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MRCP > Neuro > Flashcards

Neuro Flashcards

1
Q

Presentation of absence seizures

A

girls 3-10
provoked by stress or hyperventilation
pt unaware
EEG: bilateral sym 3Hz spike and wave pattern

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2
Q

Management and prognosis of absence seizures

A

valproate and ethosuximide
90-95% seizure free at adolescence

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3
Q

Classification of epilespy

A

generalised: motor or non motor
Focal: aware/impaired awareness/awareness unknown: motor/non motor/ other feature

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4
Q

Features of focal temporal seizure

A

aura: rising epigastric sensation, psychic, hallucinations
automatisms: lip smacking

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5
Q

features of frontal focal seizure

A

head/leg movements
posturing
post-ictal weakness

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6
Q

features of parietal focal seizure

A

paraesthesia

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7
Q

features of occipital focal seizure

A

floaters/flashes

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8
Q

When do you start management of seizures

A

after 2nd seizure unless
- neurological deficit
- structural abnormality on imaging
- epileptic activity on EEG
- risk of further seizure unacceptable

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9
Q

Management of tonic clonic seizure

A

m: valproate
f: lamotrigine or keppra

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10
Q

management of tonic or atonic seizure

A

m: valproate
f: lamotrigine

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11
Q

management of myoclonic seizure

A

m: valproate
f: keppra

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12
Q

management of focal seizure

A

1st: lamotrigine or keppra
2nd: carbamazepine

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13
Q

Which anti-epileptics can be used in pregnancy

A

carbazmazepine, lamotrigine

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14
Q

which anit-epileptics should be avoided in pregnancy

A

valproate: neural tube defects and neurodevelopment delay

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15
Q

What are the driving rules for epilepsy

A

inform DVLA
after 1st seizure - no driving 6 months
established - can drive if 1 year seizure free
withdrawing meds - no driving until 6 months after last dose

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16
Q

How does sodium valproate work

A

increase GABA activity

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17
Q

Valproate SE

A

p450 inhib
nausea, increased appetite, weight gain
ataxia, tremor
hepatotoxic, pancreatitis
thrombocytopenia, low Na

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18
Q

What causes Bells Palsy

A

unknown but associated with HSV, EBV

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19
Q

How does Bells Palsy present

A

Unilateral lower motor neuron facial nerve palsy - forehead affected
pregnant women 20-40
dry eyes

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20
Q

Management Bells Palsy

A

PO pred within 72h
Debate on anitvirals
artifical tears
tape eye if unable to close
ENT Referral at 3 weeks

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21
Q

Bells Palsy prognosis

A

most fully recover by 3/4 months

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22
Q

What is BPPV

A

vertigo triggered by change in head position can be associated with nausea

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23
Q

How is BPPV diagnosied

A

Dix-Hallpike manoeuvre

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24
Q

Management of BPPV

A

spontaneous recovery weeks-months
Epley helps with symptoms
betahistine limited valve

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25
Q

Causes of brain abscess

A

sepsis, trauma, embolic event

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26
Q

Symptoms of brain abscess

A

headache, fever, focal neurology, nausea, seizures

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27
Q

Investigation and management of brain abscess

A

CT head
Surgery, Abx and dex

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28
Q

What is Brown-Sequard syndrome

A

Lateral hemi-section of spinal cord

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29
Q

Features of Brown Sequard syndrome

A

ipsilateral weakness below lesion
ipsilateral loss of proprioception and vibration sensation
contralateral loss of pain and temperature sensation

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30
Q

Symptoms of cerebellar disease

A

Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremer
Slurred speech
Hypotonia

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31
Q

What is GBS

A

immune mediated demyelination of peripheral nerve system triggered by infection

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32
Q

Infection associated with GBS

A

Campylobacter jejuni

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33
Q

Presentation of GBS

A

leg/back pain
ascending sym limb weakness
reduced/absent reflexes
resp muscle weakness

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34
Q

Investigation of ?GBS

A

LP (increased protein, normal WCC)
nerve conduction studies
-decreased motor nerve conduction
-increased distal motor latency
-increased F wave latency

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35
Q

Management of GBS

A

IVIG
plasma exchange (more difficult and equally as effective)
FVC - monitor resp function

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36
Q

Poor prognostic factors of GBS

A

age > 40 years
poor upper extremity muscle strength
previous history of a diarrhoeal illness (specifically Campylobacter jejuni)
high anti-GM1 antibody titre
need for ventilatory support

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37
Q

Following head injury when does CTH need to be performed in 1 hr

A

GCS <13 initially
GCS <15 after 2 hrs
Suspected skull # or basal skull #
Seizure
Focal neuro deficit
>1 episode of vomiting

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38
Q

Following a head injury when does a CTH need to be performed in 8 hrs

A

loss of cons/amnesia +
>65
Hx bleeding/clotting disorder
dangerous mechanism
>30mins retrograde amnesia

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39
Q

What causes herpes simplex encephalitis and where does it affect

A

HSV1
temporal and inferior frontal lobes

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40
Q

how does HS encephalitis present

A

fever, headache, seizure, vomiting, psych
focal - aphasia

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41
Q

Investigations of herpes simplex encephalitis

A

CSF: high WCC high protein
PCR for HSV
CT: petechial haemorrhages temporal/frontal
MRI
EEG: lateral periodic discharges 2Hz

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42
Q

Management and prognosis of herpes simplex encephalitis

A

IV Aciclovir
10-20% mortality if started early compared to 80% if untreated

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43
Q

What kind of disease is Huntingtons?

A

autosomal dominant

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44
Q

Genetics of Huntingtons

A

Chromosome 4, triplet repeat CAG -> glutamine
normal is 10-35
Huntingtons >35

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45
Q

Pathophysiology of Huntingtons

A

degeneration of cholingeric and GABA neurones in striatum of basal ganglia

46
Q

Presentation of Huntingtons

A

35-40 yo
chorea
abnormal eye movements
dementia, personality change

47
Q

Management of Huntingtons

A

No treatment to alter prognosis
Tetrabenazine for chorea

48
Q

Huntingtons prognosis

A

death 20 years after the initial symptoms develop

49
Q

What is Lambert Eaton syndrome

A

antibody directed against presynaptic voltage gated calcium channel in peripheral nervous system

50
Q

What causes Lambert Eaton syndrome

A

SCLC (ovarian and breast)
autoimmune

51
Q

How does Lambert Eaton syndrome present

A

Muscle weakness that improves with use
prox muscles of lower limbs first
hypo reflexes
autonomic: dry mouth, impotence

52
Q

Lambert Eaton investigation

A

EMG: incremental response to repetitive electrical stimulation

53
Q

Management of Lambert Eaton syndrome

A

Treat any underlying cancer
Immunosuppression - pred
IVIG

54
Q

What is myasthenia gravis

A

autoimmune insufficient functioning of acetylcholine receptors

54
Q

How does myasthenia gravis present

A

women<40 or men >60
muscle fatiguability - worse at end of day
prox muscle weakness
diplopia, ptosis, dysphagia

55
Q

what is myasthenia gravis associated with

A

thymoma

56
Q

Myasthenia Gravis examination findings

A

fatiguing when
- upward gazing
- blinking
- repeated abduction

57
Q

Investigations for myasthenia gravis

A

EMG
antibodies - Ach receptor antibodies (85%)
CT thymus

58
Q

Management of myasthenia gravis

A

pyridostigmine
immunosuppression
thymectomy

59
Q

What is a myasthenia crisis

A

acute worsening of symptoms, triggered by infection, risk of resp failure requiring NIV/intubation and ventilation
Mx: IVIG

60
Q

What is Menieres disease

A

excessive pressure and progressive dilation of endolymphatic system - unknown cause

61
Q

How does Menieres present

A

vertigo tinnitus, hearing loss
aural fullness/pressure
lasts mins-hours
unilateral->bilateral

62
Q

How do you manage Menieres

A

ENT referral
inform DVLA - no driving until symptoms controlled
Acute: prochlorperazine (buc or PO)
prevent: betahistine, vestibular rehab

63
Q

Menieres prognosis

A

most resolve within 5-10 years, likely will be left with some hearing loss

64
Q

Types of MND

A

1) Amylotrophic lateral sclerosis
2) Primary lateral sclerosis
3) Progressive muscular atrophy
4) Progressive bulbar palsy

65
Q

Hows does ALS present

A

LMN signs in arms - drop things, stiffness, wasting
UMN signs in legs - foot drop, difficultly climbing stairs

66
Q

How does Primary lateral sclerosis present

A

UMN only, leg weakness

67
Q

How does progressive muscular atrophy present

A

LMN only
distal ->proximal, small muscles of hands/feet

68
Q

How does progressive bulbar palsy present

A

palsy of tongue, muscles of chewing/swallowing

69
Q

Which types of MND carry the best and worse prognosis
What is the general prognosis

A

Best: progressive muscular atrophy
Worst: progressive bulbar palsy
General: 50% died within 3 years

70
Q

Investigations for MND

A

clinical diagnosis
NCS: normal
EMG: reduced action potential with increased amplitude
MRI: exclude cervical cord compression

71
Q

Management of MND

A

Riluzole - increases life by 3 months
BiPAP at night - increases life by 8 months
PEG

72
Q

What is MS

A

chronic cell mediated autoimmune disorder characterised by CNS demyelination

73
Q

Types of MS

A

1) Relapsing remitting: most common
2) Secondary progressive: RR with symptoms between, 65% with RR develop this within 15 years
3) Primary progressive: deterioration from onset

74
Q

Presentation of MS

A

optic neuritis
optic atrophy
worsening vision following rise in body temp
pins/needles/numbness
spastic weakness
ataxia
urinary incontinence

74
Q

Investigations of MS

A

MRI: T2 lesions, periventricular plaques, Dawson fingers (white matter perpendicular to corpus callosum)
CSF: oligoclonal bands

74
Q

Management of MS relapses

A

Acute relapse: 5/7 Methypred
Reduce risk of relapse: natalizumab, ocrelizumab

75
Q

Management of fatigue in MS

A

amantadine

76
Q

Management of spasticity in MS

A

baclofen, gabapentin

77
Q

Good prognostic features of MS

A

*common presentation
female
20-30 onset
relapsing remitting
long intervals and complete recovery between relapses

78
Q

Symptoms of normal pressure hydrocephalus

A

1) urinary incontinence
2) dementia
3) gait abnormalilty

79
Q

Imaging findings of normal pressure hydrocephalus

A

hydrocephalus with ventriculomegaly

80
Q

Management of normal pressure hydrocephalus

A

ventriculoperitoneal shunt

81
Q

What is Parkinsons

A

progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in substantia nigra

82
Q

Presentation of Parkinsons

A

men,65
asym
1) bradykinesia: shuffling gait, reduced arm swelling
2) tremor: resting, pill rolling
3) rigidity: lead pipe, cog wheel

83
Q

Additional Parkinsons symptoms (Not classic trio)

A

reduced facial expressions
depression
micrographia
drooling

84
Q

Management of Parkinsons

A

Do motor symptoms affect quality of life
yes: levodopa
no: dopamine agonist, levodopa, MAO-B inhib

85
Q

SE of levodopa

A

dry mouth, anorexia, palpitations, dyskinesias

86
Q

Examples of dopmaine receptor agonists + monitoring required

A

bromocriptine, ropinirole
ECHO, CXR, Cr, ESR

87
Q

Causes of SAH

A

berry aneurysm
AVM

88
Q

Presentation SAH

A

thunderclap headache
N&V
meningism

89
Q

Investigtion of SAH

A

CT head: SAH
Normal CT: <6hrs - no LP
>6hrs: LP after 12hrs - Xanthochromia

Cta for cause

90
Q

Management of SAH

A

Supportive
Nimodipine prevents vasospasm
coil

91
Q

Types of SDH and causes

A

Acute: trauma
Chronic: rupture of bridging veins (alcoholic /elderly)

92
Q

CT findings in SDH

A

crescent shape
acute: hyperdense
chronic: hypodense

93
Q

Management of SDH

A

acute: monitor, decompressive craniectomy
Chronic: conservative if incidental, decompression if symptomatic

94
Q

describe presentation of cluster headache

A

unilateral sharp pain around eye
lasts 15m-2hr
lid swelling, redness, restlessness

95
Q

Management of cluster headache

A

acute: 100% o2, SC triptans
prophylaxis: verapamil ?pred

96
Q

Describe medication overuse headache

A

> =15days/month

97
Q

Which medications can cause medication overuse headache

A

opioids, triptans

98
Q

management of medication overuse headache

A

stop triptans/simple analgesia
slow wean of opioids

99
Q

What symptoms might a pt experience when analgesia is stopped due to medication overuse headache

A

vomiting, hypotension, increased HR, restlessness

100
Q

Migraine triggers

A

tired, stressed, alcohol, COCP, menstruation

101
Q

migraine diagnostic criteria

A

5 attacks
-4-72hrs
-N&V and/or photophobia and phonophobia
-at least 2 of: unilateral,pulsatile, mod/severe, affects routine
- no other cause

102
Q

Management of migraine

A

acute: PO triptans and NSAID/PCM *nasal in kids
prophylaxis: propranolol, topiramate, amitriptyline
acupuncture

103
Q

How to manage migraines in pregnancy

A

PCM
NSAIDS in 1st and 2nd trimester

104
Q

Cause of Wernickes

A

Thiamine def - alcoholics

105
Q

Presentation of Wernickes

A

1) opthalmoplegia
2) ataxia
3) encephalopathy

106
Q

Investigations of Wernickes

A

Decreased red cell transketolase
MRI: petechial haemorrhages

107
Q

Management of Wernickes

A

Thiamine

108
Q

Complications of untreated Wernickes

A

Korsakoffs

MRCP (19 decks)

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