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FRACP Shuyu > RPA neurology > Flashcards

RPA neurology Flashcards

1
Q

mitochondrial epilepsy - what anti-epileptic to avoid

A

valproate - will worsen epilepsy

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2
Q

EEG right vs left vs central

A

right is even
left is odd
central is z

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3
Q

normal background rhythm EEG

A

8-13Hz in occipital leads

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4
Q

where is the faster activity in normal EEG

A

frontal central region “frontal central beater”

15-25 Hz

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5
Q

normal EEEG in drowsiness

A

neat looking EEG

opening and closing - slow rolloing eye movements

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6
Q

v waves in EEG

A

normal variant
moving into stage 1 sleep
pointing towards on another in Cz

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7
Q

k complex in EEG

A

followed by stage spindle

in stage II non REM sleep

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8
Q

REM sleep EEG

A

looks more like wakeful EEG

has rectus spikes - eyes are moving

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9
Q

intermittent generalised delta slowing in EEG

A

not specific
encephalopathy
postictal

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10
Q

intermittent theta slowing in EEG

A

4-7Hz

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11
Q

continuous generalised slowing in EEG

A

mild to mod encephalopathy

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12
Q

phase reversal in EEG

A

focal slowing

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13
Q

4Hz spike and wave

A

JME

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14
Q

triphasic waves

A

hepatic encephalopathy

but also present in other forms of encephalopathy

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15
Q

PLEDs in EEG

A

period lateralised epileptiform discharges
high risk of seizure but not seizure yet
?HSV

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16
Q

GPEDs in EEG

A

generalised periodic epileptiform dishcarges
bad
severe hypoxic brain injury/other bad insults

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17
Q

enzyme inducer p$%)

A 
PHT
PB
Primidone
CBZ
OXC
TPM
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18
Q

enzyme inducer p450

A 
PHT
PB
Primidone
CBZ
OXC
TPM
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19
Q

what synergises lamotrigine

A

valproate

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20
Q

drug resistant epilepsy def

A

failing after 2 drugs at all doses

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21
Q

carbamazepine and OCP

A

makes OCP uneffective

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22
Q

Carbamazepine and bones

A

increases bone loss by increased metabolism of vit D

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23
Q

perampanel MOA

A

noncompetitive AMPA receptor antagonism
competitive AMPA receptor antagonism

liver metabolised

?for generalised epilepsy syndromes

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24
Q

lacosamide

A

slow sodium channel blocker - prevents reactivation of the neuron
metabolised by the liver
good for focal status

CAN PROLONG PR

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25
Q

clobazam

A

benzo
structurally different to benzo
better antiepileptic but less sedating

good for drug resistant focal epilepsy
sleep related epilepsy
clustering

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26
Q

brivaracetam vs levetiracetam

A

SV2A protein action like keppra
but no ampa effect
so less neutropsychiatric syndromes theorectically unlike keppra

brivaracetam metabolised by the liver

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27
Q

which part of cannibis is used for epilepsy

A

CBD for epilepsy

THC is psychoactive component but in real life exacerbates seizures

Currently some data for use in lannox gastaut syndrome but not much for adult epilepsies

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28
Q

which part of cannibis is used for epilepsy

A

CBD for epilepsy

THC is psychoactive component but in real life exacerbates seizures

Currently some data for use in lannox gastaut syndrome but not much for adult epilepsies

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29
Q

risk of epilepsy to offsprings (Generally)

A

5-8%

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30
Q

targeted therapy for tuberous sclerosis

A

everolimus because it’s due to aberrant signalling mTOR pathway

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31
Q

HLA-B*15:02

A

carbamazepine SJS

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32
Q

lamotrigine levels in pregnancy

A

lamotrigine metabolism accelerated by oestrogen

need to do levels and probably need to increase dose in pregnancy and when on OCP

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33
Q

keppra levels in pregnancy

A

increased plasma volume in pregnancy so need to monitor levels and probbaly increase dose

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34
Q

painful eye movements MS

A

optic neuritis

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35
Q

MS typical lesions (Criteria for dissemination in space) - 5

A 
periventricular
juxtacortical
infratentorial
spinal cord
cortical
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36
Q

high risk of CIS going onto MS

A

MRI brain lesions w MS features
greater number of T2 lesions is associated with a graeter risk
60-80% of MS within several years

CSF oligoclonal bands also increases risk of going onto MS

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37
Q

teriflunomide MOA

A

selectively inhibits DHOH - inhibits pyrimidine de novo synthesis
inhibits rapidly dividing cells - including activated T cells

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38
Q

tecfidera (dimethyl fumerate) MOA

A

protect oligodendrocytes from inflammatory and metabolic injury
but MOA not really know

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39
Q

fingolimod MOA

A

functional antagonist of S1P receptors on lymphocytes, fingolimod-phosphate blocks the capacity of lymphocytes to egress from lymph nodes, causing a redistribution, rather than depletion, of lymphocytes

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40
Q

fingolomod SE

A

macula oedema
lymphopenias
bradycardia/AV block

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41
Q

cladribine pros

A

oral dosing

minimal monitoring

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42
Q

cladribine MOA

A

As a purine analog, it is a synthetic chemotherapy agent that targets lymphocytes and selectively suppresses the immune system, its exact mechanism of action in MS is not clear.
CD4 preferentially depleted to CD8

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43
Q

cladribine administration

A

oral

Two treatment courses, twelve months apart

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44
Q

Tolosa-Hunt syndrome

A

It is characterized by painful ophthalmoplegia (weakness of the eye muscles) and is caused by an idiopathic granulomatous inflammation of the cavernous sinus

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45
Q

different in measuring CMAP vs SNAP amplitude

A

CMAP is onset to peak

SNAP is peak to peak

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46
Q

are reflexes lost in demyelination or axonal neuropathy

A

demyelinating due to the dispersion of nerve impulse transmission that is not sufficient to result in a reflex

e.g. GBS would have loss of reflexes but diabetics rarely do

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47
Q

IgM paraprotein in CIDP

A

bigger upper limb tremor

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48
Q

POEMS syndrome

A

Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal protein, Skin changes

all patients have peripheral neuropathy and a monoclonal plasma cell disorder, almost always of the lambda light chain type

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49
Q

CIDP IVIG vs methylpred

A

methylpred actually has decreased relapses but some people do not respond and there are more adverse effects

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50
Q

CIDP treatment options

A

IVIG, methylpred

Other immunosuppressive patients: aza, mycophenolate

rituximab

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51
Q

CMT1a

A

Most common subtype (40%) of charcot marie tooth

autosomal dominant inherited neuropathy
duplication of the PMP22 gene

Patients with point mutations usually have more prominent clinical manifestations. In these patients, PMP22 partially accumulates in the Schwann cells rather than being inserted in the myelin sheath, as occurs with gene duplication

histology: onion bulb formation (which is characteristic of all demyelination) but is uniform in this disease.

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52
Q

most common form of diabetic neuropathy

A

Distal symmetric polyneuropathy is the most common form of diabetic neuropathy. The proximate cause is a length-dependent “dying back” axonopathy, primarily involving the distal portions of the longest myelinated and unmyelinated sensory axons, with relative sparing of motor axons.

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53
Q

eye and neurology risks in gastric banding

A

B12 and thamine def -> peripheral neuropathy

Vit a def -> cataract and retinal changes

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54
Q

what is one of the only myopathies that start with distal weakness

A

myotonic dystrophy

55
Q

inclusion body myositis muscles affected

A

forearm flexors and knee extensors

56
Q

dermatomyositis biopsy

A

peripheral inflammation

57
Q

dermatomyositis antibody

A

anti Jo1

58
Q

what else to screen for in dermatomyositis

A

malignancies
brain, lung, breast

30%

often manifest after DM diagnosis

59
Q

what antibody is assoc w cancer in dermatomyositis

A

anti-TIF1gamma

50% have cancer

60
Q

inclusion body myositis pathology

A

rimmed vacuoles
characteristic inclusion bodies on EM
need multiple biopsies as the pathology is patchy

61
Q

anti-HMG-CoA reductase antibodies

A

associated with autoimmune (immune-mediated) necrotizing myopathies

More than 60% of patients with anti-HMG-CoA reductase antibodies have current or previous exposure to statin therapy

62
Q

late onset Pompe’s pathophysiology

A

glycogen storage disease type 2, acid maltase deficiency, alpha glucosidase deficiency

63
Q

Pompe genetics

A

GAA ch 17

64
Q

RYR1 gene

A 
malignant hyperthermia
exertional rhabdomylolysis
myalgias
periodic paralysis
complex syndrome`
65
Q

titin gene

A

causes muscle myopathies through sacomere something something

66
Q

drugs that can worsen myasthenias

A

aminoglycosides, tetracyclines, botox, muscle relaxants

(high dose) pred, aza in the initial period

67
Q

antibodies in myasthenia

A

anti musc
ACHR atibodies
ANti LRP4 antibodies
Titin antibodies (often present in ppl w thymoma)

68
Q

anti-musc phenotype myasthenia

A

predominantly faciobulbar weakness

69
Q

general endovascular clot retrieval time limit

A

6hr

with thrombolysis up to 4.5 hours

70
Q

thrombolysis treatment time limit stroke

A

4.5hr (but guidelines worldwide say 6hr)

71
Q

thrombolysis drug in stroke (in guidelines)

A

alteplase

however EXTEND-1A TNK campbell et al showed tenectaplase achieved greater rates of reperfusion

72
Q

clot retrieval extended time frame

A

up to 24hr <70ml core

73
Q

idarucizumab

A

antidote for dabigatran

fragmented antibody binds drug

74
Q

risk factors for recurrence after TIA/stroke

A

multiple infarcts on imaging
large atherosclerotic region
ABCD2 6-7

75
Q

best antihypertensives in stroke

A

calcium channel blockers

76
Q

what antihypertensives to avoid in stroke (Except where it is indicated by other means)

A

beta-blocker

77
Q

when to start rehab in strokes

A

after 24hr

78
Q

lifetime prevalence of stroke

A

1:6

79
Q

ICH blood pressure aim

A

uncertain
don’t go below 140
not too high

80
Q

most common mimic of a stroke

A

seizure

81
Q

definition of “minor stroke” for DAPT in minor strokes

A

NIHSS <3

82
Q

prevention of DVT in stroke

A

enoxaparin (better than heparin and TED stockings are ineffective)

83
Q

first imaging modality to perform in TIA

A

CTA

84
Q

Lewy bodies pathology

A

alpha-synucleinopathy - accumulation of intraneuronal protein aggregates

affecting substantia nigra pars compacta - dopaminergic projects to the pallidum is depleted

85
Q

dopamine agonists

A

pramipexole (D2/3), rotigotine (D3)

86
Q

rasagiline

A

monoamine oxidase B inhibitors

can increase dyskinesias

87
Q

safinamide

A

MAO B inhibitor + glutamate release inhibitor

shown to increase on time but prevents increase in dyskinesias

88
Q

entacapone

A

inhibitor of catechol-O-methyltransferase (COMT). It is used in combination with levodopa and carbidopa (Sinemet) to treat the end-of-dose ‘wearing-off’ symptoms of Parkinson’s disease

used together with levadopa/carbidopa

89
Q

apomorphine

A

apomine/movapo

Potent parenteral dopamine agonist, is an effective rescue therapy for sudden “off” periods, for early-morning “off” states, and as a bridge to shorten the “wearing off” effect between scheduled levodopa doses. Prior to regular self-administration, the effective dose for a patient is established by test administration in the office or at home with a specially trained health care professional

90
Q

best antipsychotic for parkinson’s

A

clopazine
D1/2 and noradrenergic antagonist

but in real life quetiapine

91
Q

depression in parkinson’s

A

nortriptyline

pramipexole

92
Q

parkinson’s dementia tx

A

tivastigmine
donepezil

not much evidence

93
Q

parkinson’s dementia REM sleep

A

clonazepam

amitriptyline

94
Q

lewy body dementia vs parkinsons

A

cognitive problems for 1 year before other parkinson’s symptoms

95
Q

lewy body vs parkinson’s pathology

A

lewy body predominantly cortex (but also substantia nigra)

96
Q

essential tremor frequency

A

4-12Hz (Parkinson;’s 4-6Hz)

97
Q

essential tremor characteristics clinical

A

action tremor
symmetrical
improves w alcohol
can have head tremor

98
Q

essential tremor plus

A

classic tremor +
mild neurological signs e.g. cognitive, dystonia etc

or have action + resting tremor

99
Q

treatment essential tremor

A

propanolol 1st line
primidone 2nd line (MOA unknown but probably to do with sodium channels - also used as antiepileptic)

other:

  • DBS
  • focus ultrasound thalamotomy
100
Q

MSA subtypes

A

parkinsonian vs cerebellar

101
Q

MSA characteristics

A 
autonomic dysfunction
stridor, sleep apnoea, sleep disturbance
JERKY tremor
pyramidal signs (brisk reflexes; not present in other parkinsonian conditions)
antecollis (head foward)
camptocormia (bend forward at hips)
Pisa (lean to 1 side)
REM sleep disturbance
mood instability

young age of onset

102
Q

MSA pathology

A

alpha synucleinopathy in glial cells

nigrostriatal or olivoponticerebellar

103
Q

MSA on MRI

A

parkinson’s type - putaminal rim

cerebellar type - hot cross bun

104
Q

MSA treatment

A

levodopa but can excerbate orthostatic hypotension
treat orthostatic hypotension
manage urinary dysfunction w oxybutinin

105
Q

PSP gaze palsy

A

restricted vertical eye movements but overcome w doll’s head manoeuvre

initially presenting with slow vertical saccades

106
Q

PSP characteristics

A

vertical palsy
axial rigidity
postural instability

see slides

107
Q

PSP pathology

A

tauopathy

108
Q

PSP MRI

A

Hummingbird sign - midbrain atrophy

109
Q

PSP treatment

A

usually poor response but..

levodopa
amantadine (can help w balance)
110
Q

movement disorder with long halting speech, dysgraphaesthesia, limb apraxia

A

corticobasal degeneration

111
Q

corticobasal degeneration pathology

A

tauopathy

112
Q

corticobasal degeneration MRI

A

cortical atrophy

113
Q

what parkinson like syndromes are tauopathies

A

CBD

PSP

114
Q

impersistence of tongue protrusion + depression + occular movement dysfuction

A

huntington’s

115
Q

huntington’s pathology

A

caudate atrophy

gabaergic neurons

116
Q

huntington’s treatment

A

chorea - tetrabenazine, antipsychotics
parkisonian features - levodopa
antidepressants
antipsychotics and mood stabilisers

117
Q

tx for tardive dyskinesias

A

tetrabenazine

118
Q

unilateral violent flinging movements of the limbs

A

hemiballismus

lesions usually in contralateral subthalamic nucleus
but can also happen in caudate nucleus

119
Q

what liver disease can cause movement disorders

A

wilson’s disease
presents after hepatic
ATP7B gene

120
Q

intention tremor + ataxia

+/- parkinsonian sx, peripheral neuropathy

A

fragile X assoc tremor/ataxia syndrome

121
Q

fragile X genetic defect

A

CGG repeat 55-200 is tremor/ataxia syndrome
>200 is just fragile X

X-linked dominant inheritance

122
Q

fragile X assoc tremor/ataxia syndrome pathology

A

neuronal and astrocytic inclusions

123
Q

fragile X assoc tremor/ataxia syndrome MRI

A

middle cerebellar peduncle signs

124
Q

restless legs syndrome secondary causes

A 
peripheral neuropathy
iron deficiency
ESRD
pregnancy
antiepileptics
125
Q

treatment for restless legs syndrome

A

dopamine agonist
levodopa
pregabalin, gabapentin

126
Q

brachioradialis reflex nerve root

A

c6

127
Q

medial thigh and below knee sensory deficit

A

L3 nerve root compression

128
Q

headache worse on bending over

A

increased ICP

129
Q

pure alexia without agraphia in stroke presentation

A

dominant occipital love with the involvement of the splenium of the corpus callosum

130
Q

what causes mollaret’s

A

HSV2

recurrent meningitis

131
Q

what else to give pneumococcus

A

ceft, vanc, dex 10mg IV

132
Q

Pupil-sparing 3rd nerve lesions

A

ischemic lesions such as diabetes, hypertension, or arteriosclerotic disease.

133
Q

acoustic neuroma sx

A

not discrete episodes

slowly progressive

134
Q

ear fullness + vertigo

A

meniere’s

FRACP Shuyu (65 decks)

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