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MSRA - passmed textbook > Neurology > Flashcards

Neurology Flashcards

1
Q

Huntington’s prognosis?

A

Progressive and incurable, results in death 20 years after the initial symptoms develop

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2
Q

Huntington’s genetics?

A
  1. AD
  2. Trinucleotide repeat of CAG
  3. Degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia
  4. Defect in huntingtin gene on Chromosome 4
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3
Q

Huntington’s features?

A

Typically after 35 y/o
1. Chorea
2. Personality changes
3. Dystonia
4. Saccadic eye movements

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4
Q

Guillain Barre typical organism?

A

Campylobacter jejuni

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5
Q

GBS key features?

A

Progressive, symmetrical, ascending weakness of the limbs. Sensory symptoms tend to be mild. Reflexes reduced or absent.

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6
Q

GBS other features?

A
  1. Hx of gastroenteritis
  2. Respiratory muscle weakness
  3. CN = diplopia, bilateral facial nerve palsy, oropharyngeal weakness common
  4. Autonomic = urinary retention, diarrhoea
  5. Papilloedema = reduced CSF resorption
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7
Q

GBS Ix?

A
  1. LP = raised protein with normal WCC in 66% (albuminocytologic dissociation)
  2. Nerve conduction studies = decreased motor nerve conduction velocity, prolonged distal motor latency, increased F wave latency
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8
Q

Stroke/TIA in carotid territory and pt not severely disabled?

A

Consider carotid endarterectomy

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9
Q

AF and stroke, when should anticoagulants be started?

A

14 days

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10
Q

Post-stroke when should statin be started?

A

If cholesterol > 3.5 and wait at least 48 hours due to risk of haemorrhagic transformation

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11
Q

Thrombolysis for acute stroke indications?

A
  1. Within 4.5 hours of onset of symptoms
  2. Haemorrhage excluded by imaging
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12
Q

When is thrombectomy offered for acute stroke?

A
  1. Within 6h symptoms onset and acute ischaemic stroke with confirmed occlusion of proximal anterior circulation (together with IV thrombolysis within 4.5h)
  2. 6-24 hours and confirmed occlusion of proximal anterior circulation, if there is potential to salvage brain tissue
  3. Consider < 24 hours both thrombectomy and thrombolysis for confirmed occlusion of the proximal posterior circulation (that is, basilar or posterior cerebral artery) and potential to salvage brain tissue
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13
Q

What functional status needs to be present for pts receiving thrombectomy?

A

Pre-stroke functional status of less than 3 on the modified Rankin scale and a score of more than 5 on the National Institutes of Health Stroke Scale (NIHSS)

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14
Q

Stroke secondary prevention?

A
  1. Clopidogrel
  2. Aspirin + MR dipyramidole if clopidogrel C/I
  3. MR dipyradimole if both aspirin and clopidogrel C/I
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15
Q

Carotid endarterectomy indication post-stroke?

A
  1. If suffered stroke or TIA in the carotid territory and are not severely disabled
  2. Should only be considered if carotid stenosis > 70% according ECST criteria or > 50% according to NASCET criteria
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16
Q

TIA definition?

A

A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

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17
Q

TIA features?

A

Typically resolve within 1 hour
1. Unilateral weakness or sensory loss
2. Aphasia or dysarthria
3. Ataxia, vertigo, or loss of balance
4. Visual problems = amaurosis fugax, diplopia, homonymous hemianopia

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18
Q

TIA Rx?

A

Aspirin 300mg unless:
1. Patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)
2. Already taking 75mg: continue current dose until r/v by specialist
3. Aspirin is C/I (d/w specialist team)

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19
Q

TIA specialist review?

A
  1. If >1 TIA/suspected cardioembolic source/severe carotid stenosis –> discuss need for admission/urgent observation with a stroke specialist
  2. Suspected TIA within last 7 days = assessment within 24h by stroke physician
  3. Suspected TIA >7 days = specialist assessment within 7d
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20
Q

TIA and driving?

A

Don’t drive until seen by specialist

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21
Q

TIA Neuroimaging?

A
  1. Don’t do CT unless clinical suspicion of an alternative diagnosis
  2. MRI should be done on same day as specialist assessment
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22
Q

TIA carotid imaging?

A

All pts should have urgent carotid doppler unless they are not a candidate for carotid endarterectomy

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23
Q

TIA Ix?

A
  1. Neuroimaging = MRI
  2. Carotid doppler
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24
Q

TIA Further Rx?

A

Clopidogrel

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25
Q

Neuropathic pain examples?

A
  1. DN
  2. Post-herpetic neuralgia
  3. Trigeminal neuralgia
  4. Prolapsed intervertebral disc
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26
Q

Neuropathic pain Rx?

A
  1. 1st line = Amitryptiline, duloxetine, gabapentin, pregabalin (if one doesnt work try another, typically only used as monotherapy)
  2. Tramadol as rescue therapy
  3. Topical capsaicin for localised neuropathic pain
  4. Pain management clinic if resistant
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27
Q

Trigeminal neuralgia Rx?

A

Carbamazepine 100mg BD and uptitrate slowly until pain is relieved

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28
Q

Parkinsons disease 1st line Rx?

A
  1. Motor symptoms affecting QoL = Levodopa
  2. Motor symptoms not affecting QoL = Dopamine agonist (non-ergot derived), levodopa or MAO-Bi
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29
Q

Levodopa mushkies?

A
  1. More motor symptom improvement
  2. More ADL improvement
  3. More motor complications
  4. Less specified s/e
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30
Q

Dopamine agonist mushkies?

A
  1. Less motor symptom improvement
  2. Less ADL improvement
  3. Less motor complications
  4. More specified s/e
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31
Q

MAO-B inhibitor mushkies?

A
  1. Less motor symptoms improvement
  2. Less ADL improvement
  3. Less motor complications
  4. Less specified s/e
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32
Q

Specified s/e?

A
  1. Excessive sleepiness
  2. Hallucinations
  3. Impulse control disorders
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33
Q

If pt continues to have symptoms despite optimal Levodopa Rx or has developed dyskinesia?

A

Add Dopamine agonist/MAO-B inhibitor/COMT inhibitor as adjunct

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34
Q

Amantadine evidence of motor symptoms or ADLs?

A

No evidence

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35
Q

Parkinsons and gastroenteritis risk?

A

Risk of acute Akinesia or Neuroleptic Malignant Syndrome

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36
Q

Parkinsons and impulse control disorder more common with?

A
  1. Dopamine agonist therapy
  2. History of previous impulsive behaviours
  3. History of alcohol consumption and/or smoking
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37
Q

Parkinsons and orthostatic hypotension what medication can be given?

A

Midodrine (periphral alpha adrenergic receptors to increase arterial resistance)

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38
Q

Drooling in Parkinsons Rx?

A

Glycopyrronium bromide

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39
Q

Levodopa usually given with?

A

Decarboxylase inhibitor e.g. carbidopa/benserazide = his prevents the peripheral metabolism of levodopa to dopamine outside of the brain and hence can reduce side effects

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40
Q

Levodopa s/e?

A
  1. Dry mouth
  2. Anorexia
  3. Palpitations
  4. Postural hypotension
  5. Psychosis
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41
Q

Levodopa adverse effects due to difficulty in achieving steady dose?

A
  1. End-of-dose wearing off
  2. On-off phenomenon
  3. Dyskinesias at peak dose
  4. These effects may worsen with time
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42
Q

If Parkinsons pt cannot take levodopa orally?

A

Dopamine agonist patch as rescue medication to prevent acute dystonia

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43
Q

Dopamine agonist examples?

A
  1. Bromocriptine
  2. Ropinorole
  3. Cabergoline
  4. Apomorphine
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44
Q

Ergot-derived dopamine receptor agonists?

A

Bromocriptine and cabergoline

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45
Q

Bromocriptine and cabergoline s/e?

A

Fibrosis = pulmonary, retroperitoneal and cardiac (therefore perform Echo, ESR, creatinine and CXR prior to Rx)

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46
Q

Dopamine receptor agonist s/e?

A
  1. Impulse control disorders
  2. Excessive daytime sleepiness
  3. Hallucinations
  4. Nasal congestion and postural hypotension
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47
Q

MAO-B inhibitor example?

A

Selegiline (inhibits the breakdown of dopamine secreted by the dopaminergic neurons)

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48
Q

Amantadine MOA and S/E?

A
  1. MOA = probably increases dopamine release and inhibits its uptake at dopaminergic synapses
  2. S/E = ataxia, slurred speech, confusion, dizziness, livedo reticularis
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49
Q

COMT inhibitor examples?

A

Entecapone and Tolcapone
(COMT is an enzyme involved in the breakdown of dopamine, and hence may be used as an adjunct to levodopa therapy)

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50
Q

Antimuscarinic examples?

A
  1. Procyclidine
  2. Benzotropine
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51
Q

Antimuscarinic parkinsons use?

A

Drug-induced parkinsonism

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52
Q

Most common psychiatric problem in Parkinsons?

A

Depression

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53
Q

Parkinsons disease definition?

A

Progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra. This results in a classic triad of features: bradykinesia, tremor and rigidity. Characteristically asymmetrical.

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54
Q

Parkinson’s epidemiology

A

2M:1F, mean age of diagnosis 65 y/o

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55
Q

Parkinsons tremor mushkies?

A
  1. Most marked at rest, 3-5 Hz
  2. Worse when stressed or tired, improves with voluntary movement
  3. Typically pill-rolling i.e. in thumb and index finger
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56
Q

Parkinsons autonomic dysfunction example?

A

Postural hypotension

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57
Q

Drug-induced parkinsonism features?

A
  1. Motor symptoms more rapid onset and bilateral
  2. Rigidity and rest tremor uncommon
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58
Q

Parkinsons Dx?

A

Usually clinical, but SPECT also

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59
Q

MND Features?

A
  1. Fasciculations
  2. Absence of sensory signs/symptoms
  3. Mixture of UMN and LMN signs
  4. Wasting of small hand muscles/tibialis anterior is common
  5. Does not affect external ocular muscles, no cerebellar signs
  6. Abdominal reflexes are usually preserved but sphincter dysfunction if present is a late feature
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60
Q

MND Dx?

A

Clinical

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61
Q

MND Ix?

A
  1. Nerve conduction studies = normal motor conduction, can help exclude neuropathy
  2. EMG = reduce number of action potentials with increased amplitude
  3. MRI = to exclude DDx of cervical cord compression and myelopathy
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62
Q

MS feature classification?

A
  1. Visual
  2. Sensory
  3. Motor
  4. Cerebellar
  5. Motor
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63
Q

MS Visual features?

A
  1. Optic neuritis = most common presenting feature
  2. Optic atrophy
  3. Uhthoff’s phenomenon = worsening of vision following rise in body temperature
  4. INO
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64
Q

MS sensory features?

A
  1. Pins/needles
  2. Numbness
  3. Trigeminal neuralgia
  4. Lhermitte’s syndrome = paraesthesiae in limbs on neck flexion
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65
Q

MS motor features?

A

Spastic weakness = most commonly seen in legs

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66
Q

MS cerebellar features?

A
  1. Ataxia = more often seen during an acute relapse
  2. Tremor
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67
Q

MS other features?

A
  1. Urinary incontinence
  2. Sexual dysfunction
  3. Intellectual deterioration
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68
Q

Phenytoin MOA?

A

Bind to sodium channels increasing their refractory period

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69
Q

Phenytoin s/e classification?

A
  1. Acute
  2. Chronic
  3. Idiosyncratic
  4. Teratogenic
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70
Q

Phenytoin P450?

A

Inducer

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71
Q

Phenytoin acute s/e?

A
  1. Initial = dizziness, diplopia, nystagmus, slurred speech, ataxia
  2. Later = confusion, seizures
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72
Q

Phenytoin chronic s/e?

A
  1. Common = gingival hyperplasia, hirsutism, coarsening of facial features, drowsiness
  2. Megaloblastic anaemia
  3. Peripheral neuropathy
  4. Enhanced Vitamin D metabolism causing osteomalacia
  5. Lymphadenopathy
  6. Dyskinesia
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73
Q

Phenytoin idiosyncratic s/e?

A
  1. Fever, rash (incl. TEN)
  2. Hepatitis, aplastic anaemia
  3. Dupuytren’s contracture
  4. Drug-induced lupus
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74
Q

Phenytoin teratogenic s/e?

A

A/w cleft palate and congenital heart disease

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75
Q

Phenytoin monitoring?

A

No routine monitoring needed, but trough levels, immediately before dose should be checked if:
1. Adjustment of phenytoin dose
2. Suspected toxicity
3. Detection of non-adherence to the prescribed medication

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76
Q

Status epilepticus definition?

A
  1. Single seizure > 5min
  2. > =2 seizures within a 5 min period without the person returning to normal between them
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77
Q

Status epilepticus Rx?

A
  1. 1st line = IV lorazepam, may be repeated once after 10-20 mins
  2. 2nd line = phenytoin or phenobarbital infusion
  3. Refractory (45 mins from onset) = induction of GA
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78
Q

Migraine management principles?

A

Serotonin agonists used for acute treatment, antagonists used in prophylaxis

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79
Q

Migraine acute Rx?

A
  1. 1st line = Oral triptan + NSAID/Paracetamol
  2. 12-17 y/o = consider nasal triptan
  3. If above not tolerated –> non-oral preparation of metoclopramide/prochlorperazine and consider adding a non-oral NSAID or triptan
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80
Q

Migraine prophylaxis?

A

Offered if experiencing 2 or more attacks per month: effective in about 60%
1. Topiramate/propranolol first line (Propranolol should be used in preference to topiramate in women of child bearing age as it may be teratogenic and it can reduce the effectiveness of hormonal contraceptives)
2. If these measures fail, up to 10 sessions of acupuncture over 5-8 weeks
3. Riboflavin 400mg OD may be effective in reducing migraine frequency and intensity

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81
Q

Predictable menstrual migraine Rx?

A

Zolmatriptan (2.5mg BD/TDS) or Frovatriptan (2.5mg BD) as mini-prophylaxis

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82
Q

Tuberous sclerosis inheritance?

A

AD

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83
Q

Tuberous sclerosis feature classification?

A
  1. Cutaneous
  2. Neurological
  3. Others
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84
Q

Tuberous sclerosis cutaneous features?

A
  1. Ash leaf spots which fluoresce under UV light
  2. Shagreen patches over lumbar spine
  3. Adenoma sebaceum in butterfly distribution over nose
  4. Subungual fibromata
  5. Cafe au lait spots
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85
Q

Tuberous sclerosis neurological features?

A
  1. Developmental delay
  2. Epilepsy
  3. Intellectual impairment
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86
Q

Tuberous sclerosis other features?

A
  1. Retinal hamartomas
  2. Rhabdomyomas of the hart
  3. Brain = Gliomatous changes can occur in brain lesions
  4. Kidneys = Polycystic kidneys, renal angiomyolipomata
  5. Lung = Lymphangioleiomyomatosis: multiple lung cysts
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87
Q

Epilepsy and DVLA?

A
  1. 1st unprovoked/isolated seizure = 6m off if brain imaging and EEG ok. If either abnormal then 12m off
  2. Established epilepsy/multiple unprovoked seizures = may get DL if seizure free for 12m, if there have been no seizures for 5y an until 70 license is usually restored
  3. Withdrawal of epilepsy medication = should not drive when being withdrawn and 6m after last dose
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88
Q

Syncope and driving?

A
  1. Simple faint = no restriction
  2. Single episode, explained and treated = 4 weeks off
  3. Single episode, unexplained = 6m off
  4. > = 2 episodes = 12m off
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89
Q

Stroke/TIA and driving?

A

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

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90
Q

Multiple TIAs over short period of time and driving?

A

3m off and inform DVLA

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91
Q

Craniotomy and driving?

A

1y off

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92
Q

Narcolepsy/cataplexy and driving?

A

Cease driving on Dx, can restart once ‘satisfactory control of symptoms;

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93
Q

Chronic neurological disorder e.g. MS/MND and driving?

A

DVLA should be informed, complete PK1 form (application for driving licence holders state of health)

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94
Q

Sodium valproate P450?

A

Inhibitor

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95
Q

Sodium valproate teratogenicity?

A

Neural tube defects and neurodevelopmental delay

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96
Q

Sodium valproate s/e?

A
  1. GI = nausea, increased appetite, weight gain, hepatotoxicity, pancreatitis
  2. Derm = alopecia, regrowth may be curly
  3. Neuro = ataxia, tremor
  4. Haem = thrombocytopenia
  5. Metabolic = hyponatraemia, hyperammonemic encephalopathy (L-carnitine can be used as Rx if this develops)
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97
Q

Encephalitis main cause?

A

HSV-1 responsible in 95% in adults, typically affects temporal and inferior frontal lobes

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98
Q

Encephalitis Ix?

A
  1. CXF = lymphocytosis, elevated protein
  2. PCR for HSV
  3. Neuroimaging (MRI better) = medial temporal and inferior frontal changes e.g. petechial haemorrhages, normal in 1/3rd pts
  4. EEG = lateralised periodic discharged at 2 Hz
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99
Q

Encephalitis Rx?

A

IV Aciclovir

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100
Q

Stroke assessment scoring system?

A

ROSIER (assess hypoglycaemia first), stroke is likely if score > 0

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101
Q

Stroke Ix?

A

Non-contrast CT head

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102
Q

Bell’s Palsy definition?

A

Acute, unilateral, idiopathic, facial nerve paralysis. Peak incidence 20-40 y/o, condition more common in pregnant women

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103
Q

Bell’s palsy features?

A
  1. LMN (forehead affected)
  2. Post-auricular pain may precede paralysis
  3. Dry eyes
  4. Altered tast, hyperacusis
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104
Q

Bell’s palsy Rx?

A
  1. Oral prednisolone within 72h
  2. Can add antivirals for severe facial palsy
  3. Artificial tears and eye lubricants, tape eye closed if unable to close at bedtime (to prevent exposure keratopathy)
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105
Q

Bell’s palsy f/up?

A
  1. If not improvement after 3w –> refer urgently to ENT
  2. Long-standing weakness of several months –> refer to plastics
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106
Q

Bell’s palsy prognosis?

A
  1. Most make full recovery within 3-4 months
  2. If untreated around 15% have permanent moderate to severe weakness
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107
Q

Peripheral neuropathy cause classification?

A
  1. Predominantly motor loss
  2. Predominantly sensory loss
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108
Q

Predominantly motor peripheral neuropathy causes?

A
  1. Infection = diphtheria
  2. Inflammation = GBS, HSMN (CMT), CIDP
  3. Metabolic = Porphyria, lead poisoning
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109
Q

Predominantly sensory peripheral neuropathy causes?

A
  1. Infection = Leprosy
  2. Inflammation = Amyloidosis
  3. Metabolic = Diabetes, B12 deficiency, alcohol, uraemia
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110
Q

Alcoholic neuropathy mushkies?

A
  1. Secondary to both direct toxic effects and reduced absorption of B vitamins
  2. Sensory symptoms typically present prior to motor symptoms
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111
Q

Vitamin B12 deficiency mushkies?

A
  1. SCDSC
  2. Dorsal column usually affected first (joint position, vibration) prior to distal paraesthesia
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112
Q

Cluster headache RFs?

A
  1. 3M:1F, smokers
  2. Alcohol may trigger an attack
  3. Appears to be a relation to nocturnal sleep
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113
Q

Cluster headache features?

A
  1. 1/2 a day, each episode 15m-2h
  2. Clusters last 4-12 weeks
  3. Intense sharp, stabbing pain around one eye
  4. Restless and agitated during attack
  5. Redness, lacrimation, lid swelling
  6. Nasal stuffiness (rhinorrhoea)
  7. Miosis and ptosis in a minority
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114
Q

Cluster headache Rx?

A
  1. Acute = 100% Oxygen (80% response rate within 15 mins), S/C Triptan (75% response rate within 15 minutes)
  2. Prophylaxis = Verapamil
  3. Seek neuro advice for imaging
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115
Q

Cluster headache is a type of?

A

Trigeminal autonomic cephalgia

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116
Q

Trigeminal autonomic cephalgia types?

A
  1. Cluster headache
  2. Paroxysmal hemicrania
  3. Short-lived unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT)
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117
Q

Paroxysmal hemicrania Rx?

A

Indomethacin

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118
Q

Brain abscess Rx?

A
  1. Surgery = craniotomy, debride abscess
  2. Abx = IV 3rd gen ceph + metronidazole
  3. ICP management = dexamethasone
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119
Q

When to usually start antiepileptics?

A

After second epileptic seizure

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120
Q

When to start antiepileptics after 1st seizure?

A
  1. Neurological deficit
  2. Brain imaging shows structural abnormality
  3. EEG shows unequivocal epileptic activity
  4. Pt/family/carers consider risk of having a further seizure unacceptable
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121
Q

Male GTC Rx?

A

Sodium Valproate

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122
Q

Female GTC Rx?

A

Lamotrigine or Levetiracetam

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123
Q

GTC girls < 10 y/o or women unable to have children?

A

Sodium valproate

124
Q

Focal seizure first line?

A

Lamotrigine/Levetiracetam

125
Q

Focal seizure second line?

A

Carbamazepine, oxcarbazepine or zonisamide

126
Q

Absence seizure first line?

A

Ethosuximide

127
Q

Absence seizure second line?

A
  1. Male = sodium valproate
  2. Female = lamotrigine or levetiracetam
128
Q

What drug may exacerbate absence seizures?

A

Carbamazepine

129
Q

Myoclonic seizure Rx?

A
  1. Male = sodium valproate
  2. Female = levetiracetam
130
Q

Tonic/atonic seizure Rx?

A
  1. Male = sodium valproate
  2. Female = lamotrigine
131
Q

4 major types of aphasia?

A
  1. Wernicke’s (receptive)
  2. Broca’s (expressive)
  3. Conduction
  4. Global
132
Q

Wernicke’s (receptive) aphasia mushkies?

A
  1. Due to a lesion of the superior temporal gyrus. It is typically supplied by the inferior division of the left MCA
  2. Word salad, nonsensical but speech remains fluent
  3. Comprehension is impaired
133
Q

Broca’s (expressive) aphasia mushkies?

A
  1. Due to a lesion of the inferior frontal gyrus. It is typically supplied by the superior division of the left MCA
  2. Speech is non-fluent, laboured, and halting. Repetition is impaired
  3. Comprehension is normal
134
Q

Conduction aphasia mushkies?

A
  1. aphasia Classically due to a stroke affecting the arcuate fasiculus - the connection between Wernicke’s and Broca’s area
  2. Speech is fluent but repetition is poor. Aware of the errors they are making
  3. Comprehension is normal
135
Q

Global aphasia mushkies?

A
  1. Large lesion affecting all 3 of the above areas resulting in severe expressive and receptive aphasia
  2. May still be able to communicate using gestures
136
Q

Wernicke’s which lobe?

A

Temporal lobe

137
Q

Broca’s which lobe?

138
Q

Trigeminal neuralgia definition?

A
  1. A unilateral disorder characterised by brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve
  2. The pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously
  3. Small areas in the nasolabial fold or chin may be particularly susceptible to the precipitation of pain (trigger areas)
  4. Pains usually remit for variable periods
139
Q

Pain only in ophthalmic division of trigeminal nerve (eye socket, forehead, and nose)?

140
Q

Trigeminal neuralgia Rx?

A
  1. Carbamazepine first line
  2. Failure to respond to treatment or atypical features e.g. < 50 y/o should prompt referral to neurology
141
Q

Essential tremor mushkies?

A
  1. Postural tremor = worse if arms outstretched
  2. Improved by alcohol and rest
  3. Titubation
  4. Often strong FHx
142
Q

What does sciatic nerve divide into?

A

Tibial and common peroneal nerves

143
Q

Most characteristic feature of common peroneal nerve lesion?

144
Q

Common peroneal nerve lesion features?

A
  1. Weakness of foot dorsiflexion
  2. Weakness of foot eversion
  3. Weakness of extensor hallucis longus
  4. Sensory loss over dorsum of foot and lower lateral part of the leg
  5. Weakness of anterior tibial and peroneal muscles
145
Q

What haematoma can present several weeks after the initial head injury?

A

Subdural haematoma

146
Q

Subdural haematoma classification?

A
  1. Acute
  2. Chronic (weeks to months)
147
Q

Acute subdural haematoma mushkies?

A
  1. Associated with high impact injuries
  2. Ix = CT shows hyperdense crescenteric collection, not limited by suture lines
  3. Rx = Small or incidental acute subdurals can be observed conservatively. Surgical options include monitoring of intracranial pressure and decompressive craniectomy
148
Q

Chronic subdural haematoma mushkies?

A
  1. Present for weeks to months, presents with confusion, reduced consciousness, or neurological deficit
  2. Rupture of the small bridging veins within the subdural space rupture and cause slow bleeding. Elderly and alcoholic patients are particularly at risk of subdural haematomas since they have brain atrophy and therefore fragile or taut bridging veins.
  3. Chronic subdurals are hypodense on CT imaging
  4. Rx = Confused/neurological deficit/severe imaging findings –> surgical decompression with burr holes is required
149
Q

Stroke secondary prevention if clopidogrel C/I?

A

Aspirin and dipyradimole lifelong

150
Q

Lacunar stroke features?

A
  1. Purely motor e.g. clumsy hand
  2. Purely sensory
  3. Mixed
151
Q

Oculomotor nerve palsy?

A
  1. Ptosis
  2. Down and out eye
  3. Dilated, fixed pupil
152
Q

Trochlear nerve palsy?

A

Vertical diplopia due to defective downward gaze

153
Q

Abducens nerve palsy?

A

Horizontal diplopia due to defective abduction

154
Q

Glossopharyngeal nerve palsy features?

A
  1. Hypersensitive carotid sinus reflex
  2. Loss of gag reflex
155
Q

Vagus nerve palsy features?

A
  1. Uvula deviates away from site of lesion
  2. Loss of gag reflex
156
Q

Accessory nerve palsy features?

A

Weakness turning head to contralateral side

157
Q

Hypoglossal nerve palsy features?

A

Tongue deviates towards side of lesion

158
Q

Vestibular schwannoma AKA?

A

Acoustic neuroma

159
Q

Classical history of vestibular schwannoma?

A

Vertigo, hearing loss, tinnitus, absent corneal reflex
1. CN VIII = vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
2. CN V = absent corneal reflex
3. CN VII = facial palsy

160
Q

Bilateral vestibular schwannomas?

161
Q

Vestibular schwannoma Ix?

A
  1. MRI cerebellopontine angle
  2. Audiometry as only 5% will have normal audiogram
162
Q

Vestibular schwannoma Rx?

A
  1. Urgent ENT referral, tumours are often slow growing, benign and often observed initially
  2. Rx = surgery, radiotherapy, observation
163
Q

Degenerative cervical myelopathy RFs?

A
  1. Smoking due to its effects on intervertebral discs
  2. Genetics
  3. Occupations with high axial loading
164
Q

Degenerative cervical myelopathy features?

A
  1. Pain
  2. Loss of motor function
  3. Loss of sensory function causing numbness
  4. Loss of autonomic function
  5. Hoffman’s sign
165
Q

Hoffman’s sign?

A
  1. A reflex test to assess for cervical myelopathy
  2. Performed by gently flicking one finger on a patient’s hand. A positive test results in reflex twitching of the other fingers on the same hand in response to the flick.
166
Q

Degenerative cervical myelopathy Ix?

A

MRI cervical spine = may reveal disc degeneration and ligament hypertrophy with accompanying cord signal change

167
Q

Degenerative cervical myelopathy Rx?

A
  1. Urgent referral to spinal services due to importance of early treatment, timing of surgery is important as any existing spinal cord damage can be permanent
  2. Early treatment (within 6 months of diagnosis) offers the best chance of a full recovery but at present, most patients are presenting too late.
168
Q

Degenerative cervical myelopathy Rx?

A
  1. Decompressive surgery
  2. Physiotherapy should only be initiated by specialist services, as manipulation can cause more spinal cord damage
169
Q

Guillain Barre syndrome pathogenesis?

A
  1. Cross-reaction of antibodies with gangliosides in the peripheral nervous system
  2. Correlation between anti-ganglioside antibody (e.g. anti-GM1) and clinical features has been demonstrated
  3. Anti-GM1 in 25%
170
Q

Miller Fisher syndrome?

A
  1. GBS variant
  2. Ophthalmoplegia, areflexia, ataxia (eye muscles affected first)
  3. Descending rather than ascending paralysis
  4. Anti-GQ1b antiibodies in 90%
171
Q

AED causing weight gain?

A

Sodium valproate

172
Q

Triptan s/e?

A

‘Triptan sensations’ = tingling, heat, tightness (e.g. throat and chest), heaviness, pressure

173
Q

Triptan s/e?

174
Q

Reflex roots?

A
  1. Ankle = S1-S2
  2. Knee = L3-L4
  3. Biceps = C5-C6
  4. Triceps = C7-C8
175
Q

Ulnar nerve origin?

A

Medial cord of brachial plexus (C8,T1)

176
Q

Ulnar nerve path?

A
  1. Travels through the posteromedial aspect of the upper arm to the flexor compartment of the forearm
  2. Then enters the palm of the hand via the Guyon’s canal, superficial to the flexor retinaculum and lateral to the pisiform bone
177
Q

Ulnar nerve motor and sensory function?

A
  1. Motor = All intrinsic muscles of the hand except for LOAD
  2. Sensory = medial 1 1/2 fingergs (palmar and dorsal aspects)
178
Q

Ulnar nerve patterns of damage?

A
  1. Damage at wrist
  2. Damage at elbow
179
Q

Ulnar nerve damage at wrist?

A
  1. Claw hand = hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits
  2. Wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals)
  3. Wasting and paralysis of hypothenar muscles
  4. Sensory loss to the medial 1 1/2 fingers (palmar and dorsal aspects)
180
Q

Ulnar nerve damage at elbow?

A
  1. As above + radial deviation of wrist
  2. Ulnar paradox = clawing more severe in distal lesions
181
Q

Herpes simplex encephalitis pathognomic CT change?

A

Bilateral temporal lobe changes

182
Q

Oxford Stroke Classification?

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

A. TACI = All 3 criteria, involves middle and anterior cerebral arteries
B. PACI = 2 criteria, involves smaller arteries of anterior circulation e.g. upper or lower division of MCA
C. LACI
4. POCI

183
Q

Lacunar infarct (LACI)?

A

Involved perforating arteries around the internal capsule, thalamus and basal ganglia. Presents with 1 of the following:
1. Unilateral weakness and/or sensory deficit of face and arm, arm and leg, or all three
2. Pure sensory stroke
3. Ataxic hemiparesis

184
Q

Posterior circulation infarct (POCI)?

A

Involves vertebrobasilar arteries, presents with 1 of:
1. Cerebellar or brainstem syndromes
2. LOC
3. Isolated homonymous hemianopia

185
Q

Lateral medullary syndrome?

A
  1. PICA, AKA Wallenberg’s syndrome
  2. Ipsilateral = ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
  3. Contralateral = limb sensory loss
186
Q

Weber’s syndrome?

A
  1. Ipsilateral III palsy
  2. Contralateral weakness
187
Q

Homonymous quadrantanopia lesion location?

A

PITS
1. Parietal = Inferior
2. Temporal = Superior

188
Q

Congruous and incongruous defect meaning?

A
  1. Congruous defect = Complete or symmetrical visual field loss
  2. Incongruous defect = Incomplete or asymmetric
189
Q

Homonymous hemianopia congruous defect?

A

Lesion of optic radiation/occipital cortex

190
Q

Homonymous hemianopia incongruous defect?

A

Lesion of optic tract

191
Q

Macula sparing homonymous hemianopia?

A

Lesion of occipital cortex

192
Q

Homonymous quadrantanopia locations?

A
  1. Superior = lesion of the inferior optic radiations in the temporal lobe (Meyer’s loop)
  2. Inferior = lesion of the superior optic radiations in the parietal lobe
193
Q

Bitemporal hemianopia mushkies?

A
  1. Lesion of optic chiasm
  2. Upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
  3. Lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
194
Q

Essential tremor inheritance?

195
Q

Essential tremor features?

A
  1. Postural = worse if arms outstretched
  2. Improved by alcohol and rest
  3. Most common cause of titubation (head tremor)
196
Q

Essential tremor Rx?

A
  1. Propranolol 1st line
  2. Primidone sometimes used
197
Q

Pseudoseizure AKA?

A

Psychogenic nonepileptic seizures

198
Q

MND types?

A
  1. Amyotrophic lateral sclerosis
  2. Progressive muscular atrophy
  3. Bulbar palsy
199
Q

MND Rx?

A
  1. Riluzole = prevents stimulation of glutamate receptors, mainly ALS, prolongs life by 3m
  2. Resp = Night BiPAP prolongs life by 7m
  3. Nutrition = PEG
  4. Prognosis = 50% pts die within 3 years
200
Q

FHx of early blindness and tunnel vision?

A

Retinitis pigmentosa

201
Q

Capgras syndrome?

A

A person holds a delusion that a friend or partner has been replaced by an identical-looking impostor

202
Q

Othello syndrome?

A

Irrational belief that one’s partner is having an affair with no objective evidence.

203
Q

De clerembault syndrome?

A

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

204
Q

Cotard syndrome?

A

Delusional idea that one is dead

205
Q

Fregoli syndrome?

A

Delusional idea that the various people that the patient meets are in fact the same person

206
Q

Cataplexy?

A

Sudden and transient loss of muscular tone caused by strong emotion (e.g. laughter, being frightened). Around two-thirds of patients with narcolepsy have cataplexy. Features range from buckling knees to collapse.

207
Q

Adductor pollicis innervation?

A

Ulnar nerve

208
Q

Common peroneal nerve AKA?

A

Common fibular nerve

209
Q

Saturday night palsy?

A

Compression of the radial nerve against the humeral shaft, possibly due to sleeping on a hard chair with his hand draped over the back

210
Q

Radial nerve origin?

A

Continuation of posterior cord of the brachial plexus (C5-T1)

211
Q

Radial nerve patterns of damage?

A
  1. Wrist drop
  2. Sensory loss to small area between the dorsal aspect of the 1st and 2nd metacarpals
  3. If axillary damage = as above + paralysis of triceps
212
Q

3rd nerve palsy features?

A
  1. Deviated eye down and out
  2. Ptosis
  3. If dilated = surgical
213
Q

3rd nerve palsy causes?

A
  1. Medical = DM, Vasculitis, Amyloid, MS
  2. Surgical = PICA, Cavernous sinus thrombosis, raised ICP, Weber’s syndrome
214
Q

AED causing peripheral neuropathy?

215
Q

Seizure classification 3 features?

A
  1. Where seizure begins
  2. Level of awareness during seizure
  3. Other features of seizure
216
Q

Focal seizure mushkies?

A
  1. AKA Partial seizures
  2. Start in a specific area on one side of the brain
  3. Classified into focal aware, focal impaired awareness, and awareness unknown
  4. Motor e.g. Jacksonian march, non-motor (deja vu, jamais vu), or other featurs e.g. aura
217
Q

Generalised seizure mushkies?

A
  1. Involve networks on both sides of brain at onset
  2. Consciousness lost immediately
  3. Motor e.g. tonic clonic and non-motor e.g. absence
  4. Specific types = tonic-clonic, tonic, clonic, typical absence, atonic
218
Q

Secondary generalised seizures now known as?

A

Focal to bilateral seizure

219
Q

Facial weakness with eye movements spared?

220
Q

Lambert Eaton myasthenic syndrome presentation?

A
  1. Proximal muscle weakness
  2. Autonomic features e.g. dry mouth, constipation
  3. Arreflexia
  4. Associated with underlying malignancy
221
Q

Long term prophylaxis of cluster headaches?

222
Q

Medication overuse headache mushkies?

A
  1. Present for 15 days or more per month
  2. Developed or worsened whilst taking regular symptomatic medication
  3. Patients using opioids and triptans are at most risk
  4. May be psychiatric comorbidity
223
Q

Homonymous hemianopia and paresis?

A

Always on the same side

224
Q

Neuroleptic malignant syndrome mushkies?

A

A a rare but dangerous condition seen in patients taking antipsychotic medication. It carries a mortality of up to 10% and can also occur with atypical antipsychotics. It may also occur with dopaminergic drugs (such as levodopa) for Parkinson’s disease, usually when the drug is suddenly stopped or the dose reduced

225
Q

NMS pathophysiology?

A

Dopamine blockade induced by antipsychotics triggers massive glutamate release and subsequent neurotoxicity and muscle damage.

226
Q

NMS features?

A

Occurs within hours to days of starting an antipsychotic:
1. Pyrexia
2. Muscle rigidity, hyporeflexia, normal pupils
3. Agitated delirium with confusion
4. Autonomic lability: HTN, tachycardia, tachypnoea
5. Raised CK
6. AKI secondary to rhabdomyolysis in severe cases
7. Leukocytosis may also be seen

227
Q

NMS Rx?

A
  1. Stop antipsychotic
  2. Transfer to medical bed/ITU
  3. IVF to prevent renal failure
  4. Dantrolene may be helpful in selected cases = thought to work by decreasing excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor, and decreasing the release of calcium from the sarcoplasmic reticulum
  5. Bromocriptine, a dopamine agonist, may also be used
228
Q

Most common symptoms of POCS?

229
Q

Migraine diagnosis?

A
  1. A = at least 5 attacks fulfilling criteria B-D
  2. B = 4 - 72h
  3. C = at least 2 of: unilateral, pulsating, moderate/severe, aggravation by or causing avoidance of routine physical activity
  4. D = during headache at least 1 of: nausea and/or vomiting, photophobia and phonophobia
  5. E = Not attributed to another disorder
230
Q

Migraine with aura seen in what %?

231
Q

What vessel affected in amaurosis fugax?

A

Retinal/ophthalmic artery

232
Q

What vessel affected in locked-in syndrome?

A

Basilar artery

233
Q

What vessel affected in lateral pontine syndrome?

234
Q

Anterior cerebral artery stroke effect?

A

Contralateral hemiparesis and sensory loss, lower extremity > upper

235
Q

Middle cerebral artery stroke effect?

A
  1. Contralateral hemiparesis and sensory loss, upper extremity > lower
  2. Contralateral homonymous hemianopia
  3. Aphasia
236
Q

Posterior cerebral artery stroke effect?

A
  1. Contralateral homonymous hemianopia with macular sparing
  2. Visual agnosia
237
Q

Weber’s syndrome stroke effect (posterior cerebral artery branches that supply the midbrain)?

A
  1. Ipsilateral CN III Palsy
  2. Contralateral weakness of upper and lower extremity
238
Q

PICA stroke effect?

A
  1. Ipsilateral facial pain and temperature loss
  2. Contralateral = limb/torso pain and temperature loss
  3. Ataxia, nystagmus
239
Q

Lacunar strokes mushkies?

A
  1. Present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
  2. Strong association with HTN
  3. Common sites include the basal ganglia, thalamus and internal capsule
240
Q

Anti-emetic for parkinsons?

A

Domperidone

241
Q

Causes of parkinsonism?

A
  1. Parkinson’s disease
  2. Drugs = antipsychotics, metoclopramide
  3. PSP, MSA
  4. Wilson’s disease
  5. Post-encephalitis
  6. Dementia pugilistica e.g. secondary to chronic head trauma e.g. boxing
  7. Toxins e.g. carbon monoxide, MPTP
242
Q

MS Rx goal?

A

Reducing the frequency and duration of relapses. There is no cure.

243
Q

MS acute relapse Rx?

A

High dose steroids = oral/IV methylprednisolone to shorten length of an acute relapse, do not alter the degree of recovery

244
Q

MS indications for disease-modifying drugs?

A
  1. Relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided
  2. Secondary progressive disease + 2 relapses in past 2 years + able to walk 10m aided/unaided
245
Q

5 MS disease modifying drugs?

A
  1. Natalizumab
  2. Ocrelizumab
  3. Fingolimod
  4. Beta-interferon
  5. Glatiramer acetate
246
Q

Natalizumab mushkies?

A
  1. Recombinant mAb to a4b1-integrin found on leukocyte surface
  2. Inhibit leukocyte migration across BBB
  3. Best evidence, 1st line, given IV
247
Q

Ocrelizumab mushkies?

A
  1. Humanised anti-CD20 mAb
  2. Often 1st line, given IV
248
Q

Fingolimod mushkies?

A
  1. S1P receptor modulator
  2. Prevents lymphocytes from leaving lymph nodes
  3. Oral formulations available
249
Q

Beta interferon mushkies?

A
  1. Not that effective
  2. Given S/C or IM
250
Q

Glatiramer acetate mushkies?

A
  1. Immunomodulating drug, acts as immune decoy
  2. Given S/C, along with beta-interferon considered an older drug which is less effective
251
Q

MS specific problems?

A
  1. Fatigue
  2. Spasticity
  3. Bladder dysfunction
  4. Oscillopsia
252
Q

MS fatigue management?

A
  1. Trial amantadine once other problems excluded
  2. Mindfulness training, CBT
253
Q

MS spasticity Rx?

A
  1. Baclofen and gabapentin 1st line
  2. Diazepam, dantrolene and tizanidine 2nd line
  3. Physiotherapy
  4. Cannabis and botox undergoing evaluation
254
Q

MS Bladder dysfunction Rx?

A
  1. Get an US
  2. If significant residual volume –> intermittent self catheterisation
  3. If no significant residual volume –> anticholinergics may improve urinary frequency
255
Q

MS oscillopsia Rx?

A

Gabapentin 1st line

256
Q

Median nerve supplies which muscles?

A

LOAF
Lateral 2 lumbricals, opponens pollicis, abductor pollicis brevis, flexor pollicis brevis

257
Q

Sciatic nerve supply?

A

L4-5, S1-3

258
Q

Sciatic nerve divides into?

A

Tibial and common peroneal nerves

259
Q

Sciatic nerve supplies?

A
  1. Hamstring muscles
  2. Adductor muscles
260
Q

Features of sciatic nerve lesion?

A
  1. Motor = paralysis of knee flexion and all movements below knee
  2. Sensory = loss below knee
  3. Reflexes = ankle + plantar lost, knee jerk intact
261
Q

Pudendal nerve origin?

262
Q

Femoral nerve origin?

263
Q

Causes of sciatic nerve lesions?

A
  1. Fractured NOF
  2. Posterior hip dislocation
  3. Trauma
264
Q

Loss of corneal reflex?

A

Think acoustic neuroma

265
Q

Dystrophinopathy inheritance?

A

X-linked recessive

266
Q

Dystrophinopathy pathophysiology?

A
  1. Mutation in dystrophin gene on Xp21
  2. Dystrophin is part of a large membrane associated protein in muscle which connects the muscle membrane to actin, part of the muscle cytoskeleton
267
Q

DMD mushkies?

A
  1. Frameshift mutation resulting in one or both binding sites are lost, leading to a severe form
  2. Progressive proximal muscle weakness from 5 years
  3. Calf pseudohypertrophy
  4. Gower’s sign
  5. 30% have intellectual impairment
268
Q

BMD mushkies?

A
  1. Non-frameshift insertion in the dystrophin gene resulting in both binding sites being preserved leading to a milder form
  2. Develops after 10 y/o
  3. Intellectual impairment less common
269
Q

Valley sign?

A

In DMD - there is infraspinatus and deltoid muscle enlargement with wasting of the muscles between deltoid and infraspinatus muscles causing a valley appearance

270
Q

C6 dermatome landmark?

A

Thumb + index finger

271
Q

C7 dermatome landmark?

A

Middle finger + palm of hand

272
Q

C8 dermatome landmark?

A

Ring + little finger

273
Q

Umbilicus dermatome?

274
Q

Nipple dermatome?

275
Q

Inguinal ligament dermatome?

276
Q

Genitalia deramtome?

277
Q

Absent ankle jerk and extensor plantar causes?

A

Lesion producing both UMN and LMN signs:
1. Syphilis (taboparesis)
2. SCDSC
3. MND
4. Friedrich’s ataxia
5. Syringomyelia
6. Conus medullaris lesion

278
Q

Anti-GM1 antibodies?

A

Guillain Barre Syndrome

279
Q

Pabrinex contains which vitamins?

280
Q

Thiamine is which vitamin?

A

Vitamin B1 (essential for glial cells of the nervous system)

281
Q

Wernicke’s encephalopathy definition?

A
  1. Neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics. Rarer causes include persistent vomiting, stomach cancer, and dietary deficiency.
  2. Petechial haemorrhages occur in a variety of structures in the brain including the mamillary bodies and ventricle walls
282
Q

Wernicke’s encephalopathy classical triad?

A
  1. Ophthalmoplegia/nystagmus
  2. Ataxia
  3. Encephalopathy
283
Q

Wernicke’s encephalopathy Ix?

A
  1. Decreased red cell transketolase
  2. MRI
284
Q

Wernicke’s encephalopathy Rx?

A

Urgent replacement of thiamine

285
Q

Korsakoff’s syndrome diagnosis?

A

Wernicke’s + anterograde and retrograde amnesia + confabulation

286
Q

What can cause serotonin syndrome?

A
  1. SSRIs
  2. MAOis
  3. Ecstasy/novel psychoactive stimulants
287
Q

Lhermitte’s syndrome?

A

Paraesthesiae in limbs on neck flexion

288
Q

MS deinition?

A

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

289
Q

MS epidemiology?

A
  1. 3F:1M
  2. 20-40 y/o
  3. Much more common at higher latitudes (5x more common than in tropics)
290
Q

MS subtypes?

A
  1. Relapsing-remitting
  2. Primary Progressive
  3. Secondary Progressive
291
Q

Relapsing-remitting MS?

A
  1. Most common, 85%
  2. Acute attacks (1-2m) followed by periods of remission
292
Q

Secondary-progressive MS?

A
  1. Relapsing-remitting pts who have developed neurological signs and symptoms between relapses
  2. 65% with relapsing-remitting disease go on to develop secondary progressive MS within 15y of diagnosis
  3. Gait and bladder disorders are generally seen
293
Q

Primary Progressive MS?

A
  1. 10%, progressive deterioration from onset
  2. More common in older people
294
Q

Myasthenia Gravis definition?

A

Myasthenia gravis is an autoimmune disorder resulting in insufficient functioning acetylcholine receptors. Antibodies to acetylcholine receptors are seen in 85-90% of cases. Myasthenia is more common in women (2:1)

295
Q

MG features?

A

Muscle fatigability is key feature
1. Extraocular muscle weakness: diplopia
2. Proximal muscle weakness: face, neck, limb girdle
3. Ptosis
4. Dysphagia

296
Q

MG associations?

A
  1. Thymomas in 15%, thymic hyperplasia in 50-70%
  2. AI = SLE, PA, Thyroid, RhA
297
Q

MG Ix?

A
  1. Single fibre electromyography: high sensitivity (92-100%)
  2. CT thorax to exclude thymoma
  3. CK normal
  4. Autoantibodies = Anti-ACh in 85-90%, in the remaining, 40% are anti-muscle-specific tyrosine kinase Ab +ve
  5. Tensilon test = IV edrophonium reduces muscle weakness temporarily - not commonly used any more due to the risk of cardiac arrhythmia
298
Q

MG Rx?

A
  1. Long-acting acetylcholinesterase inhibitors = pyridostigmine 1st line
  2. Immunosuppression not usually started at Dx, but majority eventually need it = prednisolone eventually –> azathioprine, cyclosporine, MMF may also be used
  3. Thymectomy
299
Q

Myasthenic crisis Rx?

A
  1. Plasmapharesis
  2. IVIG
300
Q

Rectal diazepam seizure dose?

A

10-20mg (Max 30mg), repeat once after 10-15 minutes if necessary

301
Q

Oral midazolam seizure dose?

302
Q

Facial nerve supplies?

A

Face, ear, taste, tear
1. Face = muscles of expression
2. Ear = nerve to stapedius
3. Taste = 2/3rd tongue
4. Tear = Parasympathetic fibres to lacrimal glands, also salivary glands

303
Q

Causes of bilateral facial nerve palsy?

A
  1. Infection = Lyme disease
  2. Inflammation = GBS, Sarcoidosis
  3. Malignancy = Bilateral acoustic neuromas in NF2
  4. Bilateral Bell’s
304
Q

LMN cause of unilateral facial nerve palsy?

A
  1. Bell’s, Ramsay’Hunt
  2. Acoustic neuroma, parotid tumour
  3. HIV, MS, DM
305
Q

Hoffmans sign indicated UMN or LMN?

306
Q

Common peroneal nerve AKA?

A

Common fibular nerve

MSRA - passmed textbook (25 decks)

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