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Neuro and SS > Neurology > Flashcards

Neurology Flashcards

1
Q

What are some features of a resting tremor?

A

Worse at rest
Slow tremor (freq 3-5Hz)
Pill rolling of thumb over finger

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2
Q

What are some features of a postural tremor?

A

Worse if arms outstretched

Rapid (8-12Hz)

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3
Q

What are some causes of a postural tremor?

A

Anxiety, hyperthyroidism, alcohol, drugs, benign essential tremor

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4
Q

Describe the MRC muscle power score:

A

0 - no contraction
1 - flicker of contraction
2 - active movement, with gravity eliminated
3 - active movement against gravity
4 - active movement against gravity and resistance
5 - normal power

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5
Q

What nerve roots are tested in biceps reflex?

A

C5/6

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6
Q

What nerve root is tested in triceps reflex?

A

C7

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7
Q

What nerve root is tested in supinator reflex?

A

C6

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8
Q

What nerve roots are tested in knee jerk reflex?

A

L3/4

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9
Q

What nerve roots are tested in ankle jerk reflex?

A

L5, S1

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10
Q

What nerve roots are tested in plantar reflex?

A

L5, S1/2

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11
Q

In which dermatome would you find the clavicles?

A

C3-4

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12
Q

In which dermatome would you find the thumb?

A

C6

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13
Q

In which dermatome would you find the middle finger?

A

C7

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14
Q

In which dermatome would you find the little finger?

A

C8

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15
Q

In which dermatome would you find the nipple?

A

T4

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16
Q

In which dermatome would you find the umbilicus?

A

T10

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17
Q

In which dermatome would you find the big toe?

A

L5

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18
Q

In which dermatome would you find the lateral side of the foot?

A

S1

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19
Q

How would you examine CN I?

A

Test ability of each nostril to distinguish familiar smells

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20
Q

How would you examine CN II?

A

Snellen chart, visual fields, pupil size, shape, symmetry
Direct and consensual light reflex, accommodation, swinging light test
Fundoscopy

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21
Q

How would you examine CN III, IV and VI?

A

Eye movements

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22
Q

How would you examine CN V?

A

Open mouth, move side to side, clench teeth
Check sensation in ophthalmic, maxillary and mandibular divisions
Corneal reflex

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23
Q

How would you examine CN VII?

A

Raise eyebrows, smile, puff out cheeks, shut eyes tight

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24
Q

How would you examine CN VIII?

A

Repeat whispered number, Weber’s and Rinne’s

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25
Q

How would you examine CN IX and X?

A

Say ‘ah’, gag reflex, cough

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26
Q

How would you examine CN XI?

A

Shrug shoulders and turn head against resistance

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27
Q

How would you examine CN XII?

A

Tongue movement

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28
Q

What are some diseases than can affect the CNs (generally)?

A

DM, stroke, MS, tumours, sarcoid, vasculitis

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29
Q

What might causes a CN I lesion?

A

Trauma, resp infections, meningitis, frontal lobe tumour

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30
Q

What are some causes of bitemporal hemianopia?

A

Pituitary adenoma (UQ>LQ)
Craniopharyngioma (LQ>UQ)
ICA aneurysm

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31
Q

What are some causes of homonymous hemianopia?

A

Stroke, abscess, tumour

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32
Q

What are some features of optic neuritis?

A

Pain on moving eye, loss of central vision, RAPD, disc swelling, central scotoma, colour desaturation

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33
Q

How would a pt with a CN III lesion present?

A

Ptosis, large pupil, eye down and out

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34
Q

What are some causes of a CN III lesion with pupillary sparing?

A

Diabetes, HTN, GCA, syphilis

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35
Q

What are some causes of a CN III lesion with pupillary involvement?

A

PICA aneurysm, RICP, tumours

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36
Q

How would a pt with a CN IV lesion present?

A

Diplopia on looking down and in

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37
Q

What are some causes of a CN VI lesion?

A

MS, Wernicke’s encephalopathy, false localising sign in RICP, pontine stroke

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38
Q

What is the difference between an UMN and LMN lesion of CN VII?

A

UMN spares forehead

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39
Q

What are some causes of an UMN lesion of CN VII?

A

Stroke, tumour

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40
Q

What are some causes of an LMN lesion of CN VII?

A

Bell’s, otitis media, cerebellopontine angle tumours e.g. acoustic neuroma, malignant parotid tumour, RH syndrome

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41
Q

What are some causes of a CN VIII lesion?

A

Noise damage, Meniere’s, herpes zoster, acoustic neuroma

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42
Q

What can cause dilated pupils?

A

CN III lesions, mydriatic drugs, cocaine

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43
Q

What can cause constricted pupils?

A

Old age, Horner’s, opiates, miotics

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44
Q

Describe the pathway for the pupillary light reflex:

A

Optic nerve -> superior colliculus -> Edinger-Westphal nuclei bilaterally -> parasympathetic on CNIII causes constriction

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45
Q

Describe relative afferent pupillary defect:

A

Incomplete damage to afferent pathway

Affected pupil will paradoxically dilate when light is moved from normal eye to abnormal eye

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46
Q

What is accommodation (eye)?

A

Pt first looks at distant object then at close object and eye converge and pupils constrict

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47
Q

What is Holmes-Adie pupil?

A

Affected pupil is normally moderately dilated and is poorly reactive to light
Slowly reactive to accommodation
Damage to PS fibres innervating sphincter pupillae

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48
Q

What are some causes of Holmes-Adie pupil?

A

Usually benign

Lyme disease, syphilis, parvovirus, HSV

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49
Q

What is Argyll Robertson pupil?

A

Pupil is constricted and unreactive to light but reacts to accommodation

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50
Q

What is the main cause of Argyll Roberston pupil?

A

Neurosyphilis

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51
Q

What is Hutchinson’s pupil?

A

Pupil on side of lesion first constricts then widely dilates

Due to rapidly rising unilateral intracranial pressure

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52
Q

What is internuclear ophthlamoplegia?

A

Lesion disrupts communication by MLF causing weakness in adduction of ipsilateral eye with nystagmus of contralateral eye when abducting

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53
Q

What are some causes of ptosis?

A

CNIII lesions (compleyte)
Sympathetic paralysis (partial)
MG
Congenital

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54
Q

What are some features of UMN lesions?

A

Spasticity - hypertonia and clasp knife reflex
Hyperreflexia
Plantars are upgoing (+ve Babinski sign)
Extensors affected in arm, flexors in leg

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55
Q

What are some features of LMN lesions?

A

Affected muscles show wasting +/- fasciculation
Hypotonia/flaccidity
Hyporeflexia or areflexia

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56
Q

What sensations are spinothalamic tracts responsible for?

A

Pain and temperature

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57
Q

What sensations are dorsal columns responsible for?

A

Joint-position and vibration

Two-point discrimination, light touch

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58
Q

What is meant by a level in cord lesions?

A

Sensory, motor and reflex level (e.g. power unaffected above lesion, LMN at lesion, UMN below)

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59
Q

What are some features of temporal lobe lesions?

A

Wernicke’s aphasia
Superior homonymous quadrantanopia
Amnesia
Inexplicable phenomena

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60
Q

What are some features of frontal lobe lesions?

A

Hemiparesis
Personality change
Broca’s aphasia
Executive dysfunction

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61
Q

What are some features of parietal lobe lesions?

A 
Hemisensory loss
Astereognosis
Sensory inattention
Dysphasia
Apraxia
Inferior homonymous quadrantanopia
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62
Q

What are some features of occipital lobe lesions?

A

Homonymous hemianopia with macula sparing
Polyopia (seeing multiple images)
Palinopsia (persisting images after stimulus)

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63
Q

What are some features of cerebellar lesions?

A 
Dysdiadochokinesia
Ataxia 
Nystagmus
Intention tremor
Slurred speech
Hypotonia
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64
Q

What are some features of cerebellopontine angle lesions?

A 
Ipsilateral deafness
Nystagmus
↓corneal reflex
Ipsilateral cerebellar signs
Papilloedema
7th nerve palsy
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65
Q

In dorsal column lesions, which side will signs appear?

A

Ipsilateral below lesion

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66
Q

In spinothalamic tract lesions, which side will signs appear?

A

Contralateral below lesion

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67
Q

What are some red flag signs associated with headache?

A

Thunderclap (SAH)
Unilateral with eye pain (cluster, glaucoma)
Cough initiated/worse in morning (RICP)
Persisting with tender scalp and jaw claudication (GCA)
Meningism (meningitis, SAH)
Immunosuppressed

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68
Q

What drugs can cause medication overuse headache?

A

Analgesics and triptans

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69
Q

How are cluster headaches more common in?

A

Males, smokers

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70
Q

What are the presenting features of cluster headaches?

A

Rapid-onset of excruciating pain around one eye that may become watery and bloodshot with lid swelling and miosis

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71
Q

How long do cluster headaches last for (duration of headache and clusters)?

A

15-180min

Occur once or twice a day, and often nocturnal Clusters last 4-12w

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72
Q

What is the acute treatment for cluster headaches?

A

100% O2 for 15 mins

Sumatriptan SC at onset

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73
Q

What are some preventive measures or treatments for cluster headaches?

A

Avoid triggers such as alcohol

Corticosteroids, verapamil, lithium

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74
Q

What are the features of trigeminal neuralgia?

A

Intense, stabbing pain lasting seconds in trigeminal

distribution

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75
Q

What can trigger trigeminal neuralgia?

A

Washing area, shaving, eating, talking

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76
Q

What are some secondary causes of trigeminal neuralgia?

A

Compression of trigeminal root by aneurysmal intracranial vessels
Tumour
Chronic meningeal inflamm, MS, zoster

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77
Q

What is the management for trigeminal neuralgia?

A

Carbamazepine

Lamotrigine, phenytoin or gabapentin

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78
Q

What are the features of migraine?

A

Visual/other aura lasting 15-30 min followed within 1h by unilateral, throbbing headache (4-72h)
During headache: N+V, photo/phonophobia

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79
Q

How can the aura present in migraine?

A

Visual – jumbling of lines, dots, zigzags, scotomata, hemianopia
Paraesthesia, dysarthria, ataxia, hemiparesis, dysphasia

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80
Q

What are some partial triggers for migraine?

A

CHOCOLATE

Chocolate, Hangovers, Orgasms, Cheese, Oral contraceptives, Lie-ins, Alcohol, Travel, Exercise

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81
Q

How should a migraine attack be managed?

A

Oral triptan with NSAID/paracetamol

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82
Q

What is the prophylactic treatment for migraine?

A

Propranolol, topiramate

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83
Q

What causes vasovagal syncope?

A

Occurs due to reflex bradycardia ± peripheral vasodilation provoked by emotion, pain or standing too long

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84
Q

What are some pre-syncopal symptoms in vasovagal syncope?

A

Nausea, pallor, sweating, narrowing of vf

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85
Q

What causes carotid sinus syncope?

A

Hypersensitive baroreceptors cause excessive reflex

bradycardia on minimal stimulation (e.g. head-turning, shaving)

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86
Q

What are some symptoms of spinal cord compression?

A

Bilateral leg weakness, a sensory level ± preceding back pain
Normal findings above level, LMN at level, UMN below

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87
Q

What are some causes of spinal cord compression?

A

Secondary malignancy, cervical disc prolapse,

haematoma (warfarin), myeloma, abscess

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88
Q

How should spinal cord compression be managed?

A

Urgent dex, followed by chemo/RT if cancer

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89
Q

What are the features of conus medullaris lesions?

A

Mixed UMN/LMN signs

Leg weakness, early urinary retention and constipation, back pain, sacral sensory disturbance and erectile dysfunction

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90
Q

What are the features of cauda equina lesions?

A

Back pain, radicular pain down legs, areflexic paralysis of legs, sensory loss in root distribution, ↓sphincter tone

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91
Q

What can cause unilateral foot drop?

A

DM, common peroneal nerve palsy, stroke, prolapsed disc, MS

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92
Q

What is an ataxic gait?

A

Wide based, falls, cannot walk heel to toe

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93
Q

What can cause an ataxic gait?

A

Cerebellar lesions (MS, tumours, alcohol, phenytoin) Proprioceptive sensory loss (sensory neuropathy, ↓B12)

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94
Q

Describe an intention tremor and its cause:

A

Irregular, large amplitude, worse at end of purposeful acts

Cerebellar damage

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95
Q

Describe a re-emergent tremor and its cause:

A

Postural tremor developing after delay of 10s e.g. PD

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96
Q

What is chorea?

A

Non-rhythmic, jerky, purposeless movements flitting from one place to another e.g. raising shoulders, flexing/extending fingers

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97
Q

What can cause chorea?

A

Huntington’s, Sydenham’s chorea

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98
Q

What is athetosis?

A

Slow, confluent, purposeless movements

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99
Q

What is myoclonus?

A

Sudden involuntary focal or general jerks

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100
Q

How does tardive dyskinesia present and what is commonly the cause?

A

Vacuous chewing and grimacing movements

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101
Q

What are some examples of acute dystonias?

A

Torticollis (head pulled back)
Trismus (oromandibular spasm)
Oculogyric crisis (eyes drawn up)

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102
Q

What is the Circle of Willis?

A

Anastomotic ring at base of brain fed by internal carotids and basilar artery

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103
Q

What parts of the brain are supplied by the anterior cerebral artery?

A

Supplies frontal and medial part of cerebrum

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104
Q

What parts of the brain are supplied by the middle cerebral artery?

A

Supplies lateral part of each hemisphere

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105
Q

What parts of the brain are supplied by the posterior cerebral artery?

A

Supplies occipital lobe

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106
Q

What are the features of lateral medullary syndrome?

A

Ipsilateral facial pain, temp loss, Horner’s, ataxia + nystagmus
Contralateral limb/torso pain and temp loss

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107
Q

What vessels can be affected to give rise to lateral medullary syndrome?

A

PICA or vertebra

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108
Q

Which vessel is affected to give rise to lateral pontine syndrome?

A

AICA

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109
Q

What are the features of Weber’s syndrome?

A

Ipsilateral CNIII palsy and contralateral hemiplegia

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110
Q

Which vessel is affected to give rise to Weber’s syndrome?

A

PCA branches to midbrain

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111
Q

What is subclavian steal syndrome?

A

Subclavian artery stenosis proximal to origin of
vertebral artery may cause blood to be stolen by retrograde flow down this vertebral artery into the arm causing brainstem ischemia typically after use of arm

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4
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112
Q

What are the features of a subarachnoid haemorrhage?

A

Sudden onset excruciating headache, typically occipital, ‘thunderclap’
Vomiting, collapse, seizures, coma often follow
Meningism: neck stiffness, Kernig’s sign

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113
Q

What are the main causes of a subarachnoid haemorrhage?

A 
Berry aneurysm rupture (80%)
AV malformation (15%)
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114
Q

Where are berry aneurysms often located?

A

Junctions of pos com with ICA, ant com with ACA or bifurcation of MCA

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115
Q

What are some risk factors for subarachnoid haemorrhage?

A

Previous aneurysmal SAH, smoking, alcohol, HTN, bleeding disorders, FH

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116
Q

What conditions are associated with berry aneurysms?

A

PKD, CoA and Ehlers-Danlos

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117
Q

What investigations should be performed if subarachnoid haemorrhage is suspected?

A

Urgent CT head
LP (>12h after onset to see xanthochromia)
CT angio to identify multiple aneurysms

118
Q

What is the management for subarachnoid haemorrhage?

A

Maintain cerebral perfusion through hydration
Nimodipine reduces vasospasm
Surgery: endovascular coiling v surgical clipping

119
Q

What are some complications of subarachnoid haemorrhage?

A

Rebleeding (20%), cerebral ischemia, hydrocephalus,

hyponatremia

120
Q

What are some features of dural venous sinus thrombosis (general)?

A

Symptom onset is gradual (days or weeks)

Headache, vomiting, seizures, poor vision, papilloedema, focal CNS signs

121
Q

What are some causes of intracranial venous thrombosis?

A

Pregnancy, COCP, head injury, dehydration, tumours, recent LP

122
Q

What is the management for intracranial venous thrombosis?

A

Anticoag with LMWH then warfarin

Endovascular thrombolysis/thrombectomy

123
Q

What is the cause of a subdural haematoma?

A

Bleeding from bridging veins between cortex and venous sinuses resulting in accumulating haematoma between dura and arachnoid

124
Q

Untreated, what are the consequences of a subdural haematoma?

A

↑ICP, tentorial herniation and coning

125
Q

What are some risk factors for a subdural haematoma?

A

Trauma (can be minor and long ago), falls
Low ICP
Elderly
Anticoag

126
Q

What are some presenting features of a subdural haematoma?

A

Fluctuating level of consciousness, sleepiness, headache, personality change, unsteadiness, seizures

127
Q

Describe what the imaging will show in a subdural haematoma:

A

Crescent/sickle shaped collection of blood
If acute = hyperdense (bright)
If chronic = hypodense (dark)

128
Q

What is the management for a subdural haematoma?

A

Reverse clotting abnormalities

Evacuation by craniotomy or burr hole washout

129
Q

What is the cause of an extradural haematoma?

A

Traumatic skull fracture (temporal/parietal), causing laceration of middle meningeal artery and vein
Blood accumulates between bone and dura

130
Q

What are some presenting features of a extradural haematoma?

A

Lucid interval (hours to days), ↓GCS, RICP, increasingly severe headache, vomiting, confusion, seizures

131
Q

Describe what the imaging will show in a extradural haematoma:

A

Biconvex/lens shaped haematoma

132
Q

What is the management for a extradural haematoma?

A

Clot evacuation ± ligation of bleeding vessel

133
Q

What is epilepsy?

A

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of brain, manifesting as seizures

134
Q

What are some symptoms that may be experienced in the post-ictal state?

A

Headache, confusion, myalgia, temporary weakness, dysphasia

135
Q

How is epilepsy diagnosed?

A

History, establish type of seizure, rule out provoking causes
EEG, MRI

136
Q

What advice in regards to driving should be given to those diagnosed with epilepsy?

A

Patient must contact DVLA and avoid driving until seizure-free for >1y

137
Q

What are the two main classifications of seizures?

A

Focal and generalised

138
Q

What are the main types of generalised seizures?

A

Absence
Tonic-clonic
Myoclonic
Atonic

139
Q

What is the difference between generalised and focal seizures?

A

Focal: originating within networks linked to one hemisphere
Generalised: simultaneous onset of widespread electrical discharge with no localising feature

140
Q

Lip smacking and deja vu as part of seizures are localising features to which lobe of the brain?

141
Q

What is Jackonsian March and which brain lobe is this localised to?

A

Spreading motor seizures starting with face or thumb

Frontal lobe

142
Q

What are the first line medications for focal seziures?

A

Carbamazepine or lamotrigine

143
Q

What are the first line medications for tonic-clonic seziures?

A

Valproate or lamotrigine

144
Q

What are the first line medications for absence seziures?

A

Valproate or ethosuximide

145
Q

What is the first line medication for myoclonic seziures?

146
Q

When and how should anti-epileptics be stopped?

A

If pt is seizure free for >2y

Dose must be slowly decreased over 3-6m

147
Q

What are some side effects of carbamazepine?

A

Leukopenia, diplopia, blurred vision, impaired balance, drowsiness, rash, SIADH

148
Q

What type of seizures may be exacerbated by carbamazepine?

A

Absence and myoclonic seizures

149
Q

What are the side effects of lamotrigine?

A

Rash (0.1% SJS), blurred vision, photosensitivity

150
Q

What are some side effects of sodium valproate?

A

Teratogen, nausea, liver failure, pancreatitis, hair loss, oedema, ataxia

151
Q

What are some side effects of phenytoin?

A

↓intellect, depression, acne, gingival hyperplasia, polyneuropathy

152
Q

What is the extrapyramidal triad of Parkinonism?

A

Tremor
Hypertonia
Bradykinesia

153
Q

What are some causes of Parkinsonism?

A 
Parkinson’s disease
Progressive supranuclear palsy
Multi-system atrophy
Cortico-basal degeneration
Lewy body dementia
Drugs (metoclopramide, neuroleptics)
154
Q

What is the pathophysiology of Parkinson’s disease?

A

Loss of dopaminergic neurons in substantia nigra, associated with Lewy bodies in basal ganglia, brainstem and cortex

155
Q

What are some features of Parkinson’s disease?

A

Triad
Autonomic dysfunction (postural hypotension, constipation, urinary frequency)
Sleep disturbance
Depression, dementia and psychosis

156
Q

Are Parkinson’s disease signs typically asymmetrical or symmetrical?

A

Asymmetrical

157
Q

Why should starting levodopa sometimes be delayed?

A

Efficacy reduces over time, requiring larger doses with greater SEs

158
Q

What are the consequences of sudden withdrawal of Parkinson’s disease meds?

A

Acute akinesia and neuroleptic malignant syndrome

159
Q

What is co-prescribed with levodopa?

A

Dopa-decarboxylase inhibitor as co-careldopa

160
Q

What are some side effects of levodopa?

A

Dyskinesia, painful dystonia, psychosis, visual hallucinations, N+V, postural hypotension, arrhythmias

161
Q

What is an example of a dopamine agonists used in treatment of PD?

A

Ropinirole

162
Q

What are some side effects of dopamine agonists?

A

Drowsiness, nausea, hallucinations, compulsive behaviour

163
Q

What other drugs may be used in the management of Parkinson’s disease (not levodopa)?

A

Apomorphine
Anticholinergics (younger pts)
MAO-B inhibitors (rasagiline)
COMT inhibitors

164
Q

What are some features of progressive supranuclear palsy?

A

Early postural instability, vertical gaze palsy, rigidity of trunk > limbs, symmetrical onset, speech and swallowing problems

165
Q

What are some features of multi-system atrophy?

A

Early autonomic features e.g. incontinence, postural BP drop

Cerebellar + pyramidal signs, rigidity > tremor

166
Q

What are some features of cortico-basal degeneration?

A

Akinetic rigidity involving one limb, cortical sensory loss (e.g. astereognosis), apraxia

167
Q

How is multiple sclerosis defined?

A

Inflammatory plaques of demyelination in CNS disseminated in space and time - occurring at multiple sites, with >30d between attacks

168
Q

What is the median age of onset of MS?

169
Q

What is Uhthoff’s phenomenon (think MS)?

A

Symptoms may worsen with heat

170
Q

What is Lhermitte’s sign?

A

Electric sensation through back and limbs on flexing neck

171
Q

What are some common presenting features of MS?

A 
Unilateral optic neuritis
Pins and needles
Spastic weakness
Urinary retention, incontinence
Fatigue 
Speech and swallowing problems
172
Q

How is MS diagnosed using the McDonald criteria?

A

2 or more attacks - must last >1h with >30d between attacks

2 or more lesions

173
Q

How does MS progress?

A

Most relapsing-remitting course with initial recovery
between relapse. With time, remission becomes incomplete, so disability accumulates
10% display steadily progressive disability in absence of relapses (primary progressive MS)

174
Q

What are some poor prognostic signs in MS?

A

Older male, motor signs at onset, many early relapses, many MRI lesions, axonal loss

175
Q

What lifestyle changes can be made to help with the management of MS?

A

Regular exercise, stop smoking, avoid stress

176
Q

What are some disease modifying drugs used in MS?

A

Beta-interferon, dimethyl fumarate

177
Q

What drug can be used in treating relapses in MS?

A

IV methylpred

178
Q

What are some features associated with SOLs?

A

RICP
Seizures
Evolving focal neurology
Subtle personality changes

179
Q

What are the causes of SOLs?

A

Tumour, aneurysm, abscess, chronic subdural, cysts

180
Q

Give some examples of primary brain tumours?

A

Astrocytoma, glioblastoma, oligodendroma, ependymoma, meningioma, medulloblastoma, lymphoma

181
Q

What treatments can form part of the management plan for brain tumours?

A 
Surgery if accessible
RT/chemo
Ventriculo-peritoneal shunt 
Seizure prophylaxis
Dex or IV mannitol
182
Q

What is the triad of features seen in normal pressure hydrocephalus?

A

Urinary incontinence, dementia, gait abnormality (similar to PD)

183
Q

What is the treatment for normal pressure hydrocephalus?

A

Ventriculoperitoneal shunting

184
Q

What are some presenting features of idiopathic intracranial hypertension?

A

Narrowed visual fields, blurred vision, 6th nerve palsy, enlarged blind spot if papilloedema

185
Q

What is the typical patient presenting with idiopathic intracranial hypertension?

A

Obese females in 3rd decade

186
Q

What are the management options for idiopathic intracranial hypertension?

A

Weight loss
Acetazolamide or topiramate, loop diuretics, pred
LP
Optic sheath fenestration or lumbar-peritoneal shunt if drugs fail

187
Q

Where is the lesion in Wernicke’s aphasia?

A

Superior temporal gyrus

188
Q

What are the features of Wernicke’s aphasia?

A

Sentences that make no sense, word substitution

and neologisms but speech remains fluent

189
Q

Where is the lesion in Broca’s aphasia?

A

Inferior frontal gyrus

190
Q

What are the features of Broca’s aphasia?

A

Speech is non-fluent, laboured, and halting

191
Q

What area connects Wernicke’s and Broca’s area?

A

Arcuate fasiculus

192
Q

What are the features of Bell’s palsy?

A

Abrupt onset with complete unilateral facial weakness at 24-72h
Ipsilateral numbness around ear, ageusia, hypersensitivity to sounds
Unable to wrinkle forehead

193
Q

What are some infective causes of FN palsy?

A

Ramsay-Hunt, Lyme disease, meningitis, TB, HIV

194
Q

What are some neurological causes of FN palsy?

A

Stroke, tumour, MS

Acoustic neuroma, meningioma

195
Q

What are systemic causes of FN palsy?

A

DM, sarcoid, Guillain-Barre

196
Q

What is the management for Bell’s palsy?

A

Pred within 72h
Protect eye – dark glasses, artificial tears, tape to
close eyes at night

197
Q

What is Ramsay-Hunt syndrome?

A

Latent VZV reactivating in geniculate ganglion of 7th CN

198
Q

What are some features of Ramsay-Hunt syndrome?

A

Painful vesicular rash on auditory canal, pinna, tongue, palate
Ipsilateral facial palsy, loss of taste, vertigo, tinnitus, dry mouth and eyes

199
Q

How should Ramsay-Hunt syndrome be treated?

A

Antivirals and pred

200
Q

What can cause brachial plexus injury?

A

Trauma, RT, prolonged wearing of heavy rucksack, cervical rib, thoracic outlet compression

201
Q

What investigations may be performed if polyneuropathy is suspected?

A

FBC, glucose, U+Es, LFTs, TSH, B12, electrophoresis, ANA, ANCA, CXR, urinalysis

202
Q

What are the features of sensory neuropathies?

A

Numbness, pins + needles, affects glove and stocking

Difficulty handling small objects

203
Q

What are the features of motor neuropathies?

A

Often progressive, weak/clumsy hands, difficulty walking, difficulty breathing, wasting in distal muscles of hand and feet, hyporeflexia

204
Q

What are some causes of polyneuropathy?

A

DM, renal failure, Guillain-Barre, sarcoid, B12 + folate def., Charcot-Marie-Tooth

205
Q

What drugs can causes polyneuropathy?

A

Vincristine, cisplatin, isoniazid, nitrofurantoin, phenytoin, metronidazole, amiodarone

206
Q

What are some causes of autonomic neuropathy?

A

DM, amyloidosis, GB, Sjogren’s, HIV, SLE, Lambert-Eaton

207
Q

What is the median age of onset of motor neuron disease?

208
Q

What is the pathophysiology of motor neuron disease?

A

Selective loss of neurons in motor cortex, CN
nuclei and anterior horn cells
UMN and LMN can be affected but no sensory loss
and doesn’t affect eye movements

209
Q

What are the 4 clinical patterns seen in motor neuron disease?

A

Amyotrophic lateral sclerosis (80%): combined UMN and LMN signs
Progressive bulbar palsy (10-20%): only affects CN IX-XII
Progressive muscular atrophy (<10%): LMN signs only
Primary lateral sclerosis (rare): UMN signs

210
Q

How can motor neuron disease present?

A

Stumbling spastic gait, foot drop, weak grip and shoulder abduction, or aspiration pneumonia

211
Q

What is the only drug that improves survival in motor neuron disease and what’s its MoA?

A

Riluzole: glutamate and NMDA antagonist

212
Q

What is bulbar palsy?

A

Diseases of nuclei of CN IX-XII in medulla

LMN lesion

213
Q

What are the features of bulbar palsy?

A

Flaccid fasciculating tongue, absent jaw jerk and quiet speech

214
Q

What are the causes of bulbar palsy?

A

MND, Guillain-Barre, MG, syringobulbia, brainstem tumours

215
Q

What is corticobulbar palsy?

A

UMN lesion of muscles of swallowing and talking due to bilateral lesions above the mid-pons e.g. corticobulbar tracts

216
Q

What are the features of corticobulbar palsy?

A

Slow tongue movements, slow deliberate speech, jaw jerk hypereflexia, unprovoked weeping

217
Q

What are the causes of corticobulbar palsy?

A

MS, MND, stroke, central pontine myelinolysis

218
Q

What is the pathophysiology of cervical spondylosis?

A

Degen of annulus fibrosus combined with osteophyte formation leads to narrowing of spinal canal and intervertebral foramina
As neck flexes and extends, cord is dragged over bony spurs

219
Q

How can cervical spondylosis present?

A

Neck stiffness, crepitus on moving neck, stabbing/dull arm pain, forearm/wrist pain

220
Q

How should cervical spondylosis be managed?

A

Urgent MRI, analgesia, cervical collars

Neurosurgery if no improvement in 4-6w

221
Q

What is the pathophysiology of myasthenia gravis?

A

Autoimmune disease mediated by antibodies to nicotinic ACh receptor on postsynaptic side of NMJ

222
Q

What are some presenting features of myasthenia gravis?

A

Ptosis, diplopia, weakness at end of day, myasthenic snarl on smiling, ‘peek sign’

223
Q

What can exacerbate myasthenia gravis?

A

Pregnancy, hypokalaemia, infection, exercise

224
Q

What investigations should be performed if myasthenia gravis is suspected?

A

Antibodies: ↑anti-AChR antibodies in 90%

EMG, CT (exclude thymoma)

225
Q

What is the management for myasthenia gravis?

A

Anti-cholinesterase e.g. pyridostigmine
Treat relapses with pred
Thymectomy if required

226
Q

What is a myasthenic crisis?

A

Life-threatening weakness of resp. muscles during a relapse

227
Q

How should myasthenic crisis be managed?

A

Monitor FVC, vent support

Plasmapheresis or IV Ig and treat trigger

228
Q

What is the pathophysiology of Lambert-Eaton syndrome?

A

Antibodies are to voltage gated Ca2+ channels on pre-synaptic membrane

229
Q

What are some features of Lambert-Eaton syndrome?

A

Gait difficulty, autonomic (dry mouth, constipation), hyporeflexia and weakness that improves after exercise

230
Q

What is the management for Lambert-Eaton syndrome?

A

Pyridostigmine, 3,4-diaminopyridine, IV Ig

Regular CXR/CT

231
Q

What are the features of syringomyelia?

A

Absent pain and temp sensation (cape-like
distribution) with preserved DC senses
Wasting of hands, Horner’s

232
Q

What are the features of temporal arteritis?

A

Headache, temporal artery and scalp tenderness, jaw claudication, sudden unilateral blindness, morning stiffness

233
Q

What investigations should be performed if temporal arteritis is suspected?

A

CRP, plasma viscosity ↑↑, ↑platelets, ↑ALP, ↓Hb Temporal artery biopsy within 14d of starting steroids

234
Q

What is the management for temporal arteritis?

A

Pred immediately

IV methylpred if evolving visual loss or history of amaurosis fugax

235
Q

What is the triad in Horner’s syndrome?

A

Miosis, partial ptosis and anhidrosis

236
Q

What conditions can cause Horner’s syndrome?

A 
Demyelination
Vascular disease
Syringomyelia
Pancoast’s tumour
Carotid dissection
237
Q

What is Guillain-Barre syndrome?

A

Acute inflammatory demyelinating polyneuropathy

Few weeks after an infection, symmetrical ascending muscle weakness starts

238
Q

What are some triggers for Guillain-Barre syndrome?

A

Campylobacter, CMV, mycoplasma, zoster, HIV, EBV

239
Q

What are the diagnostic features of Guillain-Barre?

A

Progressive weakness >1 limb and areflexia

Progression up to 4w

240
Q

What is the management for Guillain-Barre?

A

IV Ig or early plasmapheresis

Spirometry, vent support

241
Q

What condition presents similarly to Guillain-Barre but progresses over a time period greater than 4 weeks?

A

Chronic inflammatory demyelinating polyradiculopathy (CIDP)

242
Q

What neurological signs are seen in subacute degeneration of the cord?

A

Combination of DC loss causing sensory and LMN signs and corticospinal tract loss causing
motor and UMN signs

243
Q

What is the classic reflex triad seen in subacute degeneration of the cord?

A

Extensor plantars, absent knee jerks and absent ankle jerks

244
Q

What is the classical triad seen in Wernicke’s encephalopathy?

A

Confusion, ataxia and ophthalmoplegia

245
Q

How is Wernicke’s encephalopathy managed?

A

Thiamine (Pabrinex) IV/IM then oral supplements

246
Q

What is the consequence of Wernicke’s encephalopathy?

A

Korsakoff’s syndrome (amnesia and confabulation)

247
Q

What is the cause of Creutzfeldt-Jakob disease?

A

Prion, a misfolded form of a normal protein that can transform other proteins into prion proteins

248
Q

What are some signs of Creutzfeldt-Jakob disease?

A

Progressive dementia, focal CNS signs, myoclonus, depression, complex visual disturbances, hallucinations

249
Q

How can variant CJD be distinguished from sporadic CJD?

A 
Earlier age of presentation in vCJD (29y v 60y)
Longer survival and later dementia
Psych features are early signs
Painful sensory symptoms commoner
Normal EEG
250
Q

What are the features of complete cord transection syndrome?

A

Spinal shock and autonomic dysfunction with higher lesions
Priapism
Complete loss of sensation and paralysis below lesion

251
Q

What are some causes of complete cord transection syndrome?

A

Trauma, infarction, transverse myelitis, abscess, tumour

252
Q

What are the features of Brown-Sequard syndrome?

A

Ipsilateral loss of motor function, loss of proprioception, vibration, 2- point discrimination
Contralateral loss of pain and temp sensation

253
Q

What are some causes of Brown-Sequard syndrome?

A

Penetrating trauma, fractured vertebrae, tumour, abscess, MS

254
Q

What are the features of anterior cord syndrome?

A

Flaccid paralysis below level, loss of pain/temp, autonomic dysfunction (based on level)
Preserved dorsal columns

255
Q

What are some causes of anterior cord syndrome?

A

Flexion injury

Anterior spinal artery injury - atherosclerosis or iatrogenic secondary to cross-clamping of aorta intraop

256
Q

What are the features of central cord syndrome?

A

Motor > sensory, UL > LL, distal > proximal, bladder dysfunction and urinary retention

257
Q

What are some causes of central cord syndrome?

A

Trauma (hyperextension in elderly, hyperflexion in younger), cervical spinal stenosis, degenerative spinal disease, syringomyelia

258
Q

What are the features of posterior cord syndrome?

A

Loss of DCs but maintained motor function and pain/temp sensation

259
Q

What are some causes of posterior cord syndrome?

A

Spondylosis, spinal stenosis, infection, Vit B12 def, occlusion of paired posterior spinal arteries

260
Q

What is the general management for cord injuries?

A 
Consider intubation (C5 or above), ICU, early
immobilisation of C-spine, consider surgery
261
Q

How long must patients stop driving for after their first unprovoked seizure?

A

6m

12m if structural abnormality or epileptiform activity on EEG

262
Q

After withdrawing anti-epileptics, how long must patients wait before driving?

A

6m after last dose

263
Q

How long must patients stop driving for after an explained syncopal episode?

264
Q

How long must patients stop driving for after an unexplained syncopal episode?

265
Q

How long must patients stop driving for after an multiple syncopal episodes?

266
Q

Describe the result of electromyography in myasthenia gravis:

A

Diminished response to repetitive stimulation

267
Q

Describe the result of electromyography in Lambert-Eaton syndrome:

A

Incremental response to repetitive stimulation

268
Q

Describe the result of electromyography with regard to action potentials in neuropathy:

A

↑AP duration, ↑AP amplitude

269
Q

Describe the result of electromyography with regard to action potentials in myopathy:

A

↓AP duration, ↓AP amplitude

270
Q

What are the causes of RICP?

A

Tumours, head injury, haemorrhage, infection, hydrocephalus, cerebral oedema

271
Q

What are some features of RICP?

A

Headache (worse on coughing), vomiting, altered GCS, ↓visual acuity, papilloedema
Cushing’s response (↓HR, ↑BP), Cheyne-Stokes respiration

272
Q

What investigations should be performed if RICP is suspected?

A

FBC, U+Es, LFTs, glucose, serum osmolality, clotting, blood culture, CT head

273
Q

What is the management for RICP?

A

Elevate head of bed
Mannitol, dex
Restrict fluid <1.5L/d
Consider craniotomy or burr hole

274
Q

What is uncal herniation?

A

Lateral supratentorial mass pushes inferomedial temporal lobe (uncus) against midbrain

275
Q

What is tonsillar herniation?

A

Cerebellar tonsils through foramen magnum

276
Q

What is subfalcian herniation?

A

Cingulate gyrus (medial frontal lobe) is forced under falx cerebri

277
Q

What are some early features in meningitis?

A

Headache, fever, leg pain, cold peripheries, abnormal skin colour

278
Q

What are some features seen later in meningitis?

A

Neck stiffness, photophobia, Kernig’s sign, ↓GCS, seizures, non-blanching rash, shock

279
Q

What are some investigations that should be performed if meningitis is suspected?

A

U+Es, FBC, LFT, glucose, coagulation, swabs, CXR

CSF MC+S, protein, lactate, glucose, PCR

280
Q

What is the management for meningitis?

A

Ceftriaxone + amoxicillin if >60y or immunocompromised

281
Q

What are some features of encephalitis?

A

Bizarre behaviour, confusion, ↓GCS, fever, headache, focal neuro signs, seizures, infectious prodrome

282
Q

What are some causes of encephalitis?

A

Viral: HSV1/2, VZV, measles, mumps

Non-viral: any bacterial meningitis, TB

283
Q

What are some investigations that should be performed if encephalitis is suspected?

A

Blood culture, viral PCR, contrast-enhanced CT, LP, CSF PCR, EEG

284
Q

What is the management for encephalitis?

A

Start acyclovir within 30min of pt arriving for 14d

285
Q

What is status epilepticus?

A

Seizures lasting >30min or repeated seizures without intervening consciousness

286
Q

What is the management for status epilepticus?

A

Lorazepam slow IV bolus, if no response repeat after 10-20min
Can also give rectal diazepam or buccal midazolam
Then phenytoin infusion

287
Q

What are the features of cauda equina?

A

Lower back pain, urinary incontinence/retention, reduced sensation in perianal area, decreased anal tone

288
Q

What investigation is needed if cauda equina is suspected?

A

Urgent MRI

289
Q

What is the management for cauda equina?

A

Surgical decompression, often laminectomy

290
Q

What is the criteria for doing a head CT within 1h in regard to head injury?

A

GCS <13 on initial assessment, or <15 after 2h
Focal neuro deficit
Suspected open or depressed skull fracture or basal skull fracture
Post-traumatic seizure
Vomiting more than once

291
Q

What is the criteria for doing a head CT within 8h in regard to head injury?

A

Any LoC or amnesia AND 65+y, coagulopathy, high impact injury, retrograde amnesia of >30min

292
Q

What drugs can exacerbate myasthenia gravis?

A

Gent, opiates, tetracycline, beta blockers, quinine

Neuro and SS (5 decks)

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