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FRACP NOSH 2020 > Neurology > Flashcards

Neurology Flashcards

1
Q

Indications for thrombectomy in aute ischaemic stroke?

  • location of lesion
  • timing
A

Location: large vessel occlusion -> ICA, M1, proximal M2, basilar

Timing: less than 6 hours from symptom onset. Can perform up to 24 hours from last seen well if there is a large penumbra/core mismatch as identified by CT Perfusion (DAWN trial)

Still need to thrombolyse prior if eligible

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2
Q

Cranial nerve distribution - rule of 4s

A

4 above pons -> 1-4

4 in pons -> 5-8

4 in medulla -> 9-12 (bulbar)

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3
Q

4 medial structures in Brainstem

A

Start with M

Motor pathway

Medial lemniscus (part of dorsal column)

Medial longitudinal fasciculus

Motor nucleus (of CN 3,4,6,12)

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4
Q

4 side structures of brainstem

A

Starting with S

Spinocerebellar pathways

Spinothalamic pathways

Sensory nucleus of CN 5 (large, from pons to medulla)

Sympathetic tract

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5
Q

3rd nerve palsy

Manifestations?

Common causes?

A

3rd CN -> oculomotor nerve

Supplies:

  • levator muscle of eyelid
  • 4 extraocular muscles: medial rectus, superior rectus, inferior rectus, and inferior oblique
  • contricts pupil through parasympathetic fibres

Clinical presentation:

  • diplopia
  • ptosis
  • “down and out” position

Lesions:

  • PCA aneurysms compressing pathway
  • ischaemia (diabetes)
  • trauma
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6
Q

4th nerve palsy

Manifestations?

Common causes?

A

4th CN -> Trochlear

Supplies superior oblique muscle -> intorts, depresses in adducted position

Clinical features:

  • blurred vision / diplopia
  • eye is deviated upwards and outwards

Causes:

  • congenital
  • trauma
  • microvascular
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7
Q

6th cranial nerve palsy

Clinical features?

Causes?

A

6th CN -> abducens

Supplies lateral rectus -> abducts eye

Clinical features:

  • horizontal diplopia
  • horizontal gaze palsy
  • strabismus

Causes:

  • raised ICP causing compression
  • tumours
  • vascular disease
  • inflammation
  • trauma
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8
Q

What is Broca’s aphasia?

Other names for it

Where is the lesion?

A

Non-fluent / Expressive issue

Can’t repeat

Can comprehend perfectly, leading to intense frustration

Lesion -> dominant frontal lobe

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9
Q

What is Wernicke’s aphasia?

Where is the lesion?

A

Fluent aphasia. Receptive issue, cannot comprehend

Cannot repeat

Lesion -> Dominant temporal lobe

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10
Q

What is conduction aphasia?

Where is the lesion?

A

Mixture between Broca’s and Wernicke’s

Able to comprehend, fluent but paraphasic errors common

Not able to repeat

Lesion -> Arcute fasciculus (connection between Broca’s and Wernicke’s area)

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11
Q

What is transcortical motor / sensory aphasia?

What type of lesion?

A

Transcortical motor aphasia -> expressive aphasia but CAN repeat

Transcortical sensory aphasia -> receptive aphasia but CAN repeat

Lesion -> Classically watershed infarcts that spare main language centres of Broca’s and Wernicke’s but affect other areas

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12
Q

What is Horner’s syndrome?

Where is the lesion?

A

Triad:

Ptosis

Miosis

Anhydrosis

Lesion = in sympathetic tract. Runs with lower brachial plexus around lung apex up to brainstem

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13
Q

Internucleur ophthalmoplegia

What is the clinical finding?

Where is the lesion?

Causes?

A

INO = impaired horizontal eye movements with weak adduction of the affected eye, and abduction nystagmus of the contralateral eye

Convergence is NORMAL.

Lesion = in medial longitudinal fasciculus (usually in pons, can be midbrain). MLF connects 6th CN on one side to 3rd CN on contralateral side so eyes move in same direction horizontally

Eye that cannot adduct = side of the lesion

Causes: MS (particularly if bilateral), stroke

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14
Q

Corticospinal tract:

What does it do?

Where does it travel?

-> where do the fibres cross?

A

Key motor pathway

Long tract that descends from primary motor cortex in frontal lobe

  • through internal capsule
  • crux cerebri
  • basis pontis
  • cross over at level of pyramids in lower medulla
  • meet lower motor neurons in anterior horn
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15
Q

Spinothalamic tract

Major function?

Where does it run?

A

Responsible for pain and temperature sensation

Receives input at posterior horn

  • decussates over 2-3 spinal segments while ascending
  • through brainstem to thalamus
  • primary sensory cortex in parietal lobe
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16
Q

Dorsal Column

What is it’s main function?

Where does it run?

A

Responsible for proprioception and vibration sensation

Input through dorsal root ganglion

  • ascends entire spinal cord
  • crosses over to contralateral medial lemniscus in lower medulla
  • ascends to thalamus
  • primary sensory cortex in parietal lobe
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17
Q

What is Brown-Sequard Syndrome?

Where is the lesion?

A

Cord hemisection

  • Ipsilateral UMN weakness below level of lesion (corticospinal)
  • ipsilateral proprioception/vibration loss below level of lesion (dorsal column)
  • contralateral pain and temprature loss 1-2 levels below lesion (spinothalamic)
  • ipsilateral LMN and sensory loss AT level of lesion
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18
Q

What is Central Cord Syndrome?

Where is the lesion?

A

Central cord lesion, usually syrinx

  • suspended sensory level = loss of pain/temperature in adjacent dermatomes at level of lesion

Larger lesions -> will involve LMNs, then corticospinal tract and spinothalamic tract

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19
Q

What is Anterior Cord Syndrome?

Where is the lesion?

A

Loss of all function, except dorsal column preserved (proprioception / vibration)

Caused by occlusion of anterior spinal artery

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20
Q

Lacunar syndromes:

Name 5 classic lacunar syndromes

A
  1. Pure motor (internal capsule or basis pontis)
  2. Pure sensory (thalamic)
  3. Ataxic hemiparesis (internal capsule, basis pontis and corona radiata)
  4. Dysarthria/clumsy hand (basis pontis)
  5. Mixed sensorimotor (thalamus + internal capsule)
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21
Q

What are the absolute contraindications to thrombolysis?

A

Contraindications:

  • extensive hypoattenuation on CT
  • current or previous ICH
  • intracranial tumour
  • severe head trauma last 3 months
  • intracranial / intraspinal surgery
  • plts <100
  • INR >1.7
  • APTT >40
  • Clexane last 24 hours
  • possible endocarditis
  • active GI / other bleed
  • aortic arch dissection
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22
Q

What medication do we use for thrombolysis?

Within what time frame can it be given?

A

Alteplase 0.9mg/kg

Current guidelines -> within 4.5 hours of symptom onset

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23
Q

What should BP be before giving thrombolysis?

A

< 180 / 105

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24
Q

Thalamus =

Blood supply from which artery?

4 nuclei -> function of each?

A

Blood supply = PCA

Centre of all sensory input. Pure sensory loss-> classically thalamic injury

Anterior nuclei = language and memory

Lateral nuclei = motor and sensory

Medial nuclei = arousal and memory

Posterior nuclei = visual

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25
Q

2012 A6

63 year old man with atrial fibrillation presents with sudden onset visual changes where he is unable to recognize objects in the right lower quadrant of his visual field bilaterally. Where is the deficit?

A. Occipital lobe

B. Optic chiasm

C. Parietal lobe

D. Superior colliculus

E. Temporal Lobe

A

Optic Pathways =

Optic nerves from retina

Optic chiasm -> cross over

Lateral geniculate nucleus

Optic radiations -> upper = parietal (lower visual field) and lower = temporal (upper visual field)

Primary visual cortex in occipital lobe (upper and lower banks)

Answers =

A. Occipital lobe -> CORRECT (quadrantanopia usually results from lesions (especially infarcts) that damage either the inferior or superior banks of the occipital cortex. Less commonly, a quadrantanopia represents a lesion in the optic radiations in the temporal or parietal lobe

B. Optic chiasm

C. Parietal lobe

D. Superior colliculus (this is an area involved with spatial attention and eye movements)

E. Temporal Lobe

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26
Q

What is the indication for a hemicraniectomy in stroke?

A

Malignant MCA infarct

  • very large infarct, which will cause significant swelling and oedema, leading to brainstem compression/herniation

Improves mortality, but patients will have significant disability

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27
Q

What is the drug of choice for getting BP into target prior to thrombolysis?

A

IV labetalol 10mg

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28
Q

What is the most significant risk factor for stroke?

A

Hypertension (both for ischaemic and haemorrhagic)

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29
Q

What is the BP aim post stroke for secondary prevention?

A

BP < 130 (120-140) / 90

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30
Q

Antiplatelets for secondary stroke prevention:

What are the short-term and long-term regimes?

A

Short-term -

Minor strokes or TIAs = DAPT with Aspirin + Clopidogrel for first 3 weeks

Intracranial large vessel atherosclerosis = DAPT for 90 days

Long-term = single antiplatelet (clopidogrel OR aspirin/dipyridamole OR aspirin alone)

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31
Q

What are the indications for a carotid entarterectomy?

A

Symptomatic carotid stenosis:

  • 70-99% in everyone
  • 50-99% in males

Should be done within 2 weeks of stroke/TIA

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32
Q

Post stroke/TIA, what would be indication for carotid stenting over CEA?

A

  • Unfavourable anatomy
  • Re-stenosis after CEA
  • previous radiotherapy
  • younger patients (<70)
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33
Q

What is the management of symptomatic intracranial atherosclerosis?

A

Aggressive medical management:

  • DAPT for 90 days
  • single APT lifelong thereafter
  • statin
  • BP control

No role for intracranial stenting

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34
Q

Which imaging modality are MS lesions best seen on?

A

White matter lesions -> best seen on T2 flair

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35
Q

What is the treatment approach for acute MS attack?

A

Steroids -> methylpred pulse

Plasmapheresis if severe

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36
Q

Following ischaemic stroke in AF, when can anticoagulation be restarted?

A

Warfarin - within 24 hours

NOACs - a few days

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37
Q

When is PFO closure indicated in the post stroke setting?

A

In patients <60 years, with no other cause found for stroke, who have associated atrial septal aneurysm or moderate-large R to L shunt

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38
Q

What is the definition of a TIA?

How do you stratify risk?

A

Brief episode of neurological dysfunction, resulting from focal cerebral ischaemia not associated with permanent cerebral infarction. Usually less than 1 hour in duration

Risk stratified by ABCD3 score

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39
Q

What is amaurosis fugax?

Where is the lesion?

A

Transient monocular vision loss, descending curtain

Due to hypoperfusion / blockage of ophthalmic artery from ICA

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40
Q

What is the classical presentation of cerebral amyloid angiopathy?

A

  • lobar haemorrhages
  • cortical microhaemorrhages
  • cortical superficial siderosis (may present with positive TIA symptoms)
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41
Q

What is the management of ICH due to cerebral amyloid angiopathy?

A

Avoid anticoagulation / antiplatelets

Treat HTN

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42
Q

What is the treatment of cerebral venous thrombosis?

A

Anticoagulation

  • heparin initially
  • transition to warfarin (3-6 months provoked, 6-12 months unprovoked)
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43
Q

What may prolonged or absent F waves indicate in NCS?

A

Early sign of Guillian-Barre

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44
Q

How should patients with GBS be monitored for respiratory failure?

A

2 hourly FVC on ward

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45
Q

What are some typical nerve biopsy findings in CIDP?

A

Segmental demyelination + remyelination, clusters of macrophages

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46
Q

What is the approach to treatment of CIDP?

A

1st line -> IVIG, plasma exchange, steroids.

2nd line -> immunosuppressive drugs (eg mycophenolate mofetil, cyclosporin, cyclophosphamide, rituximab) may be used.

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47
Q

What are the favoured medical therapies for painful diabetic neuropathy?

A

TCAs

Duloxetine

Pregabalin

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48
Q

Nitrous oxide as a recreational drug can have what link with peripheral neuropathy?

A

Functional inactivation of B12, causing peripheral neuropathy

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49
Q

What are the classic histopathologic findings in MND?

A

Cytoplasmic eosinophilic intracellular inclusions, positive for TDP 43

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50
Q

What is the mode of genetic transmission in most forms of Charcot-Marie-Tooth?

A

Autosomal dominant

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51
Q

What are the 2 antibodies involved in immune-mediated necrotising myopathy?

A

HMG-CoA reductase Ab

Anti-SRP

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52
Q

What is the approach to managing a statin-associated immune-mediated myopathy?

A

Cease the statin

Commence immunosuppression -> stopping the medication is not enough

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53
Q

What is the classic histopath finding in dermatomyositis?

A

Perivascular inflammatory infiltrate

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54
Q

Which muscles are classically involved in inclusion-body myositis?

A

Long finger flexors

Also involves quads, ankle dorsiflexors, can involve bulbar

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55
Q

What antibodies are involved in myasthenia gravis?

A

80-90% have IgG autoantibodies against the acetyl choline receptor (AChR)

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56
Q

Where are the antibodies in myasthenia gravis thought to originate?

A

Thought to originate in hyperplastic germinal centres in the thymus

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57
Q

What is the key to treatment of Bell’s palsy?

A

Steroid treatment within 72 hours

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58
Q

What are the indications for thymectomy in myasthenia gravis?

A

Indicated if thymoma, or if <60 with AChR antibodies

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59
Q

What is the classic triad of Wernicke’s encephalopathy?

A

Encephalopathy

Oculomotor dysfunction

Gait ataxia

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60
Q

What is the cause of Wernicke’s encephalopathy?

A

Thiamine (Vitamine B1) deficiency

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61
Q

What are Anti-Yo ab associated with?

A

A paraneoplastic cerebellar syndrome

Cancers = breast, ovarian, SCLC

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62
Q

What malignancy is KELCH-11 ab encephalitis associated with?

A

Testicular seminoma

63
Q

What malignancy is commonly found in NMDA encephalitis?

A

Ovarian teratomas

64
Q

What do positive sharp waves and fibrillation potentials on EMG indicate?

A

Spontaneous electrical activity - active denervation/ imflammatory myopathy

65
Q

What may be the earliest abnormality on NCS in GBS?

A

Prolonged F wave latency

66
Q

What is the role of steroids in AIDP?

A

NO ROLE - worse outcomes

67
Q

What is the classic LP finding in AIDP / CIDP ?

A

Albuminocytologic dissociation

68
Q

What is the key ab in AIDP (Miller-Fisher)?

What is the key ab in CIDP?

A

AIDP - GQ1b

CIDP - NF-155

69
Q

What condition is classically associated with dorsal root ganglionopathy?

A

Sjogren’s Syndrome

70
Q

Which anti-epileptic drug has highest association with birth defects?

What can occur?

A

Sodium valproate

Increases the risk of spina bifida up to ten-fold, associated with other serious malformations.

Can cause lower intelligence and greater risk of learning difficulties

71
Q

What is the commonest identifiable cause of epilepsy in older adults?

A

Previous strokes

72
Q

What are the EEG findings in juvenile myoclonic epilepsy?

A

4 to 6 Hz bilateral polyspike and slow wave discharges with frontal predominance

73
Q

What is the gold standard treatment of juvenile myoclonic epilepsy?

What are alternatives?

A

Sodium valproate

Lamotrigine, Keppra (these are options in pregnancy / young females of childbearing age)

74
Q

Which anti-epileptic can cause neurocognitive SEs?

A

Topiramate

75
Q

Are fasciculations present in UMN or LMN lesions?

A

LMN

76
Q

On NCS what is indicated by slowed conduction velocity?

A

Demyelination

77
Q

On NCS what is indicated by decreased amplitude?

A

Axon loss

78
Q

What is the usual pattern seen on NCS with nerve entrapment?

A

Focal demyelination ->

  • delayed or absent F waves
  • slowed conduction velocity
  • conduction block
79
Q

What is Wallerian degeneration?

When does this happen for

  • motor nerves?
  • sensory nerves?
A

Active process of degeneration that results when a nerve fiber is cut or crushed and the part of the axon distal to the injury (i.e. farther from the neuron’s cell body) degenerates.

Motor - Day 3-7

Sensory - Day 6-10

80
Q

What is Saturday Night Palsy?

A

Radial neuropathy, classically at spiral groove

Clinical features = wrist drop, finger extensor and brachioradialis weakness

81
Q

What is the key way to differentiate between radial neuropathy and central lesion?

A

Brachioradialis will be spared in Stroke

82
Q

On EMG, what do fibrillations and positive sharp waves indicate?

How long do they take to develop?

A

Abnormal spontaneous activity -> active denervation, can be present in inflammatory myopathies

Over 10-42 days

83
Q

In Myopathy, what pattern is seen on EMG?

A

Recruitment -> early

Amplitude -> reduced

84
Q

In chronic denervation, what pattern is seen on EMG?

A

Recruitment -> reduced

Amplitude -> increased

85
Q

What is the earliest finding usually seen in GBS on NCS?

A

Loss of F waves

86
Q

What HLA allelle is associated with SJS/TENs with carbamazepine use?

A

HLA-B*1502

87
Q

What is split hand syndrome?

What is it found in?

A

Thenar and 1st dorsal interosseous wasting

MND

88
Q

Multifocal motor neuropathy with conduction block

  • classical features?
  • How is it treated?
A

Features: progressive LMN signs, peripheral weaknes

Unusual sites of demyelination

Rx: IVIG

89
Q

What is the most common gene associated with CMT?

A

PMP22

(CMT1A - most common type)

90
Q

What is the classic phenotype of Anti-MuSK ab positive myasthenia gravis?

A

Bulbar involvement, respiratory crises, less ocular involvement

91
Q

What is the classic finding seen on single fibre EMG in myasthenia gravis?

A

Increased jitter

92
Q

What is the initial treatment for mild to moderate myasthenia gravis?

A

Pyridostigmine

93
Q

What anti-epileptic medication is preferred in pure absence seizures?

A

Ethosuximide

94
Q

What is the anti-epileptic agent of choice in focal epilepsies?

A

Carbamazepine

95
Q

What is the treatment of choice in myasthenic crisis?

A

PLEX or IVIG (equal)

Usually need to add glucocorticoids for lasting effect

96
Q

How does fingolimod work?

What is the classic SE to be aware of?

A

Sphingosine-1-phosphate receptor modulator

Inhibits migration of T cells from lymphoid tissue into CNS

AE -> first dose bradycardia

97
Q

Which MS drugs are contraindicated in pregnancy?

A

Fingolimod

Dimethyl fumerate

Teroflunomide

98
Q

What is area postrema syndrome?

A

Episode of unexplained hiccups or nausea and vomiting

99
Q

What are the auto antibodies found in NMOSD?

A

AQP4 ab

MOG ab

100
Q

In which Parkinsons Plus syndrome is hummmingbird sign and Mickey Mouse appearance seen on MRI?

A

PSP

101
Q

In which Parkinson’s Plus syndrome is alien hand found?

A

Corticobasal degenration

102
Q

Where in the brain does HSV encephalitis tend to affect?

A

Mesial temporal lobe

103
Q

What is the most common cause of rhomboencephalitis?

A

LIsteria

104
Q

What is seen in Myasthenia Gravis on repetitive nerve stimulation?

ON single fibre EMG?

A

Decrementing amplitudes

sfEMG -> “Jitter”

105
Q

Neuropathic Root lesions

A
106
Q

L5 vs Common Peroneal drop ?

A

Common peroneal

  • inversion preserved

L5 -

INVERSION also affected

Sciatic -

issues ABOVE the knee

107
Q

Neurogenic vs vascular claudication

A

Neurogenic

  • better with sitting down and going up hills
108
Q

Brachial neuritis features?

A

Unil shoulder pain then weakness

Winging of scapular

109
Q

What are F waves on NCS trying to detect?

A

Proximal demyelination

110
Q

What is the finding on CSF of GBS?

A

Albumino-cytological dissociation

  • high protein, but no inflammatory cells
111
Q

Split hand sign?

What condition?

A

Wasting of thenar eminence + FDI with preservation of hypothenar

MND

112
Q

When can you thrombolyse a stroke (time frame)?

What agent do you use?

A
  • Within 4.5hrs of onset
  • Within 9 hours of onset / midpoint of sleep if wake-up stroke -> pending CT perfusion with large penumbra

Alteplase

113
Q

When can you do thrombectomy for stroke?

A

Defs within 6 hours in large vessel stroke

Within 24 hours -> pending CT perfusion findings

114
Q

Classic features of Menieres?

A

Episodic Vertigo

Tinnitus

Aural fullness

Sensorineural hearing loss

115
Q

How to differentiate between posterior stroke and vestibular neuronitis?

A
116
Q

What is the initial management of IIH?

What is the treatment for IIH with visual compromise?

A

Weight loss, acetazolamide, topiramate

Optic nerve sheath fenestrations

117
Q

Most SPECIFIC sign of Bell’s palsy vs central cause?

A

Loss of taste (chorda tympani)

118
Q

CADASIL? What is it?

MRI findings?

Gene?

A

Cerebral Autosomal Dominant Arteriopathy Subcortical Infarcts & Leucoencephalopathy

Features:

  1. Migraine with aura (20-40%, 5x population)
  2. Stroke (60-85%, mean age~50)
  3. Dementia

Anterior temporal white matter changes on MRI

Notch 3 gene mutation

119
Q

Recurrent thunderclap headaches?

A

Reversible cerebral vasoconstriction

DDx SAH

120
Q

Key classes of chemoTx which cause peripheral neuropathy?

A

Platinums

Taxanes

Vincristine

Bortezomib

121
Q

Which MS drugs are contraindicated in pregnancy? (3)

A

Teriflunamide

Dimethyl Fumarate

Fingolimod

122
Q

In migraine, what vasoactive substance is thought to be central to vasodilation and inflammation?

A

Calcitonin Gene Related Peptide (CGRP) - from trigeminal fibres

123
Q

What is the key area of the brain involved in trigeminal autonomic cephalgias?

Why must an MRI be performed?`

A

Hypothalamus

To assess for pituitary and posterior fossa lesions

124
Q
A
125
Q

What is the recommended 1st line agent for prevention in cluster headaches?

A

Verapamil IR TDS

126
Q

Which of the trigeminal autonomic cephalgias are exquisitely responsive to indomethacin?

A

Paroxysmal hemicrania

Hemicrania continua

127
Q

What makes up the lentiform nucleus?

What is its clinical relevance?

A

Globus pallidus + putamen

Part of basal ganglia

128
Q

What is the preferred treatment option for SUNCT?

A

Lamotrigine

129
Q

What is the usual pathophysiology of trigeminal neuralgia?

What is the 1st line agent?

A

Neurovascular compression

Carbamazepine

130
Q

Which side do eyes deviate in cortical infarcts?

A

Towards lesion

131
Q

Where is the lesion in locked-in syndrome?

What function is spared?

A

Bilateral ventral pons (basilar artery)

Paralysis of all movements except vertical gaze and eyelid opening

Fully conscious

132
Q

What innervates posterior 1/3 of tongue?

A

Glossopharyngeal nerve (CN 9)

133
Q

In tongue weakness, what side does the tongue deviate to in

  • UMN lesion?
  • LMN lesion?
A

UMN - away from side of lesion

LMN - towards side of lesion

134
Q

At what level does the spinal cord end?

A

L1/L2

135
Q

What part of CNS does polio affect?

A

Anterio horn cells

136
Q

What is the lesion / where?

  • Loss of elbow extension
  • weakness of supination
  • loss of hand/finger extension, wrist drop
  • loss of sensation to lateral arm, and lateral dorsum of hand
A

Radial nerve

Proximal, at GH joint, can occur in crutch injury

137
Q

What is the lesion / where?

  • normal triceps
  • weakness of supination
  • loss of hand/finger extension, wrist drop
  • loss of sensation to lateral arm, and lateral dorsum of hand
A

Radial nerve

  • humeral fracture at radial groove
138
Q

What is the lesion?

  • weakness in extension of hand and fingers
  • finger drop, partial wrist drop
  • no sensory deficit
A

Radial nerve

Entrapment in arcade of Frohse

139
Q

What is the lesion?

  • no motor deficit
  • Numbness and tingling in radial half of hand dorsum
A

Radial nerve

Laceration of forearm

140
Q

What are the LOAF muscles?

What are they innervated by?

A

Lumbricals (1st and 2nd)

Opponens pollicis

Abductor pollicis brevis

Flexor pollicis brevis

Median nerve

141
Q

What is the deficit in ‘hand of Benediction’?

A

Median nerve

When attempting to form a fist, cannot flex 1st two fingers

142
Q

What is the lesion?

  • loss of pronation, weak wrist flexion, loss of thumb opposition
  • Benediction sign
  • loss of sensation lateral 3.5 digits and thenar area
A

Median nerve

Pronator teres syndrome or supracondylar fracture

143
Q

What is the lesion?

  • weakness in flexion of lateral digits and thumb flexion/opposition
  • numbness lateral 3.5 digits, sparing thenar eminence
A

Median nerve

Carpal tunnel

144
Q

What is the lesion?

  • no sensory deficit
  • loss of pronation
  • loss of flexion of lateral digits and thumb
A

Median nerve -> anterior interosseous branch

145
Q

Why is there paradoxical worsening of claw hand with more peripheral ulnar lesions?

A

The extent of clawing of digits four and five can be worse with lesions at the wrist than at the elbow as a result of sparing of the flexor digitorum profundus and weakness of the third and fourth lumbricals, resulting in greater muscle imbalance.

146
Q

In what lesion will there be foot drop but preserved eversion?

A

Deep branch of peroneal nerve

147
Q
A
148
Q

What does a positive head impulse test suggest?

A

Vertigo - peripheral cause

149
Q

What are the findings on HINTS screen that would suggest a central cause of vertigo?

A

Negative head impulse

Direction-changing nystagmus

Positive test of skew

**also new hearing loss

150
Q

What condition is vestibular neuritis commonly associated with?

What is the treatment, if required?

A

Herpes SImplex 1 reactivation

Rx: Pred 1mg/kg for 5 days, then taper over 2 weeks

151
Q

What is the recommended prophylactic treatment for episodic vertigo of Meniere’s DIsease?

A

Thiazide diuretic -> to lower endolymphatic pressure

Can be combined with potassium-sparing diuretic e.g. amiloride

Low salt diet, avoid caffeine

152
Q

What is the Semont manoeuvre?

A

Manoeuvre for BPPV.

Equally effective to Epley’s.

However, the Semont manoeuvre is usually easier to perform on patients with limited neck movement or a prominent cervical kyphosis.

153
Q

Management of Status Epilepticus

At what time frame is medication given?

What options?

A

After 5 minutes of continuous seizing / repeated activity with incomplete recovery

  1. Midazolam 10 mg IV OR Diazepam 10 mg IV OR Clonazepam 1 mg IV
  2. Unless cause easily reversed, start an anti-epileptic:
    - Phenytoin 20 mg/kg IV

OR

  • Sodium valproate 40 mg/kg IV

Consider need for HDU/ICU

154
Q
A

FRACP NOSH 2020 (18 decks)

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