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Neurology > Pasmedicine/Pastest > Flashcards

Pasmedicine/Pastest Flashcards

1
Q

most common complication of meningitis

A

sensorineural hearing loss

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2
Q

what is hoovers sign

A

Hoover’s sign of leg paresis is a specific manoeuvre used to distinguish between an organic and non-organic paresis of a particular leg. This is based on the concept of synergistic contraction. If a patient is genuinely making an effort, the examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg. Noticing this is indicative of an underlying organic cause of the paresis. If the examiner, however, fails to feel the ‘normal’ limb pushing downwards as the patient tries to raise their ‘weak’ leg, then this is suggestive of an underlying functional weakness, also known as ‘conversion disorder’.

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3
Q

causes of restless leg syndrome

A 
there is a positive family history in 50% of patients with idiopathic RLS
iron deficiency anaemia
uraemia
diabetes mellitus
pregnancy
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4
Q

treatment of restless leg syndrome

A

simple measures: walking, stretching, massaging affected limbs
treat any iron deficiency
dopamine agonists are first-line treatment (e.g. Pramipexole, ropinirole)
benzodiazepines
gabapentin

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5
Q

blood test used to differentiate between seizures and peudoseizures

A

prolactin

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6
Q

features of temporal lobe seizure

A

“HEAD”

Hallucinations (auditory/gustatory/olfactory), Epigastric rising/Emotional, Automatisms (lip smacking/grabbing), Deja vu/Dysphasia post-ictal)

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7
Q

frontal lobe seizure

A

Head/leg movements , posturing, post-ictal weakness

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8
Q

parietal lobe seizurw

A

parasthesia

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9
Q

occipital lobe seizures

A

flashers/floaters

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10
Q

vein commonly used for a venous cut down

A

long saphenous vein

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11
Q

who needs CT head immediately after injury

A

GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
suspected open or depressed skull fracture.
any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
post-traumatic seizure.
focal neurological deficit.
more than 1 episode of vomiting

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12
Q

who needs a CT head within 8 hours of injury

A
  • for adults with any of the following risk factors who have experienced some loss of consciousness or amnesia since the injury:
    age 65 years or older
    any history of bleeding or clotting disorders
    dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
    more than 30 minutes’ retrograde amnesia of events immediately before the head injury

also .- warfarin regardless of other risk factors

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13
Q

what should be given in a SAH to reduce risk of cerebral vasospasm

A

nimodepine

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14
Q

suspected SAH but CT normal - what is next investigation

A

LP at 12 hours

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15
Q

best investigation from diffuse axonal injury

A

MRI brain

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16
Q

who needs urgent neurosurgical review even before CT

A

patients with a GCS or 8 or less

penetrating injury e.g. gunshot wound

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17
Q

investigation of choice to clear the C spine in trauma

A

CT spine

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18
Q

where is brocas area and what type of aphasia do you get

A

frontal lobe - expressive aphasia

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19
Q

where is wernickes and what type of aphasia do you get

A

temporal lobe - receptive aphasia

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20
Q

exmaination signs in meningitis

A

kernigs sign - cannot straighten leg when hip flexed at 90 dgreesb
brudinskis sign - when neck flexed knees and hips will flex

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21
Q

treatment of generalised tonic clonic

A

1st line sodium valproate/lamotrogine

2nd carbamazepine

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22
Q

absence seizures

A

1st ethosuxemide or sodium valproate

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23
Q

myoclonic seizures

A

sodium valproate

2nd line - lamotrigine

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24
Q

focal seizures

A

carbamazepine or lamotrigine

second line: levetiracetam, oxcarbazepine or sodium valproat

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25
Q

what type of seizure can carbamazepine make worse

A

absence

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26
Q

sodium valproate adverse affecrs

A 
increased appetite and weight gain
alopecia: regrowth may be curly
P450 enzyme inhibitor
ataxia
tremor
hepatitis
pancreatitis
thrombocytopaenia
teratogenic (neural tube defects)
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27
Q

carbemazepine adverse effects

A 
P450 enzyme inducer
dizziness and ataxia
drowsiness
leucopenia and agranulocytosis
syndrome of inappropriate ADH secretion
visual disturbances (especially diplopia)
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28
Q

lamotrigine adverse effects

A

Steven johnson syndrome

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29
Q

phenytoin adverse effects

A 
P450 enzyme inducer
dizziness and ataxia
drowsiness
gingival hyperplasia, hirsutism, coarsening of facial features
megaloblastic anaemia
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
30
Q

Brief spasms beginning in first few months of life
1. Flexion of head, trunk, limbs → extension of arms (Salaam attack); last 1-2 secs, repeat up to 50 times
2. Progressive mental handicap
3. EEG: hypsarrhythmia
usually 2nd to serious neurological abnormality (e.g. TS, encephalitis, birth asphyxia) or may be cryptogenic
poor prognosis

A

infantile spasms (West syndrome)

31
Q 
May be extension of infantile spasms (50% have hx)
onset 1-5 yrs
atypical absences, falls, jerks
90% moderate-severe mental handicap
EEG: slow spike
ketogenic diet may help
A

Lennox-Gastaut syndrome

32
Q

paraesthesia (e.g. unilateral face), usually on waking up

A

benign rolandic epilepsy

33
Q

Typical onset in the teens, more common in girls
1. Infrequent generalized seizures, often in morning
2. Daytime absences
3. Sudden, shock like myoclonic seizure
usually good response to sodium valproate

A

juvenile myoclonic epilepsy

34
Q

antibody which may be seen in GBS

A

Anti GM 1 (25 percent)

35
Q

antibody which may be seen in Miller fisher

A

ant GQ1b

36
Q

management of GBS

A

plasmapheresis and IV Ig

37
Q

treatment of chronic inflammatory demyelinating polyneuropathy

A

steroids and immunosuppression

38
Q

acute treatment of myaesthenia

A

plasmaphereses and iV IG

39
Q

long term treatment of myaesthnia gravis

A

anti cholinersterase inhibitors - pyrdostymine
thymectomy
steroids

40
Q

investigation of myaesthenia gravis

A

EMG
CT thorax
CK normal
autoantibodies: around 85-90% of patients have antibodies to acetylcholine receptors. In the remaining patients, about about 40% are positive for anti-muscle-specific tyrosine kinase antibodies
Tensilon test: IV edrophonium reduces muscle weakness temporarily - not commonly used anymore due to the risk of cardiac arrhythmia

41
Q

drugs which may exacerbate myaesthenia

A 
penicillamine
quinidine, procainamide
beta-blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines
42
Q

what is lambert eaton syndrome

A

seen in association with small cell lung cancer, and to a lesser extent breast and ovarian cancer. It may also occur independently as an autoimmune disorder. Lambert-Eaton myasthenic syndrome is caused by an antibody directed against pre-synaptic voltage gated calcium channel in the peripheral nervous system

43
Q

features of lambert eaton

A

repeated muscle contractions lead to increased muscle strength* (in contrast to myasthenia gravis)
limb girdle weakness (affects lower limbs first)
hyporeflexia
autonomic symptoms: dry mouth, impotence, difficultly micturating
ophthalmoplegia and ptosis not commonly a feature (unlike in myasthenia gravis)

44
Q

treatment of lambert eaton

A

treat underlying cancer
immunisupressionw ith steroids or azothiaprine
intravenous immunoglobulin therapy and plasma exchange may be beneficial

45
Q

what artery is affected in a POCS

A

vertebrobasilar

46
Q

what artery is affected in lateral medullary syndrome ie Wallenburg

A

posterior inferior cerebellar artery

47
Q

how long can you not drive for after a TIA

A

a month

48
Q

how long can you not drive after multiple TIAs

A

3 months

49
Q

What is glabella tap

A

tap on forhead - myerson sign is when blinking fails to cease with tapping
its an extrapyramidal sign

50
Q

what is cogwheel rigidity

A

tremor superimposed in increased resting tone

51
Q

what is multi system atrophy

A

parkinsonism
autonomic disturbance (atonic bladder, postural hypotension, erectile dysfunction)
cerebellar signs

52
Q

what is progressive supranuclear palsy

A 
parkinsonism 
supranuclear ophthalmoplegia
Neck dystonia
Parkinsonism
Pseudobulbar palsy - swallowing difficulties
Behavioral and cognitive impairment
Imbalance and walking difficulty
Frequent falls
53
Q

what is corticobasilar degeneration

A

Parkinsonism
Alien hand syndrome
Apraxia (ideomotor apraxia and limb-kinetic apraxia)
Aphasia

54
Q

what investigation can you do for parkisnons

A

clinical diagnosis

but if doubt then SPECT

55
Q

first line treatment of parkinson’s

A

if the motor symptoms are affecting the patient’s quality of life: levodopa
if the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived), levodopa or monoamine oxidase B (MAO‑B) inhibitor

56
Q

what is the risks with dopamine agonists/levodopa

A

psychosis/hallucinations - more likely with dopamine agonists
neuroleptic malignant syndrome if drug abruptly stopped
impulsively
postural hypotension
excessive daytime somolence (dopamine agonists)

57
Q

name a comt inhibitor

A

carbidopa

58
Q

what is given if levodopa alone does not control motor symptoms

A

addition of a dopamine agonist, MAO‑B inhibitor or catechol‑O‑methyl transferase (COMT) inhibitor as an adjunct

59
Q

what is the specific downside to levodopa

A

decreased efficacy with time

dyskinesia

60
Q

what do antimuscarinics help with in parkinsons

A

tremor and rigidity

used to treat drug induced parkinsons

61
Q

what anticonvulsant cause hyperammonaemia

A

sodium valproate

62
Q

what anticonvulsant causes a visual field defect

A

vigabatrin

63
Q

what fluid should be avoided in patients with a head injury

A

dextrose

64
Q

where does herpes simplex encephalitis tend to affect

A

temporal lobes

65
Q

small vs large sensory fibre neuropathy

A

small- only burnign sensation

large - glove and stocking sensation loss and loss of reflexes

66
Q

what type of visual field defect occurs most commonly in MS

A

central scotoma

67
Q

what type of visual field defect occurs most commonly in papilloedema

A

increased blind spot

68
Q

drowsiness, bradycardia and slowrelaxing refexes + hypothermia indicates

A

hypothyroid coma

69
Q

nerve at risk in carotid endartectomy

A

hypoglossal

70
Q

pupils in brainstem death

A

unreative dilated pupils

Neurology (36 decks)

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