypersensitive carotid sinus reflex
  • Loss of gag reflex (afferent)
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46
Q

CN X aka

A

Vagus

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47
Q

CN X function

A
  • Phonation
  • Swallowing
  • Innervates viscera
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48
Q

CN X lesion presentation

A
  • Deviated uvula from site of lesion
  • Loss of gag reflex
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49
Q

CN XI aka

A

Accessory

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50
Q

CN XI function

A

Head and shoulder movement

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51
Q

CN XI lesion presentation

A

Weakness turning head to contralateral side

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52
Q

CN XII aka

A

Hypoglossal

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53
Q

CN XII function

A

Tongue movement

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54
Q

CN XII lesion presentation

A

Tongue deviates towards side of lesion

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55
Q

Afferent limb of corneal reflex

A

Opthalmic (division of trigeminal) nerve

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56
Q

Efferent limb of corneal reflex

A

Facial nerve

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57
Q

Afferent limb of jaw jerk reflex

A

Mandibular reflex

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58
Q

Efferent limb of jaw jerk reflex

A

Mandibular nerve

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59
Q

Afferent limb of gag reflex

A

Glossopharyngeal nerve

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60
Q

Efferent limb of gag reflex

A

Vagal nerve

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61
Q

Afferent limb of carotid sinus reflex

A

Glossopharyngeal nerve

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62
Q

Efferent limb of carotid sinus reflex

A

Vagal nerve

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63
Q

Afferent limb of pupillary light reflex

A

Optic nerve

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64
Q

Efferent limb of pupillary light reflex

A

Oculomotor nerve

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65
Q

Afferent limb of lacrimation reflex

A

Ophthalmic nerve

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66
Q

Efferent limb of lacimation reflex

A

Facial nerve

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67
Q

Anterior cerebral artery stroke features

A
  • Contralateral hemiparesis and sensory loss
  • Lower extremity > upper
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68
Q

Middle cerebral artery stroke features

A
  • Contralateral hemiparesis and sensory loss
  • Upper extremity > lower
  • Contralateral homonymous hemianopia
  • Aphasia
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69
Q

Posterior cerebral artery stroke features

A
  • Contralateral homonymous hemianopia with macular sparing
  • Visual agnosia
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70
Q

What arteries affected in Weber’s syndrome

A

Branches of posterior cerebral artery supplying the midbrain

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71
Q

Weber’s syndrome features

A
  • Ipsilateral CN III palsy
  • Contralateral weakness of upper and lower extremity
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72
Q

What arteries infected in Wallenberg syndrome (lateral medullary syndrome)

A

Posterior inferior cerebellar artery

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73
Q

Wallenberg (lateral medullary) syndrome features

A

Ipsilateral - facial pain and temperature loss
Contralateral - limb/torso pain and temperature loss
Ataxia
Nystagmus

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74
Q

Artery affected in lateral pontine syndrome

A

Anterior inferior cerebellar arteryF

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75
Q

Features of lateral pontine syndrome

A

Ipsilateral - facial pain and temperature loss, facial paralysis, deafness
Contralateral - limb/torso pain and temperature loss
Ataxia
Nystagmus

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76
Q

Retinal artery stroke features

A

Amaurosis fugax

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77
Q

Basilar artery stroke features

A

Locked in syndrome

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78
Q

Lacunar stroke features

A

Either isolated hemiparesis, hemisensory loss, or hemiparesis with limb ataxia

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79
Q

Capgras syndrome

A

Delusion that friend or partner has been replaced by identical looking imposter

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80
Q

Othello syndrome

A

Irrational belief partner is having affair with no objective evidence

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81
Q

De clerambault syndrome

A

Delusional idea that person whom they consider to be of higher social and/or professional standing is in love with them

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82
Q

Cotard syndrome

A

Delusional idea one is dead

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83
Q

Examples 5-HT3 antagonists

A

Ondansetron
Palanostetron

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84
Q

Use 5-HT3 antagonists

A

Mainly management of chemotherapy related nausea

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85
Q

SEs 5HT3 receptor antagonists

A

Prolonged QT interval
Constipation

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86
Q

Advantage palanosetron over ondansetron

A

Reduced effect on QT interval

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87
Q

Inheritance ataxia telangiectasia

A

Autosomal recessive

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88
Q

When does ataxia telangiectasia present

A

Early childhood

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89
Q

Features ataxia telangiectasia

A

Cerebellar ataxia
Telangiectasia
IgA deficiency → recurrent chest infections

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90
Q

Malignancy and ataxia telangiectasia

A

10% risk of developing malignancy - lymphoma, leukaemia, non-lymphoid tumours

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91
Q

What is Bell’s palsy

A

Acute, unilateral, idiopathic facial nerve paralysis

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92
Q

Features Bell’s palsy

A

Lower motor neuron facial nerve palsy → forehead affected
Post-auricular pain
Altered taste
Dry eyes
Hyperacusis

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93
Q

Management Bells palsy

A

Oral pred within 72 hours of onset
?Antivirals if severe facial nerve palsy
Eye care - artificial tears, eye lubricants, tape eye closed at bedtime

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94
Q

Importance of eye care Bell’s palsy

A

Prevent exposure keratopathy

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95
Q

Referral criteria Bell’s palsy

A

If paralysis shows no signs of improvement after 3 weeks, refer urgently to ENT

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96
Q

When to consider referral to plastic surgery Bell’s palsy

A

For more long-standing weakness, e.g. several months

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97
Q

Prognosis Bell’s palsy

A

Most people make full recovery within 3-4 months
If untreated, around 15% of patients have permanent moderate to severe weakness

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98
Q

Causes brain abscess

A
  • Extension of sepsis from middle ear or sinuses
  • Trauma or surgery to scalp
  • Penetrating head injuries
  • Embolic events from endocarditis
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99
Q

Presentation brain asbcess

A

Depends on site of abscess, those in critical sites, e.g. motor cortex will present earlier

Headache
Fever (may be absent, usually not swinging)
Focal neurology
Nausea
Papilloedema
Seizures

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100
Q

Investigation brain abscess

A

CT scanning

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101
Q

Management brain abscess

A

Craniotomy and debridement of abscess
IV antibiotics
ICP management

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102
Q

Limitation of craniotomy and debridement of brain abscess

A

Abscess may reform because head is closed following drainage

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103
Q

IV antibiotics used in brain abscess

A

3rd gen cephalosporin + metronidazole

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104
Q

What is used for ICP management in brain abscess

A

Dexamethasone

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105
Q

Use of carbamazepine

A

Epilepsy, particularly partial seizures - most common use
Trigeminal neuralgia
Bipolar disorder

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106
Q

Adverse effects carbamazepine

A

P450 enzyme inducer
Dizziness and ataxia
Drowsiness
Headache
Visual disturbance, esp diplopia
Steven-Johnson syndrome
Leucopenia and agranulocytosis
Hyponatraemia secondary to SIADH

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107
Q

What is cataplexy

A

Sudden transient loss of muscular tone caused by strong emotion

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108
Q

What is Charcot-Marie-Tooth disease

A

Most common hereditary peripheral neuropathy, resulting in predominant motor loss

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109
Q

Management Charcot-Marie-Tooth disease

A

No cure, management focused on physical and occupational therapy

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110
Q

Features Charcot-Marie-Tooth disease

A
  • Foot drop
  • High arched feet
  • Hammer toes
  • Distal muscle weakness
  • Distal muscle atrophy
  • Hyporeflexia
  • Stork leg deformity

May be history of frequently sprained ankles

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111
Q

Risk factors cluster headaches

A

Male
Smoker

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112
Q

Triggers cluster headaches

A

Alcohol
Noctural sleep

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113
Q

Features cluster headaches

A

Intense sharp, stabbing pain around one eye, each episode lasting 15 mins - 2 hours
Redness, lacrimation, and lid swelling
Nasal stuffiness
Miosis and ptosis in minority

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114
Q

How long do clusters last in cluster headaches

A

4-12 weeks

Occur around once a year

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115
Q

Investigations cluster headaches

A

MRI with gadolinium contrast - underlying brain lesions sometimes found

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116
Q

Referral cluster headaches

A

Should speak specalist advice from neurologist if patient develops cluster headaches

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117
Q

Acute management cluster headaches

A

100% oxygen
SC triptan

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118
Q

Prophylaxis cluster headaches

A

Verapamil

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119
Q

Treatment paroxysmal hemicrania

A

Indomethacin

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120
Q

What does sciatic nerve divide into

A

Tibial and common peroneal nerves

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121
Q

Where does injury to common peroneal nerve occur

A

Neck of fibula

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122
Q

Features common peroneal nerve

A

Foot drop
Weakness of foot dorsiflexion
Weakness of foot eversion
Weakness of extensor hallucis longus
Sensory loss over dorsum of foot and lower lateral part of leg
Wasting of anterior tibial and perioneal muscles

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123
Q

Risk factors degenerative cervical myelopathy

A
  • Smoking
  • Genetics
  • Occupations exposing patients to high axial loading
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124
Q

Degenerative cervical myelopathy symptoms

A

Pain affecting neck, upper, or lower limbs
Loss of motor function - loss of digital dexterity, arm or leg weakness/stiffness leading to impaired gait and imbalance
Loss of sensory function causing numbness
Loss of autonomic function (urinary or faecal incontinence and/or impotence)

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125
Q

What is Hoffmans sign

A

Gently flicking one finger on a pateints hand → reflex twitching of other fingers on same hand

Suggests cervical myelopathy

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126
Q

Investigation degenerative cervical myelopathy

A

MRI of cervical spine

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127
Q

Findings MRI cervical spine in degenerative cervical myelopathy

A

Disc degeneration and ligament hypertrophy, with cord signal change

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128
Q

Referral degenerative cervical myelopathy

A

All patients need urgent referral for assessment by specialist spinal services (neurosurgery or ortho spinal)

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129
Q

Why is timing of surgery important in DCM

A

Any existing spinal cord damage can be permanent, early treatment (within 6 months of diagnosis) offers best chance of full recovery

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130
Q

Treatment DCM

A

Decompressive surgery

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131
Q

Role of observation in DCM

A

Close observation is option for mild stable disease

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132
Q

Role of physio in DCM

A

Should only be initiated by specialist services, as manipulation can cause more spinal cord damage

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133
Q

C2 dermatome landmark

A

Posterior half of skull (cap)

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134
Q

C3 dermatome landmark

A

High turtleneck shirt

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135
Q

C4 dermatome landmark

A

Low-collar shirt

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136
Q

C5 dermatome landmark

A

Ventral axial line of upper limb

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137
Q

C6 dermatome landmark

A

Thumb and index finger

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138
Q

C7 dermatome landmark

A

Middle finger and palm of hand

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139
Q

C8 dermatome landmark

A

Ring and little finger

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140
Q

T4 dermatome landmark

A

Nipples

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141
Q

T5 dermatome landmark

A

Inframammary fold

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142
Q

T6 dermatome landmark

A

Xiphoid process

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143
Q

T10 dermatome landmark

A

Umbilicus

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144
Q

L1 dermatome landmark

A

Inguinal ligament

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145
Q

L4 dermatome landmark

A

Knee caps

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146
Q

L5 dermatome landmark

A

Big toe, dorsum of foot

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147
Q

S1 dermatome landmark

A

Lateral foot, small toe

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148
Q

S2-3 dermatome landmark

A

Genitalia

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149
Q

Drugs causing peripheral neuropathy

A

Amiodarone
Isoniazid
Vincristine
Nitrofurantoin
Metronidazole

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150
Q

DVLA advice first unprovoked/isolated seizure

A

6 months off if no relevant structural abnormalities on brain imaging, and no definite epileptiform activity on EEG
If these conditions not met, 12 months

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151
Q

DVLA advice established epilepsy or multiple unprovoked seizures

A

May qualify for driving license if seizure free for 12 months

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152
Q

DVLA advice withdrawal of epilepsy medication

A

Should not drive whilst anti-epilepsy medication being withdrawn, and for 6 months after last dose

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153
Q

DVLA advice simple faint

A

No restriction

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154
Q

DVLA advice single episode syncope, explained and treated

A

4 weeks off

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155
Q

DVLA advice single episode unexplained syncope

A

6 months off driving

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156
Q

DVLA advice two or more episodes syncope

A

12 months off

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157
Q

DVLA advice stroke/TIA

A

1 month off, may not need to inform DVLA if no residual neurological deficit

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158
Q

DVLA advice multiple TIAs over short period of time

A

3 months off, inform DVLA

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159
Q

DVLA advice pituitary tumour

A

If craniotomy, 6 months
If trans-sphenoidal, can drive when no debarring residual impairment likely to affect safe driving

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160
Q

DVLA advice narcolepsy/cataplexy

A

Cease driving on diagnosis, can restart once satisfactory control of symptoms

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161
Q

DVLA advice chronic neurological disorders, e.g. MS, MND

A

Inform DVLA, complete PK1 form (application for driving license holders state of health)

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162
Q

Inheritance pattern dystrophinopathies

A

X linked recessive

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163
Q

DMD presentation

A

Progressive proximal muscle weakness from 5 years
Calf pseudohypertrophy
Gower’s sign
30% have intellectual impairment

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164
Q

What is Gower’s sign

A

Child uses arms to stand up from squatted position

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165
Q

Beckers muscular dystrophy age of presentation

A

After 10 years

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166
Q

Features encephalitis

A

Fever
Headache
Psychiatric symptoms
Seizures
Vomiting
Focal features, e.g. aphasia

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167
Q

Most common cause encephalitis

A

HSV-1 - 95% of cases in adults

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168
Q

Areas of brain affected in encephalitis

A

Temporal and inferior frontal lobes typically

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169
Q

CSF in encephalitis

A

Lymphoctosis
Elevated protein

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170
Q

Neuroimaging in encephalitis

A

Medial temporal and inferior frontal changes, e.g. petechial haemorrhages
Normal in 1/3

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171
Q

Best imaging modality in encephalitis

A

MRI

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172
Q

EEG in encephalitis

A

Lateralised periodic discharges at 2Hz

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173
Q

Management encephalitis

A

IV aciclovir

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174
Q

Features of temporal lobe seizures

A

May occur with or without impairment of consciousness
Aura in most patients
Typically last around one minute - automatisms, e.g. lip smacking/grabbing/plucking

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175
Q

Auras in temporal lobe seizures

A

Typically a rising epigastric sensation
Psychic or experiential phenomena, e.g. deja vu, jamais vu
Less commonly hallucinations - auditory, gustatory, olfactory

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176
Q

Features of frontal lobe seizures

A

Head/leg movements
Posturing
Post-ictal weakness
Jacksonian march

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177
Q

Features of parietal lobe seizures

A

Paraesthesia

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178
Q

Features occipital lobe seizures

A

Floaters/flashes

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179
Q

Inheritance pattern essential tremor

A

Autosomal dominant

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180
Q

Essential tremor

A

Postural tremor, worse if arms outstretched
Improved by alcohol and rest
Affects upper limbs and titubation (head tremor)

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181
Q

Management essential tremot

A

Propanolol first line
Primidone sometimes used

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182
Q

What is supplied by the facial nerve

A

Face - muscles of expression
Ear - nerve to stapedius
Taste - anterior 2/3 of tongue
Tear - parasympathetic fibres to lacrimal glands, also salivary g lands

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183
Q

Causes of bilateral facial nerve palsy

A

Sarcoidosis
Guillain-Barre syndrome
Lyme diseae
Bilateral acoustic neuromas, e.g. in NF2
Bilateral Bells palsy

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184
Q

Difference between LMN and UMN facial nerve palsy

A

UMN spares upper face (forehead), LMN affects all facial muscles

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185
Q

Causes of LMN facial nerve palsy

A

Bell’s palsy
Ramsay-Hunt syndrome
Acoustic neuroma
Parotid tumours
HIV
MS
Diabetes mellitus

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186
Q

Causes of UMN facial nerve palsy

A

Stroke
MS

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187
Q

Inheritance Friedreich’s ataxia

A

Autosomal recessive

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188
Q

Genetic defect in Friedreich’s ataxia

A

Trinucleotide repeat disorder - GAA repeat in X25 gene on chromosome 25

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189
Q

What is unusual about Friedreich’s ataxia

A

It does not demonstrate anticipation

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190
Q

Age of onset Friedreich’s ataxia

A

10-15

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191
Q

Most common presenting features Friedreich’s ataxia

A

Gait ataxia
Kyphoscoliosis

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192
Q

Neurological features Friedreich’s ataxia

A

Absent ankle jerks/extensor plantars
Cerebellar ataxia
Optic atrophy
Spinocerebellar tract degeneration

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193
Q

Other features Friedreich’s ataxia

A

Hypertrophic obstructive cardiomyopathy (90%)
Diabetes mellitus
High arched palate

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194
Q

GCS motor scoring

A

6 - obeys commands
5 - localises to pain
4 - withdraws from pain
3 - abnormal flexion to pain
2 - extending to pain
1 - none

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195
Q

GCS verbal scoring

A

5 - orientated
4 - confused
3 - words
2 - sounds
1 - none

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196
Q

GCS eye scoring

A

4 - spontaneous
3 - to speech
2 - to pain
1 - none

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197
Q

What is Guillain-Barre syndrome

A

Immune-mediated demyelination of the peripheral nervous system often triggered by an infection

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198
Q

Infection classically triggering Guillian-Barre syndrome

A

Campylobacter jejuni

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199
Q

Antibody correlated with clinical features in Guillian-Barre syndrome

A

Anti-GM1

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200
Q

What is Miler Fisher syndrome

A

Variant of Guillain-Barre syndrome, associated with opthalmoplegia, areflexia, and ataxia. Eye muscles usually affected first

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201
Q

Guillain-Barre syndrome vs Miller Fisher syndrome

A

Guillain-Barre ascending paralysis, Miller Fisher syndrome descending paralysis

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202
Q

Antibody seen in Miller Fisher syndrome

A

Anti-GQ1b (90%)

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203
Q

Presentation Guillain-Barre

A

65% experience back/leg pain in initial stages of the illness
Progressive, symmetrical weakness of all limbs, classically ascending, reflexes reduced or absent, sensory symptoms mild with few sensory signs
Resp muscle weakness
Cranial nerve involvement (diplopia, bilateral facial nerve palsy, oropharyngeal weakness)
Autonomic involvement (urinary retention, diarrhoea)
Less commonly, papilloedema (secondary to reduced CSF resorption)

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204
Q

Investigations in Guillain-Barre syndrome

A

Lumbar puncture
Nerve conduction studies

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205
Q

LP findings Guillain-Barre syndrome

A

Rise in protein with normal WCC

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206
Q

Nerve conduction studies findings Guillain-Barre syndrome

A

Decreased motor nerve conduction velocity
Prolonged distal motor latency
Increased F wave latency

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207
Q

Features tension headache

A

Recurrent, non-disabling, bilateral headache, often described as tight-band

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208
Q

Features medication overuse headache

A

Present for 15 days or more per month
Developed or worsened whilst taking regular symptomatic medication
May be psychiatric co-morbidity

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209
Q

Highest risk medicines for medication overuse headache

A

Opioids
Triptans

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210
Q

Where in brain characteristically affected by herpes simplex encephalitis

A

Temporal (and inferior frontal) lobes

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211
Q

Features herpes simplex encephalitis

A

Fever
Headache
Psychiatric symptoms
Seizures
Vomiting
Focal features, e.g. aphasia

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212
Q

Are peripheral lesions e.g. cold sores related to HSV encephalitis

A

No

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213
Q

CSF findings HSV encephalitis

A

Lymphocytosis
Elevated protein

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214
Q

CT findings HSV encephalitis

A

Medial temporal and inferior frontal changes, e.g. petechial haemorrhages

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215
Q

EEG pattern HSV encephalitis

A

Lateralised periodic discharges at 2Hz

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216
Q

Treatment HSV encephalitis

A

IV aciclovir

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217
Q

Inheritance pattern Huntington’s disease

A

Autosomal dominant

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218
Q

Genetic defect Huntington’s disease

A

Trinucleotide repeat disorder - repeat expansion of CAG

219
Q

Pathophysiology Huntington’s disease

A

Degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia

220
Q

Age of onset Huntington’s disease

A

35

Anticipation may be seen, where the disease presents at an earlier age in successive generations

221
Q

Features Huntington’s disease

A

Chorea
Personality changes, e.g. irritability, apathy, depression
Intellectual impairment
Dystonia
Saccadic eye movements

222
Q

Risk factors idiopathic intracranial hypertension

A

Obesity
Female
Pregnancy
Drugs

223
Q

Drugs increasing risk of IIH

A

COCP
Steroids
Tetracyclines
Retinoids (isotretinoin, tretinoin), vitamin A
Lithium

224
Q

Features IIH

A

Headache
Blurred vision
Papilloedema
Enlarged blind spot
6th nerve palsy may be present

225
Q

Management IIH

A

Weight loss
Carbonic anhydrase inhibitors, e.g. acetazolamide
Topiramate
Repeated lumbar puncture for short term management
Surgery

226
Q

Medications for weight loss in IIH

A

Semaglutide
Topiramate (particularly good as inhibits carbonic anhydrase)

For specialist consideration

227
Q

Surgery IIH

A

Optic nerve sheath decompression and fenestration - prevent damage to optic nerve
Lumboperitoneal or ventriculoperitoneal shunt - reduce intracranial pressure

228
Q

What is internuclear opthalmoplegia

A

Horizontal disconjugate eye movement due to a lesion in the medial longitudinal fasciculus

229
Q

What is internuclear opthalmoplegia

A

Horizontal disconjugate eye movement due to a lesion in the medial longitudinal fasciculus

230
Q

What is the role of the medial longitudinal fasciculus

A

Controls horizontal eye movements by interconnecting the 3rd, 4th, and 6th cranial nerve

231
Q

Where is the medial longitudinal fasciculus located?

A

In the paramedian area of the midbrain and pons

232
Q

Features internuclear opthalmoplegia

A

Impaired adduction of the eye on the same side as the lesion
Horizontal nystagmus of the abducting eye on the contralateral side

233
Q

Causes internuclear opthalmoplegia

A

Multiple sclerosis
Vascular disease

234
Q

Location of intracranial venous thrombosis

A

50% have isolated sagittal sinus thromboses
Remainder have co-existent lateral sinus thromboses and cavernous sinus thromboses

235
Q

Features intracranial venous thrombosis

A

Headache, may be sudden onset
Nausea and vomiting
Reduced consciousness

236
Q

Investigation intracranial venous thrombosis

A

MRI venography gold standard, CT venography alternative

237
Q

D-dimer in intracranial venous thrombosis

A

May be elevated

238
Q

Management intracranial venous thrombosis

A

Anticoagulation - typically low molecular weight heparin → warfarin for longer term anticoagulation

239
Q

Presentation sagittal sinus thrombosis

A

May present with seizures and hemiplegia

240
Q

Imaging findings sagittal sinus thrombosis

A

‘Empty delta sign’ on venography
Parasagittal biparietal or bifrontal haemorrhagic infarctions sometimes seen

241
Q

Causes other than intracranial venous thrombosis of cavernous sinus syndrome

A
  • Local infection, e.g. sinusitis
  • Neoplasia
  • Trauma
242
Q

Features cavernous sinus thrombosis

A

Periorbital erythema and oedema
Opthalmoplegia - 6th nerve damage typically occurs before 3rd and 4th
Trigeminal nerve involvement may lead to hyperaesthesia of upper face and eye pain
Central retinal vein thrombosis

243
Q

Features lateral sinus thrombosis

A

6th and 7th nerve palsies

244
Q

What vessels involved in lacunar stroke

A

A single penetrating branch of a large cerebral artery

245
Q

What structures affecting in lacunar stroke

A
  • Internal capsule
  • Thalamus
  • Basal ganglia
246
Q

Potential lacunar stroke syndromes

A
  • Purely motor (most common)
  • Purely sensory
  • Sensorimotor stroke
  • Ataxic hemiparesis
  • Dysarthria-clumsy hand syndrome
247
Q

Features ataxic hemiparesis caused by lacunar stroke

A

Ipsilateral weakness and limb ataxia that is out of proportion to motor deficit

248
Q

What do lacunar strokes typically lack

A

Cortical findings, such as aphasia, agnosia, neglect, apraxia, or hemianopsia

249
Q

Causes Lambert-Eaton syndrome

A

Small cell lung cancer (most common)
Breast cancer
Ovarian cancer

May occur independently as autoimmune disorder

250
Q

Pathophysiology Lambert-Eaton syndrome

A

Antibody directed against presynaptic voltage-gated calcium channel in the peripheral nervous system

251
Q

Features Lambert-Eaton syndrome

A
  • Repeated muscle contractions lead to increased muscle strength
  • Limb-girdle weakness, affecting lower limbs first
  • Hyporeflexia
  • Autonomic symptoms - dry mouth, impotence, difficulty micturating
252
Q

EMG findings Lambert-Eaton syndrome

A

Incremental response to repetitive electrical stimulation

253
Q

Treatment Lambert-Eaton syndrome

A

Treatment of underlying cancer if present
Immunosuppression, e.g. pred and/or azathioprine
3,4-diaminopyridine
IV immunoglobulin
Plasma exchange

254
Q

Lambert-Eaton syndrome vs myasthenia gravis

A

Muscle strength in Lambert-Eaton, weakness in MG
Opthalmoplegia and ptosis in MG, not LES

255
Q

Use lamotrigine

A

Second line anti-epileptic for variety of generalised and partial seizures

256
Q

Mechanism of action lamotrigine

A

Sodium channel blocker

257
Q

Adverse effects lamotrigine

A

Stevens-Johnson syndrome

258
Q

Complications meningitis

A

Sensorineural hearing loss (most common)
Seizures
Focal neurological deficit
Sepsis, intracerebral abscess
Brain herniation, hydrocephalus

259
Q

Complications meningococcal meningitis

A

Waterhouse-Friderichsen syndrome

260
Q

What is Waterhouse-Friderichsen syndrome

A

Adrenal insufficiency secondary to adrenal haemorrhage

261
Q

Diagnostic criteria migraine

A

A - at least 5 attacks fulfilling B-D
B - headache lasting 4-72 hours
C - at least two of;
- unilateral location
- pulsating quality
- moderate or severe
- aggravation by/causing avoidance of routine activity
D - during headache, at least one of
- nausea/vomiting
- photophobia/phonophobia
E - not attributed to another disorder

262
Q

Differences in migraines in children

A
  • Shorter lasting
  • More commonly bilateral
  • GI disturbance
263
Q

Migraine aura symptoms requiring investigation/referral

A
  • Motor weakness
  • Double vision
  • Visual symptoms affecting only one eye
  • Poor balance
  • Decreased consciousness
264
Q

First line acute treatment migraine

A

Combo therapy with;
- Oral triptan and NSAID, or
- Oral triptan and paracetamol

265
Q

Acute migraine treatment in 12-17y/o

A

Nasal triptan rather than oral

266
Q

Second line treatment acute mgiraine

A

Non-oral metaclopramide or prochlorperazine
Considering adding non-oral NSAID or triptan

267
Q

Why caution in prescribing metaclopramide to young patients

A

Acute dystonic reactions may develop

268
Q

When to give migraine prophylaxis

A

Migraine attacks having significant impact on quality of life and daily function, e.g. more than once a week on average, or prolonged and severe despite optimal acute treatment

269
Q

First line options for migraine prophylaxis

A

Propanolol
Topiramate (not women of childbearing age)
Amitriptyline

270
Q

Second line treatment migraine prophylaxis

A

Course of up to 10 sessions of acupuncture over 5-8 weeks

271
Q

Treatment predictable menstrual migraine

A

Frovatriptan 2.5mg twice a day, or
Zolmitriptan 2.5mg BD-TDS

272
Q

Specialist treatment options for migraine prophylaxis

A

Candesartan
Monoclonal antibodies directed against calcitonin gene-related peptipe receptor, e.g. erenumab

273
Q

Use of pizotifen migraine prophylaxis

A

No longer recommended

274
Q

What is multiple sclerosis

A

Chronic cell-mediated autoimmune disorder characterised by demyelination in the CNS

275
Q

Demographics MS

A

3x more common in women
20-40 years
Higher latitudes

276
Q

Features relapsing remitting MS

A

Acute attacks (1-2 months) following by periods of remission

277
Q

Features secondary progressive MS

A

Relapsing-remitting patients who have deteriorated and have developed neurological signs and symptoms between relapses
Gait and bladder disorders generally seen

278
Q

Features primary progressive disease

A

Progressive deterioration from onset
More common in older people

279
Q

Diagnostic criteria MS

A

Two or more relapses, and either;
- Objective clinical evidence of two or more lesions
- Objective clinical evidence of one lesion, together with reasonable historical evidence of an additional relapse

280
Q

Visual features MS

A
  • Optic neuritis
  • Optic atrophy
  • Uhthoff’s phenomenon
  • Internuclear opthalmoplegia
281
Q

What is Uhthoff’s phenomenon

A

Worsening of vision following rise in body temperature

282
Q

Sensory features MS

A
  • Pins/needles
  • Numbness
  • Trigeminal neuralgia
  • Lhermitte’s syndrome
283
Q

What is Lhermitte’s syndrome

A

Parasthesiae in limbs on neck flexion

284
Q

Motor features MS

A

Spastic weakness - most commonly seen in legs

285
Q

Cerebellar features MS

A

Ataxia
Tremor

286
Q

Other features MS

A

Urinary incontinence
Sexual dysfunction
Intellectual deterioration

287
Q

MRI findings MS

A

High signal T2 lesions
Periventricular plaques
Dawson fingers - hyperintense lesions penpendicular to the corpus callosum

288
Q

CSF findings MS

A

Oligoclonal bands (and not in serum)
Increased intrathecal synthesis of IgG

289
Q

Visual evoked potentials in MS

A

Delayed, but well preserved waveform

290
Q

Management acute relapse MS

A

High dose steroids (oral or IV methylpred) may be given for up to 5 days

291
Q

Action of steroids in acute relapse MS

A

Shorten the duration of relapse, but do not alter the degree of recovery

292
Q

Indications for disease modifying drugs in MS

A
  • Relapsing remitting disease + 2 relapses in the past 2 years + able to walk 100m unaided
  • Secondary progressive disease + 2 relapses in the past 2 years + able to walk 10m (aided or unaided)
293
Q

Disease modifying drug options MS

A

Natalizumab
Ocrelizumab
Fingolimod
Beta-interferon
Glatiramer acetate

294
Q

Usual first line disease modifying drug MS

A

Natalizumab or ocrelizumab

295
Q

Route of administration natalizumab

296
Q

Route of administration ocrelizumab

297
Q

Route of administration fingolimod

A

Oral formulations available

298
Q

Route of administration beta-interferon

299
Q

Route of administration glatiramer acetate

300
Q

What disease modifying drugs for MS considered less effective

A

Beta-interferon and glatiramer acetate

301
Q

Treatment fatigue in MS

A

Once other problems, e.g. anaemia, thyroid, depression ruled out, trial amantadine

302
Q

First line treatment spasticity MS

A

Baclofen
Gabapentin

Physio

303
Q

Other options spasticity MS

A

Diazepam
Dantrolene
Tizanidine

304
Q

Treatment bladder dysfunction in MS

A

Ultrasound to assess bladder emptying

If significant residual volume - intermittent self-catheterisation
If no significant residual volume - anticholinergics

305
Q

What is oscillopsia

A

When visual fields appear to oscillate

306
Q

Treatment oscillopsia MS

A

Gabapentin

307
Q

Types of multiple system atrophy

A

MSA-P - predominant Parkinsonian features
MSA-C - predominant cerebellar features

308
Q

Features multiple systems atrophy

A

Parkinsonism
Autonomic disturbance - erectile dysfunction, postural hypotension, atonic bladder
Cerebellar signs

309
Q

Drugs exacerbating myasthenia gravis

A

Penicillamine
Quinidine
Procainamide
Beta-blockers
Lithium
Phenytoin
Gentamicin, macrolides, quinolones, tetracyclines

310
Q

Age of onset myotonic dystrophy

A

20-30 years

311
Q

Inheritance myotonic dystrophy

A

Autosomal dominant

312
Q

Genetics myotonic dystrophy

A

Trinucleotide repeat disorder

313
Q

Myotonic dystrophy DM1 vs DM2

A

Distal weakness more prominent in DM1
Proximal weakness more prominent DM2, severe congenital form not seen

314
Q

Facial features myotonic dystrophy

A

Myotonic facies (long, haggard appearance)
Frontal balding
Bilateral ptosis
Cataracts
Dysarthria

315
Q

Other features myotonic dystrophy

A

Myotonia (tonic spasm of muscle)
Weakness of arms and legs (distal initially)
Mild mental impairment
Diabetes mellitus
Testicular atrophy
Cardiac involvement - heart block, cardiomyopathy
Dysphagia

316
Q

Inheritance neurofibromatosis

A

Autosomal dominant

317
Q

Features neurofibromatosis type 1

A

Cafe-au-lait spots (≥6 15mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas (Lisch nodules)
Scoliosis
Phaeochromocytomas

318
Q

Features neurofibromatosis type 2

A

Bilateral vesticular schwannomas
Multiple intracranial schwannomas, meningiomas, ependymomas

319
Q

Drugs causing neuroleptic malignant syndrome

A

Antipsychotics
Dopaminergic drugs, e.g. levodopa (usually when stopped or suddenly reduced)

320
Q

When does neuroleptic malignant syndrome occur

A

Usually hours to days of starting an antipsychotic

321
Q

Features neuroleptic malignant syndrome

A

Pyrexia
Muscle rigidity
Autonomic lability - hypertension, tachycardia, tachypnoea
Agitated delirium with confusion

322
Q

Bloods neuroleptic malignant syndrome

A

Raised AKI
AKI in severe cases
Leukocytosis

323
Q

Management neuroleptic malignant syndrome

A

Stop antipsychotic
IV fluids
Dantrolene

324
Q

First line treatment neuropathic pain

A

Amitriptyline
Duloxetine
Gabapentin
Pregabalin

325
Q

Second line treatment neuropathic pain

A

Switch to one of the other first line drugs (not add)

326
Q

‘Rescue therapy’ for exacerbations of neuropathic pain

327
Q

Treatment localised neuropathic pain

A

Topical capsaicin

328
Q

Causes normal pressure hydrocephalus

A

Reduced CSF absorption at arachnoid villi, may be secondary to head injury, SAH, or meningitis

329
Q

Features normal pressure hydrocephalus

A

Urinary incontinence
Dementia and bradyphrenia (slowing of mental processes)
Gait abnormality

330
Q

Timeline of symptom development normal pressure hydrocephalus

A

Develop over a few months

331
Q

Imaging normal pressure hydrocephalus

A

Hydrocephalus with ventriculomegaly in absense of, or out of proportion to, sulcal enlargement

332
Q

Management normal pressure hydrocephalus

A

Ventriculoperitoneal shunting

333
Q

Complications VP shunt in normal pressure hydrocephalus

A
  • Seizures
  • Infection
  • Intracerebral haemorrhages
334
Q

Cause Parkinson’s disease

A

Degeneration of dopaminergic neurons in the substantia nigra

335
Q

Features Parkinson’s disease

A

Bradykinesia
Tremor
Rigidity

336
Q

Characteristic of symptoms in Parkinsons

A

Classically asymmetrical

337
Q

Features of bradykinesia in Parkinson’s disease

A

Poverty of movement (hypokinesia)
Short, shuffling steps, reduced arm swing
Difficulty in initiating movement

338
Q

Features of tremor in Parkinson’s disease

A

Most marked at rest, 3-5Hz
Worse when stressed or tired, improves with voluntary movement
Typically pill-rolling

339
Q

Features of rigidity in Parkinsons disease

A

Lead pipe
Cogwheel - due to superimposed tremor

340
Q

Other features of Parkinson’s disease

A

Mask like facies
Flexed posture
Micrographia
Drooling of saliva
Psychiatric features
Impaired olfaction
REM sleep behaviour disorder
Fatigue
Autonomic dysfunction - postural hypotension

341
Q

Drug induced Parkinsonism vs Parkinson’s disease

A

Motor symptoms generally rapid onset and bilateral
Rigidity and rest tremor uncommon

342
Q

Investigation Parkinsons disease

A

Diagnosis usually clinical
If difficulty differentiating between essential tremor and Parkinson’s disease, consider SPECT

343
Q

First line treatment Parkinson’s disease

A

If motor symptoms affecting patients quality of life - levodopa
If motor symptoms not affecting patients quality of life - dopamine agonist, levodopa, or monoamine oxidase B

344
Q

Levodopa vs dopamine agonists vs MAO-B inhibitors

A

Levodopa more improvement in motor symptoms. and ADL than dopamine agonists/MAO-B inhibitors
Levodopa more motor complications
Dopamine agonists greatest adverse effects

345
Q

Treatment Parkinsons when continued symptoms despite optimal levodopa treatment, or developed dyskinesia

A

Add dopamine agonist, MAO-B inhibitor or COMT inhibitor

346
Q

Dopamine agonists vs MAO-B inhibitors vs COMT inhibitors

A

Dopamine agonists most off-time reduction
COMT most adverse events, MAO-B least
Dopamine agonists most risk of hallucinations

347
Q

Risk if Parkinsons medication not taken/not absorbed/drug holiday

A

Acute akinesia or neuroleptic malignant syndrome

348
Q

Risk factors for impulse control disorders with Parkinsons medication

A
  • Dopamine agonist therapy
  • History of previous impulsive behaviours
  • History of alcohol consumption and/or smoking
349
Q

Management excessive daytime sleepines Parkinson’s disease

A

Adjust medications
Modafinil if alternative medications fail

Should not drive

350
Q

Management orthostatic hypotension in Parkinson’s

A

Medication review
If symptoms persist, midodrine

351
Q

Management drooling in Parkinsons

A

Glycopyrronium bromide

352
Q

What medication is levodopa combined with

A

Decarboxylase inhibitor, e.g. carbidopa, benserazide

353
Q

Why is levodopa combined with decarboxylase inhibitor

A

Prevents peripheral metabolism of levodopa to dopamine outside the brain, hence can reduce SEs

354
Q

Common adverse effects levodopa

A
  • Dry mouth
  • Anorexia
  • Palpitations
  • Postural hypotension
  • Psychosis
355
Q

Adverse effects due to difficulty in achieving steady dose levodopa

A
  • End of dose wearing off (symptoms worsen towards end of dosage interval → decline in motor activity)
  • On-off phenomenon (large variations in motor performance
  • Dyskinesias at peak dose - dystonia, chorea, athetosis
356
Q

Management if patients unable to take levodopa orally

A

Dopamine agonist patch as rescue medication

357
Q

Examples ergot derived dopamine receptor agonists

A

Bromociptine
Cabergline

358
Q

Examples non-ergot derived dopamine receptor agonists

A

Ropinirole
Apomorphine

359
Q

Adverse effects ergot-derived dopamine receptor agonists

A

Pulmonary, retroperitoneal, and cardiac fibrosis

360
Q

Monitoring ergot-derived dopamine receptor agonists

A

Echo, ESR, creatinine and CXR obtained prior to treatment
Patients should be closely monitored

361
Q

Other adverse effects dopamine receptor agonists

A
  • Impulse control disorders
  • Excessive daytime somnolence
  • Hallucinations
  • Nasal congestion
  • Postural hypotension
362
Q

Example MAO-B inhibitor

A

Selegiline

363
Q

SEs amantidine

A

Ataxia
Slurred speech
Confusion
Dizziness
Lived reticularis

364
Q

Examples COMT inhibitors

A

Entacapone
Tolcapone

365
Q

Use of COMT inhibitors in Parkinsons

A

Used in conjunction with levodopa - COMT is enzyme involved in breakdown of dopamine

366
Q

Use of antimuscarinics in Parkinsons

A

Now used more to treat drug-induced Parkinsonism rather than idiopathic Parkinson’s disease

367
Q

Examples antimusarinics used in Parkinsons

A

Procyclidine
Benzotropine
Trihexyphenidyl

368
Q

Causes of Parkinsonism

A

Parkinson’s disease
Drug induced, e.g. antipsychotics, metoclopramide
Progressive supranuclear palsy
Multiple systems atrophy
Wilson’s disease
Post-encephalitis
Dementia pugilistica
Toxins - carbon monoxide, MPTP

369
Q

What causes dementia pugilistic

A

Chronic head trauma, e.g. boxing

370
Q

Causes of peripheral neuropathy with predominantly motor loss

A

Guillain-Barre syndrome
Porphyria
Lead poisioning
Hereditary sensorimotor neuropathies, e.g. Charcot-Marie-Tooth
Chronic inflammatory demyelinating polyneuropathy
Diptheria

371
Q

Causes of peripheral neuropathy causing predominantly sensory loss

A

Diabetes
Uraemia
Leprosy
Alcoholism
Vitamin B12 deficiency
Amyloidosis

372
Q

Cause of alcohol neuropathy

A

Direct toxic effects of alcohol and reduced absorption of B vitamins

373
Q

Alcohol neuropathy sensory vs motor symptoms

A

Sensory symptoms typically present prior to motor symptoms

374
Q

How does vitamin B12 deficiency cause peripheral neuropathy

A

Subacute combined degeneration of the spinal cord

375
Q

Order of presentation peripheral neuropathy secondary to vitamin B12 deficiency

A

Dorsal column usually affected first (joint position, vibration) prior to distal parenthesis

376
Q

Effect of phenytoin on P450

377
Q

Acute SEs phenytoin

A
  • Dizziness
  • Diplopia
  • Nystagmus
  • Slurred speech
  • Ataxia
  • Confusion
  • Seizures
378
Q

Common chronic SEs phenytoin

A
  • Gingival hyperplasia
  • Hirsutism
  • Coarsening of facial features
  • Drowsiness
379
Q

Other chronic SEs phenytoin

A
  • Megaloblastic anaemia
  • Peripheral neuropathy
  • Enhanced vitamin D metabolism causing osteomalacia
  • Lymphadenopathy
  • Dyskinesia
380
Q

Idiosyncratic SEs phenytoin

A
  • Fever
  • Rashes, inc severe reactions e.g. TEN
  • Hepatitis
  • Dupuytren’s contracture
  • Aplastic anaemia
  • Drug induced lupus
381
Q

Teratogenic effects phenytoin

A
  • Cleft palate
  • CHD
382
Q

Monitoring phenytoin

A

Check trough levels (immediately before dose) if;
- Adjustment of phenytoin dose
- Suspected toxicity
- Suspicion of non-adherence

383
Q

Features progressive supranuclear palsy

A
  • Postural instability and falls, stiff broad-based gait
  • Impairment of vertical gaze - down gaze worse than up gaze
  • Parkinsonism, bradykinesia prominent
  • Cognitive impairment, primarily frontal lobe dysfunction
384
Q

L-dopa in progressive supranuclear palsy

A

Poor response to L-dopa

385
Q

Factors favouring psychogenic non-epileptic seizures

A
  • Pelvic thrusting
  • Family member with epilepsy
  • Much more common in females
  • Crying after seizure
  • Don’t occur when alone
  • Gradual onset
386
Q

Factors favouring true epileptic seizures

A
  • Tongue piting
  • Raised serum prolactin
387
Q

Roots of radial nerve

388
Q

Muscle affected in injury to radial nerve at shoulder

A

Long head of triceps

389
Q

Effect of injury to radial nerve at shoulder

A

Minor affects on shoulder stability in abduction

390
Q

Muscle affected in injury to radial nerve at arm

391
Q

Effect of injury to radial nerve at arm

A

Loss of elbow extension

392
Q

Muscle affected in injury to radial nerve at forearm

A
  • Supinator
  • Brachioradialis
  • Extensor carpi radialis longus and brevis
393
Q

Effect of injury to radial nerve at forearm

A

Weakening of supination of prone hand and elbow flexion in mid prine position

394
Q

Sensory loss in radial nerve injury

A

Small area between dorsal aspect of 1st and 2nd metacarpals

395
Q

Normal ICP when supine

396
Q

What is the cerebral perfusion pressure

A

The net pressure gradient causing cerebral blood flow to the brain

397
Q

How to calculate cerebral perfusion pressure

398
Q

Causes raised ICP

A
  • Idiopathic intracranial hypertension
  • Traumatic head injuries
  • Infection, e.g. meningitis
  • Tumours
  • Hydrocephalus
399
Q

Features raised ICP

A
  • Headache
  • Vomiting
  • Reduced level of consciousness
  • Papilloedema
  • Cushing’s triad
400
Q

What is Cushing’s triad

A
  • Widening pulse pressure
  • Bradycardia
  • Irregular breathing
401
Q

Investigations raised ICP

A
  • Neuroimaging (CT/MRI) to determine underlying cause
  • Invasive ICP monitoring
402
Q

Cut off for intervention in invasive ICP monitoring

403
Q

Management raised ICP

A
  • Treat underlying cause
  • Head elevation to 30
  • IV mannitol
  • Controlled hyperventilation
  • Removal of CSF
404
Q

How does controlled hyperventilation help in raised ICP

A

Reduce pCO2 → vasoconstriction of cerebral arteries → reduced ICP

405
Q

Limitation of controlled hyperventilation in raised ICP

A
  • Temporary
  • May reduce blood flow to already ischaemic parts of the brain
406
Q

Methods for CSF removal

A
  • Drain from intraventricular monitor
  • Repeat LP
  • VP shunt
407
Q

Root of ankle reflex

408
Q

Root of knee reflex

409
Q

Root of biceps reflex

410
Q

Root of triceps reflex

411
Q

What is restless legs syndrome

A

Syndrome of spontaneous, continuous lower limb movements, may be associated with paresthesia

412
Q

Features restless leg syndrome

A
  • Uncontrollable urge to move legs - initially at night, but progress to occur during day, worse at rest
  • Paresthesias, e.g. crawling or throbbing sensations
  • Movements during sleep - periodic limb movements of sleep
413
Q

Associations with restless leg syndrome

A
  • Iron deficiency anaemia
  • Uraemia
  • Diabetes mellitus
  • Pregnancy
414
Q

Basic management restless legs syndrome

A
  • Simple measures - walking, stretching, massaging affected limbs
  • Treat any iron deficiency
415
Q

First line drug treatment restless legs syndrome

A

Dopamine agonists, e.g. pramipexole, ropinorole

416
Q

Other drug treatments restless legs syndrome

A

Benzodiazepines
Gabapentin

417
Q

What is Reye’s syndrome

A

Severe progressive encephalopathy affecting children, accompanied by fatty infiltration of the liver, kidneys, and pancreas

418
Q

Cause Reye’s syndrome

A

Unclear

Association with aspirin use
Potential viral cause

419
Q

Peak incidence Reye’s syndrome

420
Q

Features Reye’s syndrome

A
  • Encephalopathy - confusion, seizures, cerebral oedema, coma
  • Fatty infiltration of the liver, kidneys, and pancreas
  • Hypoglycaemia
421
Q

Managment Reye’s syndrome

A

Supportive

422
Q

Roots sciatic nerve

A

L4-5, S1-3

423
Q

What does sciatic nerve divided into

A

Tibial and common peroneal nerves

424
Q

Muscles supplied by sciatic nerve

A
  • Hamstrings
  • Adductors
425
Q

Motor features of sciatic nerve lesion

A

Paralysis of knee flexion and all movements below knee

426
Q

Sensory features of sciatic nerve lesion

A

Loss below knee

427
Q

Reflexes in sciatic nerve lesion

A

Ankle and plantar lost
Knee jerk in tact

428
Q

Causes sciatic nerve lesion

A
  • Fracture neck of femur
  • Posterior hip dislocation
  • Trauma
429
Q

Teratogenic effects of sodium valproate

A
  • Neural tube defects
  • Neurodevelopmental delay
430
Q

P450 and sodium valproate

A

P450 inhibitor

431
Q

SEs sodium valproate

A
  • Nausea
  • Increased appetite and weight gain
  • Alopecia
  • Ataxia
  • Tremor
  • Hepatotoxicity
  • Pancreatitis
  • Thrombocytopenia
  • Hyponatraemia
  • Hyperammonaemic encephalopathy
432
Q

Definition status epilepticus

A

Single seizure lasting >5 minutes
≥2 seizures within 5 min period without person returning to normal

433
Q

First line treatment status epilepticus in pre-hosp setting

A

PR diazepam or buccal midazolam

434
Q

First line treatment status epilepticus in hospital

A

IV lorazepam

435
Q

Second line treatment status epilepticus in hospital

A

Repeat IV lorazepam after 5-10 mins

436
Q

Third line treatment status epilepticus

A

Levetiracetam, phenytoin, or sodium valproate

437
Q

Advantages levetiracetam as third line treatment for status

A

May be quicker to administer and have fewer adverse effects than other options

438
Q

Fourth line treatment for status epilepticus, and when to give

A

Induction of general anaesthesia or phenobarb

If no response within 45 mins from onset - refractory status

439
Q

Effect of stroke of anterior cerebral artery

A

Contralateral hemiparesis and sensory loss
Lower extremity>upper

440
Q

Effect of stroke of middle cerebral artery

A

Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

441
Q

Effect of stroke of posterior cerebral artery

A
  • Contralateral homonymous hemianopia with macular sparing
  • Visual agnosia
442
Q

What artery is affected in Weber’s syndrome

A

Branches of posterior cerebral artery that supply the midbrain

443
Q

Effect of stroke affecting branches of PCA supplying midbrain

A
  • Ipsilateral CN III palsy
  • Contralateral weakness of upper and lower extremity
444
Q

What is lateral medullary syndrome

A

Stroke affecting posterior inferior cerebellar artery

445
Q

Effect of stroke affecting posterior inferior cerebellar artery

A
  • Ipsilateral facial pain and temp loss
  • Contralateral limb/torso pain and temp loss
  • Ataxia
  • Nystagmus
446
Q

What is lateral pontine syndrome

A

Stroke affecting inferior cerebellar artery

447
Q

Effect of stroke affecting anterior inferior cerebellar artery

A
  • Ipsilateral facial paralysis and deafness
  • Contralateral limb/torso pain and temp loss
  • Ataxia
  • Nystagmus
448
Q

Effect of stroke affecting retinal/opthalmic arteyr

A

Amaurosis fugax

449
Q

Effect of stroke affecting basilar artery

A

Locked in syndrome

450
Q

Common sites of lacunar strokes

A

Basal ganglia
Thalamus
Internal capsule

451
Q

Criteria in Oxford Stroke Classification

A
  1. Unilateral hemiparesis and/or hemisensory loss of face, arm, and leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction, e.g. dysphasia
452
Q

What arteries does total anterior circulation infant involve

A

Middle and anterior cerebral artery

453
Q

Oxford criteria and TACI

A

All 3 Oxford criteria present

454
Q

What arteries does partial anterior circulation infarct involve

A

Smaller arteries of anterior circulation, e.g. upper or lower division of middle cerebral artery

455
Q

Oxford criteria in PACI

A

2 Oxford criteria are present

456
Q

What arteries involve in lacunar infarcts

A

Perforating arteries around internal capsule, thalamus, and basal ganglia

457
Q

Presentation lacunar infarcts

A

One of;
- Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg, or all 3
- Pure sensory stroke
- Ataxic hemiparesis

458
Q

What arteries involved in posterior circulation stroke

A

Vertebrobasilar arteries

459
Q

Presentation posterior circulation stroke

A

1 of;
- Cerebellar or brainstem syndromes
- Loss of consciousnes
- Isolated homonymous hemianopia

460
Q

Features suggesting more like haemorrhagic stroke

A
  • Reduced consciousness level
  • Headache
  • N&V
  • Seizures
461
Q

Common management TIA

A

Aspirin 300mg immediately unless contraindicated

462
Q

When is urgent admission indicated TIA

A
  • More than 1 TIA (crescendo TIA)
  • Suspected cardioembolic source
  • Severe carotid stenosis
  • Bleeding disorder or anticoagulant (imaging to r/o haemorrhage)
463
Q

Management TIA within last 7 days

A

Assessment within 24 hours by stroke specialist

464
Q

Management TIA over a week ago

A

Specialist assessment ASAP, within 7 days

465
Q

Management haemorrhagic stroke

A

Neurosurgical review ?surgical intervention

Usually supportive - stop anticoag/antithrombotics, reversal
Lower BP

466
Q

Management of BP in acute ischaemic stroke

A

Should not be lowered in acute phase unless complications,e .g. hypertensive encephalopathy, being considered for thrombolysis

467
Q

Common management acute ischaemic stroke

A

Aspirin 300mg ASAP once haemorrhage excluded

468
Q

Management of AF in ischaemic stroke

A

Should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days after onset

469
Q

Management hypercholesterolaemia in stroke

A

If cholesterol >3.5, statin

Delay until at least 48 hours after due to risk of haemorrhagic transformatino

470
Q

Criteria for thrombolysis in acute ischaemic stroke

A
  • Can be administered within 4.5 hours of onset of stroke symptoms
  • Imaging has excluded haemorrhage
471
Q

When can thrombolysis be considered beyond 4.5 hours

A

If;
- Treatment can be started between 4.5 and 9 hours of known onset, or within 9 hours of the midpoint of sleep when they have woken with symptoms, and
- Evidence on CT/MR perfusion or MRI of the potential to salvage brain tissue

472
Q

What agent should be used for stroke thrombolysis

A

Alteplase or tenecteplase

Alteplase if >4.5 hours

473
Q

Should thrombolysis be performed if a patient is having thrombectomy

474
Q

BP and thrombolysis

A

BP should be lowered to 185/110 before thrombolysis

475
Q

Absolute contraindications to thrombolysis

A
  • Previous intracranial haemorrhage
  • Seizure at onset of stroke
  • Intracranial neoplasm
  • Suspected SAH
  • Stroke or TBI in prev 3 months
  • LP in past 7 days
  • GI haemorrhage in past 3 weeks
  • Active bleeding
  • Oesophageal varices
  • Uncontrolled hypertension >200/120mmHg
476
Q

Relative contraindications to thrombolysis

A
  • Pregnancy
  • Concurrent anticoagulation (INR >1.7)
  • Haemorrhagic diathesis
  • Active diabetic haemorrhagic retinopathy
  • Suspected intracardiac thrombus
  • Major surgery/trauma in prev 2 weeks
477
Q

Which patients are eligible for thrombectomy

A
  • Pre-stroke functional status of less than 3 on modified Rankin scale
  • Score of more than 5 on National Institutes of Health Stroke Scale (NIHSS)
478
Q

Timeline thrombectomy

A

Less than 6 hours

Offer if 6-24 hours from when last known well and imaging shows salvagable brain

479
Q

Which arteries thrombectomy

A

Proximal anterior circulation

Consider if proximal posterior circulation (basilar of posterior cerebral artery) and imaging showing salvageable brain

480
Q

Antiplatelet in secondary prevention of stroke

A

Clopidogrel
Aspirin if CI/not tolerated

481
Q

When should carotid endarterectomy be considered in stroke

A
  • Stroke or TIA in carotid territory
  • Not severely disabled
  • Stenosis >50%
482
Q

Timeline carotid endarterectomy stroke

A

ASAP within 7 days

483
Q

Cause subacute degeneration of spinal cord

A
  • Vitamin B12 deficiency
  • Recreational nitrous oxide inhalation (because it causes B12 def)
484
Q

Structures affected in subacute degeneration of the spinal cord

A
  • Dorsal column
  • Lateral corticospinal tract
  • Spinocerebellar tract
485
Q

Features of subacute degeneration of the spinal cord due to dorsal column involvement

A
  • Distal tingling/burning/sensory loss, symmetrical, legs>arms
  • Impaired proprioception and vibration sense
486
Q

Features of subacute degeneration of the spinal cord due to lateral corticospinal tract involvement

A
  • Muscle weakness, hyperreflexia, spasticity
  • Upper motor neuron signs
  • Brisk knee reflexes
  • Absent ankle jerks
  • Extensor plantars
487
Q

Features of subacute degeneration of the spinla cord due to spinocerebellar involvement

A
  • Sensory ataxia → gait abnormalities
  • Positive Romberg’s sign
488
Q

What is syringomyelia

A

A collection of CSF in the spinal cord

489
Q

What is syringobulbia

A

Fluid-filled cavity within medulla of brainstem

490
Q

Causes syringomyelia

A
  • Chiari malformation
  • Trauma
  • Tumours
  • Idiopathic
491
Q

Features syringomyelia

A
  • Cape like (neck, shoulders, arms) loss of sensation to temp, but preservation of light touch, proprioception, and vibration
  • Spastic weakness, predominantly lower limbs
  • Neuropathic pain
  • Upgoing plantars
  • Autonomic features
  • Horner’s syndrome
  • Bladder and bowel dysfunction
492
Q

Investigations syringomyelia

A

Full spine MRI - exclude tumour or tethered cord
Brain MRI - exclude Chiari malformation

493
Q

Treatment syringomyelia

A

Treat cause of syrinx
If persistent or symptomatic, shunt into syrinx

494
Q

Features third nerve palsy

A
  • Eye is deviated ‘down and out’
  • Ptosis
  • Pupil may be dilated
495
Q

Causes third nerve palsy

A
  • Diabetes mellitus
  • Vasculitis, e.g temporal arteritis, SLE
  • Posterior communicating artery aneurysm
  • Cavernous sinus thrombosis
  • Weber’s syndrome
  • Amyloid
  • MS
496
Q

When might third nerve palsy be a false localising sign

A

Uncal herniation through tentorium if raised ICP

497
Q

TIA mimics

A

Hypoglycaemia
Intracranial haemorrhage

498
Q

Role of CT brain in TIA

A

Should not be done unless clinical suspicion of alternative diagnosis that CT could detect, e.g. exclude haemorrhage

499
Q

Role of MRI brain in TIA

A
  • Determine territory of ischaemia
  • Detect haemorrhage or alternative pathologies
500
Q

Initial management TIA

A

Aspirin 300mg

501
Q

Ongoing management TIA

A

Clopidogrel + aspirin (or ticagrelor) for 21 days, then clopi ongoing

502
Q

Management TIA if not suitable for DAPT

A

Clopidogrel

503
Q

Management AF in TIA

A

Anticoagulate as soon as haemorrhage excluded

504
Q

Statin in TIA

A

High intensity statin, e.g. atorvastatin 20-80mg daily

505
Q

Features of tremor in Parkinsonism

A

Resting pill rolling tremor

506
Q

Features of tremor in essential tremor

A

Postural tremor, worse if arms outstretched
Improved by alcohol and rest
Titubation (nodding head movement)

507
Q

Features of tremor in cerebellar disease

A

Intention tremor
Occurs with cerebellar signs, e.g. past-pointing, nystagmus

508
Q

Features of trigeminal neuralgia

A
  • Brief electric shock like pains, abrupt onset and termination, limited to one or more divisions of trigeminal nerve
  • Pain commonly evoked by light touch
  • Small areas in nasolabial fold or chin may be particularly susceptible (trigger areas)
  • Main usually remit for variable periods
509
Q

Red flags for serious underlying cause in trigeminal neuralgia

A
  • Sensory changes
  • Deafness or other ear problems
  • History of skin or oral lesions that could spread perineurally
  • Pain only in opthalmic division of trigeminal near (eye socker, forehead, nose) or bilaterally
  • Optic neuritis
  • FHx MS
  • Age of onset before 40
510
Q

Management trigeminal neuralgia

A

Carbamazepine first line

511
Q

Referral trigeminal neuralgia

A
  • Failure to respond to treatment
  • Atypical feature
512
Q

Adverse effects triptans

A
  • Tingling
  • Heat
  • Tightness of throat and chest
  • Heaviness
  • Pressure
513
Q

CIs triptans

A

History of or significant risk factors for IHD or CVD

514
Q

Inheritance tuberous sclerosis

A

Autosomal dominant

515
Q

Cutaneous features tuberous sclerosis

A
  • Depigmented ash leaf spots which flouresce under UV light
  • Shagreen patches - roughened patches of skin over lumbar spine
  • Adenoma sebaceum (angiofibromas) - butterfly distribution over nose
  • Subungal fibromata (under nails)
  • Cafe-au-lait spots
516
Q

Neurological features tuberous sclerosis

A
  • Developmental delay
  • Epilepsy
  • Intellectual impairment
517
Q

Other features tuberous sclerosis

A
  • Retinal hamartomas (dense white areas on retina)
  • Rhabdomyomas of heart
  • Polycystic kidneys, renal angiomyolipomata
  • Multiple lung cysts
518
Q

Roots ulcer nerve

519
Q

Sensory function ulnar nerve

A

Medial 1 1/2 fingers (palmar and dorsal)

520
Q

Presentation ulnar nerve damage at wrist

A
  • Claw hand
  • Wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals)
  • Wasting and paralysis of hypothenar muscles
  • Sensory loss to medial 1 1/2 fingers
521
Q

What is claw hand

A

Hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits

522
Q

Presentation ulnar nerve damage at elbow

A
  • Claw hand (less severe than at wrist)
  • Wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals)
  • Wasting and paralysis of hypothenar muscles
  • Sensory loss to medial 1 1/2 fingers
  • Radial deviation of wrist
523
Q

Presentation vestibular schwannoma (acoustic neuroma)

A
  • Vertigo
  • Unilateral sensorineural hearing loss
  • Unilateral tinnitus
  • Absent corneal reflex
  • Facial palsy
524
Q

Cause bilateral acoustic neuroma

A

Neurofibromatosis type 2

525
Q

Investigation acoustic neuroma

A

MRI of cerebellopontine angle

526
Q

Management acoustic neuroma

A

Surgery, radiotherapy, or observation

527
Q

What causes homonymous hemianopia

A

Lesion of the opposite optic tract (e.g. left homonymous hemianopia = right optic tract)

528
Q

What is an incongruous visual field defect

A

Incomplete or asymmetric visual loss

529
Q

What does an incongruous visual field defect suggest

A

Optic tract lesion

530
Q

What is a congruous visual field defect

A

Complete or symmetrical visual loss

531
Q

What does a congruous visual field defect suggest

A

Optic radiation lesion or occipital cortex lesion

532
Q

What does macula sparing suggest

A

Lesion of occipital cortex

533
Q

Cause of superior homonymous quadrantanopia

A

Lesion of inferior optic radiations in temporal lobe (Meyer’s loop)

534
Q

Cause of inferior homonymous quadrantanopia

A

Lesion of superior optic radiations in parietal lobe

535
Q

Cause of bitemporal hemianopia

A

Lesion of optic chiasm

536
Q

Cause of bitemporal hemianopia upper quad > lower quad

A

Inferior chiasmal compression, commonly pituitary tumour

537
Q

Cause of bitemporal hemianopia lower quad > upper quad

A

Superior chiasmal compression, commonly craniopharyngioma

538
Q

What is Wernicke’s encephalopathy

A

Neuropsych disorder caused by thiamine deficiency

539
Q

Causes Wernicke’s encephalopathy

A
  • Alcoholic (most common)
  • Persistent vomiting
  • Anorexia
  • Stomach cancer
  • Dietary deficiency
540
Q

Features Wernicke’s encephalopathy

A
  • Oculomotor dysfunction - nystagmus, ophthalmoplegia
  • Gait ataxia
  • Encephalopathy - confusion, disorientation, indifference, inattentiveness
  • Peripheral sensory neuropathy
541
Q

Opthalmoplegia in Wernicke’s encephalopathy

A
  • Lateral rectus palsy
  • Conjugate gaze palsy
542
Q

Investigation Wernicke’s encephalopathy

A
  • Red cell transketolase - reduced
  • MRI
543
Q

Treatment Wernicke’s encephalopathy

A

Urgent replacement of thiamine

544
Q

Features Korsakoff syndrome

A
  • Antero and retrograde amnesia
  • Confabulation

1 - MSRA (23 decks)

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