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Phase 3a Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

Define Essential Tremor

A

autosomal dominant condition affecting both upper limbs

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2
Q

features of essential tremor

A

postural tremor : worse if arms outstretch

improved by alcohol and rest

mc cause of titubation (head tremor)

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3
Q

management of essential tremor

A

propanolol - beta blocker - 1st line

sometimes used primidone

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4
Q

what is narcolepsy?

A

neurological disorder associated with excessive daytime sleeping

associated with HLA-DR2
associated with low levels of orexin (hypocretin) - this protein is responsible for controlling appetite and sleep patterns.

early onset of REM sleep

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5
Q

features of narcolepsy

A

typical onset: teenagers
hypersomnolence

cataplexy - sudden loss of muscle tone often triggered by emotion
sleep paralysis
vivid hallucinations on going to sleep or waking up

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6
Q

how would you investigate narcolepsy

A

multiple sleep latency EEG

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7
Q

Management of narcolepsy

A

daytime stimulants - eg MODAFINIL

nightime : sodium oxybate

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8
Q

what is normal pressure hydrocephalus?

A

reversible cause of dementia in elderly.

secondary to reduced CSF absorption at the arachnoid villi.

could be secondary to head injury, subarachnoid haemorrhage or meningitis.

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9
Q

classic triad of symptoms seen in normal pressure hydrocephalus?

A

urinary incontinence
dementia and bradyphrenia (slow in thinking and processing info)
gait abnormality - similar to PD

60% of pts will have all 3 at time of diagnosis.

sx typically develop over a few months.

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10
Q

imaging for normal pressure hydrocephalus

A

hydrocephalus with venticulomegaly in the abscence of or out of proportion to, sulcal enlargement

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11
Q

how would you manage normal pressure hydrocephalus?

A

ventriculoperitoneal shunting
10% pts that have shunts get significant comps like seizures, infection and intracerebral haemorrhages

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12
Q

What is a TIA?

A

transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia, without acute infarction.

usually lasting less than 24 hrs signs.

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13
Q

causes of tia

A

vascular cause - transient decrease in blood flow to the brain

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14
Q

clinical features of tia

A

sudden onset, focal neurological deficit - typically resolve within an hr

unilateral weakness or sensory loss
aphasia or dysarthria (difficulty forming/pronouncing words)
ataxia, vertigo, loss of balance

visual problems:
- diplopia
- homonymous hemianopia
- sudden transient loss of vision in 1 eye (amaurosis fugax)

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15
Q

what to do with patient that has acute focal neurological symptoms that resolve completely within 24 hrs of onset

A

aspirin 300mg immediately unless CI’d

assess within 24 hrs by stroke specialist

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16
Q

give 2 examples of TIA mimics

A

hypoglycaemia

intracranial haemorrhage : all pts on anticoagulants or with similar rf should be admitted for urgent imagine to exclude haemorrhage

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17
Q

what to do if a pt presents more than 7 days ago with tia?

A

see stroke specialist asap within 7 days

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18
Q

imaging for tia

A

ct - only useful if clinical suspicion of haemorrhage bc pt is taking anticoagulants

MRI - including diffusion-weighted and blood-sensitive sequences- determines the territory of ischaemia, or to detect haemorrhage or alternative pathology.

do same day as stroke specialist seen

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19
Q

medication for tia?

A

pts within 24 hrs of tia or minor ischaemic stroke , with low bleeding risk : dapt regime -
clopidogrel 300mg initial then 75 mg od + aspirin 300mg initial then 75mg od for 21 days. then continue clopidogrel
ticagrelor + clopi = alternative

if cant have DAPT:
clopi 300mg loading + 75 mg od forever.

could you PPI

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20
Q

what other drugs can you give to help with tia?

A

if AF pt. : anticoagulated as soon as intracranial haemorrhage excluded.

high intensity statin - atorvastatin 20-80 mg daily - reduce non-hdl cholesterol by more than 40%

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21
Q

why is it necessary to do carotid imaging for TIA patient?

A

atherosclerosis in carotid artery could be emboli source.

if carotid intervention, do carotid imagine within 24 hrs of assessment. - CAROTID DUPLEX USS, CT ANGIOGRAPHY OR MR ANGIOGRAPHY

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22
Q

what is the surgery for tia and when would you do it?

A

carotid endarterectomy - if pt suffered stroke/tia in carotid territory and isnt severely disabled.

if stenosis over 50%.
some have cut off of 70%

perform asap within 7 days

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23
Q

What is MND and what are the types?

A

neurological condition.
unknown cause.
presents with UMN and LMN signs.

rare before 40.

types:
amyotrophic lateral sclerosis (ALS)
primary lateral sclerosis
progressive muscular atrophy
progressive bulbar palsy

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24
Q

tell me what signs you see in ALS

A

50% of mnd cases

LMN signs in arms and UMN in legs

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25
Q

tell me what signs you see in primary lateral sclerosis (mnd)

A

umn signs only

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26
Q

tell me what signs you see in progressive muscular atrophy (MND)

A

LMN signs only

affects distal muscles before proximal

carries best prognosis

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27
Q

tell me the signs you see in progressive bulbar palsy (MND)

A

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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28
Q

features of ALS specific MND

A

assymetric limb weakness
mixed lmn and umn

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29
Q

features of mnd

A

wasting of small hand muscles/tibialis anterior common

fasciculations

absense of sensory signs/symptoms - vague sensory sx early in disease like limb pain- never sensory signs

doesnt affect external ocular muscles- eye movement

no cerebellar signs

abdominal reflexes preserved
sphincter dysfunction present (LATE FEATURE)

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30
Q

how to diagnose MND?

A

clinical

nerve conduction studies = normal motor conduction.

electromyography - reduced number of action potentials with increased amplitude.

MRI - exclude differentials : cervical cord compression and myelopathy.

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31
Q

how to manage MND?

A

Riluxole : prevents glutamate receptor stimulation. used in ALS. - prolongs life by 3 months

Resp: BIPAP - non invasive ventilation - @ night : survival benefit of 7 months

nutrition: PEG - percutaneous gastrostomy tube

prognosis: 50% pts die within 3 yrs

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32
Q

what is multiple sclerosis?

A

chronic cell-mediated autoimmune disorder characterised in CNS.

3* more common i women.
20-40 yrs old
higher latitudes more common

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33
Q

genetics associated with multiple sclerosis

A

monozygotic twin concordance = 30%

dizygotic twin concordance = 2%

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34
Q

subtypes of multiple sclerosis

A

relapsing remitting - 85% pts - acute attacks 1-2mths - followed with remission periods

secondary progressive : relapsing remitting deteriorated pts - neurological signs and sx between relpase.
65% of RR pts develop this within 15 yrs of diagnosis
gait and bladder disorders too

primary progressive : 10% pts - progressive deterioration from start. older people

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35
Q

features of multiple sclerosis

A

visual : optic neuritis, optic atrophy, internuclear opthalmoplegia, UHTOFF PHENOMENON: worsening of vision with rise in body temp.

sensory : pins/needles , numbness, trigeminal neuralgia, LHERMITTES SYNDROME: sharp pain/electric shock down spine (parasthesiae) in limbs on neck flexion forward.

motor: spastic weakness - in legs

cerebellar: ataxia (acute relapse not presenting sx) , tremor

others: urinary incontinence, sexual dysfunction intellectual deterioration

non specific: LETHARGY

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36
Q

criteria for diagnosing multiple sclerosis

A

2 or more relapses and
either

clinical evidence of 2 or more lesions
or
objective clinical evidence of 1 lesion together with reasonable historical evidence of previous relapse.

LESIONS DISSEMINATED IN TIME AND SPACE

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37
Q

investigations of multiple sclerosis

A

diagnosis requires demonstration of lesions DISSEMINATED IN TIME AND SPACE

MRI:
high signal T2 lesions.
periventricular plaques.
DAWSON FINGERS: FLAIR images : hyperintense lesions perpendicular to corpus callosum

CSF:
oligoclonal bands (and not in serum)
increased intrathecal synthesis of IgG

Visual Evoked Potentials:
- delayed but well preserved waveform

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38
Q

How would you manage an acute relapse of multiple sclerosis?

A

high dose steroids - eg oral/iv methylpredinosolone
5 days TO SHORTERN LENGTH OF ACUTE RELAPSE.

dont alter degree of recovery. (whether pt return to baseline function)

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39
Q

what are the indications for disease modifying drugs for multiple sclerosis?

A

relapsing remitting disease + 2 relapses in past 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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40
Q

what are the different drug options for reducing relapse risk in MS.

how would you administer each?

A

natalizumab - strongest evidence base for reducing relapse - iv

ocrelizumab - iv

fingolimod - oral formulation

beta-interferon - subcut/intramuscularly

glatiramer acetate - subcut

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41
Q

tell me a little bit about natalizumab (MS tx drug)

A

recombinant monoclonal antibody that antagonises alpha 4 -beta-1 integrin found on surface of leucocytes

inhibit migration of leucocytes across endothelium across blood brain barrier.

1st LINE

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42
Q

tell me a little bit about ocrelizumab (MS TX)

A

humanized anti-cd20 monoclonal antibody

like natalizumab - high efficacy

natalizumab and ocrelizumab both used 1st line.

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43
Q

tell me a little bit about fingolimod (MS TX)

A

spingosine 1-phosphate (S1P) receptor modulator

prevents lymphocytes leaving lymph nodes

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44
Q

tell me a little bit about beta-interferon (MS TX)

A

not as effective as alternatvie disease modifying drugs like natalizumab and ocrelizumab

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45
Q

tell me a little bit about glatiramer acetate (MS TX)

A

immunomodulating drug - acts as immune decoy.

older drug - less effective than 1st line drugs

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46
Q

how would you treat fatigue in MS patients?

A

AMANTADINE

exclude anaemia, thyroid and depression first though.

other options: mindfulness training, CBT

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47
Q

how would you treat spasticity in MS patient?

A

baclofen and gabapentin : 1st LINE

other options:
diazepam, dantrolene and tizanidine

physio is important

cannabis and Botox - under evaluation

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48
Q

how would bladder dysfunction in MS pts?

A

could be urgency incontinence or overflow

GET USS to assess bladder emptying - anticholinergics could worsen sx in some pts

if signifcant residual volume - intermittent self catherisation

if no significant residual volume - anticholinergics - may improve urinary frequency

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49
Q

how would you treat oscillopsia (visual fields oscillate) in MS pts?

A

GABAPENTIN - 1ST LINE

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50
Q
A
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51
Q

features of duchenne muscular dystrophy

A

progressive proximal muscle weakness from 5 years

calf pseudohypertrophy (fat/connective tissue replacing muscle tissue so weak)

GOWERS sign: child uses arms to stand up from squatted position

30% of pts - intellectual impairement

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52
Q

how to investigate duchenne muscular dystrophy?

A

raised creatinine kinase

genetic testing replaced muscle biopsy for definitive diagnosis

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53
Q

how to manage duchenne muscular dystrophy?

A

largely supportive

no effective tx

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54
Q

prognosis of duchenne muscular dystrophy?

A

most children cant walk by 12 yrs old

patients typically survive to approx 25-30

associated with dilated cardiomyopathy

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55
Q

most common heart lesion associated with duchenne muscular dystrophy

A

dilated cardiomyopathy

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56
Q

tell me a little about becker muscular dystrophy?

A

develops after 10 yrs old

intellectual impairment much less common

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57
Q

talk to me about the genetics behind dystrophinopathies (duchenne and becker)

A

X LINKED

MUTATION IN GENE ENCODING DYSTROPHIN, dystrophin GENE ON Xp21.

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58
Q

what is dystrophin?

A

part of large membrane associated protein in muscle.

connects muscle membrane to actin. - part of muscle cytoskeleton.

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59
Q

genetic mutation in duchenne muscular dystrophy vs becker muscular dystrophy?

A

duchenne: frameshift mutation resulting in 1 or both of binding sites lost leading to severe form

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

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60
Q

what is myotonic dystrophy?

A

inherited myopathy.

features develop at 20-30 yrs old.

affects skeletal, cardiac and smooth muscle.

2 types: DM1 AND DM2.

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61
Q

genetics of myotonic dystrophy

A

autosomal dominant

trinucleotide repeat disorder

DM1 : CTG repeat and the end of DMPK (dystrophia myotonica-protein kinase) gene on chromosome 19

DM2: repeat expansion of ZNF9 gene on chromosome 3.

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62
Q

key differences between DM1 AND DM2 - myotonic dystrophy?

A

dm1: DMPK gene on chr 19. DISTAL WEAKNESS more prominent

dm2: ZNF9 gene on chr3. Proximal weakness more prominent. severe congenital form not seen.

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63
Q

general features of myotonic dystrophy

A

myotonic facies, long, haggard appearance. atrophy of facial muscles and narrow face.

frontal balding

bilateral ptosis - eye lids drop down.

cataracts

dysarthria

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

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64
Q

What is huntingtons disease??

A

neurodegenerative condition inherited.

progressive. incurable.

results in death 20 yrs after initial symptoms develop.

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65
Q

genetics of huntingtons disease

A

autosomal dominant

trinucleotide repeat disorder : repeat expansion of CAG - phenomenon of anticipation seen - disease presents earlier age in successive generations

results in degeneration of cholinergic and gabaergic neurons in the striatum of the basal ganglia

due to defect in huntingtin gene on chromosome 4

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66
Q

features of huntingtons disease

A

typically after 35

chorea

personality changes - irritability, apathy, depression , intellectual impairement

dystonia

saccadic eye movement - quick shifts of both eyes that change point of fixation

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67
Q

how would you manage huntingtons disease

A

no tx.

supportive:
genetic counselling
physio - mobility improve , joint function and prevent contractures

SALT speech language therapy

tetrabenazine - chorea
antidepressant - ssri - depression

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68
Q

what is a brain abscess?

A

pus filled swelling in brain .

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69
Q

causes of brain abscess

A

extension of sepsis from middle ear or sinuses.

trauma

surgery to scalp

penetrating head injuries

embolic events from endocarditis.

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70
Q

presenting symptoms of brain abscess

A

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

headache - dull, persistent

fever - possibly absent - usually not swinging pyrexia (large temp fluctuations) seen with abscesses at other sites.

focal neurology - oculomotor nerve palsy or abducens nerve palsy secondary to raised intracranial pressure

raised intracranial pressure:
nausea
papilloedema
seizures

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71
Q

if a patient has headache fever and focal neurology what should i think?

A

brain abscess

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72
Q

if someone says oculumotor nerve palsy what should i think?

A

drooping of eyelid - ptosis.

difficulty moving eye in certain directions

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73
Q

if someone says abducens nerve palsy what should i think?

A

difficulty moving affected eye laterally - inward deviation - esotropia

double vision.

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74
Q

investigations for brain abscess

A

imaging with CT scan

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75
Q

how would you manage brain abscess

A

surgery - craniotomy - abscess cavity debrided
abscess might reform because head is closed following abscess drainage

iv abx: iv 3rd gen cephalosporin + metronidazole

intracranial pressure mx : dexamethasone

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76
Q

meningitis organisms in children

A

neonatal to 3 months:
group B streptococcus : usually acquired from mother at birth. more common in low birth weight babies and following prolonged rupture of membranes. breaking of the amniotic sac more than 18-24 hours before delivery

1month to 6 yrs -
neisseria meningitidis - meningococcus
streptococcus pneumoniae - pneumococcus
haemophilus influenzae

greater than 6 years:
neisseria menigitidis - meningococcus
streptococcus pneumoniae - pneumococcus

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77
Q

tell me a little bit about meningitis vaccine

A

children always immunised against serotype A,C.

so B became mc cause of bacterial meningitis in UK.

BEXSERO released. - added to nhs immunisation
2 months
4 months
12-13 months.

also available to pts @ high risk of meningococcal disease like ppl with asplenia, splenic dysfunction or complement disorder.

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78
Q

symptoms of meningitis

A

headache
fever
n+v
photophobia
drowsiness
seizures

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79
Q

signs of meningitis

A

neck stiffness
purpuric rash - particularly with invasive meningococcal disease

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80
Q

csf findings for bacterial meningitis

appearance
glucose
protein
white cells

A

cloudy appearance

glucose : Low - <1/2plasma

Protein: high >1g/L

White cells: 10-5000 polymorphs/mm3

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81
Q

csf findings for viral meningitis

appearance
glucose
protein
white cells

A

clear/cloudy appearance

glucose: 60-80% of plasma glucose

protein: normal/raised

white cells: 15-1000 lymphocytes/mm3

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82
Q

csf findings in tuberculous meningitis

appearance
glucose
protein
white cells

A

slight cloudy, fibrin web

glucose: low <1/2 plasma

protein : high >1 g/L

white cells: 10-1000 lymphocytes/mm3

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83
Q

for detection of tuberculous meningitis what is used?

A

PCR - sensitivity 75%

ziehl-neelsen stain only 20% sensitive.

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84
Q

for viral meningitis, what are the exceptions to the rule for csf findings of glucose?

A

mumps and herpes encephalitis - has low glucose level in some cases.

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85
Q

why might it be hard to diagnose meningitis clinically?

A

classical signs are often absent in infants in bacterial meningitis

sx can progress rapidly and often become more specific and severe with time.

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86
Q

causative agents of meningitis

A

0-3 months:
group B streptococcus - mc in neonates
e.coli
listeria monocytogenes

3mnths- 6yrs:
neisseria meningitidis
streptococcus pneumonia
haemophilus influenzae

6yrs - 60 yrs:
neisseria meningitidis
streptococcus pneumonia

> 60yrs:
streptococcus pneumoniae
Neisseria meningitidis
listeria monocytogenes

immunosuppressed:
listeria monocytogenes

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87
Q

complications of meningitis

A

seizures
focal neurological deficit

infective: sepsis, intracerebral abscess
pressure: brain herniation, hydrocephalus

sensorineural hearing loss (MC) - inner ear/auditory nerve damage = difficulty hearing faint sounds and understanding speech.

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88
Q

what are patients with meningococcal meningitis at risk of

A

waterhouse - friderichsen syndrome - adrenal insufficiency secondary to adrenal haemorrhage

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89
Q

what would be some contraindications to carrying out a lumbar puncture for meningitis?

A

any signs of raised ICP

focal neurological signs - impairments in the function of the brain, spinal cord, or nerves that affect a specific area of the body

papilloedema - SWELLING OF OPTIC DISK DUE TO INCREASE ICP

significant bulging of fontanelle

disseminated intravascular coagulation

signs of cerebral herniation

PATIENTS WITH MENINGOCOCAL SEPTICAEMIA - DO BLOOD CULTURES AND PCR INSTEAD.

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90
Q

how to manage meningitis

A
  1. abx - if under 3months: iv amoxicilllin (or ampiciliin) + iv cefotaxime
    if over 3 months: iv cefotaxime (or ceftriaxone)
  2. steroids - NOT FOR CHILDREN UNDER 3 MONTHS.
    dexamethasone if lumbar puncture shows:
    - frankly purulent csf
    -csf wbc over 1000/microleter
    - raised csf wbc with protein conc over 1g/L
    - bacteria on gram stain
  3. fluids - treat any shock eg with colloid
  4. cerebral monitoring - mechanical ventilation if resp impairement
  5. public health - notify and abx prophylaxis of contacts.
    GIVE CIPROFLOXACIN OVER RIFAMPICIN.
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91
Q

WHAT IS MENINGITIS

A

INFLAMMATION OF LEPTOMENINGES AND CSF IN SUBARACHNOID SPACE.

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92
Q

what is viral meningitis

A

inflammation by viral agent in leptomeninges

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93
Q

causes of viral meningitis

A

non-polio enteroviruses eg - coxsackie virus, echovirus

mumps

herpes simplex virus - HSV, cytomegalovirus (CMV), herpes zoster viruses

HIV
MEASLES

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94
Q

risk factors of viral meningitis

A

patients at extremes of age - under 5 and elderly

immunocompromised - eg patients with renal failure with diabetes

iv drug users.

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95
Q

clinical presentation of viral meningitis

A

headache
neck stiffness
photophobia - often milder than that of bacterial meningitis
confusion
fever

less common:
focal neurological deficit on exam
seizures: suggests meningoencephalitis

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96
Q

investigations for viral meningitis

A

csf :
opening pressure - 10-20cm3 h20
cell count - 10-300 cells/uL
cell diff: lymphocytes
glucose : 2.8-4.2 mmol/l or 2/3 serum glucose mmol/L
protein : 0.5-1 g/dL (0.15-0.45 g/L)

viral pcr - underlying organism

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97
Q

how to manage viral meningitis

A

whilst waiting on lumbar puncture: supportive . if you think bacterial/encephalitis then start broad spec abx with cns penetration : CEFTRIAXONE AND ACICLOVIR IV. particularly in elderly, immunocompromised

viral meningitis self limiting, sx improving over the course of 7-14 days. comps are rare in immunocompetent patients.

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98
Q

what to use if the patient is suspected of having meningitis secondary to HSV?

A

Aciclovir

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99
Q

managing suspected bacterial meningitis?

initial approach in hospital

A

if patient in gp : give IM benzylpenicillin as long as it dont delay hospital transit.

ABC - initially
airway
breathing
circulation
disability : gcs, focal neurological signs: seizures, papilloedema

senior review if warning signs are present

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100
Q

give some warning signs of meningitis as per investigation/mx of it (bacterial)

A

rapidly progressive rash

poor peripheral perfusion

rr : less than 8 or over 30/min or pulse rate under 40 or over 140/min

ph less than 7.3
wbc less than 4*10 power of 9/L or lactate over 4 mmol/L

gcs under 12 or drop of 2 pts

poor response to fluid resus.

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101
Q

in what circumstances should a lumbar puncture be delayed?

A

signs of severe sepsis or rapidly evolving rash

severe respiratory/cardiac compromise

significant bleeding risk

signs of raised icp:
focal neurological signs
papilloedema
continuous/uncontrolled seizures
GCS 12 OR MORE.

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102
Q

how would you manage bacterial meningitis patients without indication for delayed LP?

A

iv access = take bloods and blood cultures
NO NEED FOR CT

lumbar puncture : if you cant in 1st hr, iv abx after blood cultures

iv abx: 3mnths-50yrs : cefotaxime (or ceftriaxone)
over 50: cefotaxime (or ceftriaxone) + amoxicillin (or ampicillin) for adults.

iv dexamethasone (consider adjuncting with it if pneumoccocal meningitis). start before or with 1st dose of antibacterial. not later than 12 hrs after.

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103
Q

in what case would you avoid iv dexamethasone in bacterial meningitis pt ?

A

septic shock
meningococcal septiciaemia

immunocompromised

meningitis following surgery

104
Q

how would you manage patients with bacterial meningitis that have signs of raised intracranial pressure?

A

critical care input

secure airway + high flow oxygen

iv acess= take blood + blood cultures
iv dexamethasone
iv abx cefotaxime or ceftriaxone
arrange neuroimagine

105
Q

how would you manage bacterial meningitis patients that have signs of severe sepsis or rapidly evolving rash?

A

critical care input

secure airway + high flow o2
iv access = bloods+ blood culture
iv fluid resus
iv abx

106
Q

when you take bloods for bacterial meningitis pt, what should they include?

A

fbc
renal function
glucose
lactate
clotting profile
crp

107
Q

if an LP is done for suspected bacterial meningitis , what should the csf be tested for?

A

glucose protein microscopy and culture
lactate
meningococcal and pneumococcal PCR
enteroviral, herpes simples and varicella zoster PCR

consider ix for tb meningitis

108
Q

other than blood and an LP what tests could be useful in a bacterial meningitis suspected pt?

A

blood gases
throat swab for meningococcal culture

109
Q

pt has been found to have bacterial meningitis : pneumoccal meningitis. what is the treatment?

A

iv cefotaxime (of ceftriaxone)

110
Q

pt has been found to have bacterial meningitis, specifically meningococcal meningitis. how would you treat?

A

iv benzylpenicillin or cefotaxime (or ceftriaxone)

111
Q

pt has been found to have bacterial meningitis specifically meningitis caused by haemophilus influenze. how to treat?

A

iv cefotaxime (of ceftriaxone)

112
Q

patient has bacterial meningitis, caused by listeria. how to treat?

A

iv amoxicillin (or ampicillin) + gentamicin

113
Q

who should prophylaxis of meningitis (bacterial) be offered to?

how long does risk last for?

A

households and close contacts of pts with meningococcal meningitis.

exposed to resp secretion , regardless of closeness.

risk is highest in 1st 7 days but stays for 4 weeks.

114
Q

what is the prophylactic tx for close contacts?

A

give within 7 days before onset.

oral ciprofloxacin or rifampicin.
cipro only requires 1 dose.

meningoccocal vaccination offered to close contacts when serotype results are available including booster doses.

pneumoccocal meningitis: no prophylaxis needed. only if cluster of cases give abx.

115
Q

what is guillain-barre syndrome?

A

immune mediated demyelination of peripheral nervous system often triggered by infection

CAMPLYOBACTER JEJUNI

116
Q

what is the pathogenesis of guillain-barre syndrome?

A

cross reaction of antibodies with gangliosides in the peripheral nervous system.

correlation between anti-ganglioside antibody (anti-GM1) and clinical features has been demonstrated.

anti- GM1 antibodies in 25% of pts.

117
Q

what is miller fisher syndrome?

A

variant of guillain-barre syndrome

associated with:
opthalmoplegia
areflexia
ataxia.

eye muscles typically affected first.

presents with descending paralysis rather than ascening.

anti- GQ1B antibodies in 90% of cases.

118
Q

what initial symptoms will you notice with guillain- barre syndrome?

A

65% pts experience back/leg pain in initual stages

119
Q

characteristic features of gullain-barre syndrome

A

progressive symmetrical weakness of all the limbs.

ASCENDING. - legs affected first.

reflexes reduced/absent

sensory symptoms tend to be mild (distal paresthesia) - very few sensory signs

120
Q

general other features of guillain- barre syndrome

A

history of gastroenteritis

respiratory muscle weakness

cranial nerve involvement: diplopia, bilateral facial nerve palsy, oropharyngeal weakness common

autonomic involvement: urinary retention, diarrhoea

less common: papilloedema: secondary to reduced csf resorption

121
Q

what investigations would you do for guillain-barre syndrome?

A

lumbar puncture- rise in protein with normal wbc (ALBUMINOCYTOLOGIC DISSOCIATION) - found in 66%

nerve conduction studies -
decreased motor nerve conduction velocity - due to demyelination
prolonged distal motor latency
increased F wave latency

122
Q

how would you manage guillain barre syndrome?

A

supportive

vte prophylaxis - pe leading cause of death

iv immunoglobulines - IVIG - 1st line

plasmapharesis - alternative to 1st line

severe cases might have resp failure: intubate, ventilate, admit to icu.

123
Q

prognosis of guillain-barre

A

months to years.

continue regaining function 5 yrs after acute illness.

most get full recovery or have minor sx.
some have significant disability.

mortality 5% - due to resp or cardio complications

124
Q

features of encephalitis

A

fever headache psychiatric symptoms, seizures vomiting

focal features: aphasia (language disorder)

peripheral lesions (cold sores) - have no relation to Prescence of HSV encephalitis

125
Q

pathophysiology of encephalitis

A

hsv-1 responsible for 95% of cases in adults

typically affects temporal and inferior frontal lobes

126
Q

how would you investigate encephalitis?

A

csf: lymphocytosis, elevated protein,
PCR FOR HSV,VSV AND ENTEROVIRUSES.

neuroimaging:
- medial temporal and inferior frontal changes (eg petechial haemorrhages)
- normal in 1/3 of pts
- MRI is better

EEG:
- lateralised periodic discharges at 2 Hz

127
Q

how would you manage encephalitis

A

IV Aciclovir - started in all cases of suspected encephalitis

128
Q

ct head shows temporal lobe changes, and pt has temporal lobe signs like aphasia. what should i think

A

herpes simplex encephalitis

129
Q

prognosis of encephalitis

A

depends on if aciclovir is commenced early.

if started promptly, mortality 10-20%.

untreated it goes to 80%.

130
Q

what is shingles?

A

herpes zoster infection.

acute unilateral painful blistering rash caused by reactivation of varicella-zoster virus (vzv).

after primary infection - chicken pox (VZV) - the virus lies dormant in the dorsal root or cranial nerve ganglia.

131
Q

risk factors of shingles

A

increasing age

HIV - strong risk factor.
15 times more common

other immunosuppressive conditions (eg steroids, chemo)

132
Q

most commonly affected dermatomes for shingles

A

T1-L2

133
Q

features of shingles

A

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

rash:
- initially erythematous , macular rash over affected dermatome
- quickly becomes vesicular
- well demarcated by dermatome. doesnt cross midline. some “bleeding” into adjacent areas might be seen.

134
Q

diagnosis of shingles

A

clinical

135
Q

management of shingles

A

tell pts its infectious! - avoid pregnant and immunosuppressed. infectious until vesicles cruster over, 5-7 after onset

analgesia:
para and nsaids = 1st line
if not then : neuropathic agent : amitriptyline
oral corticosteroids - consider in 1st 2 weeks in immunocompetent adults with localised shingles if pain is severe and not responding to above.

antivirals - GIVE WITHIN 72 HOURS unless if pt. is under 50 and has “mild” truncal rash associated with mild pain and no underlying risk factors.

examples:
aciclovir, famciclovir, valaciclovir

136
Q

give a benefit of prescribing antivirals for shingles pt

A

reduced incidence of post-herpetic neuralgia - particularly in older people

137
Q

complications for shingles

A

post-herpetic neuralgia:
- most common complications
- more common in older pts
- affects between 5-30% of pts depending on age.
- most commonly resolves with 6 months but may last longer

herpes zoster ophthalmicus - (shingles affecting affecting the ocular division of trigeminal nerve)

herpes zoster oticus (Ramsay hunt syndrome)- may results in ear lesions and facial paralysis

138
Q

define malaria

A

a disease caused by plasmodium protozoa which is spread by the female anopheles mosquito.

139
Q

4 different species that cause malaria

A

plasmodium falciparum
plasmodium vivax
plasmodium ovale
plasmodium malariae

140
Q

which plasmodium for malaria causes most severe malaria?

A

plasmodium falciparum.

after that vivax is most common, causes “benign” malaria

141
Q

protective factors for malaria

A

sickle-cell trait.

g6pd deficiency
hla-b53
absense of duffy antigens (proteins on surface of rbc involved in entry of malaria vivax into cells)

142
Q

clinical features of the most common and severe type of malaria : falciparum

A

sx like flu. (malaise, headache and myalgia)

classic triad: paroxysms of fever, chills and sweating.

sx occur every 48 hrs. - correspond to erythrocytic cycle of plasmodium falciparum parasite.

fever high and intermittent. - poss rigors too.

143
Q

general features of falciparum malaria

A

fever: cyclical. poss sweating and rigors

gi: anorexia, n+v + abdo pain. diarrhoea (sometimes in kids), poss mild jaundice and pruritus

resp: cough, poss mild tachypnoea.

msk: general body aches and joint pain

neuro: headache prominent and severe. dizziness and sleep disturbance.

cv: tachycardia poss, hypotension typical of more severe malaria.

haem: thrombocytopenia, can happen in absence of severe disease. mild anaemia poss

renal: aki associated with severe malaria. non severe could have mild to moderate increases in creatinine or blood urea nitrogen levels.

144
Q

features of severe falciparum malaria

A

schizonts on a blood film

parasitaemia over 2%

hypoglycaemia

acidosis

temperature over 39

severe anaemia

complications (another card)

145
Q

complications of falciparum malaria

A

cerebral malaria: seizures, coma

acute renal failure: blackwater fever, secondary to intravascular haemolysis

acute resp distress syndrome (ARDS)

hypoglycaemia

disseminated intravascular coagulation (DIC)

146
Q

how would you manage uncomplicated falciparum malaria

A

strains resistant to chloroquine are prevalent in some parts of asia and africa

artemisinin-based combination therapy: 1st line

eg: arthemer + lumefantrine.
artesunate + amodiaquine
artesunate + mefloquine
artesunate + sulfadoxine- pyrimethamine
dihydroartemisinin + piperaquine

147
Q

how would you treat severe falciparum malaria?

A

if parasite count over 2% then parenteral tx regardless of clinical state.

iv artesunate better than iv quinine

if parasite count over 10% - exchange transfusion consider

shock might indicate coexistent bacterial septicaemia = malaria rarely causes haemodynamic collapse

148
Q

most common nonfalciparum malaria

A

vivax

then ovale and malariae

149
Q

where is non falciparum vivax found

ovale?

knowlesi?

A

central america

indian subcontinent

ovale from africa

knowlesi - causes clinical pathology - south east asia

150
Q

features of non falciparum malaria

A

fever headache splenomegaly

vivax/ovale: cyclical fever every 48 hrs
malariae: cyclical fever every 72 hrs. nephrotic syndrome association

151
Q

why might ovale and vivax malaria relapse after treatment

A

they have a hypnozoite stage

152
Q

treatment of non falciparum malaria

A

if chloroquine sensitive then artemisinin based combo therapy or chloroquine

if chloroquine resistant then defo ACT. avoid in pregnancy

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

153
Q

what is acoustic neuroma? (vesitbular schwannoma)

A

accounts for 5% of intracranial tumours and 90% of cerebellopontine angle tumours.

154
Q

classic history of acoustic neuroma

A

combo of vertigo, hearing loss, tinnitus with absent corneal reflex.

155
Q

features of acoustic neuroma can be predicted by the affected cranial nerves. tell me about this.
cranial nerve 8,5,7

A

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

CN V : absent corneal reflex

CN VII: facial palsy

156
Q

in what condition would you see bilateral vestibular schannomas (acoustic neuromas)

A

neurofibromatosis type 2

157
Q

what to do if suspected vestibular schwannoma (acoustic neuroma)?

include investigations

A

refer urgent to ENT. some tumours are slow, benign and often observed initially.

MRI of cerebellopontine angle.

audiometry - only 5% pts will have normal audiogram.

158
Q

management of acoustic neuroma (vestibular schwannoma)

A

surgery

radiotherapy

or observation

159
Q

what is a subdural haemorrhage?

A

colleciton of blood deep to the dural layer of meninges.

its not within the substance of the brain so its called “extra-axial” or “extrinsic” lesion.

can be uni/bi lateral.

160
Q

how can you classify subdural haematoma:

acute
sub acute
chronic

A

in terms of its age

acute: sx develop within 48 hrs of injury - rapid neurological deterioration

subacute: sx manifest within days to weeks post-injiury - gradual progression

chronic: common in elderly - weeks to months. - pts might not remember specific head injury

161
Q

typical presentation of subdural haematoma

A

hx of head trauma minor-severe.

lucid interval - temp recovery of gcs after initial loss. - then gradual decline in conciousness. (very common in chronic sdh)

headache
confusion
lethargy

162
Q

neurological symptoms of subdural haemorhage

A

altered mental status: mild confusion - deep coma. fluctuations in level of gcs common.

focal neurological deficit: weakness on 1 side of body, aphasia (ability to speak), visual field defects, depending on haematoma location.

headache : often localised to 1 side, worsening over time.

seizures: possible, more chance in acute/expanding haematoma.

163
Q

what physical examination findings would you find in subdural haematoma patient?

A

papilloedema: shows raised ICP

pupil changes: unilateral dilated pupil (side of haematoma)- shows compression of 3rd cranial nerve

gait abnormalities: including ataxia or weakness in 1 leg.

hemiparesis(partial paralysis 1 side of body)/hemiplegia (full paralysis 1 side of body): reflecting mass effect and midline shift

164
Q

what behavioural and cognitive changes would you see in subdural haemorrhage patient?

A

memory loss : esp in chronic SDH

personality changes: irritability, apathy, depression

cognitive impairment: attention difficulty, problem-solving, other executive functions

165
Q

general features of subdural haemorrhage

A

n+v : secondary to raised ICP

drowsiness: progressing to supor and coma in severe cases.

signs of icp : bradycardia, hypertension, respiratory irregularities (cushings triad)

166
Q

tell me about an acute subdural haematoma

A

collection of blood in subdural space. high impact trauma. possible underlying brain injuries too.

spectrum of sx and presentation depends on size of compressive acute subdural haematoma.

ranges from incidental finding in trauma to severe coma and coning due to herniation.

167
Q

what investigation to do for acute subdural haematoma? and findings?

A

CT : 1st line

crescentic collection not limited by suture lines.

hyperdense (bright) compared to brain, .

large acute subdural haematoma will push on the brain (mass effect) and cause midline shift/herniation.

168
Q

how to manage acute subdural haematoma?

A

small/incidental acute subdural: conservatively observe.

surgery: monitor of ICP and decompressive craniectomy

169
Q

tell me a little bit about chronic subdural haematoma

A

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

rupture of small bridging veins in subdural space - slow bleeding.

170
Q

who is at risk of chronic subdural haematoma?

why?

A

elderly and alcoholic pts.

they have brain atrophy - so fragile or taut bridging veins.

infant: shaken baby syndrome. fragile bridging veins

171
Q

presentation of chronic subdural haematoma

A

several week to month progressive hx of either confusion, reduced gcs or neurological deficit.

172
Q

how would you investigate chronic subdural haemorrhage?

findings

A

CT - crescentic in shape not restricted by suture lines and compress the brain (mass effect)

different to acute bc:
hypodense (Dark) compared to substance of brain

173
Q

management of chronic subdural haemorrhage

A

if incidental finding or small in size with no neurological deficit : conservative mx. hope itll dissolve with time.

if pt confused, has associated neurological deficit or has severe imagine findings: SURGICAL DECOMPRESSION WITH BURR HOLES. (burr hole evacuation)

174
Q

what is a subarachnoid haemorhage?

A

intracranial haemorrhage.

blood within subarachnoid space - deep to subarachnoid layer of meninges.

175
Q

causes of subarachnoid haemorrhage

A

most common : head injury (traumatic SAH)

if not trauma then spontaneous.

spontaneous:
- intracranial aneurysm (saccular “berry” aneurysm) - 85%.
- arteriovenous malformation
- pituitary apoplexy
- mycotic (infective) aneurysm

176
Q

conditions associated with berry aneurysms (subarachnoid haemorrhage)

A

htn
adult polycystic kidney disease (ADPKD)
ehlers-danlos syndrome
coarctation of aorta

177
Q

classic presenting features of subarachnoid haemorrhage

A

headache - sudden onset, thunderclap, severe(worst of life), occipital, typically peaks in intensity within 1-5 mins.
could be hx of less-severe sentinel headahce weaks prior.

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

178
Q

investigations of subarachnoid haemorrhage

A

non-contrast CT head : 1st line. - acute blood hyperdense bright. - distributed in basal cisterns, sulci and in severe case ventricular system.

if ct head done within 6hrs and normal - no LP. consider alternative diagnosis

if ct head done more than 6 hrs after and is normal - do LP. LP at least 12 hrs after sx start to allow xanthochromia to develop. ( result of rbc breakdown)

if ct shows evidence of SAH: refer to neurosurgery.

179
Q

what does xanthochromia help to distinguish in LP for SAH patient?

A

traumatic tap (blood introduced by LP procedure)

180
Q

what csf findings are consistent with SAH?

A

xanthochromia

normal or raised opening pressure

181
Q

what investigations to do once spontaneous SAH is confirmed?

why?

A

identify causative pathology that needs urgent tx

CT intracranial angiogram - identify vascular lesion (aneurysm or AVM)

+/- digital subtraction angiogram (catheter angiogram)

182
Q

how would you manage a confirmed aneurysmal subarachnoid haemorrhage?

A

supportive: bed rest, analgesia, VTE prophylaxis, discontinue antithrombotics (reversal of anticoagulation if present)

oral nimodipine: prevent vasospasm

COIL: intracranial aneursym - bc of risk of bleeding. small minority need craniotomy and clipping. - WITHIN 24 HRS

182
Q

complications of aneurysmal SAH

A

seizures
re-bleeding - 10% in 1st 12hrs. if suspected so sudden worsened sx then repeat CT. high morality 70%

hydrocephalus - temp tx with external ventricular drain (csf diverted into bag at bedside) - long term : ventriculoperitoneal shunt)

vasospasm: (delayed cerebral ischaemia) - typically 7-14 days after onset.

hyponatremia - typically due to SIADH

183
Q

what would you do to treat vasospasm as comp of aneurysmal SAH?

A

ensure euvolemia - normal blood volume

consider tx with vasopressor if sx persist.

184
Q

name 3 important predictive factors in SAH

A

age
amount of blood on CT head
conscious level on admission

185
Q

what is an extradural haematoma?

where is the collection usually?

A

collection of blood between skull and dura.

almost always trauma - most typically low impact. (blow to head/fall).

collection: temporal region because the thin skull at pterion overlies the MIDDLE MENINGEAL ARTERY = vulnerable to injury.

186
Q

classic presentation of patient with extradural haematoma

A

loses,gains,loses gcs after low impact injury. (brief regain is called lucid interval)

you lose it again due to expanding haematoma and brain herniation.

187
Q

treatment of extradural haematoma

A

if no neurological deficit: cautious clinical and radiological obs appropriate.

definitive: craniotomy and evacuation of haematoma

188
Q

imaging of extradural haematoma

A

ct

biconvex (or lentiform) hyperdense collection around surface of brain.

limited by suture lines of the skull.

189
Q

explain why you lose the lucid interval in patient with extradural haemorrhage/haematoma?

A

expanding haematoma and brain herniation.

As haematoma expands the uncus of temporal lobe herniates around tentorium cerebelli

pt develops fixed and dilated pupil due to compression of parasympathetic fibers of 3rd cranial nerve.

190
Q

what is a febrile convulsion?

A

seizure provoked by fever in otherwise normal kids.

6months - 5 years
3% of kids

191
Q

clinical features of febrile convulsions

A

usually occur early in viral infection as temp rises rapidly

brief, lasting less than 5 mins

most commonly tonic-clonic

192
Q

types of febrile convulsions

A

simple : under 15 mins. generalised seizure. typically no recurrence within 24 hrs. should be complete recovery within nan hr.

complex: 15-30 mins. focal seizure. might have repeat seizures within 24hrs

febrile status epilepticus : over 30 mins

193
Q

how would you manage a febrile convulsion seizure?

A

if 1st seizure / complex seizure - admit to paeds

parents phone ambulance is seizure over 5 mins

regular antipyretics dont reduce change of febrile convulsion happening

if recurrent febrile convulsion then benzodiazepine rescue med. - RECTAL DIAZEPAM/BUCCAL MIDAZOLAM

194
Q

risk of further febrile convulsion.

what does it depend on?

A

1/3

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

195
Q

can you tell me a little bit about the link between epilepsy and febrile convulsions?

A

fhx of epilepsy, complex febrile seizures and background of neurodevelopmental disorder

196
Q

what is trigeminal neuralgia?

causes

A

pain syndrome characterised by severe unilateral pain.

idiopathic
could get compression of trigeminal roots by tumours or vascular problems

197
Q

presentation of trigeminal neuralgia

how is pain evoked

A

unilateral
brief electric shock pain
limited to 1 or more division of trigeminal nerve.

pain evoked by light touch : washing, shaving, smoking, talking, brushing teeth.

198
Q

where is pain usually evoked in trigeminal neuralgia?

A

small areas in nasolabial fold or chin.

199
Q

name some red flag symptoms that suggest serious underlying cause of trigeminal neuralgia?

A

sensory changes
fhx of MS
onset before 40
optic neuritis
deafness/other ear problems

hx of skin/oral lesions that could sprewad perineurally

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

200
Q

how would you manage trigeminal neuralgia?

A

carbamazepine - 1st line

if they dont respond or have atypical features - like under 50: refer to neuro

201
Q

tell me about diabetic neuropathy

A

glove and stocking sensory loss.

no motor loss.

lower legs affected 1st due to length of sensory neurones supplying the area.

sometimes you see painful diabetic neuropathy

202
Q

how would you manage neuropathic pain (diabetic neuropathy managed same way)

A

1st line: amitryptiline, duloxetine, gabapentin, pregabalin

if 1st line dont work, try one of others

tramadol - rescue therapy - for exacerbations of neuropathic pain.

topical capsaican :: localised neuroapthic pain - post-herpetic neuralgia

pain management clinic?

203
Q

why does gastro-oeseophageal reflux disease happen?

A

decreased lower esophageal sphincter (les) pressure

204
Q

what happens in GI autonomic neuropathy

A

gastroparesis - 2ndary to autonomic neuropathy. erratic bg , bloating + vomiting. mx: metoclopramide, domperidone or erythromycin (prokinetic agents)

chronic diarhoea - @ night

GORD

205
Q

what is giant cell arteritis: temporal arteritis?

A

vasculitis of unknown cause - affecting medium + large sized vessels arteries.

over 50.
peak incidence: 70’s

206
Q

features of temporal arteritis

A

typical patient over 60.

rapid onset (under month)

headache (found in 85%)

jaw claudication (65%)

anterior ischaemic optic neuropathy .

possible temporary vision loss - amaurosis fugax

permanent visual loss - feared comp of gca and could suddenly happen.

diplopia - results from involvement of any part of oculomotor system - eg cranial nerves

  • tender , palpable temporal artery
  • 50% pts have features of PMR: aching, morning stiffness in proximal limb muscles (not weakness)
  • also lethargy , depression, low-grade fever, anorexia, night sweats
207
Q

in giant cell arteritis , why does anterior ischaemic optic neuropathy occur?

A

occlusion of posterior ciliary artery - branch of opthalmic artery.

ischaemia of optic nerve head.

fundoscopy shows swollen pale disc and blurred margins.

208
Q

what investigations would you do for gca?

A

raised inflammatory markers:
- esr >50 mm/hr (esr under 30 in 10% pts)
crp could be elevated

temporal artery biopsy: skip lesions possibly present

creatine kinase and EMG normal

209
Q

how to treat GCA?

A

urgent high-dose glucocorticoids asap when diagnosis suspected before temporal artery biopsy

if no visual loss: high dose prednisolone

if evolving visual loss - iv methylprednisolone prior to starting high-dose pred

should be dramatic response

urgent opthalmology review :
- pts with visual sx same day review bc visual damage often irreversible.

other tx:
bone protection - bisphosphonates as long as required - tapering course of steroids.
low dose aspirin - sometimes.

210
Q

what is bells palsy?

A

acute
unilateral
idiopathic
facial nerve paralysis.

unknown aetiology.

peak incidence: 20-40.

more common: pregnant women

211
Q

features of belly palsy

A

lower motor neuron facial nerve palsy - forehead affected. - in contrast to umn lesion spares the upper face.

patients also notice:
- altered taste
-dry eyes
-post-auricular pain (may precede paralysis)
- hyperacusis

212
Q

how would you manage bells palsy?

A

oral prednisolone within 72 hours of onset.

debate about adding antiviral meds (esp if severe facial paralysis)

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

213
Q

follow up for bells palsy

A

if paralysis no sign of improvement after 3 weeks, refer urgently to ENT

refer to plastics for pts with more long standing weakness- eg several months

214
Q

prognosis of bells palsy

A

most ppl full recovery within 3-4 months

if untreatred, 15% pts permanent moderate to severe weakness

215
Q

what is cerebral palsy?

A

disorder of movement and posture due to non-progressive lesion of motor pathways in developing brain.

2/1000 live births
MC cause of major motor impairement

216
Q

causes of cerebral palsy

A

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

intrapartum (10%) - birth asphyxia/trauma

postnatal (10%) - intraventricular haemorrhage, meningitis, head trauma

217
Q

classifications of cerebral palsy

A

spastic - 70% - hemiplegia, diplegia, or quadriplegia

dyskinetic

ataxic

mixed

218
Q

manifestations of cerebral palsy

A

abnormal tone early infancy

delayed motor milestones

abnormal gait

feeding difficulty

219
Q

what non-motor problems do children with cerebral palsy have?

A

learning difficulty - 60%

epilepsy (30%)

squints (30%)

hearing impairment (20%)

220
Q

how would you manage a pt with cerebral palsy

A

multidisciplinary approach - child - chronic

tx:
spasticity - oral diazepam , oral and intrathecal baclofen, botulinum toxin type A , orthopaedic surgery and selective dorsal rhizotomy

  • anticonvulsants , analgesia as required
221
Q

what is hypoxic-ischaemic encephalopathy?

A

serious neuro condition due to inadequate cerebral oxygen supply.

associated with perinatal asphyxia in neonates.

can occur in adults due to cardiac arrest or severe systemic hypoxia.

2 types : primary energy and secondary energy failure

222
Q

tell me about primary energy failure - hypoxic ischaemic encephalopathy?

A

occurs immediately during HIE.

leading to anaerobic metabolism, lactic acidosis and cytotoxic oedema.

after initial resus and reoxygenation , a period of latent phase occurs where the brain appears to recover.

223
Q

tell me about secondary energy failure - HIE

A

hours to days later occurs

renewed accumulation of toxic metabolites and free radicals causing further neuronal death.

clinically, HIE presents with

altered consciousness levels ranging from lethargy to coma, seizures, abnormal tone and reflexes

224
Q

how would you manage HIE?

A

supportive care :
- maintaining normal body temp
blood glucose
seizure control.

therapeutic hypothermia : shown benefits in neonatal HIE if initiated within 6 hrs of birth.

225
Q

1st line ix for HIE

A

ABG - extent of met acidosis, hypercapnia, hypoxemia.

complete blood count - underlying infection, anaemia, polycythaemia

serum electrolytes and glucose - sodium potassium calcium and glucose - detect imbalances that can exacerbate neuro injury

lft + renal function test: liver enzymes and renal function markers eg creatinine and urea.

226
Q

what neuroimaging would you do for HIE

A

cranial ultrasound:
in neonates non-invasive 1st line. detects intracranial haemorrhage or structural abnormality.
sensitivity is limited in early HIE

MRI brain : diffusion weighted imaging - gold standard.
within 2-5 days post injury. assess brain injury.

look for patterns like :
watershed infarcts
basal ganglia/thalamic involvement

227
Q

tell me some amplicative ix for HIE?

A

EEG : check subclinical seizures. brain activity.
continuous if suspect seizures or severe encephalopathy.

aEEG: amplitude - integrated eeg - continuous bedside monitoring in neonatal units. rapid assessment of cerebral function over time.

228
Q

what to do if there are atypical features of HIE suggesting metabolic disorder?

A

do met screening

ammonia levels
lactate
pyruvate
plasma A.A
urine organic acids
tandem mass spectrometry for acylcarnitine profile analysis.

also do if:
- inborn error of metabolism based on clinical presentation/fhx.
- if mitochondrial disorders like elevated lactate-to-pyruvate ratio. specific neuroimaging findings like basal ganglia lesions.

229
Q

name some complications of HIE

A

cerebral palsy - common outcome - often involving spastic quadriplegia or dyskinetic form.

poor growth - feeding difficulty - neurological impairement

microcephaly - reduced head circumference - due to impaired brain growth.

behavioural disorders: adhd, asd

sensory : visual , auditory deficit frequent. cortical visual impairment and sensorineural hearing loss.

congitive impairement: mild learning difficulty to severe intellectual disability.

seizure disorders: neonates develop symptomatic seizures intially and later epilepsy.

severe cases:

multisystem organ failure - cv,renal,hepatic,respiratory systems.

230
Q

what is a migraine?

A

common headache.

severe unilateral throbbing

nausea
photophobia
phonophobia

attacks can last upto 72 hrs.

pts usually go into dark,quiet room during attack

231
Q

what is an aura?

A

happens before headache. precipitates migraine.

1/3 of migraine pts.

visual progressive last 5-60 mins .

characterised by transient hemianopic disturbance or a spreading scintillating scotoma.(flashing lights)

232
Q

epidemiology of migraine

A

3 times more in women

233
Q

common triggers of migraine

A

tiredness, stress

alcohol
combined oral ccp
lack of food/dehydration
cheese,chocolate,red wines, citrus fruits
menstruation
bright lights

234
Q

migraine diagnostic criteria

A

at least 5 attacks fulfilling b-d

b - lasts 4-72 hrs - untx or unsucessfully tx

c headache at least 2 of following:
- unilateral
- pulsating
-moderate/severe pain
- aggravation bby or causing avoidance of routine physical activity

d - during headache at least one of:
- nausea and/or vomiting
- photophobia and phonophobia

e - no other cause.

235
Q

what is a hemiplegic migraine?

A

variant.

motor weakness manifestation of aura in some attacks.

half pts have strong fhx

very rare - 0.01%
more common in adolescent females

236
Q

aura sx

A

fully reverisble, develop over 5 mins, last 5-60 mins

motor weakness
double vision
poor balance
decreased gcs
visual sx affecting only 1 eye

237
Q

how to manage migraine

A

5-ht receptor agonist in acute tx

5-ht receptor antagonist -prophylaxis

acute
1st line : combination - oral triptan and nsaid , or

oral triptan + paracetamol

if 12-17 - nasal triptan

if not effective

non-oral prep of metoclopramide or prochlorperazine and can add non-oral nsaid or triptan.

238
Q

what can develop when giving metoclopramide in young pts with migraine?

A

acute dystonic reaction

239
Q

prophylaxis of migraine

A

propranolol
topiramate - avoid in women of child bearing age - teratogenic - reduces hormonal contraceptive effectiveness
amitriptyline

10 sessions of accupuncture over 5-8 weeks

riboflavin 400mg od - can reduce frequency and intensity for some.

240
Q

for women with predictable menstrual cycle, how to prophylaxis for migraine?

A

frovatriptan 2.5 mg twice a day

zolmitriptan 2.5 mg twice or 3 times a day

miniprophylaxis

241
Q

why isnt pizotifen no longer recommended for migraine prophylaxis?

A

weight gain
drowsiness

242
Q

how to treat migraine during pregnancy?

A

paracetamol 1g : 1st line

nsaids second line in 1st and second trimester

avoid aspirin and opioids eg codeine

243
Q

pt has migraine with aura, wants to take oral contraceptive, what to do ?

A

contraindicated due to increased risk of stroke

244
Q

can i prescribe hormone replacement therapy for migraine pt?

A

safe but might make migraines worse

245
Q

link between migraine and menstruation

A

lots pts say frequency and severity increase around menstruation

tx with mefanamic acid

or combo of

aspirin paracetamol and caffeine.

triptans also in acute situation

246
Q

clinical features of tension headache

A

tight band around head or pressure sensation.

bilateral

lower intensity than migraine

no aura, n+v, or aggravated by physical activity.

could be stress related

could co-exist with migraine

247
Q

what is a chronic tension-type headache ?

A

tension headache 15 or more days a month

248
Q

how would you manage tension type headache?

A

acute: aspirin, paracetamol or an nsaid - 1st line

prophylaxis: 10 sessions acupuncture over 5-8 weeks

low dose amitriptyline - prophylaxis.

249
Q

categories of tension headaches

A

infrequent - less than 1 day per month

frequent - 10 times in less than 15 days a month for more than 3 months

chronic: 15 days or more a month, more than 3 months - no med overuse

250
Q

what is a cluster headache?

A

one of most painful .

occur in clusters lasting several weeks.
clusters typically once a yr.

251
Q

epi of cluster headaches

A

50-60 yrs

more in males : 3-1

252
Q

causes of cluster headache

A

male
smoking

alcohol could trigger

also nocturnal sleep

253
Q

features of cluster headache

A

4-12 weeks lasts

pain : intense sharp stabbing pain around 1 eye - recurrent attack always same side.
typically once or twice a day - 15min-2 hrs

pt restless and agitated during attack.

redness
nasal stuffiness
lacrimation
lid swelling

miosis (constriction of pupils) and ptosis (drooping of upper eyelid) in minority

254
Q

how would you investigate for cluster headache?

A

neuroimaging - underlying brain lesions can be found even if clinical sx are typical for cluster headache

MRI with gadolinium contrast

255
Q

how to diagnose cluster headache : criteria

A

at least 5 attacks meeting criteria B-D

b - severe/very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 mins (when untreated)

c - either or both of:

  1. 1 of following symptoms or signs , ipsilateral to headache:
    - eyelid oedema
    - forehead and facial sweating
    - miosis and/or ptosis
    - nasal congestion and/or rhinorrhoea
    - conjunctival infeciton and/or lacrimation
  2. sense of restlessness or agitation

d. - frequency between 1 every other day and 8 per day.

e - no better diagnoses.

256
Q

how to manage cluster headache?

A

acute: 100% oxygen (80% response rate within 15 mins), subcut triptan (75% response rate within 15 mins)

prophylaxis:
verapimil
some say tapering dose of prednisolone

Phase 3a Medicine (16 decks)

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