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Phase 3a Finals > Neurology > Flashcards

Neurology Flashcards

1
Q

Most common cause of dementia

A

alzheimers

then
vascular
lewy body

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2
Q

What is Alzheimers?

risk factors-

A

progressive degnerative disease of the brain.

  • age
  • fhx
  • autosomal dominant 5% - amyloid precursor protein (chr21), presenlin 1 (chr 14) , presenilin 2 (chr 1)
  • apoprotein E allele E4 - encodes cholestrol transport protein
  • caucasian
  • downs
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3
Q

Pathological Changes of Alzheimers

A

macroscopic:
- widespread cerebral atrophy, involves more the cortex and hippocampus

Microscopic:
- Cortical plaques due to deposition of type A beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of tau protein.
- hyperphosphorylation of tau protein - linked to AD

biochemical:
- deficit of acetylcholine from damage to ascending forebrain projection

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4
Q

What are neurofibrillary tangles?
(Alzheimer’s)

A
  • paired helical filaments partly made from tau protein

tau = protein interacts with tubulin stabilising microtubules and promoting tubulin assembly into microtubules.

AD: tau proteins hyperphosphorylated = impaired function

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5
Q

How would you manage Alzheimers?

A

non pharm:
- cognitive stimulation therapy
- cognitive rehab
- group reminiscence therapy

pharm:
- acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) - mild - moderate AD

  • memantine (NMDA receptor antagonist)- 2nd line
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6
Q

when would you give memantine as AD tx?

A

moderate AF intolerant or CI to acetylcholinesterase inhibitor

as add on drug for mod-severe

monotherapy in severe

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7
Q

when can you give an antipsychotic in AD?

A

to manage noncognitive sx

pt at risk of harming themselves or others.

when agitation hallucination or delusions causing them severe distress

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8
Q

how is donepezil contraindicated in and what is the adverse effecct?

AD TX

A

bradycardic pts

insomnia

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9
Q

characteristic pathological feature of lewy body dementia?

where are they found?

A

alpha-synuclein cytoplasmic inclusions (lewy body)

in substantia nigra, paralimbic and neocortical areas.

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10
Q

relationship with alzheimers and lewy body?

A

upto 40% of of alzheimers have lewy bodies.

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11
Q

features of Lewy body dementia?

A

progressive cognitive impairment: typically before parkinsonism but both occur within a yr of each other.

FLUCTUATING COGNITION

parkinsonisms

visual hallucinations

  • poss delusions and nonvisual hallucinations

REM sleep disorder?

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12
Q

how can lewy body be differentiated from parkisons disease?

A

in parkinsons motor symptoms occur at least a yr before cognitive sx.

in lewy body first cognitive impaired then motor.

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13
Q

How would you diagnose Lewy body dementia?

A

clinical

single photon emission computed tomography - SPECT. (called DaTscan)
90% sensitivity 100% specificity

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14
Q

How would you manage Lewy Body Dementia?

A

both acetylchoinesterase inhibtors (donepezil, rivastigmine) and memantine.

NO TO NEUROLEPTICS

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15
Q

why should you avoid neuroleptics in Lewy body dementia?

A

can get irreversible parkinsonism.

if hx of pt with deteriorated after antipsychotic agent

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16
Q

What is Vascular Dementia?

A

second most common form after AD.

group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease.

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17
Q

subtypes of vascular dementia

A

stroke related - multi infarct or single infarct dementia

subcortial vd - caused by small vessel disease

mixed dementia - both vd and ad

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18
Q

rf of vascular dementia

A

hx of tia
af
htn
dm
hyperlipidemia
smoking
obesity
coronary heart disease
fhx of storke/cv issue

rare: CADASIL - inherited - cerebral autosomal dominant ateriopathy with subcortical infarcts and leukoencephalopathy

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19
Q

pt comes with vascular dementia. how is he presenting?

A

several months/years of hx of a sudden or stepwise deterioration of cognitive function

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20
Q

symptoms of vascular dementia

A

focal neurological abnormalities: visual disturbance, sensory or motor sx

difficulty with attention and concentration

seizures

memory disturbance
gait disturbance
speech disturbance
emotional disturbance

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21
Q

how would you make a diagnosis of vascular dementia?

A

hx and exam
formal screen for cognitive impairment
med review - exclude medication cause of cognitive decline

MRI - may show infarcts and extensive white matter changes

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22
Q

what criteria used for diagnosis of vascular dementia

A

NINDS-AIREN

presence of cognitive declines interferes with adls not due to secondary effects of cerebrovascular event

cerebrovascular disease - defined by neurological signs/brain imaging

relationship between above 2 disorders inferred by:

onset of dementia within 3 months after recognised stroke
abrupt deterioriation in cognitive function
fluctuating stepwise progressive cognitive deficits

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23
Q

how would you mange vascular dementia?

A

non pharm:
- cognitive stimulation
- multisensory stimulation
-music and art
-animal assisted therapy

pharm:
- no specific ones
- only ache inhibitors or memantine if they have AD too, parkinsons dementia or dementia with lew body.

  • aspirin isnt effective in tx of vd PATIENTS.
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24
Q

rare causes of dementia

A

huntingtons
CJD
picks disease - atropy of frontal and temporal lobes
HIV - 50% of aids pts.

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25
Q

name some differentials of dementia

A

hypothyroidism, addisons
b12 folate thiamine def
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use - alcohol, barbiturates

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26
Q

assessment tools for dementia in non specialist setting

A

10-point cognitive screener : (10-CS)

6- item cognitive impairment test (6CIT)

others: not recommended for non-specialist setting
- AMTS
-GPCOG
-MMSE - 24 or less/30 = suggests dementia

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27
Q

what to investigate initially when thinking dementia?

A

fbc
u+e
lft
calcium
glucose
esr crp
tft
vit b12
folate

neuroimagine - rule out subdural haematoma, normal pressure hydrocephalus

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28
Q

factors favouring delirium over dementia

A

acute onset
impairment of consciousness
fluctuation of sx: worse at night, periods of normality

abnormal perception - illusions and hallucinations

agitation,fear, delusions

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29
Q

What is frontotemporal lobar degeneration?

3 types

A

3 MC cortical dementia after AD and lewy body

3 types:
-frontotemporal dementia (picks disease)

  • progressive non fluent aphasia - chronic progressive aphasia, CPA
  • semantic dementia
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30
Q

common features of frontotemporal lobar dementias

A
  • onset before 65
  • insidious onset
  • relatively preserved memory and visuospatial skills
  • personality change
  • social conduct problems
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31
Q

What is Picks Disease - frontotemporal dementia?

A

personality change
impaired social conduct.

hyperorality
disinhibition
increased appetite
preservation behaviours

behaviour
speech
language

can be familial.

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32
Q

characteristic appears of picks disease - frontotemporal dementia?

A

focal gyral atrophy with knife blade appearance

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33
Q

tell me the macroscopic changes in picks and the microscopic changes

A

Macroscopic:
atrophy of frontal and temporal lobes

Microscopic:
Pick Bodies - spherical aggregations of tau protein - silver staining
Gliosis
Neurofibrillary Tangles
Senile Plaques

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34
Q

how would you manage picks disease?

A

AchE inhibitors or memantine

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35
Q

features of chronic progressive aphasia

A

non fluent speech.

short utterances that are agrammatic.

preserved comprehension

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36
Q

features of semantic dementia?

A

fluent progressive aphasia.

fluent speech but empty and conveys little meaning.

memory between for recent than remote events unlike AD.

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37
Q

name the meds with anticholinergic effect

A

anticholinergic urological drugs - oxybutynin, solifenacin and tolterodine

antihistamine - chlorphenamine and promethazine

tricyclic antidepressants - amitriptyline

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38
Q

what is ace-III - addenbrooke cognitive examination

domains

points

A

assessment tool for memory impairement.

5 domains:
attention
memory
language
visuospatial function
verbal fluency

100 points
88 or less = possible dementia.

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39
Q

name some behavioural and psychological sx of dementia

how would you tx?

A

depression anxiety agitation aggression disinhibition hallucinations delusions slep disturbance

ssri
antipsychotic - risperidone

benzodiazepine - only for crisis.

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40
Q

predisposing factors for delirium

A

age over 65
dementia background
significant injury eg- hip fracture

frailty or multimorbidity

polypharmacy

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41
Q

features of delirium

A

memory disturbances (loss of short> long term)

could be agitated or withdrawn

disorientation
mood change
visual hallucinations
disturbed sleep cycle
poor attention

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42
Q

precipitating events of dementia

A

infection - uti
severe pain
alcohol withdrawal
constipation
any cv,resp,neuro,endo condition

metabolic: hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration

change of environment

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43
Q

how would you manage delirium

A

tx underlying cause.

haloperidol 0.5 mg - 1st line sedative

or olanzapine

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44
Q

what can antipsychotic prescribing be challenging for parkinson patient?

A

worsen parkinsonian sx

careful reduction of parkinson meds may be helpful

if sx need urgent tx : atypical antipsychotic quetiapine and clozapine preffered

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45
Q

What is benign essential tremor?
genetic

most notable where?

A

autosomal dominant - affected both upper limbs
associated with older age.

fine tremor affecting all voluntary muscles.

hands but also: head (TITUBATION)!!!, jaw and vocal tremors

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46
Q

features of benign essential tremor

A

POSTURAL TREMOR - WORSE IF ARMS OUTSTRETCHED

fine tremor - 6-12 hx
symmetrical
more prominent with voluntary movement

worse when tired,stressed or after caffeine

improved by alcohol
absent during sleep

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47
Q

differentials of benign essential tremor

A

parkinsons
MS
Huntingtons chorea
hyperthyroidism
fever
dopamine antagonists - eg antipsychotics

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48
Q

how would you manage benign essential tremor?

A

nothing definitive.

to improve sx:
propranolol 1st line - non selective beta blocker

primidone - barbiturate antiepileptic med

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49
Q

Name some causes of parkinsonisms

A

parkinsons

drug induced - antipsychotics,metoclopramide

progressive supranuclear palsy

multiple system atrophy
wilsons disease

post-encephalitis
dementia pugilistica - chronic head trauma cause like boxing

toxins: carbon monoxide, MPTP

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50
Q

domperidone
class of drug
function
why doesn’t it cause extrapyramidal side effects

A

antisickness
dopamine antagonist

doesnt cross blood brain barrier

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51
Q

What is Parkinson’s disease?

A

progressive neurodegenerative conditions

caused by degeneration of dopaminergic neurons in substantia nigra.

progressive reduction in dopamine in basal ganglia - so you get disorder of movements

ASYMMETRICAL

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52
Q

classical triad of features: parkinsons

other general picture

A

REDUCTION IN DOPAMINERGIC OUTPUT CAUSES:
bradykinesia - slowness of movement
resting tremor - tremor worst at rest
rigidity - resisting passive movement

ASSYMETRICAL

forward tilt
stooped posture
facial masking
shuffling gait

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53
Q

epidemiology of parkinsons

A

twice as common in men
mean age: 65

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54
Q

talk to me about the triad of sx in parkinsons: bradykinesia

A

poverty of movement - hypokinesia

short shuffling (gait) steps with reduced arm swing

difficulty in initiating movement

micrographia

festinating gait - rapid frequency of steps to comp for small steps and not fall

reduced facial movements and expressions(hypomimia)

difficulty initiating movement

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55
Q

Pathophsyiology of Parkinsons

A

basal ganglia are group of structures near centre of brain.
coordinate habitual movements like walking controlling voluntary movements etc.

dopamine plays major role. - in pd you have a drop of dopamine.

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56
Q

talk to me about triad of sx in parkinsons: tremor
WHAT EXAGGERATES THE PILLROLLING TREMOR

A

most marked at rest, 3-5 hz

worse when stressed/tired, IMPROVES WITH VOLUNTARY MOVEMENT (unilateral)

PILL-ROLLING ie in the thumb and index finger. worse at rest better with voluntary movement. worse if pt distracted.

miming act of painting a fence

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57
Q

tell me about sx in parkinsons: rigidity

A

resistance to passive movement of a joint

lead pipe
cogwheel: due to superimposed tremor

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58
Q

other general features of parkinsons

A

mask-like facies
flexed posture
micrographia
drooling of saliva
REM sleep behaviour disorder

fatigue
autonomic dysfunction: postural hypotension due to autonomic failure

psychiatric feature: depression is MC feature (40%) - psychosis and sleep disturbances poss

impaired olfaction
cognitive impairement.

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59
Q

how are drug induced parkinsonism presenting features to parkinsons?

A

motor symptoms are generally rapid onset and bilateral

rigidity and rest tremor are uncommon

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60
Q

How would you differentiate between essential tremor and Parkinson’s?

A

123 I - FP - CIT single photon emission computed tomography (SPECT)

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61
Q

What stain shows alpha synuclein of substantia nigra in parkinsons?

A

lewy body brown stain positive for alpha synuclein

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62
Q

How would you treat parkinsons?

A

if motor sx affected QoL: levodopa
if motor sx not affecting QoL: dopamine agonist (non-ergot derived), levodopa, monoamine oxidase B (MAO-B) inhibitor

if optimal levodopa and still sx or developed dyskinesia, add dopamine agonist, MAO-B inhibitor or catechol-o-methyl transferase (COMT) inhibitor as adjunct.

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63
Q

out of parkinson treatments rank them for motor symptoms, activities of daily living and motor complications

adverse events - what are they too

A

levodopa - fever adverse events
dopamine agonist - more adverse
MAO-B inhibitors - fever adverse

1st - more improvement and more motor comps
2nd and 3rd - less improvement and fever motor comps

adverse: excessive sleep, hallucination, impulse control disorder

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64
Q

when adding a drug as an adjunct in parkinsons you need to make a few decisions based on

motor sx
adl
off time
adverse events
hallucinations

make them for dopamine agonist, MAO-B inhibitors, COMT inhibitors, Amantadine.

A

Motor Symptoms, ADL : dopamine agonist, MAO-Bi COMTi - improvement in both.
Amantadine: no evidence in improvement of either.

Off time: dopamine agonist : more off-time reduction, MAO-Bi and COMTi - off-time reduction
Amantadine : no evidence

Hallucinations:
DA - more risk
MAO-Bi/COMTi : lower risk of them
Amantadine: no evidence

Adverse events :
DA - intermediate risk
MAO-Bi/COMTi : fever adverse events/more adverse events

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65
Q

what can happen to a patient if parkinson tx medication is not absorbed/taken?

give a reason why this could happen

A

risk of acute akinesia or neuroleptic malignant syndrome

gastroenteritis

NO DRUG HOLIDAY

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66
Q

what therapy/treatment can impulse control disorder happen with?

A

dopamine agonist therapy

hx of previous impulsive behaviours

hx of alcohol consumption and/or smoking

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67
Q

parkinson patient is day time sleepy but drives what to do?

A

modafinil - Atypical dopamine reuptake inhibitor

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68
Q

if orthostatic hypotension in parkinson patient what to give?

how does it work?

A

midodrine - acts of peripheral alpha-adrenergic receptors to increase arterial resistance

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69
Q

parkinson pt drooling of saliva - how to tx?

A

glycopyrronium bromide

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70
Q

common adverse effects of levodopa

reduced effectiveness over what period of time?

A

dry mouth
anorexia
palpitations
postural hypotension
psychosis
reddish discolouration of urine upon standing
n+V
cardiac arrhythmias
on off effect
dyskinesia

by 2 yrs

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71
Q

how is levodopa usually prescribed? parkinsons

why?

A

usually with a decarboxylase inhibitor - eg carbidopa or benserazide

levo+benserazide : MADOPA
levo+carbi: SINEMET

prevents peripheral metabolism of levodopa to dopamine outside of brain - reduce side effects

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72
Q

can you name some adverse effects of levodopa due to difficulty in achieving a steady dose of levodopa?

A

end of dose wearing off. - decline of motor activity.

on-off phenomenon: large variation in motor performance. - weakness and restricted mobility during off.

dyskinesia at peak dose: dystonia,chorea and athetosis (involuntary writhing)

effects worsen over time

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73
Q

you are at peak dose of levodopa in parkinson tx and develop dyskinesias

what are they?

A

dystonia
chorea
athetosis - involuntary writhing movements

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74
Q

why shouldnt you acutely stop levodopa

what to do if they cant take orally

A

acute dystonia

give dopamine agonist patch as rescue medication

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75
Q

give me 4 examples of dopamine receptor agonists

side effects of ergot derived= what to do if prescribing these?

A

bromocriptine - ergot derived
ropinirole
cabergoline - ergot derived
apomorphine

ergot derived: pulmonary,retroperitoneal and cardiac fibrosis

echocardiogram
esr
creatinine
cxr

all above before tx and closely monitor during.

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76
Q

side effects of dopamine receptor agonists

A

congestion and postural hypotension in some

more likely than levodopa in older pts to cause hallucinations

potential: impulse control disorder and excessive daytime somnolence

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77
Q

give the the MoA of MAO-B inhibitor and an example

A

Selegiline/Rasagiline.

inhibits breakdown of dopamine secreted by dopaminergic neurons

used to delay use of levodopa, then with levodopa to reduce end of dose worsening sx.

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78
Q

How does amantadine work and what is its side effects? parkinsons

class of drug

use

A

glutamate antagonist - treat dyskinesia associated with levodopa

increases dopamine release and inhibits its uptake at dopaminergic synapses

ataxia
slurred speech
confusion
dizziness
livedo reticularis

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79
Q

give me 2 examples of COMTi - catechol-o-methyl transferase inhibitors

and what is it?

how and when used?

A

entacapone, tolcapone

enzyme breaks down dopamine.
use with levodopa esp in established PD patients to slow breakdown of levodopa in brain. extends effective duration of levodopa

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80
Q

how do antimuscarinics work in parkinsons?

give examples

what sx do they help with

A

block cholinergic receptors

used more to tx drug-induced parkinsons

help tremor and rigidity

procyclidine
benzotropine
trihexyphenidyl - (benzhexol)

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81
Q

what is multiple system atrophy?

symptoms

A

rare

neurones of brain degenerate including basal ganglia. - parkinsons presentation

but you get autonomic dysfuntcion (postural hypotension,constipation, abnormal sweating and sex dysfunction) too

cerebellary dysfunction (ataxia)

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82
Q

prolonged use dopamine agonist treat side effect

A

pulmonary fibrosis

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83
Q

What is motor neuron disease and types?

with the types theyre main signs

A

progressive group of diseases affecting motor nerves not sensory.
rarely before 40.

ALS - MC - 50% pts - LMN signs in arms and UMN signs in legs.
if familial : gene responsible lies on chr 21 and codes for superoxide dismutase

Primary Lateral Sclerosis: UMN signs only

Progressive muscular atrophy: LMN signs only, distal muscles before proximal, best prognosis

Progressive Bulbar Palsy: palsy of tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei. Worst prognosis.

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84
Q

features of mnd

A

assymetric limb weakness - ALS

mixed lmn and umn signs

wasting of small hand muscles/tibialis anterior
fasciculations

absence of sensory signs/sx:
- vague sensory symptoms early in disease poss? - eg limb pain but never sensory sign

no cerebellar signs
dont affect external ocular muscles
abdo reflexes preserved.

SPINCTER DYSFUNCTION - LATE FEATURE

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85
Q

how to diagnose MND?

A

clinical

nerve conduction studies - normal motor conduction.

electromyography - reduced no. of action potentials with increased amplitude.

MRI: exclude cervical cord compression and myelopathy

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86
Q

how would you manage MND

A

riluzole
- ALS
- prolongs life by 3 months
- prevents glutamate receptor stimulation

Resp care:
- non invasive ventilation - BIPAP - at night
- 7 month survival benefit

Nutrition
- PEG - percutaneous gastrostomy tube

Prognosis: poor
50% pts die within 3 yrs

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87
Q

any associated risk factors for mnd

A

fhx - 5-10%
smoking
heavy metals and certain pesticides

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88
Q

signs of lower mnd

A

muscle wasting
reduced tone
fasciculations
reduced reflexes

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89
Q

signs of upper mnd

A

increased tone or spasticity
brisk reflexes
upgoing plantar reflex

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90
Q

What is Multiple Sclerosis?

A

chronic and progressive autoimmune condition involving demyelination in cns.

immune system attacks myelin sheath of myelinated neurones

typically under 50 . more in women 20-40 peak.

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91
Q

causes of MS

A

Genetics:
monozygotic twin concordance = 30%
dizygotic twin concordance = 2%

EBV
low vit d
smoking
obesity

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92
Q

types of MS

A

relapsing remitting - mc - 85%
acute attacks - last1-2 months followed by periods of remission

secondary progressive disease:
- relapsing remitting pts deteriorated and got neurological signs and symptoms between relapses.
- 65% of RR patients get this within 15 yrs
- gait and bladder disorders

primary progressive
-10% pts
- progressive deterioration from onset
- mc in older ppl

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93
Q

Pathophysiology of MS

A

affects cns - oligodendrocytes.
inflammation and immune cell infiltration damages myelin.

pt gets ms attack - episode of optic neuritis. therell be other demyelinating lesions in cns but not causing sx.

re-myelination can happen in early disease so sx resolve. later on in disease re-myelination is incomplete for sx get more permanent.

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94
Q

characteristic feature of MS

onset of sx - ms

A

disseminated in time and space

lesions vary in location - affected sites and sx change over time

progress over more than 24hrs. sx last days to weeks at 1st presentation and then improve.

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95
Q

how would you investigate MS?

A

diagnosis need proof of lesions disseminated in time and space

MRI:
- high signal T2 LESIONS
- periventricular plaques
- Dawson fingers: often seen on FLAIR images - hyperintense lesions perpendicular to corpus callosum

CSF:
- oligoclonal bands IgG - not in serum
- increased intrathecal synthesis of IgG

Visual Evoked Potentials:
- delayed, but well preserved waveform

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96
Q

features of MS

A

75% lethargy

visual:
- optic neuritis - unliateral reduced vision hours to days.
-optic atrophy
-Uhtoff’s phenomenon: worsening of vision (all sx) after body temp rise
- internuclear opthalmoplegia - impaired adduction and nystagmus in contralateral abducting eye

Sensory
- pins/needles
-numbness
-trigeminal neuralgia
- Lhermitte’s Syndrome: paresthesiae in limbs on neck flexion

Motor:
- spastic weakness: mc legs

cerebellar:
-ataxia : more during acute relapse than presenting sx
- tremor

Other:
- urinary incontinence
-sex dysfunction
- intellectual deterioration

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97
Q

key features of optic neuritis

A

central scotoma - enlarged central blind spot

pain with eye movement

impaired colour vision
relative afferent pupillary defect

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98
Q

explain what a relative afferent pupillary defect is

OPTIC NEURITIS

A

pupil in affected eye constricts more when shining a light in contralateral eye.

reduced pupil response to shining light in affected eye - direct pupillary reflex check.

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99
Q

in MS , lesion in abducens cnVI causes?

A

conjugate lateral gaze disorder.

conjugate just means connected.

lateral gaze where both eyes move laterally to lef tor right.

when they look in a direction of affected eye, affected eye cant abduct.

eg: lesion in left eye. when looking to left the right eye will adduct ( move towards nose) the left eye will stay middle.

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100
Q

MS presents with focal weakness. give examples

A

incontinence
horner syndrome
facial nerve palsy
limb paralysis

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101
Q

ms presents with focal sensory sx. give examples

A

trigeminal neuralgia
numbness
paraesthesia
lhermittes sign

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102
Q

what is lhermittes sign?

what does it tell you?

how is it caused?

A

ms

electric shock sensation travels down spine and into limbs when flex neck.

tells you disease in cervical spinal cord in dorsal column.

caused by stretching demyelinated dorsal column

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103
Q

MS issue with ataxia - 2 types and differences

A

ataxia - coordinated movement issue

sensory: loss of proprioception. - positive rombergs test. - lose balance when standing with eyes closed. -
cause psedoathetosis - involuntary writhing movements.
lesion in dorsal columns of spine can cause sensory ataxia.

cerebellar: problems with cerebellum coordinating movement, indicating cerebellar lesion.

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104
Q

how would you manage an acute relapse of MS?

A

acute relapse:
- high dose steroid: oral/iv methylprednisolone 5 days. - short length of acute relapse

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105
Q

when would you give disease modifying drugs for ms ?

A

relapsing remitting disease + 2 relapses in last 2 yrs + able to walk 100m unaided

secondary progressive disease + 2 relapses in past 2 yrs + able to walk 10m (Aided/unaided)

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106
Q

drug options for reducing relapse risk - MS

A

Natalizumab - 1st line - iv

ocrelizumab - iv - also used first line

fingolimod - oral formula

beta-interferon - subcut/IM - not as effective as other drugs

glatiramer acetate - subcut - immunomodulating drug - immune decoy

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107
Q

natalizumab - ms tx
MoA

A

recombinant monoclonal antibody that antagonises alpha 4 beta 1 integrin found on leucocyte surface.

inhibit migration of leucocytes across endothelium across blood brain barrier.

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108
Q

ocrelizumab - ms tx
MoA

A

humanised anti-cd20 monoclonal antibody

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109
Q

fingolimod - ms tx
MoA

A

sphingosine 1-phosphate receptor modulator (S1P)

prevents lymphocytes from leaving lymph nodes

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110
Q

if an ms pt experiences fatigue what to give?

A

exclude anaemia thyroid and depression

then give amantadine

or mindfulness training and cbt

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111
Q

if an ms pt has spasticity what to give?

A

baclofen and gabapentin: 1st line

others:
diazepam,dantrolene and tizanidine

physio

cannabis and botox: under evaluation

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112
Q

how would you tx oscillopsia (when visual fields oscillate) in ms pt?

A

gabapentin : 1st line

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113
Q

how would you manage bladder dysfunction in ms pt?

A

could be urgency incontinence or overflow

get uss first to assess bladder emptying - anticholinergic could worsen sx in some pts

if significant residual vol: intermittent self-catheterise

if not: anticholinergics improve urinary frequency

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114
Q

What is duchenne muscular dystrophy?

A

x linked recessive inherited disorder in the dystrophin genes required for normal muscular function.

dystrophinn gene on Xp21

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115
Q

features of duchenne muscular dystrophy

A

progressive proximal muscle weakness from 5 yrs

calf pseduohypertrophy

gowers sign: child uses arms to stand up from squatted position because muscles around pelvis not strong enough to get body erect.

30% pts - intellectual impairement

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116
Q

how would you investigate duchenne muscular dystrophy?

A

raised creatinine kinase

genetic testing replaced muscle biopsy to get definitive diagnosis

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117
Q

how would you manage duchenne muscular dystrophy?

prognosis

A

supportive
no effective tx

prognosis:
- most kids cant walk by 12 yrs
- survive till 25-30
- have dilated cardiomyopathy!!

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118
Q

tell me about becker muscular dystrophy

A

develops after 10 yrs
intellectual impairment much less common
also x linked recessive.

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119
Q

difference between duchenne muscular dystrophy and becker muscular dystrophy - genetics

A

duchenne: frameshift mutation = 1 or both of binding sites are lost = severe form

becker: non-frameshift insertion in dystrophin gene = both binding sites preserved = milder form

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120
Q

Tell me about myotonic dystrophy

A

inherited myopathy.
20-30 yrs old.

skeletal cardiac and smooth muscle affects.

2 types: dm1 and dm2

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121
Q

genetic component to myotonic dystrophy

A

autosomal dominant
trinucleotide repeat disorder

DM1 caused by CTG repeat at end of DMPK gene on chr 19

DM2 caused by repeat expansion of ZNF9 gene on chr3.

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122
Q

key difference between dm1 and dm2 for myotonic dystrophy

A

dm1: dmpk gene on chr 19. distal weakness more prominent

dm2 : znf9 gene on chr3. proximal weakness more. severe congenital form not seen

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123
Q

general features of myotonic dystrophy

A

myotonic facies - long “HAGGARD” appearance
frontal balding
bilateral ptosis
cataracts
dysarthria

myotonia (tonic spasm of muscle)
weakness of arms and legs - initially distal
mild mental impairement
DM
testicular atrophy
cardiac: heart block, cardiomyopathy
dysphagia

PROLONGED MUSCLE CONTRACTION.

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124
Q

briefly tell me about facioscapulohumeral muscular dystrophy

A

in childhood present

weakness around face - progress to shoulders and arms

sleep with eyes slightly open
weakness pursing lips.

cant blow cheeks out without air leaking from mouth

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125
Q

briefly tell me about oculopharyngeal muscular dystrophy

A

late adulthood weakness of ocular muscles and pharynx.

bilateral ptosis
restricted eye movement
swallowing problems

muscles around limb girdles affected to varying degrees.

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126
Q

briefly tell me about limb girdle muscular dystrophy

A

teenage years

progressive weakness around limb girdle - hips and shoulders

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127
Q

briefly tell me about emery-dreifuss muscular dystrophy

A

childhood with contractures - elbows and ankles.

contracture: shorterning of muscle and tendons – restrict range of movement in limb.

progressive weakness and wasting of muscle - upper arm and lower legs first

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128
Q

What is huntingtons disease?

A

inherited neurodegenerative condition.

progressive
incurable

death 20yrs after initial sx start.

autosomal dominant
defect in huntingtin gene on chr 4 - genetic mutation of HTT

trinucleotide repeat disorder: repeat expansion of CAG - PHENOMENON OF ANTICIPATION

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129
Q

what is the phenomenon of anticipation in huntingtons disease?

A

disease presents earlier age in sucessive generations

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130
Q

features of huntingtons disease

age of presentation

A

typically develop after 35 yrs old

chorea - involuntary random irregular abnormal body movements.
personality change - irritable, apathy, depression and intellectual impairment

dystonia - abnormal muscle tone - abnormal posture
saccadic eye movements

dysarthria - speech issue
dysphagia

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131
Q

how would you manage huntingtons?

A

physio - for contractures

speech and language - speech and swallowing difficulty

tetrabenazine - chorea

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132
Q

why might someone get a brain abscess?

A

extension of sepsis from middle ear or sinuses

trauma or surgery to scalp

penetrating head injury

embolic event from endocarditis

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132
Q

what is someone most likely going to die with when they have huntingtons disease?

A

aspiration pneumonia.

or suicide.

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133
Q

presenting sx of brain abscess

A

depend on site of abscess - if motor cortex will present earlier

mass effect on brain and raised icp

headache: dull persistent
fever: poss absent. not swinging pyrexia though
focal neurology: oculomotor nerve palsy or abducens nerve palsy secondary to raised icp

nausea
papilloedema
seizures

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134
Q

how would you investigate for brain abscess

A

ct scanning

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135
Q

how would you manage for brain abscess

A

surgery - craniotomy - debride abscess cavity.
abscess can reform because head is closed after abscess drainage

iv abx: 3rd gen cephalosporin+ metronidazole

icp manage: dexamethasone

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136
Q

causative organisms of meningitis

A

neonatal to 3 months:
- group b strept : from mother at birth. mc in low birth weight babies and after prolonged rupture of membranes
-ecoli and other gram negative organisms
- listeria monocytogenes

1mnth- 6yrs:
- neisseria menigitidis - meningococcus
- strept pneumoniae - pneumococcus
-haemophilus influenzae

over6:
- Neisseria meningitidis - meningococcus
-streptococcus pneumoniae - pneumococcus

over 60 :
streptococcus pneumonia
neisseria meningitidis

immunosupresed:
listeria monocytogenes

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137
Q

meningitis vaccination includes which serotypes and given when

A

2 months 4 months 12-13 months

a and c and b (bexsero)

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138
Q

symptoms and signs of meningitis

A

symptoms:
headache fever n+v, photophobia drowsiness seizures

signs:
neck stiffness
purpuric rash - particular with invasive meningococcal disease

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139
Q

what stain is used to find tuberculous meningitis ?

A

ziehl neelsen

20% sensitive

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140
Q

csf findings in meningitis

bacterial
viral
tuberculous
fungal

appearance
glucose
protein
white cells

A

bacterial:
cloudy
low - (<1/2 plasma)
high (>1 g/l)
10 -5000 polymorphs /mm3

viral:
clear/cloudy
60-80% of plasma glucose
normal/raised
15-1000

tuberculous:
slight cloudy,fibrin web
low
high
10-1000

cloudy
low
high
20-200

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141
Q

complications of meningitis

A

neurological sequlae:

sensorineural hearing loss - mc

seizures
focal neurological deficit

infective: sepsis, intracerebral abscess

pressure: brain herniation, hydrocephalus

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142
Q

pt has meningococcal meningitis, risk of what syndrome?

A

waterhouse-friderichsen

adrenal insufficiency secondary to adrenal haemorrhage

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143
Q

in what patients would you not do lumbar puncture for suspected meningitis?

what to do instead

A

focal neurological signs
papilloedema
significant bulging of fontanelle
disseminated intravascular coagulation
signs of cerebral hernation

blood cultures and pcr

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144
Q

how would you manage meningitis in kids?

A

abx
under 3 months: iv amox (or ampiciliin) + iv cefotaxime
over 3 months: iv cefotaxime - of ceftriaxone

steroids
- not to under 3 mnths
- dexamethasone - if LP shows:
frankly purulent csf.
csf wbc over 1000/microlitre
protein over 1g/l
bacteria on gram stain

fluids: treat shock eg with colloid

cerebral monitoring - mechanical ventilation if resp impairment

public health notify

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145
Q

what abx would you give as prophylaxis to contacts of meningitis

A

ciprofloxacin

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146
Q

what is meningitis?

A

inflammation of leptomeninges and csf of subarachnoid space.

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147
Q

viral causes of meningitis

A

non-polio enteroviruses: coxsackie, echovirus

mumps

hsv, cytomegalovirus, herpes zoster

hiv
measles

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148
Q

risk factors of viral meningitis

A

pt at extremes of age under 5 and old

immunocompromised - pt with renal failure, with dm

ivdu

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149
Q

clinical features of viral meningitis

A

common:
headache
neck stiffness
photophobia - milder than bacterial
confusion
fever
NON BLANCHING RASH

less common:
- focal neurological deficit on exam
- seizure: suggest meningoencephalitis

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150
Q

how would you investigate viral meningitis

A

LP - csf

opening pressure - 10-20cm3 h20
cell count - 10-300 cells/ul
cell differential - lymphocytes

glucose - 2.8-4.2 mmol/l
protein - 0.5-1 g/dl

viral pcr - underlying organism

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151
Q

how would you manage viral meningitis?

A

if thinking bacterial or encephalitis: start broad spect abx with cns pentration: ceftriaxone and aciclovir IV.

viral meningitis self limiting - immproves 7-14 days.

aciclovir - if pt suspected to have meningitis secondary to hsv.

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152
Q

pt with meningitis - hospital approach

A

a - irway
b - reathing
c - circulation
d - disability : gcs - focal neuro signs, seizures, papilloedema

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153
Q

warning signs for acute presentation meningitis

A

rapidly progressing rash
poor peripheral perfusion
resp rate under 8 or over 30 or pulse under 40 over 140

ph under 7.3
wbc under 4*10(9) or lactate over 4 mmol/l
gcs under 12 or drop of 2 pts
poor response to fluid resus

154
Q

in what circumstance would you delay a lumbar puncture - meningitis - bacterial suspected?

A

signs of severe sepsis or rapidly evolving rash

severe resp/cardiac compromise

significant bleeding risk

signs of raised icp : focal neuro signs,papilloedema,continuous/uncontrolled seizures, gcs 12 or less.

155
Q

how would you manage bacterial meningitis with pt without indication for delayed lp

A

iv access - blood and blood cultures

lp: if not in 1st hr - iv abx after blood cultures taken

iv abx: 3mth-50 : cefotaxime - or ceftriaxone

over 50: above + amox (or ampicillin) for adults

iv dex : adjunctive - esp if pneumoccocal menin in adults - start before or with first dose of antibac, but not later than 12 hours after.

NO CT

156
Q

in what case would you avoid dex - meningitis bacterial case?

A

septic shock,
meningococcal septiciaemia
immunocompromised
or meningitis after surgery.

157
Q

how would you manage a bacterial meningitis case with raised icp? same if severe sepsis or rapidly evolving rash

A

secure airway + high flow ox

iv access - bloods and blood cultures

iv dex
iv abx
neuroimagine

158
Q

what bloods to test for suspected bacterial meningitis?

other tests

A

fbx
renal
flucose
lactate
clotting profile
crp

blood gases
throat swab for meningococcal culture

159
Q

bacterial meningitis pt : initial empirical therpay undr 3 months or over 50

A

iv cefotaxime + amoxicillin

160
Q

bacterial meningitis - initial empiral therapy 3mths - 50 yrs

A

iv cefotaxime - or ceftriaxone

161
Q

meningococcal meningitis - bactieral scenario mx

A

iv benzylpenicillin or cefotaxime (or ceftriaxone)

162
Q

pneumococcal meningitis - bacterial meningitis scenario mx

meningitis caused by h influenzae

A

iv cefotaxime (or ceftriaxone)

163
Q

meningitis caused by listeria - mx

A

iv amox or amp - + gentamicin

164
Q

what to do in bacterial meningitis mx if pt history of immediate hypersensitivity to penicillin to cephalosporins?

A

chloramphenicol

165
Q

prophylaxis for contacts of bacterial meningitis

A

if exposed to resp secretion.

risk highest in 1st 7 days- lasts for 4 weeks.

if confirmed: give if close within 7 days before onset.
oral ciprofloxacin or rifampicin.

give meningococcal vaccination. - give booster if they had it in infancy.

no prophylaxis for pneumococcal.

166
Q

2 tests for meningeal irritation

A

both pt lies on back

kernigs - flex 1 hip and knee to 90 degree. slowly straighten knee keep hip flexed. spinal pain or resistance?

brudzinkis - use hand to life head and neck off bed and flex chin to chest. - causes pt to involuntarily flex hips and knees

167
Q

what is guillain barre syndrome?

triggers

A

acute paralytic polyneuropathy affects pns.

immune mediated demyelination of pns.

acute, symmetrical ascending weakness.

sensory symptoms.

triggered by infections:
- campylobacter jejuni
-cytomegalovirus (cmv)
-epstein-barr virus (ebv)

168
Q

pathophysiology of guillain barre syndrome

A

cross reaction of antibodies with gangliosides in pns

correlation between anti-ganglioside antibody (anti-gm1) and clinical features seen

anti-gm1 antibodies - seen in 25% pts

169
Q

what is miller fisher syndrome?

A

variant of guillain-barre syndrome

opthalmoplegia, areflexia, ataxia. - eye muscles affected first.

descending paralysis not ascending.

anti-gq1b antibodies in 90% pts

170
Q

initial symptoms of gullain barre syndrome
characteristic features
other features

lesson common findings:

A

back/leg pain

-progressive symmetrical weakness of all limbs. ascending - legs affected first.
- reflexes reduced/absent
-sensory sx mild - distal paresthesia with very few sensory signs

other:
- hx of gastroenteritis
-respiratory muscle weakness
- cranial nerve involvement - diplopia, bilateral facial nerve palsy, oropharyngeal weakness
- autonomic involvement: - urinary involvement, diarrhoea

less common:
- papilloedema : secondary to reduced csf resorption

171
Q

how would you investigate guillain barre syndrome?

A

lp : rise in protein. normal wbc count - albuminocytologic dissociation

nerve conduction studies : decreased motor nerve conduction velocity - due to demyelination

prolonged distal motor latency
increased f wave latency

172
Q

what criteria to diagnose guillain barre?

A

brighton criteria

173
Q

how would you manage guillain barre syndrome?

A

vte prophylaxis - pulmonary embolism

iv immunoglobulins - IVIG - 1st line

plasmapheresis - alternative to IVIG

severe: if resp failure require intubation, ventilation and admit to icu.

174
Q

features of encephalitis

A

fever headache psychiatric sx , seizures, vomiting

focal features: aphasia

altered cognition/conciousness. unusual behaviour.

peripheral lesions: like cold sores no relationship to presence of HSV encephalitis

175
Q

pathophysiology of encephalitis

A

hsv-1 - 95% adult cases

affects temporal and inferior frontal lobes

176
Q

how would you investigate encephalitis

A

csf - lymphocytosis, elevated protein
pcr: HSV,VSV,ENTEROVIRUSES

neuroimaging:
CT - medial temporal and inferior frontal changes - eg petechial haemorrhages
normal in 1/3 of patients
MRI is better
hiv test
swabs - causative organism, throat and vesicle swab

EEG: lateralised periodic discharges at 2Hz

177
Q

how would you manage encephalitis

A

intravenous aciclovir start in all suspected encephalitis cases - hsv and vsv
ganciclovir - cmv

178
Q

complications of encephalitis

A

lasting fatigue/prolonged recovery
headache, chronic pain, learning disability, change to memory, personality, mood , cognition.

movement disorder
sensory disturbance
siezure
hormonal imbalance

179
Q

contraindications of lp in encephalitis in kids

A

gcs below 9
haemodynamiccaly unstable
active seizures
post-ictal

180
Q

causes of encephalitis in kids

A

non infective: autoimmune

mc : viral
bacterial and fungal - rare

mc: hsv. hsv-1 from cold sores.
in neonates: hsv-2 from genital herpes from birth.

vzv: chicken pox,cmv associated with immunodeficiency.
ebv: infectious monucleosis, adenovirus, influenza virus.

polio, mumps, rubella, measles - all can cause it too.

181
Q

hsv encephalitis - typically affects with lobes

A

temporal

182
Q

what is shingles herpes zoster?

A

acute unilateral painful blistering rash

caused by reactivation of varicella-zoster virus - vzv.

(following vzv infection, chickenpox)
virus lies dormant in dorsal root or cranial nerve ganglia.

183
Q

risk factors of shingles

A

increasing age
hiv: strong rf 15* more common

other immunosuppressive conoditions: steroids, chemo

184
Q

most common affected dermatomes in shingles

A

t1-l2

185
Q

features of shingles

A

prodromal period:
- burning pain over affected dermatome for 2-3 days.
-pain might be severe and sleep
- 20% pts experience fever, headache, lethargy

rash
- erythematous, macular rash over affected dermatome
-quickly becomes vesicular
- characteristically well demarcated by dermatome dont cross midline. “ bleeding” in adjacent areas might be seen.

clinical diagnosis

186
Q

how would you manage shingles - herpes zoster

A

avoid pregnant women and immunosuppresed - contagious

infectious until vesicles crusted over, 5-7 days after onset. covering lesions reduces risk.

analgesia:
- 1st line para and nsaids
- if not : neuropathic agent like amitriptyline
- oral corticosteroids - in 1st 2 weeks in immunocompetent adults with localised shingles if pain severe.

antivirals
- within 72 hrs for most patients, unless pt under 50 and mild truncal rash with mild pain
- aciclovir , famciclovir, valaciclovir

187
Q

benefit of prescribing antiviral in shingles - herpes zoster

A

reduced incidence of post-herpetic neuralgia

188
Q

complications of shingles -herpes zoster

A

postherpetic neuralgia

herpes zoster opthalmicus - ocular division of trigeminal nerve

herpes zoster oticus - ear lesions and facial paralysis

189
Q

malaria is caused by?

A

plasmodium protozoa spread by female anopheles mosquito:
4 diff :

plasmodium falciparum - most.
plasmodium vivax - 2nd - benign malaria
plasmodium ovale
plasmodium malariae

190
Q

malaria protects from what diseases?

A

sickle-cell trait

g6pd deficiency
hla b53
absence of duffy antigens

191
Q

falciparum malaria - mc - most severe type: features - classic triad

why do they occur every 48 hrs?

A

paroxysms of fever chills and sweating.

every 48 hrs because erythrocytic cycle of plasmodium falciparum parasite.

fever high intermittent. - possible rigors too.

non specific:
malaise,headache,myalgia

192
Q

general features of falciparum malaria

A

fever - cyclical - sweating and sometimes rigors.

gi:
-anorexia,n+v, abdo pain. diarhoea poss , mc in kids. poss mild jaundice and occasional pruritus

resp: cough, poss mild tachypnoea

msk: generalised body aches and joint pain

neuro: headache. dizziness and sleep disturbance.

cv: tachy, hypotension more typical of severe malaria.

haem: thrombocytopenia most significant haematological finding. mild anaemia poss

renal: aki associated with severe malaria. non severe : mild-moderate increase in creatinine or blood urea nitrogen levels

193
Q

features of severe falciparum malaria

how to treat

A

schizonts on blood film

parasitaemia >2%

hypogly
acidosis
temp over 39
severe anaemia

iv artesunate
if parasite count over 10% then exchange tranfusion

shock might show bacterial septicaemia

194
Q

comps of malaria falciparum

A

cerebral malaria: seizures, coma
acute renal failure: blackwater fever, secondary to intravascular haemolysis

ards
hypogly
dic

195
Q

how would you manage falciparum malaria?

A

uncomplicated falciparum:
1st line: artemisinin-based combo therapy (acts) - artemether+ lumefantrine, artesunat+ amodiaquine, artesunate+ mefloquine, artesunate + sulfadoxine-pyrimethamine, dihydroartemisinin + piperaquine

196
Q

mc non falciparum malaria

A

vivax - central america and indian subcontinent.
then ovale (africa) and malariae.

knowlesi - south east asia

197
Q

features of non falciparum malaria

A

fever headache splenomegaly

vivax/ovale: cyclical fever every 48 hrs.
malariae: cyclical fever every 72 hours. associated with nephrotic syndrome.

ovale and vivax: hypozoite stage : relapse after tx.

198
Q

how would you treat non falciparum malaria?

A

artemisinin-based combo therapy (act) or chloroquine
if chloroquine resistant.

act avoid in pregnancy.

ovale/vivax: primaquine after acute tx with chloroquine to destroy liver hypnozoites and prevent relapse

199
Q

incubation period of malaria

A

1-4 weeks after exposure.

vivax and ovale can lie dormant upto 4 yrs

200
Q

how do you diagnose malaria

A

blood film.
edta bottle.

3 negative samples over 3 consecutive days needed to exclude.

201
Q

side effect of primaquine

A

can cause severe haemolysis in g6pd pts

202
Q

doxycline - use in malaria when to give etc

side effedcts

A

broad spect abx

se: diarrhoea , thrush. skin sensitivity to sun

take 2 days before until 4 weeks after endemic area travel.

203
Q

antimalarial meds

A

proguanil with atovaquone
doxycycline
mefloquine - psych side effects. - anxiety,dep,abnormal dreams
chloroquine with proguanil

204
Q

general advice preventing malaria

A

mosquito spray 50% DEET spray
nets and barriers
antimalarial meds

205
Q

metastatic brain cancer can spread from?

A

lung - MC
breast
bowel
skin - namely melanoma
kidney

206
Q

features of brain tumour

A

poss asx

progressive focal neurological symptoms

raised icp

207
Q

features of raised icp

A

headache contant worse at night or on waking or coughing/straining.
vomiting
papilloedema on fundoscopy (paton lines)

altered mental state
ptosis unilateral
visual field defect
3rd and 6th nerve palsy

208
Q

with papilloedema what do u see on fundoscopy?

A

blurring of optic disc margin

engorged retinal veins

haemorrhages around optic disc

paton lines - creases in retina around optic disc

loss of venous pulsation

elevated optic disc

209
Q

what is a glioma?

A

tumour of glial cells in brain/spinal cord.

support/surround neurones.

include: astrocytes,oligodendrocytes, ependymal cells.

grade 1-4.
4 (glioblastoma multiforme)

210
Q

3 types of glioma

A

astrocytoma - mc and aggressive is glioblastoma

oligodendroglioma
ependymoma

211
Q

what is a meningioma?

histology
ix
tx

A

tumour of meninges.
benign
mass effect. = raised icp

arise from arachnoid cap and typically located next to dura.

spindle cells in concentric whirls and calcified psammoma bodies.

CT: contrast enhancement
MRI

tx: RADIO/ SURGERY

212
Q

gliobastoma multiforme

prognosis
imaging
histology
tx

A

solid tumour with central necrosis and a rim that enhances contrast.

pleomorphic tumour cells border necrotic areas

surgery and postop chemo and/or radio.

dex: oedema

213
Q

what is an acoustic neuroma?

classical history of it

A

vestibular schwannoma (benign tumour of schwann cells surrounding auditory nerve)

slow growing benign

intracranial tumour.

combo of :
vertigo
hearing loss
tinnitus
absent corneal reflex

214
Q

features of acoustic neuroma

A

CN VIII :
vertigo, unilateral sensorineural hearing loss, unilateral tinnitus

cranial nerve V: absent corneal reflex

cranial nerve VII: facial palsy

215
Q

bilateral vestibular schwannoma are seen in what condition?

A

neurofibromatosis type 2

216
Q

ix of acoustic neuroma

mx

A

MRI of cerebelllopontine angle.

audiometry : only 5% of pts will have a normal one

surgery, radio.

217
Q

where do acoustic neuromas occur?

A

cerebellopontine angle

218
Q

unknown primary of metastatic disease what to do?

A

fbc u+E, lft, calcium, urinalysis, ldh

cxr
ct chest abdo pelvis
AFP , hCG

myeloma screen - if lytic bone lesions

endoscopy

psa - men
ca 125 - women with peritoneal malignancy or ascites

testicular US - men with germ cell tumour

mammography

219
Q

tell me about pituitary tumours.

press on what?

sx?

mx

A

benign
optic chiasm press - bitemporal hemianopia

cause hormone def or release excessive hormones lead to:
- acromegaly
-hyperprolactinaemia
- cushings disease
- thyroxicosis

transphenoidal surgery
radio
bromocriptine - block excess prolactin
somatostatin analogue - block excess GH

220
Q

symptoms of cerebellar disease

A

D - dysdiadokinesia, dysmetria, “drunk”
A - ataxia - limb,truncal
N - nystagmus - horizantal = ipsilateral hemisphere
I - intention tremor
S - slurred staccato speech, scanning dysarthria
H - hypotonia

221
Q

unilateral cerebellar lesions cause what signs?

A

ipsilateral

222
Q

causes of cerebellar disease

A

friedreichs ataxia

neoplastic: cerebellar haemangioma

stroke
alcohol
ms
hypothyroid
drugS: phenytoin, lead poisoning

paraneoplastic: 2 to lung cancer

223
Q

What is normal pressure hydrocephalus?

A

reversible cause of dementia in elderly.

2 to reduced csf absorption at arachnoid villi.

could be due to head injury, subarachnoid haemorrhage or meningitis

224
Q

classic triad of normal pressure hydrocephalus

A

urinary incontinence

dementia and bradyphrenia

gait abnormality

sx develop over a few months

225
Q

imaging for normal pressure hydrocephalus

A

hydrocephalus with ventriculomegaly in absence of ,or out of proportion to , sulcal enlargement

226
Q

how would you manage normal pressure hydrocephalus

comps of this tx

A

ventriculoperitoneal shunting

seizures
infection
intracerebral haemorrhage

227
Q

mc cause of hydrocephalus

A

aqueductal stenosis = insuffiency drainage of csf.

chromosomal abnormality
arachnoid cysts

arnold-chiari malformation

228
Q

presentation of normal pressure hydrocephalus

A

cranial bones in babies not fused at sutures until 2.

outward pressure on cranial bones so have enlarged and rapid increasing head circumference: occipitofrontal circumference

bulging anterior fontanelle
poor feeding and vomiting
poor tone
sleepiness

229
Q

how does a ventriculoperitoneal shunt work?

A

drain csf from ventricles to other body cavity.

usually perioneal cavity.

230
Q

what is neurofibromatosis?

A

genetic condition causing nerve tumours - neuroma

benign

type 1
type 2

231
Q

neurofibromatosis type 1

gene found on which chromosome?

genetic component

A

chr 17
codes for neurofibromin - tumour suppressor protein.

autosomal dominant

232
Q

features of neurofibromatosis type 1

A

C - cafe au lait spots (more than 15 mm diameter)
R - relative with nf1
A - axillary/inguinal freckling
BB - bony displasia, bowing of long bone or sphenoid wing dysplasia
I - iris hamartomas - lisch nodules - yellow-brown spots on iris
N - neurofibromas
G - glioma of optic pathway

233
Q

what are neurofibromas?

plexiform neurofibroma?

A

skin coloured
raised
nodules / papules

smooth regular surface.

2 or more.

plexiform : larger irregular complex with multiple cell types.

234
Q

neurofibromatosis type 2 on what chr?

tx
associations
genetic component
what it codes for

A

chr 22

codes for merlin - tumour supressor protein in schwann cells.

autosomal dominant.

associated with acoustic neuroma.

bilateral vestibular schwannoma
multiple intracranial scwannomas, meningiomas, ependymomas

surgery: resect tumour.
permanent nerve damage

235
Q

comps of neurofibromatosis

A

malignant peripheral nerve sheath

gi stromal tumour

brain tumour
spinal cord tumour
increased cancer risk - breast and leuk

vision loss
scoliosis
behaviour/ld
renal artery stenosis
migraine
epilepsy

236
Q

What is myasthenia gravis?

A

autoimmune affecting neuromuscular junction.

acetycholine receptor antibody blocks postsynaptic receptor block muscle activity.

237
Q

features of myasthenia gravis

link with what condition

A

worse with activity

improves with rest

men and women - typically women under 40 men over 60

thymomas!!
autoimmune: pernicious anaemia, autoimmune thyroid disorder, rheumtoid, sle
thymic hyperplasia in 50-70%

more in women

238
Q

2 antibodies that can cause myasthenia gravis

A

muscle specific kinase (MuSK) antibodies

Low density lipoprotein receptor related protein 4 (LRP4) antibody

239
Q

how would you investigate for myasthenia gravis?

A

single fibre electromyography : high sensitivity

ct thorax - exclude thymoma

CK normal

antibodies to acetylcholine receptors - 85% pts and 40% for anti muscle specific tyrosine kinase antibodies

tensilon test: iv edrophonium reduces muscle weakness temp - dont use because of cardiac arrhythmia risk

240
Q

mx of myasthenia gravis

A

long acting acetylcholinesterase inhibitor: pyridostigmine - 1st line

immunosuppression not started at diagnosis, but eventually need:
- prednisolone
- azathioprine, cyclosporine, mycophenolate mofetil

  • thymectomy
241
Q

how would you manage myasthenic crisis

A

plasmapheresis

iv immunoglobulins

242
Q

symptoms of myasthenia gravis

A

affect proximal muscles of limbs and small muscles of head and neck :

hard to climb stairs , stand from seat , raise hand above head

diplopia
ptosis
facial movement weakness
dysphagia
fatigue chewing
slurred speech.

243
Q

what examinations could you do for myasthenia gravis?

A

check for thymectomy scar

test for fvc

repeat blinking - ptosis

prolonged upward gaze - diplopia

repeat abduction of 1 arm 20 times - unilateral weakness

244
Q

what drugs can exacerbate myasthenia

A

penicillamine

quinidine, procainamide

beta block
lithium
phenytoin
abx: gentamicin, macrolides, quinolones, tetracycline

245
Q

what is narcolepsy

A

chronic neuro disorder affects brain ability to control sleep wake cycle

hla dr2

low levels of orexin (hypocretin) - protein responsible for controlling appetite and sleep patterns

early onset of REM sleep

246
Q

features of narcolepsy

A

teenage

hypersomnolence

cataplexy - sudden loss of muscle tone often triggered by emotion

sleep paralysis

vivid hallucinations on going sleep/waking

247
Q

ix for narcolepsy

A

multiple sleep latency EEG

248
Q

mx for narcolepsy

A

daytime stimulants - modafinil

nightime sodium oxybate

249
Q

What is chronic fatigue syndrome?

epidemiology

A

at least 3 months of disabling fatigue affecting mental and physical function over 50% of time in absence of other disease.

more in females
past psych hx isnt rf

250
Q

features of chronic fatigue syndrome

A

sleep problems: insomnia, hypersomina, unrefreshing sleep, disturbed sleep-wake cycle

headache
muscle/joint pain
painful lymph node no enlarged

sore throat
nausea
palpitations
dizziness
general malaise
physical/mental exertion

cognitive dysfunction : difficulty thinking, concentration issue, impairement of short term memory.

251
Q

how would you investigate chronic fatigue syndrome

A

screening bloods

fbc
u e
lft
glucose
tft
esr
crp
calcium
ck
ferritin
coeliac
urinalysis

252
Q

how would you diagnose chronic fatigue syndrome?

how would you manage?

A

if sx persist 3 months

refer to cfs

energy mx: self management

physical activity- if they feel ready. (and if part of cfs only)
graded exercise therapy

cbt: supportive rather than curative

253
Q

What is wernickes encephalopathy?

rarer causes

A

thiamine deficiency caused by alcoholism.

neuropsychiatric

persistent vomiting
stomach cancer
diet def

254
Q

classic triad of wernickes encephalopathy

A

opthalmoplegia
nystagmus

ataxia
encephalopathy

petechial haemorrhage in mamillary bodies and ventricular walls

255
Q

features of Wernickes encephalopathy

A

oculomotor dysfunction- nystagmus , Opthalmoplegia: lateral rectus palsy, conjugate gaze palsy

gait ataxia
encephalopathy: confusion, disorientation, indifference, inattentiveness

peripheral sensory neuropathy

256
Q

Investigations of Wernicke’s Encephalopathy

tx

A

decreased red cell transketolase

MRI

urgent replacement of thiamine

257
Q

relationship of wernickes with korsakoff

A

addition of antero and retrograde amnesia and confabulation.

258
Q

calculation of alcohol units

A

volume ml * alcohol content % /1000 = units of alcohol

259
Q

units of alcohol

A

no more than 14
spread even over 3 or more days
no more than 5 units in single day.

binge: 6 or more women. 8 or more men.

260
Q

typical triad of menieres disease

A

hearing loss
vertigo
tinnitus

261
Q

what is menieres disease?

A

long term inner ear disorder.

recurrent attacks

fullness in ear

excessive buildup of endolymph in labyrinth of inner ear - higher pressure than normal.

excessive pressure and progressive dilation of endolymphatic system.

262
Q

presentation of menieres disease

A

typical 40-50 can happen to anyone.

unilateral episode of vertigo hearing loss and tinnitus

vertigo: episodes. 20 mins.

hearing loss: fluctuates at first, then more pernanent.

tinnitus: episodes of vertigo. eventually permenant. unilaterla.

fullness
unexplained falls - without loss of consciousness
imbalance - after vertigo.

spontaneous nystagmus - during acute attack.

263
Q

how would you diagnose menieres disease

how would you manage?

A

clinical.

audiology asessment

manage sx
prophylaxis

acute: buccal/intramuscular prochlorperazine, antihistamines (cyclizine, cinnarizine, promethazine)

prophylaxis: betahistine or vestibular rehab

264
Q

what is diabetic neuropathy?

how to tx

A

sensory loss
glove and stocking

lower legs first.

1st line: amitriptyline, duloxetine, gabapentin or pregabalin

tramadol: rescue for neuropathic pain

topical capsaicin - localised neuropathic pain - post herpetic neuralgia.

pain management clinic

265
Q

what does gastroperesis occur secondary to ?

sx?

mx?

A

autonomic neuropathy

erratic bg control, bloating, vomiting

metoclopramide, domperidone, erythromycin

266
Q

what is trigeminal neuralgia?

A

pain syndrome.
severe unilateral pain.

can be idiopathic.
compression of trigeminal roots by tumours or vascular problems poss.

brief electric shock like pain - abrupt in start and finish.

267
Q

how would you manage trigeminal neuralgia?

A

1st line: carbamazepine

268
Q

red flag sx suggesting serious illness to do with trigeminal neuralgia

A

age before 40
fhx of ms
optic neuritis
deafness
sensory changes
hx of skin/oral lesions that could spread perineurally

pain only in opthalmic division of trigeminal nerve (eye socket, forehead, nose) or bilaterally

269
Q

particularly susceptible areas for trigeminal neuralgia

pain evoked by

pain remited?

A

small areas in nasolabial fold

light touch
washing
shaving
smoking
talking
brushing teeth

pain remits for variable periods

270
Q

what is horners syndrome?

A

combo of sx that happen when group of nerves known as sympathetic trunk is damaged.
eye and surrounding area on 1 side of face.

271
Q

features of horners syndrome

A

miosis - small pupil

ptosis

enophthalmos - sunken eye

anhidrosis - loss of sweating one side

272
Q

using anhidrosis to decipher where the lesion is for horners syndrome

A

face arm and trunk: central lesion

face: pre-ganglionic

no anhidrosis: post-ganglionic

273
Q

central lesion causes of horners

pre ganglionic

post ganglionic

A

stroke, syringomyelia, ms, tumour, encephalitis

pancoasts tumour , thryoidectomy, trauma, cervical rib

carotid artery dissection, carotid anerusym, cavernous sinus thrombosis, cluster headache

274
Q

heterochronic - difference in iris colour is seen in what?

A

congenital horners

275
Q

horners - what are apraclonidine drops

A

alpha adrenergic agonist

cause pupillary dilation

produces mild pupillary construction in normal pupil.

276
Q

what is gca? temporal arteritis?

what condition is it associated with

mc in who?

key comp?

A

medium and large artery vasculitis systemic.

strong link with polymyalgia rheumatica

mc: older white pts

vision loss - often irreversible

277
Q

presentation of temporal arteritis - gca

A

unilateral headache - severe around temple and forehead.

scalp tenderness - brushing hair

jaw claudication
blurred/double vision
loss of vision in untx.

temporal artery tender and thickened to palpation with reduced or absent pulsation

278
Q

what other features might you have for gca?

A

sx of pmr: shoulder and pelvic girdle pain and stiffness

systemic sx: wt loss, fatigue, low grade fever

muscle tenderness

carpel tunnel syndrome

peripheral oedema

279
Q

how would you diagnose gca?

A

raised esr - 50mm/hr

temporal artery biopsy : multinucleated giant cells (skip lesions)

CK and EMG - normal

duplex uss - hypoechoic halo sign and stenosis of temporal artery

vision testing

280
Q

what should you expect to see in vision testing in gca?

A

anterior ischaemic optic neuropathy - occlusion of posterior ciliary artery. - FUNDOSCOPY SHOWS SWOLLEN PALE DISC, BLURRED MARGINS

poss amaurosis fugax

permanent vision loss poss? - sudden

diplopia

281
Q

how would you manage gca?

A

steroids straight away.
- 40-60 mg pred daily with no visual sx or jaw claudication
- 500mg - 1000mg methylpred if above

steroid slowly weaned over 1-2 yrs.

aspirin 75mg - decrease vision loss/strokes

ppi - omeprazole - gastroprotection on steroids

bisphosphonates and calcium and vit d - bone protection

282
Q

What is meralgia paresthetica ?

A

localised sensory sx of outer thigh caused by compression of lateral femoral cutaneous nerve.

mononeuropathy - one nerve

283
Q

presentation of meralgia paresthetica?

A

abnormal sensation - dysaesthesia
and loss of sensation - anaesthesia inlateral femoral cutaneous nerve distribution.

skin of upper outer thigh affected.

burning
numbness
pins and needles
cold sensation
localised hair loss.

284
Q

in meralgia paresthetica , sx aggravated by?

A

walking
standing long time
improve when sit down.

worse with extension of hip on affected side.

285
Q

how to manage meralgia paresthetica?

A

rest
looser clothing
wt loss
physio

para
nsaids
neuropathic analgesia - amitriptyline, gabapentin, pregabalin, duloxetine

steroid/anaesthetic local nijection

surgery: decompression, transection, resection

286
Q

lateral femoral cutaneous nerve originates from?

A

l1 l2 and l3 nerve roots.

being psoas muscle

around surface of iliacus muscle

under inguinal ligament onto thigh.

287
Q

What is Cerebral Palsy?

A

non-progressive lesion motor pathways in developing brain.

disorder of movement and posture.

288
Q

causes of cerebral palsy

antenatal

intrapartum

postnatal

A

antenatal 80%
- cerebral malformation
-congenital infection (rubella, toxoplasmosis, CMV)

intrapartum 10% =
- birth asphyxia/trauma
-preterm birth

postnatal 10%
- intraventricular haemorrhage
-meningitis
-head trauma

289
Q

classifying cerebral palsy
4 different types

A

spastic 80%
- hemiplegia, diplegia or quadriplegia
-increased tone (hypertonia) and reduced function resulting from damage to UMN

dyskinetic:
- damage to basal ganglia and substantia nigra
-athetoid movements and oro-motor problems . muscle tone problems (hypertonia/hypotonia) causing the athetoid etc.

ataxic:
- caused by damage to the cerebellum with typical cerebellar signs
- problems with coordinated movement due to above.

mixed: mixed of spastic,dyskinetic and/or ataxic features.

290
Q

patterns of spastic cerebral palsy

A

monoplegia: 1 limb affected

hemiplegia: one side of body affected

diplegia: 4 limbs affected by mostly legs

quadriplegia: neck down all 4 limbs - with seizures, speech disturbance and other impairements

291
Q

what non-motor problems might a cerebral palsy patient have?

A

learning difficulties - 60%

epilepsy 30
squints 30%

hearing impairement 20

292
Q

How would you manage cerebral palsy?

A

tx spasticity:
-oral diazepam
-oral and intrathecal baclofen (muscle relaxant), botulinum toxin type A , orthopaedic surgery and selective dorsal rhizotomy.

  • anticonvulsants, analgesia prn

physio - stretch and strength muscles prevent muscle contractures.

OT
SLT
DIETICIAN - peg feeding poss?
ORTHO SURGEON - release contractures or length tendons (tenotomy)

glycopyrronium bromide: excessive drooling.
anti-epileptic - seizures

293
Q

what condition makes children at risk of developing cerebral palsy?

A

hypoxic-ischaemic encephalopathy

294
Q

signs and symptoms of cerebral palsy

A

failure to meet milestones

learning difficulty

feeding or swallowing problems

problems with coordination, speech or walking

increased/decreased tone, generally or in specific limbs

hand preference below 18 months .

295
Q

based on neuro exam what to each of these indicate:

hemi/di plegic gait

broad based gait/ataxic gait

high stepping gait

waddling gait

antalgic gait

A

UMN lesion

cerebellar lesion

foot drop/lmn lesion

pelvic muscle weakness due to myopathy

indicates localised pain

296
Q

with a UMN lesion tell me about:

inspection
tone
power
reflexes

A

muscle bulk preserved
hypertonia
slightly reduced
brisk

297
Q

with a lmn tell me about:
inspection
tone
power
reflex

A

reduced muscle bulk with fasciculations
hypotonia
dramatically reduced
reduced

298
Q

complications and associated conditions of cerebral palsy

A

learning disability

epilepsy

kyphoscoliosis

muscle contractures

hearing and visual impairment

gastro-oesophageal reflux

299
Q

what is hypoxic ischaemic encephalopathy?

A

neonates.
hypoxia during birth.

300
Q

causes of HIE

A

anything that leads to asphyxia (deprivation of oxygen) to the brain.

eg:

  • maternal shock
    -intrapartum haemorrhage
    -prolapsed cord - causing compression of the cord during birth
  • nuchal cord - where the cord is wrapped around the neck of the baby
301
Q

grading HIE

mild
moderate
severe

A

Sarnat Staging

mild:
- poor feeding, generally irritability and hyper-alert
-resolves within 24 hours
-normal prognosis

moderate:
- poor feeding, lethargic, hypotonic, seizures
-can take weeks to resolve
-up to 40% develop cerebral palsy

severe:
- reduced gcs, apnoeas, flaccid and redcued or absent reflexes
-upto 50% mortality
-upto 90% develop cerebral palsy

302
Q

when to suspect HIE

A

neonate

acidosis (ph under 7) on umbilical abg

poor Apgar score

features of mild,mod,severe HIE

evidence of multi organ failure.

303
Q

how would you manage HIE

A

supportive care with neonatal resus

optimal ventilation, circulatory support, nutrition, acid base balance and seizure tx.

therapeutic hypothermia - protect brain from hypoxic injury.

304
Q

explain therapeutic hypothermia?

how to do it

ideal temp

intention of it.

reduces the risk of ?

A

baby near/at term that have HIE.

cool core temp of baby.

transfer baby to neonatal ICU. - cooling blankets and cooling hat.

target : 33 and 34 - measure using rectal probe.

continue for 72 hours

then warm baby to normal temp over 6 hours.

reduce inflammation and neurone loss after acute hypoxic injury.

reduces risk of cerebral palsy, developmental delay, LD, blindness and death

305
Q

What is Bell’s Palsy?

A

acute unilateral idiopathic facial nerve paralysis.

unknown aetiology

herpes simplex virus poss?

peak incidence: 20-40 yrs.

condition mc in pregnant women.

306
Q

features of bell’s palsy

A

lmn facial nerve palsy - forehead affected
- in contrast, umn lesions spares the upper face

post-auricular pain (may precede paralysis)

altered taste

dry eyes
hyperacusis

307
Q

how would you manage bells palsy?

A

no tx
prednisolone only

antivirals + prednisolone

all pts: oral pred (50mg for 10 days or 60 mg for 5 days followed by 5 day reducing regime of 10mg a day ) within 72 hrs of onset.

debate about adding antiviral: alone not recommendation. - give for severe facial palsy

eye care important: prevent exposure keratopathy.
- artificial tears and eye lubricant.
- if cant close eye at bedtime tape it with microporous tape

308
Q

follow -up for bells palsy

A

if paralysis shows no improvement after 3 weeks, refer to ent

plastic surgery: long standing weakness: several months

309
Q

prognosis of bells palsy

A

full recovery 3-4 months.

if untx 15% - permanent moderate to severe weakness

310
Q

What is epilepsy?

types

A

seizure tendency.

transient episodes of abnormal electrical activity in brain.

generalised tonic-clonic
focal seizures
absence
atonic
myoclonic
infantile spasms
febrile convulsions

311
Q

What are febrile convulsions?

age of onset

mc type of seizure here

clinical features

A

seizures provoked by fever in otherwise normal kids.

6 months and 5 years.

tonic-clonic

usually occur early in viral infection as temp rises rapidly

seizures brief: last less than 5 mins

312
Q

types of febrile convulsion

simple
complex
febrile status epilepticus

A

simple:
- less than 15 mins
-generalised seizure
-typically no recurrence within 24 hours
-should be complete recovery within an hr

complex:
- 15-30 mins
-focal seizure
-may have repeat seizures within 24 hours

febrile status epilepticus :
- over 30 mins

313
Q

Mx of Febrile Convulsion

following a seizure

ongoing

A

admit if first or features of complex seizure

phone ambulance if seizure over 5 mins.

benzodiazepine rescue med: rectal diazepam or bvuccal midazolam

regular antipyretics: dont reduce chance of them occuring

314
Q

prognosis of febrile convulsions

A

risk of another one is 1 in 3. depends on:

age of onset under 18months
fever under 39
shorter duration of fever before seizure
fhx of them

315
Q

rf for developing epilepsy post febrile convulsions

A

fhx of epilepsy

complex febrile seizures.

background of neurodevelopmental disorder

if no rf@ 2.5% risk of developing it.

if kids have all 3 features 50% risk

316
Q

what is benign rolandic epilepsy?

how to ix and what does it show

prognosis

features

A

form of childhood epilepsy occurs between 4 and 12.

EEG - centrotemporal spikes

excellent prognosis - seizures stop by adolescence

seizures at night.
partial seizures (paresthesia affect face) but secondary generalisation may occur (parents may only report tonic-clonic movements)

317
Q

Using Contraception in epilepsy what factors are to be considered?

A

effect of contraceptive on effectiveness of anti-epileptic

effect of anti-epileptic on effectiveness of contraceptive

potential teratogenic effects of anti-epileptic if women becomes pregnant

318
Q

if women is taking phenytoin carbamazepine barbiturates primidone topiramate oxcarbazepine what to do?

for contraception in epileptic pt

A

ukmec 3 : the COCP and POP

ukmec 2 : implant

ukmec 1 : depo-provera, IUD,IUS

use condom

if COCP : min of 30 ug of ethinylestradiol

319
Q

for lamotrigine if women takes what to do?

contraceptionin epileptic pt

A

use condom

ukmec 3 : cocp
ukmec 1: pop, implant, depo-provera, Iud, ius

if COCP: min or 30 ug of ethinylestradiol

320
Q

what conditions are associated with epilepsy?

A

cerebral palsy: 30% have it

tuberous sclerosis

mitochondrial diseases

321
Q

what is an alcohol withdrawal seizure?

mechanism

tx

A

pt hx of alcohol excess suddenly stopped drinking.

36 hours after drink cessation.

give benzodiazepine after stopping.

chronic alcohol enhances gaba mediated inhibition in cns and inhibits nmda-type glutamate receptors.

alcohol withdrawal dose the opposite

322
Q

what are psychogenic non-epileptic seizures?

A

pseudoseizures

epileptic-like seizures but no electrical discharges.

hx of mental health or personality disorder

323
Q

define a focal seizure

A

partial seizure.- start in temporal lobe.

start in a specific area , one 1 side of brain.

varied awareness.

30 yr old women told by her husband she wakes at night, grunting sound, lip smacking, non responsive during ep. after minute falls asleep again.

focal impaired awareness - explained above.

classified into
motor: jacksonian march

non-motor : deja vu, jamais vu

or other features like aura

sx: affect hearing speech memory and emotions.

  • hallucinations
    -memory flashbacks
    -deja vu
  • doing strange things on autopilot
324
Q

generalised seizure define

A

involve networks on both sides of the brain at onset.

lose conciousness immediately.

motor: tonic clonic
non motor: absence

specific types:
-tonic clonic - grand mal
- tonic
-clonic
-typical absence - petit mal
- myoclonic: brief,rapid muscle jerks
- atonic

325
Q

unknown onset seizure - what is it?

A

unknown origin of seizure

326
Q

focal to bilateral seizure - what is it

A

starts on 1 side of brain in specific area before spreading to both lobes

previously called secondary generalised seizure

327
Q

what is infantile spasms - wests syndrome

features

eeg:

secondary to what?

prognosis

A

brief spasms in first few months of life.

  1. flexion of head, trunk, limbs - extension of arms (salaam attack) : 1-2 secs, repeat upto 50 times
  2. progressive mental handicap
  3. eeg: hypsarrhythmia
  4. 2nd to serious neuro abnormality like: TS,encephalitis, birth asphyxia) or cryptogenic

poor prognosis

328
Q

what is lennox-gastaut syndrome?

onset

eeg

tx

A

1-5 years

poss extension of infantile spasms - 50% have hx

eeg: slow spike

ketogenic diet poss

90% moderate-severe mental handicap

atypical absences, falls, jerks

329
Q

what is juvenile myoclonic epilepsy (janz syndrome)

features

tx

A

typical onset: teens, more in girls

  1. infrequent generalised seizures
  2. often in morning
  3. daytime absences
  4. sudden shock like myoclonic seizure

responds well to sodium valproate

330
Q

tell me about typical absence seizures: petit mal

onset

duration

eeg

tx

prognosis

A

onset: 4-8 years

duration : few-30 seconds. no warning, quick recovery: often many per day

eeg: 3Hz, generalised, symmetrical

sodium valproate, ethosuximide

good prognosis: 90-95% become seizure free in adolescence

331
Q

if a focal seizure happens starts in occipital lobe (visual) what happens?

A

floaters/flashes

332
Q

if a focal seizure happens in parietal lobe what happens ? (sensory)

A

paresthesia

333
Q

if a focal seizure happens in frontal lobe? (motor)

A

head/leg movements, posturing
post-ictal weakness (todd’s paresis),

jacksonian march (clonic movements travelling proximally)

334
Q

if a focal seizure starts in temporal lobe what can i expect?

A

last around 1 min - automatisms (lip smacking/grabbing/plucking) common

with/without impairement of conciousness or awareness

aura in most:
- rising epigastric sensation
-psychic or experiental phenomena like deja vu , jamais vu
-less common: hallucination (auditory,gustatory,olfactory)

335
Q

sodium valproate is associated with what issue for maternal kids?

A

neural tube defects

risk of neurodevelopmental delay in kids after maternal use of it.

DONT USE IN PREGNANCY AND WOMEN OF CHILDBEARING AGE UNLESS NECESSARY.

336
Q

which of the epileptic drugs is seen as least teratogenic or older antiepileptics?

A

carbamazepine

337
Q

phenytoin is associated with what issue?

antiepileptic

what to give with it. this is to prevent what?

A

cleft palate

vit k
last month of pregnancy
prevent clotting disorders in newborn

338
Q

is breast feeding safe for mothers taking anti-epileptics?

is there an exception to the rule?

A

yes
NO BARBITURATES

339
Q

women want to get pregnant epileptic what should they take and why?

A

folic acid 5mg per day well before pregnancy

minimise risk of neural tube defects

340
Q

briefly explain what an absence seizure is?

tx

A

in kids.

pt becomes blank stares into space and abruptly returns to normal.

unaware of surroundings, wont respond.

10-20 seconds.

stop when they get older

1st line: ethosuximide
2nd line:
m - sodium valproate
f: lamotrigine or levetiracetam

carbamazepine - exacerbate absence seizures

341
Q

how would you tx focal seizures ?

A

1st line : lamotrigine or levetiracetam

2nd line: carbamazepine, oxcarbazepine or zonisamide

342
Q

the rules are you start antiepileptics after second seizure.

in what case would you start after first?

A

pt has neuro deficit

brain imaging shows structural abnormality

EEG shows unequivocal epileptic activity.

pt or their fam or carer consider the risk of having a further seizure unacceptable

343
Q

generalised tonic clonic seizure tx?

A

male: sodium valproate

female: lamotrigine or levetiracetam

under 10, unlikely to need tx when old enough to have kids or women unable to have children can be given sodium valproate first line.

344
Q

how to atonic seizures present?

tx?

A

drop attacks.

brief lapse in muscle tone.

no more than 3 minutes.
childhood begin.

indicative of lennox-gastaut syndrome.

mx:
- m: sodium valproate
- f: lamotrigine

345
Q

how do myoclonic seizures present?

tx?

A

sudden brief muscle contractions - sudden jump.

awake during.

happen in kids as part of juvenile myoclonic epilepsy.

tx:
- m - sodium valproate
- f : levetiracetam

346
Q

rule for patient who drives on anti-epileptic

rule for patient taking other meds

women wishing to get pregnant

A

cant drive for 6 months after seizure. if established epilepsy must be fit free for 12 months.

antiepileptics induce/inhibit p450 system - varied metabolism of meds like warfarin.

teratogenic esp sodium valproate. breastfeeding safe except barbiturates.

347
Q

sodium valproate

MoA

uses

Adverse effects

A

increases GABA activity

used for generalised seizures in males

increased apetite
weight gain
alopecia: regrowth may be curly
p450 enzyme inhibitor
ataxia
tremor
hepatitis
pancreatitis
thrombocytopenia
teratogenic - neural tube defects - dont use in women of reproductive age

348
Q

carbamazepine

moa

uses

adverse effects

A

binds to sodium channels increasing their refractory period

2nd line for focal seizures

p450 enzyme inducer
dizziness and ataxia
drowsiness
leucopenia
agranulocytosis
SIADH
visual disturbances (especially diplopia)
aplastic anaemia

349
Q

lamotrigine

moa

uses

adverse effects

A

sodium channel blocker

used for variety of generalised and focal seizures

stevens johnson syndrome or DRESS SYNDROME. - life threatening skin rashes.

leukopenia

350
Q

phenytoin

moa

uses

adverse effects

A

binds to sodium channels increasing their refractory period

no longer first line due to side effect profile

p450 enzyme inducer
dizziness and ataxia
drowsiness
gingival hyperplasia, hirsutism, coarsening of facial features
megaloblastic anaemia (folate and vit d def)
peripheral neuropathy
enhanced vit d metabolism causing osteomalacia (vit d def)
lymphadenopathy

351
Q

rescue medication for epilepsy if they dont terminate spontaneously ie after 5-10 mins

A

benzodiazepines like diazepam

administer rectally or intranasally/under tongue.

if still fits: status epilepticus. - medical emergency - hospital tx required.

mx: further benzodiazepine med, infusion of antiepileptic or general anesthetic.

352
Q

ix for epilepsy

A

good history

eeg: typical patterns of it. after the second simple tonic clonic do.

MRI brain: structure of brain.

ecg - exclude heart problems

blood electrolytes - sodium, potassium, calcium , magnesium

bg: hypoglycaemia and diabetes

blood cultures, urine cultures and lp where sepsis, encephalitis or meningitis is suspected

353
Q

general advice for epileptic patients

A

take showers not baths

cautious with heights, traffic, heavy/hot/electric equipment

be very catious with swimming unless seizures well controlled and they are closely supervised.

354
Q

2 side effects of ethosuximide

A

night terrors
rashes

355
Q

mx of seizures physically

A

pt in safe position - carpeted floor

recovery position if poss

something soft under head

remove obstacles that could lead to injury

note the time at start and end

call ambulance if more than 5 mins or 1st seizure.

356
Q

what is status epilepticus?

mx:

medical options in community ?

A

med emergency

seizure lasting more than 5 mins or 2 or more seizures without regaining consciousness in interim.

ABCDE approach
secure airway
high conc ox
assess cardiac and resp function
check bg levels
iv access - insert cannula
iv lorazepam - repeated after 10 mins if the seizure continues.

if persist final step is iv phenobarbital or phenytoin. intubation and ventilation to secure airway- transfer to icu.

med options in community:
- buccal midazolam
- rectal diazepam

357
Q

What is an extradural haematoma?

caused by?

collection of blood most likely where?
what artery?

A

collection of blood between skull and dura.

trauma - low impact. - blow to head or fall.

in temporal region since the thin skull at pterion overlies the middle meningeal artery - vulnerable to injury

358
Q

classic presentation of extradural haematoma?

and why

A

pt initially loses, briefly regains and then again loses consciousness after low-impact head injury.

brief regain in conciousness termed lucid interval.
lost due to expanding haematoma and brain herniation.

as haematoma expands the uncus of temporal lobe herniates around tentorium cerebelli and pt gets:
fixed and dilated pupil due to compression of parasympathetic fibres of 3rd cranial nerve

359
Q

imaging of extradural haematoma

A

biconvex - lentiform hyperdense collection around surface of brain. limited by the suture lines of the skull.

360
Q

how would you manage extradural haematoma?

A

if no neurological deficit, cautious clinical and radiological observation is appropriate.

definitive: craniotomy and evacuation of the haematoma.

361
Q

what is a subdural haemorrhage?

A

collection of blood deep to the dural layer of meninges.

blood not within substance of brain - extra-axial or extrinsic lesion.

can be unilateral or bilateral

362
Q

classifying subdural haemorrhage by age

A

acute: sx develop within 48 hrs of injury, characterised by rapid neurological deterioration

subacute: sx manifest within days to weeks post-injury, with more gradual progression

chronic: common in elderly, develop over weeks to months. pts may not recall specific head injury

363
Q

typical presentation of subdural haematoma

A

hx of head trauma - minor to severe.

pt exhibit lucid interval followed by gradual decline in consciousness.
this pattern common in chronic sdh.

headache
confusion
lethargy

364
Q

clinical features of subdural haematoma

neurological sx

other associated features

A

altered mental status: mild confusion to deep coma. fluctuations in level of conciousness common.

focal neuro deficits: weakness on 1 side of body, aphasia, visual field defects, depending on haematoma location

headache: often localised to 1 side, worsening over time

seizures: may occur, particularly in acute/expanding haematoma.

365
Q

behavioural and cognitive changes in subdural haemorrhage

A

memory loss: especially in chronic sdh

personality change: irritability, apathy, depression

cognitive impairement: difficulty with attention, problem-solving and other executive functions

366
Q

physical examination findings in subdural haemorrhage

A

papilloedema: indicates raised icp

pupil changes: unilateral dilated pupil, especialy on side of the haematoma, indicated compression of 3rd cranial nerve.

gait abnormalities: including ataxia or weakness in 1 leg

hemiparesis or hemiplegia: reflecting the mass effect and midline shift

367
Q

talk to me about acute subdural haematoma

ct imaging

tx

A

collection of fresh blood within subdural space caused by high impact trauma. - often other brain underlying injuries.

sx depends on size of the compressive acute sdh.
could be from indental finding to severe coma and coning due to herniation.

ct: 1st line - crescentic collection not limited by suture lines.
hyperdense (bright) in comparison to brain.

large acute subdural haematomas: push on brain (mass effect) cause midline shift or herniation.

tx:
- small/incidental: observe
surgery: monitor icp and decompressive craniectomy

368
Q

tell me about chronic subdural haematoma

who can have it and why?

presentation

imaging

tx

A

collection of blood within subdural space present for weeks to months.

rupture of small bridging veins within subdural sapce rupture, slow bleeding.

elderly and alcoholic - they have brain atrophy so fragile/taut bridging veins

px:
- several week to month progressive hx of either confusion, reduced gcs or neuro deficit.

infants have fragile bridging veins to and can rupture in shaken baby syndrome.

ct:
- crescentic in shape, not restricted by suture lines and compress the brain (mass effect)
- hypodense (dark) compared to substance of brain.

  • small in size and no neuro deficit: conservatively manage
  • if pt confused and associated neuro def or severe imaging findings: - surgical decompression with burr holes.
369
Q

What is a subarachnoid haemorrhage

mc cause

A

intracranial haemorrhage , blood in subarachnoid space - deep to the subarachnoid layer of meninges.

head injury. - traumatic sah.
if not trauma its called sponteneous sah

370
Q

causes of spontaneous sah

A

intracranial aneurysm - saccular berry aneursym - 85% cases - conditions associated with this are
- htn
-adults pkd
- ehlers-danlos
-coarctation of aorta

  • arteriovenous malformation
    -pituitary apoplexy
    -mycotic (infective) aneurysms
371
Q

classic presenting features of subarachnoid haemorrhage

A

headache - sudden onset thunderclap (hit with baseball bat) - severe worst of life occipital
- peak in intensity within 1-5 mins
- poss hx of a less severe sentinel headache weeks prior to presentation

n+ v
meningism - photophobia, neck stiffness
coma
seizures
ecg - st elevation - secondary to either autonomic neural stimulation from hypothalamus or elevated levels of circulating catecholamines

372
Q

how would you ix for subarachnoid haemorrhage

A

non-contrast ct head: 1st line
- acute blood (hyperdense/bright on ct) - distributed in basal cisterns, sulci and if severe ventricular system

if ct head done within 6 hours of sx onset and is normal : dont do LP consider alternative diagnosis.

if ct head done more than6 hrs after sx onset and normal do a LP: should be done at least 12 hrs after sx to allow development of xanthochormia (rbc breakdown)
xanthochromia help distinguish true sah from traumatic tap (blood introduced by lp procedure)

csf findings: normal or raised opening pressure

if ct shows evidence of sah: refer to neurosurgery

373
Q

once i have confirmed a spontaneous sah what other ix doi need to do and why?

A

to identify causative pathology

ct intracranial angiogram - identify vascular lesion eg aneurysm or AVM

+/- digital subtraction agiogram - catheter angiogram

374
Q

important predictive factors for SAH

A

conscious level on admission
age
amount of blood visible on CT head

375
Q

how would you manage sah?

A

supportive:
- bed rest
- analgesia
-vte prophylaxis
- discontinuation of antithrombotics (reversal of anticoagulation if present)

  • vasospasm is prevented using : oral nimodipine
  • intracranial aneurysms at risk of rebleeding so require intervention within 24 hrs - coil by interventional neuroradiologists, minority need craniotomy and clipping
376
Q

complications of aneurysmal sah

A

re-bleeding: 10% cases within 1st 12 hrs.
if suspected - sudden worsening of neuro sx - repeat ct - high mortality 70%

hydrocephalus - tx temp with external ventricular drain (csf divert to bag at bedside) or long term ventriculoperitoneal shunt

vasospasm - delayed cerebral ischaemia - 7-14 days after osnet
- ensure euvolemia - normal blood vol
- consider tx with vasopressor if sx persist

hyponatremia - due to siadh

seizures

377
Q

general risk factors for all intracranial bleeds

A

head injuries
htn
aneurysms
ischaemic strokes
brain tumour
thrombocytopenia
bleeding disorder s- haemophilia

anticoag - doac or warfarin

378
Q

what is the glasgow coma scale?

total score
min score

score that is diagnostic
and what to do if so and why?

A

tool for consciousness

based on eyes verbal response and motor response.
15/15 max
min 3/15 -
8/15 - needs airway support , risk of airway obstruction or aspiration = hypoxia and brain injury

6 - obeys commands
5 - oriented, localises pain
4 - spontaneous eyes, confused verbal response, normal flexion
3 - speech, inappropriate words, abnromal flexion
2 - pain, incomprehensible sounds, extends
1 - none none none

379
Q

What is cauda equina?

presentation main

late diagnosis lead to

A

rare
where lumbosacral nerve roots that extend below the spinal cord are compressed.

any pt presenting with new/worsening lower back pain.

late diagnosis lead to permanent nerve damage results in long term leg weakness and urinary/bowel incontinence.

380
Q

causes of cauda equina

A

mc cause: central disc prolapse - occurs at l4/l5 or l5/s1

tumours: primary or mets
infection: abscess, discitis
trauma
haematoma

381
Q

presentation of cauda equina

A

low back pain
bilateral sciatica - 50% pts
reduced sensation/pins and needles in perianal area

decreased anal tone:
- good practice to check anal tone in pts with new-onset back pain.
- poor sensitivity and specificity

urinary dysfunction:
- incontinence, reduced awareness of bladder filling, loss of urge to void
- incontinence is a late sign that may indicate irreversible damage

382
Q

ix for cauda equina

mx of cauda equina

A

urgent MRI

surgent decompression

Phase 3a Finals (25 decks)

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