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Zero to Finals: Medicine A.S. > Neurology > Flashcards

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
  • pre-existing CVD
  • AF
  • carotid artery disease
  • HTN
  • DM
  • smoking
  • vasculitis
  • thrombophilia
  • COCP
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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
  • Age
  • BP
  • Clinical features
  • Duration of symptoms
  • DM
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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
  • head injury
  • HTN
  • aneurysms
  • ischaemic stroke (progressing to haemorrhage)
  • brain tumours
  • anticoagulation (warfarin)
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18
Q

presentation of intracranial bleed?

A
  • sudden onset headache
  • seizures
  • weakness
  • vomiting
  • reduced consciousness
  • any other sudden onset neuro sign
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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
  • 1 = none
  • 2 = extends
  • 3 = abnormal flexion
  • 4 = normal flexion / withdraws from pain
  • 5 = localises to pain
  • 6 = obeys command
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21
Q

verbal scoring in GCS?

A
  • 1 = none
  • 2 = incomprehensible sounds
  • 3 = inappropriate words
  • 4 = confused conversation
  • 5 = orientated
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22
Q

eye opening scoring in GCS?

A
  • 1 = none
  • 2 = open to pain
  • 3 = open to speech
  • 4 = open spontaneously
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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
  • rupture of middle meningeal artery in temporo-parietal region
  • between skull and dura mater
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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
  • young pt with traumatic head injury
  • lucid interval first
  • followed by rapid decline as haematoma grows and compresses things
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29
Q

where can an intracerebral bleed occur?

A
  • lobes
  • intraventricular
  • basal ganglia
  • cerebellar
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30
Q

management of intracranial bleeds?

A
  • immediate CT head (diagnostic)
  • check FBC and clotting
  • admit to specialist stroke unit
  • consider intubation and ventilation if low GCS
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31
Q

pathophysiology of a subarachnoid haemorrhage?

A
  • bleed in the subarachnoid space, where the CSF is
  • between pia mater and arachnoid membrane
  • typically due to ruptured cerebral aneurysm
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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
  • HTN
  • smoking
  • excessive alcohol consumption
  • cocaine use
  • FHx
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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
  • CT
  • LP
  • CT / MRI angiography
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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
  • admit to specialist neurosurgical unit
  • intubate and ventilate if low GCS
  • coiling / clipping of aneurysms
  • nimodipine to prevent vasospasm
  • LP / shunt insertion to treat hydrocephalus
  • AEDs for seizures
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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
  • relapsing-remitting
  • secondary progressive (follows on from RRMS)
  • primary progressive
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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
  • flexion of the neck causes electric shock sensations in the trunk and limbs
  • MS
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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
  • done by neurologist
  • symptoms must have been progressive over a year for primary progressive MS diagnosis
  • must exclude other causes
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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
  • MS (most likely)
  • sarcoidosis
  • SLE
  • DM
  • syphilis
  • measles, mumps
  • lyme disease
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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
  • exercise (maintains strength)
  • amitriptyline / gabapentin for neuropathic pain
  • SSRIs for depression
  • tolterodine / oxybutynin for urge incontinence
  • baclofen / gabapentin / physio for spasticity
57
Q

most common form of MND?

A

amyotrophic lateral sclerosis (ALS)

58
Q

name some different types of MND

A
  • ALS
  • progressive bulbar palsy (second most common)
  • progressive muscular atrophy
  • primary lateral sclerosis
59
Q

risk factors for MND?

A
  • FHx of MND
  • smoking
  • heavy metal exposure (lead)
  • pesticide exposure
60
Q

typical patient affected by MND?

A

man in 60s with affected relative

61
Q

presentation of MND?

A
  • insidious, progressive weakness
  • affects: limbs, trunk, face and speech (dysphasia)
  • typically starts off in upper limbs
  • Hx clumsiness, dropping things, tripping over
  • mixed UMN and LMN signs
62
Q

signs of LMN disease?

A
  • muscle wasting
  • reduced tone
  • fasciculations
  • reduced reflexes
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
  • riluzole slows disease progression
  • NIV to support breathing at night
  • advanced directives put in place
  • end of life care planning
66
Q

what are the 2 main causes of death in MND?

A
  • respiratory failure

- pneumonia

67
Q

pathophysiology of parkinson’s disease?

A
  • progressive reduction of dopamine production from substantia nigra
  • found in the basal ganglia
  • leads to disordered movement
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
  • pill-rolling tremor
  • cogwheel rigidity
  • micrographia
  • shuffling gait
  • difficulty in initiating movement (chair to standing)
  • difficulty in turning when walking
  • hypomimia / masked facies
  • depression
  • sleep disturbance, insomnia
  • anosmia
  • postural instability
  • cognitive impairment
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
  • multiple system atrophy
  • lewy body dementia
  • progressive supranuclear palsy
  • corticobasal degeneration
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
  • fine tremor
  • symmetrical
  • worse on voluntary movement
  • worse when tired / stressed / caffeinated
  • improved by alcohol
  • absent in sleep
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
  • EEG
  • MRI brain
  • ECG (exclude heart problems)
89
Q

what are the different types of seizure?

A
  • generalised tonic clonic
  • focal / partial
  • absence
  • atonic
  • myoclonic
  • infantile spasms (west syndrome)
90
Q

features of a generalised tonic clonic seizure?

A
  • LOC
  • muscle tensing (tonic)
  • muscle jerking (clonic)
  • tongue biting
  • incontinence
  • groaning
  • irregular breathing
91
Q

features of post-ictal period following a GTC seizure?

A
  • confusion
  • feeling drowsy
  • irritability
  • feeling depressed
92
Q

management of tonic clonic seizures?

A

1st: valproate
2nd: 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
  • hallucinations
  • memory flashbacks
  • deja vu, jamais vu
  • doing strange things on autopilot
95
Q

management of focal seizures? hint: opp. to GTC

A

1st: carbamazepine or lamotrigine
2nd: 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: valproate
2nd: 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: valproate
2nd: 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
  • teratogenic (must be on contraception)
  • liver damage, hepatitis
  • hair loss
  • tremor
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
  • post-herpetic neuralgia from shingles (dermatomal)
  • nerve damage from surgery
  • MS
  • diabetic neuralgia (feet)
  • trigeminal neuralgia
  • complex regional pain syndrome
117
Q

features of neuropathic pain?

A
  • burning
  • tingling
  • pins and needles
  • electric shocks
  • loss of touch sensation in affected areas
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
  • headache
  • associated vomiting
  • visual disturbance
128
Q

describe the headache caused by idiopathic intracranial hypertension

A
  • non-pulsatile
  • bilateral
  • worse in the morning
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
  • COCP
  • steroids
  • tetracycline
  • vit A
  • lithium
132
Q

management of idiopathic intracranial hypertension?

A

weight loss

133
Q

causes of spinal cord compression?

A
  • trauma
  • tumour
  • infection (esp TB)
  • disc prolapse
  • epidural haematoma

Zero to Finals: Medicine A.S. (11 decks)

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