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MBBS Y5 > Medicine - Neurology > Flashcards

Medicine - Neurology Flashcards

1
Q

define a TIA

A

transient neurological dysfunction secondary to ischaemia without infarction

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2
Q

what is a crescendo TIA?

A

2 or more TIAs within a week

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3
Q

features of stroke?

A

typically sudden onset:- limb weakness - facial weakness - dysphasia - visual / sensory loss

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4
Q

risk factors for stroke?

A

NAME?

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5
Q

what is the ROSIER tool for? what is a significant score?

A
  • recognition of stroke in the emergency room| - anything above 0
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6
Q

what is the ABCD2 score used for?

A

to calculate risk of subsequent stroke in patients with suspected TIA

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7
Q

what are the components of ABCD2?

A

NAME?

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8
Q

immediate management steps for a suspected stroke?

A
  • admit to specialist stroke unit- exclude hypoglycaemia- CT head to rule out haemorrhage - aspirin 300mg to be continued for 2 weeks
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9
Q

what can be offered immediately after a CT head has ruled out an intracranial haemorrhage in suspected stroke? hint: within 4.5h

A
  • thrombolysis| - done with alteplase
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10
Q

what is the window for thrombolysis?

A

4.5 hours

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11
Q

what is done following thrombolysis?

A

repeat CT heads to check for complications (e.g. haemorrhage)

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12
Q

should HTN be controlled at the time of a stroke?

A
  • no| - the extra perfusion keeps brain tissue alive
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13
Q

management of TIA?

A
  • aspirin 300mg daily for 2 weeks- then lifelong clopidogrel - start secondary prevention of CVD- get ABCD2 score- diffusion-weighted MRI (gold standard)- carotid USS (look for stenosis, offer endarterectomy if present)
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14
Q

how is the ABCD2 score interpreted?

A
  • 3 or less = specialist assessment within a week| - >3 = specialist assessment within 24h
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15
Q

secondary prevention of stroke?

A
  • clopidogrel 75mg daily- atorvastatin 80mg (after 2 weeks)- endarterectomy for carotid stenosis- treat modifiable RFs (e.g. DM) - offer rehabilitation
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16
Q

what % of strokes are intracranial bleeds?

A

10-20%

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17
Q

risk factors for an intracranial bleed?

A

NAME?

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18
Q

presentation of intracranial bleed?

A

NAME?

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19
Q

how is GCS interpreted?

A

8 or less = consider intubation

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20
Q

motor scoring in GCS?

A

NAME?

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21
Q

verbal scoring in GCS?

A

NAME?

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22
Q

eye opening scoring in GCS?

A

NAME?

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23
Q

pathophysiology of subdural haemorrhage?

A
  • rupture of bridging veins| - between dura mater and arachnoid mater
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24
Q

SDH appearance on CT?

A
  • crescent (moon) shaped| - crosses suture lines
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25
Q

which patient demographics are more affected by SDH?

A
  • elderly| - alcoholics
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26
Q

pathophysiology of an extradural haemorrhage?

A

NAME?

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27
Q

appearance of EDH on CT?

A
  • biconvex (lens) shaped| - does not cross suture lines
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28
Q

typical history of EDH?

A

NAME?

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29
Q

where can an intracerebral bleed occur?

A

NAME?

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30
Q

management of intracranial bleeds?

A

NAME?

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31
Q

pathophysiology of a subarachnoid haemorrhage?

A

NAME?

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32
Q

features of SAH?

A
  • sudden onset occipital “thunderclap” headache- neck stiffness- photophobia- neuro changes (vision, speech, weakness, seizures, LOC)
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33
Q

risk factors for SAH?

A

NAME?

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34
Q

which other medical conditions are associated with SAH?

A
  • HTN- sickle cell anaemia- marfan’s syndrome- ehlers-danlos syndrome- neurofibromatosis
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35
Q

appearance of SAH on CT?

A
  • star-shaped hyperattenuation| - if normal, does NOT rule out SAH
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36
Q

investigations for SAH?

A

NAME?

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37
Q

findings on LP in SAH?

A
  • raised RBC| - xanthochromia
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38
Q

management of SAH?

A

NAME?

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39
Q

typical demographic affected by MS?

A

white women <50

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40
Q

when might symptoms improve in MS?

A
  • during pregnancy| - postpartum
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41
Q

describe the pathophysiology of MS

A

oligodendrocytes of the CNS end up demyelinated

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42
Q

how are the lesions in MS described?

A
  • white matter plaques| - disseminated in space and time
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43
Q

how can MS be classified?

A

NAME?

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44
Q

when might symptoms worsen in MS? what is this called?

A
  • heat - exercise- uhthoff’s phenomenon
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45
Q

presentation of MS?

A

lots of different presentations: - unilateral vision loss (optic neuritis, most common)- double vision (internuclear ophthalmoplegia, conjugate gaze disorder, CN6-related)- focal weakness - focal sensory symptoms- ataxia (sensory or cerebellar)

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46
Q

examples of focal weakness seen in MS?

A
  • bells palsy- horner’s synrome- limb paralysis- incontinence
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47
Q

examples of focal sensory symptoms seen in MS?

A
  • trigeminal neuralgia- numbness- parasthesia- lhermitte’s sign
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48
Q

describe lhermitte’s sign. which condition is this seen in?

A

NAME?

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49
Q

sign O/E of sensory ataxia?

A

positive romberg’s test

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50
Q

after the first presentation of demyelination, what determines progression to MS?

A
  • presence of lesions on MRI = high risk of MS| - if no further episodes, this is called “clinically isolated syndrome”
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51
Q

how is MS diagnosed?

A

NAME?

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52
Q

potential causes of MS?

A

true cause unknown but the following might contribute:- certain genes- EBV- low vit D (lowest rates at equator)- smoking- obesity

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53
Q

causes of optic neuritis?

A

NAME?

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54
Q

findings on LP in MS?

A
  • raised protein| - oligoclonal bands
55
Q

management of relapses in MS?

A
  • 500mg methylprednisolone PO for 5 days - given IV if severe - DMARDs (natalizumab, ocrelizumab)
56
Q

management of symptoms in MS?

A

NAME?

57
Q

most common form of MND?

A

amyotrophic lateral sclerosis (ALS)

58
Q

name some different types of MND

A

NAME?

59
Q

risk factors for MND?

A

NAME?

60
Q

typical patient affected by MND?

A

man in 60s with affected relative

61
Q

presentation of MND?

A

NAME?

62
Q

signs of LMN disease?

A

NAME?

63
Q

signs of UMN disease?

A
  • increased tone / rigidity- spasticity (velocity-dependent)- brisk reflexes- upgoing plantar reflex
64
Q

how is MND diagnosed?

A
  • clinically O/E| - done by specialist
65
Q

management of MND?

A

NAME?

66
Q

what are the 2 main causes of death in MND?

A
  • respiratory failure| - pneumonia
67
Q

pathophysiology of parkinson’s disease?

A

NAME?

68
Q

classic triad of parkinson’s disease?

A

asymmetrical, unilateral:- resting tremor- rigidity - bradykinesia

69
Q

presentation of parkinson’s disease? hint: there’s a LOT

A

NAME?

70
Q

typical demographic affected by parkinson’s disease?

A

man >70

71
Q

what are the 4 parkinson’s plus syndromes to know?

A

NAME?

72
Q

features of multiple system atrophy?

A
  • parkinsonian presentation, but also:- autonomic signs (postural hypotension, constipation, sweating, sexual dysfunction)- cerebellar signs (ataxia)
73
Q

features of lewy body dementia?

A
  • parkinsonian presentation, but also:- progressive cognitive decline- visual hallucinations - delusions - REM sleep disorders- fluctuating consciousness
74
Q

management of parkinson’s disease?

A
  • levodopa (co-benyldopa includes benserazide, co-careldopa includes carbidopa)- COMT inhibitor (entacapone, taken with levodopa)- DA agonists (bromocriptine, cabergoline) - MAO-B inhibitors (selegiline, rasagiline)
75
Q

what is a disadvantage of starting levodopa early in parkinson’s treatment?

A
  • it becomes less effective over time| - best to reserve it for when other treatments have stopped working
76
Q

adverse effects of levodopa?

A

dyskinesias:- dystonia- chorea- athetosis

77
Q

describe athetosis

A

involuntary twisting, writhing movements in hands and feet

78
Q

describe dystonia

A

excessive muscle contractions causing abnormal postures / exaggerated movements

79
Q

describe chorea

A

abnormal, involuntary, jerking movements

80
Q

important benefit of COMT inhibitor?

A

extends effective duration of levodopa action

81
Q

key adverse effect of DA agonists?

A

pulmonary fibrosis

82
Q

key risk factor for benign essential tremor (BET)?

A

ageing

83
Q

features of BET?

A

NAME?

84
Q

what are the differential causes of tremor?

A
  • BET- parkinson’s- MS - huntington’s chorea- hyperthyroidism- fever- antipsychotics
85
Q

management of BET?

A

can try the following for symptomatic relief:- propanolol- primidone

86
Q

define epilepsy

A

umbrella term for condition where there is a tendency to have seizures

87
Q

what is a seizure?

A

a transient episode of abnormal electrical activity in the brain

88
Q

investigations in epilepsy?

A

NAME?

89
Q

what are the different types of seizure?

A

NAME?

90
Q

features of a generalised tonic clonic seizure?

A

NAME?

91
Q

features of post-ictal period following a GTC seizure?

A

NAME?

92
Q

management of tonic clonic seizures?

A

1st: valproate2nd: lamotrigine or carbamazepine

93
Q

where do focal seizures start in the brain?

A

temporal lobe

94
Q

how could a focal seizure present?

A

NAME?

95
Q

management of focal seizures? hint: opp. to GTC

A

1st: carbamazepine or lamotrigine2nd: valproate or levetiracetam

96
Q

which demographic is typically affected by absence seizures? how might it present?

A
  • children| - look blank, stare into space for 10-20 secs, then recover
97
Q

prognosis for absence seizures?

A

> 90% of children stop getting them as they grow up

98
Q

management of absence seizures?

A

valproate or ethosuximide

99
Q

presentation of atonic seizure?

A
  • “drop attack”- brief drop in muscle tone- typically lasts <3 mins - seen in children
100
Q

which condition is associated with having atonic seizures?

A

lennox-gastaut syndrome

101
Q

management of atonic seizures?

A

1st: valproate2nd: lamotrigine

102
Q

presentation of myoclonic seizure?

A

sudden, brief muscle contraction

103
Q

which condition is myoclonic seizures seen in?

A

juvenile myoclonic epilepsy

104
Q

management of myoclonic seizures?

A

1st: valproate2nd: lamotrigine, levetiracetam or topiramate

105
Q

which age is west syndrome seen at?

A

6 months

106
Q

prognosis of west syndrome?

A
  • poor- 1/3 die by age 25- 1/3 go on to live seizure free
107
Q

management of west syndrome

A
  • prednisolone| - vigabatrin
108
Q

important adverse effects of valproate?

A

NAME?

109
Q

important adverse effects of carbamazepine?

A
  • agranulocytosis| - aplastic anaemia
110
Q

important adverse effects of phenytoin?

A
  • folate and vit D deficiency| - therefore: megaloblastic anaemia and osteomalacia
111
Q

side effects of ethosuximide?

A
  • night terrors| - rashes
112
Q

important adverse effects of lamotrigine?

A
  • stevens-johnson syndrome (DRESS syndrome)| - leukopenia
113
Q

define status epilepticus

A
  • seizures lasting > 5 minutes| - OR >3 seizures in 1 hour
114
Q

management of status epilepticus in hospital?

A
  • ABCDE - high flow O2- check glucose- insert cannula- IV lorazepam 4mg - repeat after 10 mins if seizure continues- then: IV phenobarbital or phenytoin
115
Q

management of status epilepticus in community?

A
  • buccal midazolam| - rectal diazepam
116
Q

causes of neuropathic pain?

A

NAME?

117
Q

features of neuropathic pain?

A

NAME?

118
Q

what is the DN4 questionnaire used for?

A

to assess characteristics of pain to determine if it’s neuropathic

119
Q

management of neuropathic pain? name the drug class for each one

A

pick one of the following and if it fails, try another instead:- amitriptyline (TCA)- duloxetine (SNRI)- gabapentin (anticonvulsant)- pregabalin (anticonvulsant)

120
Q

what can be tried if all 4 neuropathic pain drugs fail?

A
  • tramadol (short-term)- capsaicin cream (chilli pepper)- physio- psychological input
121
Q

which drug is used to manage trigeminal neuralgia?

A
  • carbamazepine| - not a conventional neuropathic pain drug
122
Q

typical presentation of complex regional pain syndrome?

A
  • area of skin becomes hypersensitive to even simple clothing - neuropathic pain and abnormal sensation - usually restricted to 1 limb- follows injury to area
123
Q

what is syringomyelia?

A

a collection of CSF within the spinal cord itself

124
Q

what is syringobulbia?

A

collection of fluid in medulla of brainstem

125
Q

presentation of syringomyelia?

A
  • cape-like distribution (neck, shoulders, arms) - loss of temp sensation - pt could accidentally burn hands- spastic weakness of LLs- upgoing plantars- horner’s syndrome - scoliosis
126
Q

which demographic is most likely to get idiopathic intracranial hypertension?

A

young, obese women

127
Q

features of idiopathic intracranial hypertension?

A

NAME?

128
Q

describe the headache caused by idiopathic intracranial hypertension

A

NAME?

129
Q

describe the vision changes in idiopathic intracranial hypertension

A

transient visual darkening

130
Q

findings on fundoscopy in idiopathic intracranial hypertension?

A

bilateral papilloedema

131
Q

which drugs are associated with idiopathic intracranial hypertension?

A

NAME?

132
Q

management of idiopathic intracranial hypertension?

A

weight loss

133
Q

causes of spinal cord compression?

A

NAME?

MBBS Y5 (27 decks)

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