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Semester 2 (3rd year) > case 22: headache and funny turns > Flashcards

case 22: headache and funny turns Flashcards

1
Q

what is epilepsy

A

repeated seizures due to abnormal electrical activity in the brain

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2
Q

what does post ictal mean

A

period immediately after seizure

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3
Q

risk factors for epilepsy

A

family history

febrile convulsions in childhood

motor/developmental delay

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4
Q

specific causes of epilepsy

A

developmental= cerebral palsy, downs syndrome

traumatic brain injury= however, seizures within 30 days aren’t classified as epilepsy and often those occurring many years later aren’t related to the injury

structural= space occupying lesion, stroke, hippocampal sclerosis (aka mesial temporal sclerosis seen in Alzheimers), tuberous sclerosis

infections/autoimmune diseases= these cause chronic brain injury which can lead to epilepsy (meningitis, syphilis, neurocysticerosis, SLE, PAN and sarcoidosis

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5
Q

typical migraine presentation

A

severe (build up in severity)

episodic

may last several (but up to several days)

most commonly in young women

come on over minutes/hours

premonitory symptoms in hours-days leading up to pain (fatigue, aching, aura, yawning or altered appetite)

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6
Q

subarachnoid haemorrhage pain description

A

sudden onset

severe pain

reaches maximal intensity within a few minutes

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7
Q

trigeminal neuralgia pain description

A

recurrent brief jabs of pain in one side of face

may be triggered by touching affected area

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8
Q

cluster headache pain description

A

recurrent unilateral pain around eye and temple on only one side

rapid onset over minutes

brief duration (15mins)

occurring several times in a night

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9
Q

raised intracranial pressure pain description

A

progressively worsening headache over days/weeks

worse on bending over/lying down

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10
Q

episodic headaches lasting between 4hrs and 3 days

occurs intermittently with headache free days in between

A

migraine

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11
Q

dozens of brief jabbing pains each day with periods of spontaneous remission lasting weeks to months

A

trigeminal neuralgia

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12
Q

headaches gradually worsening over weeks, present daily

patient wakes from sleep but eases when arisen

A

raised intracranial pressure

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13
Q

spells of brief (15-30) minute headaches lasting a few weeks at a time

during a spell headaches occur multiple times a day, commonly at night

periods of remission last weeks to months

A

cluster headache

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14
Q

what other features are common with migraine

A

photophobia

visual disturbance spreading across field prior to headache - aura symptoms could be positive (sparkles, flashes, zigzags) or negatives (loss of vision), can also get pins and needles or word finding difficulties, these usually last less than 1hr

mechanophobia- sensitivity to movement

photophobia- sensitivity to sound

nausea and vomiting

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15
Q

with what type of headache might you experience redness of eye with watering and nasal stuffiness

A

more typical of cluster headache (but may also happen with migraine)

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16
Q

red flag symptoms for headache

A

fever- indicates infective cause

new onset seizures- suggests structural brain disease

pain triggered by cough, sneeze, valsava- suggests raised intracranial pressure

episodes of transient visual loss when changing posture- aka transient visual obscuration and can be a sign of raised intracranial pressure

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17
Q

migraine risk factors

A

family history of similar headaches

caffeine excess

dehydration

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18
Q

medication overuse headache risk factors

A

regular use of codeine/paracetamol

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19
Q

CNS infection risk factors

A

history of immunosuppression

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20
Q

intracranial metastases risk factors

A

history of cancer

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21
Q

intracranial haemorrhage risk factors

A

recent neurosurgery

oral anticoagulant medication

fragility and minor trauma

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22
Q

red flag signs for new headaches

A

almost any abnormal UMN sign would be worrying

papillodema- sign of raised ICP (this may be the only sign)

restricted visual fields- sign of raised ICP (may not be aware of this until tested)

oculoparesis- patient would have diplopia (VI nerve palsy may be sign of raised ICP)

nystagmus- for raised ICP this would help localise the lesion to the cerebellum or its connections

increased tone- UMN sign, increased tone in left arm would suggest right sided brain lesion

brisk reflexes- UMN sign, brisk reflexes in left arm suggests right sided brain lesion

pyramidal drift- downward pronating movement of outstretched arm is seen with lesions of contralateral brain hemisphere

limb/gait ataxia- for raised ICP helps localise lesion to cerebellum or its connections

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23
Q

what PMH is important for headaches

A

cancer
immunosuppression

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24
Q

what is oral hair leukoplakia and what does it suggest

A

white patches on tongue which cannot be scraped off

caused by EBV and seen almost exclusively in immunocompromised

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25
Q

what is livedo recticularis

A

rash (looks like mottled skin)

seen in those with antiphospholipid antibody syndrome

increases risk of clotting

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26
Q

what % of women have migraines

A

25% at some point in their life

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27
Q

examples of migraine triggers

A

food (chocolate/cheese)
caffeine
sleep deprivation
missed meals

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28
Q

what medications can tigger medication overuse headache

A

analgesia overuse
opiate
triptan
paracetamol

(if used over 10 days in the month)

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29
Q

what number of migraine attacks per month would warrant acute treatment

A

less than 4 disabling attacks per month

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30
Q

acute treatment for migraines

A

paracetamol + NSAID +/- antiemetic

triptans (nasal, oral, injection)

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31
Q

what number of migraine attacks per month would warrant preventative treatment

A

if more than 4 disabling attacks per month or chronic migraine

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32
Q

preventative treatment for migraines

A

b-blocker
tricyclic
topiramate

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33
Q

what can you do for treatment resistant migraines

A

botulinum toxin
anti-CGRP (antibody) drugs

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34
Q

key features of cluster headaches

A

unilateral

severe

in and around the eye, temporal

restless

red/watery eye

partial ptosis/horners

nasal stuffiness/runny nose

15-180 minutes

1-8 per day (typically at night)

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35
Q

are more men or women affected by cluster headaches

A

more men
4:1

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36
Q

management of acute cluster headache attack

A

high flow O2

injectable triptan

maybe steroids at the start of a cluster

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37
Q

prophylaxis management of cluster headaches

A

verapamil

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38
Q

key features of trigeminal neuralgia

A

unilateral

there is disruption of CN V

very brief (1s-120s)

lancinating pain

touch sensitive/chewing

neuro exam normal

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39
Q

are more men or women affected by trigeminal neuralgia

A

women
3:2

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40
Q

management of trigeminal neuralgia

A

need to investigate cause

carbamazepine/oxcarbazepine

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41
Q

key features of tension headaches

A

bilateral

pressing

featureless

episodic- less than 15 days per month

chronic- more than 15 days per month for 3 out of 12 months

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42
Q

management of tension headaches

A

simple analgesia

tricyclics

non-pharmacological measures

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43
Q

lifestyle measures for migraine management

A

caffeine avoidance
good hydration
regular exercise

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44
Q

acute treatments for migraine management

A

paracetamol
naproxen
triptans
aspirin and metoclopramide

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45
Q

preventative treatment for migraine management

A

propranolol
amitriptyline
topiramate

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46
Q

what pain drug can actually worsen migraines

A

codeine

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47
Q

issues with propranolol

A

contraindicated in asthma and COPD

in those with IHD or bradyarrythmias may not be possible to use drug

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48
Q

issues with topiramate

A

(antiepileptic)

not safe in pregnancy (women of child bearing age should use contraception)

reduces appetite so may cause weight loss

risk of kidney stones and acute angle closure glaucoma- so in those with previous history of these should be avoided

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49
Q

issues with amitriptyline

A

(sedative medication- taken at night)

has benefits for nocturnal sleep but can cause drowsiness in morning

caution for driving and machinery use

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50
Q

what is giant cell arthritis/temporal arthritis

A

arteries at the temples become inflamed

serious form of vasculitis

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51
Q

typical history of giant cell arthritis/temporal arthritis

A

over 55
malaise
sweats
proximal muscle aching

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52
Q

causes of raised intracranial pressure

A

space occupying lesion

intracranial bleeding

CSF flow obstruction

brain swelling

venous sinus thrombosis

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53
Q

signs and symptoms of raised ICP

A

headache- postural (worse bending over and lying down, therefore worse at night and can wake them up), valsalva (coughing/straining can tigger it)

vision- peripheral field loss, blurring, transient visual obscuration (loss of vision when standing up), diplopia

neurological- focal dysfunction, confusion, reduced GCS (can be due to brain herniation- temporal lobe can squash brainstem)

also:

papilloedema, constricted peripheries and enlarged blind spot on visual fields, UMN signs and CN VI palsy

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54
Q

what is the most common cause of subarachnoid haemorrhage

A

trauma

55
Q

other causes of subarachnoid haemorrhage

A

aneurysmal
perimesencephalic (where no aneurysm can be found- milder and have better prognosis)
vasculitis

56
Q

typical presentation of subarachnoid haemorrhage

A

thunderclap headache (sudden and severe- maximal intensity within 1-5mins)

photophobia and vomiting (due to meningeal irritation)

reduced GCS

focal symptoms

57
Q

management of subarachnoid haemorrhage

A

stabilise patient

CT ASAP

if the CT is negative do lumbar puncture after 12hrs (spectrophotometry to detect bilirubin and oxyhaemaglobin as these are formed by the breakdown of subarachnoid blood)

if confirmed refer to neurology for angiography to identify the cause

58
Q

role of nimodipine in subarachnoid haemorrhage

A

prevents secondary complication of vasospasm

59
Q

what is meningitis

A

inflammation of the meningeal tissue
caused by infectious or non-infectious triggers

60
Q

most severe meningitis type

A

bacterial

61
Q

mortality of bacterial meningitis

A

20-30%
requires prompt recognition and treatment

62
Q

the bacterias which most commonly cause community acquired bacterial meningitis

A

streptococcus pneumoniae and neisseria meningitides

63
Q

most common cause of bacterial meningitis in immunocompromised over 50s

A

listeria monocytogenes

64
Q

what other infection can cause meningitis

A

TB can disseminate and cause meningitis

65
Q

most common causes of bacterial meningitis in neonates

A

group B streptococcus, E.coli and less commonly listeria monocytogenes

66
Q

what are the most common causes of bacterial health-care associated meningitis

A

after neurosurgery or cranial trauma, where there is internal or external ventricular drains

staphylococci or aerobic gram -ve bacilli are most common causes

67
Q

most common bacterial cause of meningitis in returning travellers

A

penicillin-resistant streptococcus pneumoniae

68
Q

viral causes of meningitis

A

enteroviruses
mumps (and other paramyxoviruses)
herpes simplex virus (primary HSV infection or disseminated HSV)

69
Q

most common fungal cause of meningitis

A

cryptococcus neoformans

70
Q

in which patients does fungal meningitis typically occur

A

in those with severe deficiencies in cell-mediated immunity (such as HIV patients)

71
Q

clinical features of meningitis

A

fever above 38

severe headache

nausea

neck stiffness

change in mental status (GCS less than 14)

usually sudden onset and are acutely unwell

those who are younger might not have the above

meningococcal rash or petechial inflammation

less common= seizures, aphasia, or hemi- or monoparesis, coma, cranial nerve palsy, rash and papilloedema

72
Q

in what type of meningitis is meningococcal rash or petechial inflammation typically seen

A

neisseria meningitides (meningococcal disease)

73
Q

what protocol should be followed in meningitis patients

A

surviving sepsis protocol

74
Q

how can you check for the clinical signs of meningitis

A

neck stiffness- passively flex patient neck, resistance indicates positive sign

kernigs sign- position patient on their back with hips flexed to 90 degrees, positive if there is pain on passive leg extension at knee joint

brudzinskis sign- position patient on their back and passively flex their neck, positive if patient involuntarily bends their knees

cant be relied upon for diagnosis but they have high specificity (but low sensitivity)

75
Q

differentials for meningism

A

bacterial meningitis

viral meningitis- common and can occur at any age (most common in children), management is supportive and most cases are self-limiting with good prognosis

fungal meningitis- life-threatening but rare, seen in immuncompromised

tuberculous meningitis- consider TB risk factors, can have similar findings to bacterial meningitis

drug-induced meningitis- history of drugs such as NSAIDs, trimethoprim/sulfamethoxazole, amoxicillin, ranitidine

encephalitis- suggested by abnormal cerebral function such as altered behaviour, speech or motor function (especially if associated with fever)

malignancy

CNS abscess

HIV- risk factors and immune system history

subarachnoid haemorrhage

autoimmune disorders- such as systemic lupus erythematosus (which can cause aseptic meningitis) and Behcets syndrome

76
Q

lumbar puncture and meningitis management

A

LP within 1hr of hospital arrival (if safe and patient haemodynamically stable)

antibiotics commenced immediately after LP

if LP cannot be performed within 1hr, blood cultures should be taken, antibiotics started and LP when safe

77
Q

what to do if you suspect sepsis with meningitis

A

in those with sepsis or rapidly evolving rash- commence SEPSIS 6

LP when patient is stabilised

78
Q

what vertebral level would you do LP

A

between L3 and L4 or L4 and L5 (this is below the level at which the spinal cord terminates)

79
Q

precautions to rule of before doing LP

A

make sure not on anticoagulants and doesnt have clotting disorder

rule out raised ICP with risk of herination or suspected spinal epidural abscess

80
Q

risk factors which would make you do CT head before performing lumbar puncture

A

immunocompromised

history of CNS infection, masses or stroke

new-onset seizure

papilloedema

altered consciousness

focal neurologic deficit

81
Q

what are you looking for in the CSF

A

cell count and differential

glucose concentration

protein concentration

gram stain, bacterial culture and PCR

viral PCR

82
Q

how many specimen pots do you need for the CSF

A

minimum of 4 samples

83
Q

treatment of bacterial meningitis

A

urgent IV antibiotics (often cetriaxone with additional amoxicillin if listeria is likely, chloramphenicol if penicillin allergy)

also dexamethasone 10mg IV 4 times daily for 4 days (within 12 hours of commencing antibiotics)

if confirmed meningococcal meningitis need oropharyngeal eradication (either ceftriaxone or ciporfloxacin) alongside treatment

84
Q

treatment of viral meningitis

A

once confirmed it is viral, stop antibiotics if they have already been administered

no treatment necessary

can give supportive IV fluids if needed

85
Q

what can be seen on fundoscopy with papilloedema

A

blurred edges of the optic disc (due to swelling)
haemorrhagic changes around the disc margins

86
Q

what does pronator drift mean

A

means there is subtle pyramidal tract dysfunction (issue is in contralateral hemisphere)

87
Q

is there is pronator drift is the issue unilateral or contralateral

A

contralateral

88
Q

what type of rays do CT scans use

A

X-rays

89
Q

which artery is most commonly compromised with extra-dural haematomas

A

middle meningeal artery (is at the temporoparietal area)

90
Q

typical presentation of extra-dural haematomas

A

may regain consciousness following a brief loss of consciousness at the time of the injury

initial loss of consciousness is usually due to cerebral concussion

level of consciousness then begins to deteriorate as the haemotoma develops

‘lucid level’ is when the patient may appear normal- this can lead to miss diagnoses

91
Q

the difference between sub-dural and extra-dural haematoma

A

sub-dural= inner surface of the dura developing within a few days of head injury and is venous

extra-dural= outer surface of dura and arterial usually straight after injury

92
Q

typical presentation of sub-dural haematoma

A

may be after not major injury but in people who are vulnerable- elderly, alcoholics

haematoma develops very slowly- ‘venous ooze’ therefore presentation may be after weeks/months

headaches, drowsiness and confusion are all late signs

there is a typical varying fluctuation in consciousness due to the haematoma contracting and expanding due to osmotic effects

93
Q

do primary brain tumours metastasise

A

no

94
Q

classification of brain tumours

A

primary= arise from intracranial structures such as meninges (miningeoma) or glial cells (gliomas or astrocytomas)

secondary metastases= from primary tumours usually arising in the bronchus, breast, stomach, prostate, thyroid or kidneys

95
Q

growth speed of miningeomas vs gliomas

A

meningeomas= slow growth

gliomas= range of growth (multiforme is the worst)

96
Q

what is the treatment given for brain oedema

A

steroids (dexamethasone)

97
Q

questions to ask about before attack (potentially seizure)

A

what they were doing before

position

feeling unwell (warning signs)

light headedness, nausea, altered vision, pale/clammy

twitching/jerking

98
Q

questions to ask about during attack (potentially seizure)

A

memory of event

hearing anyone talking

body stiffness

floppy body

shaking

breathing

blue around lips

eyes open/closed

length of attack

99
Q

questions to ask about after attack (potentially seizure)

A

feeling when came round

injury (tongue bite)

incontinence

did you know where you were

how long did you take to come round

100
Q

management after first seizure

A

neurological and cardiovascular examination

routine bloods

12 lead ECG

refer to first fit clinic

stop driving until definitive diagnosis and treatment

101
Q

features of temporal lobe seizures

A

limbic- deja vu and memory loss

abdominal rising sensation (from epigastric region)

vomiting, flushing, pallor, altered HR

altered language

102
Q

features of frontal lobe seizures

A

motor signs, hyperkinetic (unwanted excess movements)- head turn (head is pushed away from the side where its happening), eye movements, peddling movements or motor arrest

nocturnal (often occurs at night)

speech arrest

recovery is typically rapid but post-ictal phase can have weakness (Todds palsy)

103
Q

features of parietal lobe seizures

A

may begin with odd sensations (tingling/numbness)

may have complex visual hallucinations

104
Q

features of occipital lobe seizures

A

visual symptoms (shapes and/or flashes)

shapes are often more colourful and circular than migraine

105
Q

focal vs generalised seizures

A

focal= partial and may suggest underlying structural disease, abnormal activity is in one hemisphere

generalised= simultaneous discharge in both hemispheres, abnormal activity in both hemispheres

106
Q

focal seizures classification

A

aware (simple partial)= seizure with retained consciousness

impaired awareness (dyscognitive/complex partial)= seizure with impaired consciousness which may manifest as blank stare and/or behavioural arrest

focal to bilateral tonic-clonic (partial seizure with secondary generalisation)= starts focal then becomes generalised (this is the only time a generalised seizure can have aura)

107
Q

what is aura

A

warning sign- symptoms before the main seizure

symptoms= flashing lights, strange gut feeling, deja vu, sensing smells

108
Q

aura is most common in seizures affecting which lobe

A

temporal

109
Q

what is benign rolandic epilepsy

A

commonest epilepsy in children (5-10)

nocturnal seizures- facial twitches, eye flickering, lip smacking

110
Q

what types of primary generalised seizures are there

A

absense seizures (aka petit mal, nonmotor)

generalised tonic-clonic seizures (GTCS, aka grand mal, motor)

atonic seizures (aka akinetic)

myoclonic seizures

111
Q

absence seizures features

A

behavioural pause (usually less than 10 secs)
starts in childhood
Hz spike and slow-wave complexes on ECG

112
Q

generalised tonic-clonic seizures features

A

loss of consciousness
limbs stiffen (tonic) and then rhythmically jerk (clonic)
starts with cry and/or biting side of tongue
may be cyanosed due to chest spasm
urine and/or faecal incontinence
post-ictal confusion and drowsiness

113
Q

atonic seizures features

A

sudden brief loss of tone and consciousness
will fall or regain consciousness and catch themselves

114
Q

myoclonic seizures features

A

sudden jerk of bilateral limbs (usually arms) face, or trunk which may lead to fall
single/multiple
may occur on waking

115
Q

triggers for seizures (especially generalised)

A

lack of sleep
alcohol
fever
flickering light
drugs/drug withdrawal

116
Q

causes for seizures which isn’t epilepsy

A

non-epileptic attack disorder

acute trauma (concussive seizure)

cardiovascular= stroke, haemorrhage, pre-clampsia, arrhythmia (true epilepsy is recurrent seizures and can develop later as a result of a stroke)

metabolic= reduced oxygen, alerted sodium, decreased calcium, altered glucose, uraemia

infection= meningitis, encephalitis, fever

drugs= alcohol or benzodiazepine withdrawal, tricyclic antidepressants, cocaine, tramadol, theophylline

other= raised ICP and liver disease

117
Q

types of focal seizures and types of generalised seizures

A

focal= focal aware seizure, focal unaware seizure, focal to bilateral tonic clonic seizure

generalised= primary generalised tonic clonic seizure, absence seizure, generalised myoclonic seizure

118
Q

what are function seizures

A

they are non-epileptic dissociative seizures

aka psychogenic non epileptic seizures (PNES) or non epileptic attach disorder (NEAD)

119
Q

what do function seizures typically look like

A

rapid twitching- tremor or rigor-like movements

funny feeling

swoon- unresponsive without motor manifestations

complex movements- back arching and pelvic thrusting (classes NEAD)

violent movements

120
Q

risk factors for epileptic seizures

A

alcohol misuse
febrile convulsions in childhood
perinatal brain injury
family history of epilepsy
traumatic brain injury
previous CNS infection
recreational drug use

121
Q

management of epilepsy once diagnosis has been made

A

MRI brain- needed for any adult who develops seizures (probably won’t show anything)

inform DVLA- refrain my driving until seizure free for one year

offer anti epileptic (for example lamotrigine)

ECG

122
Q

what effects need to be discussed with a patient when starting them on lamotrigine

A

risk of rash- can develop hypersensitivity rash and is associated with dermatological conditions such as stevens Johnson syndrome

need for regular dosing- needs to be taken at regular intervals

requirement for long-term therapy- most likely needed life-long

123
Q

what may be observed in cariogenic syncope

A

collapse in floppy manner

myoclonic jerking may occur, especially if in upright position

124
Q

features of epileptic seizures (length, initial movements, nature of jerking and eyes)

A

2-5mins

whole body stiffening

there is rhythmic jerking, then reducing amplitude and frequency

eyes are open

125
Q

features of non-epileptic seizures (length, initial movements, nature of jerking and eyes)

A

over 10mins

back arching movements

asynchronous limb movements

eyes may be tightly closed

126
Q

features of syncope (length, initial movements, nature of jerking and eyes)

A

less than 1min

floppy collapse

brief jerking of low amplitude

eyes closed

127
Q

what is syncope

A

transient loss of consciousness due to temporary reduction in cerebral blood flow

128
Q

2 types of syncope

A

vaso-vagal (fainting)
cariogenic syncope

129
Q

features of vasodilation-vagal syncope

A

symptoms before- dizziness, light-headedness, clamminess, visual blurring

there is postural correction on falling

consciousness regained in 30-60secs

well orientated on recovery

130
Q

what could cause cardiogenic syncope

A

underlying cardiac arrhythmia/structural heart disease

131
Q

does cariogenic syncope have preceding warning symptoms

A

typically no

132
Q

what would you do when finding out someone had complete heart block

A

refer urgently to cardiology
consider permanent pacemaker

133
Q

vital initial test when someone presents with altered conscious level

A

blood glucose

Semester 2 (3rd year) (12 decks)

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