case 22: headache and funny turns Flashcards
what is epilepsy
repeated seizures due to abnormal electrical activity in the brain
what does post ictal mean
period immediately after seizure
risk factors for epilepsy
family history
febrile convulsions in childhood
motor/developmental delay
specific causes of epilepsy
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
typical migraine presentation
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)
subarachnoid haemorrhage pain description
sudden onset
severe pain
reaches maximal intensity within a few minutes
trigeminal neuralgia pain description
recurrent brief jabs of pain in one side of face
may be triggered by touching affected area
cluster headache pain description
recurrent unilateral pain around eye and temple on only one side
rapid onset over minutes
brief duration (15mins)
occurring several times in a night
raised intracranial pressure pain description
progressively worsening headache over days/weeks
worse on bending over/lying down
episodic headaches lasting between 4hrs and 3 days
occurs intermittently with headache free days in between
migraine
dozens of brief jabbing pains each day with periods of spontaneous remission lasting weeks to months
trigeminal neuralgia
headaches gradually worsening over weeks, present daily
patient wakes from sleep but eases when arisen
raised intracranial pressure
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
cluster headache
what other features are common with migraine
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
with what type of headache might you experience redness of eye with watering and nasal stuffiness
more typical of cluster headache (but may also happen with migraine)
red flag symptoms for headache
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
migraine risk factors
family history of similar headaches
caffeine excess
dehydration
medication overuse headache risk factors
regular use of codeine/paracetamol
CNS infection risk factors
history of immunosuppression
intracranial metastases risk factors
history of cancer
intracranial haemorrhage risk factors
recent neurosurgery
oral anticoagulant medication
fragility and minor trauma
red flag signs for new headaches
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
what PMH is important for headaches
cancer
immunosuppression
what is oral hair leukoplakia and what does it suggest
white patches on tongue which cannot be scraped off
caused by EBV and seen almost exclusively in immunocompromised
what is livedo recticularis
rash (looks like mottled skin)
seen in those with antiphospholipid antibody syndrome
increases risk of clotting
what % of women have migraines
25% at some point in their life
examples of migraine triggers
food (chocolate/cheese)
caffeine
sleep deprivation
missed meals
what medications can tigger medication overuse headache
analgesia overuse
opiate
triptan
paracetamol
(if used over 10 days in the month)
what number of migraine attacks per month would warrant acute treatment
less than 4 disabling attacks per month
acute treatment for migraines
paracetamol + NSAID +/- antiemetic
triptans (nasal, oral, injection)
what number of migraine attacks per month would warrant preventative treatment
if more than 4 disabling attacks per month or chronic migraine
preventative treatment for migraines
b-blocker
tricyclic
topiramate
what can you do for treatment resistant migraines
botulinum toxin
anti-CGRP (antibody) drugs
key features of cluster headaches
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)
are more men or women affected by cluster headaches
more men
4:1
management of acute cluster headache attack
high flow O2
injectable triptan
maybe steroids at the start of a cluster
prophylaxis management of cluster headaches
verapamil
key features of trigeminal neuralgia
unilateral
there is disruption of CN V
very brief (1s-120s)
lancinating pain
touch sensitive/chewing
neuro exam normal
are more men or women affected by trigeminal neuralgia
women
3:2
management of trigeminal neuralgia
need to investigate cause
carbamazepine/oxcarbazepine
key features of tension headaches
bilateral
pressing
featureless
episodic- less than 15 days per month
chronic- more than 15 days per month for 3 out of 12 months
management of tension headaches
simple analgesia
tricyclics
non-pharmacological measures
lifestyle measures for migraine management
caffeine avoidance
good hydration
regular exercise
acute treatments for migraine management
paracetamol
naproxen
triptans
aspirin and metoclopramide
preventative treatment for migraine management
propranolol
amitriptyline
topiramate
what pain drug can actually worsen migraines
codeine
issues with propranolol
contraindicated in asthma and COPD
in those with IHD or bradyarrythmias may not be possible to use drug
issues with topiramate
(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
issues with amitriptyline
(sedative medication- taken at night)
has benefits for nocturnal sleep but can cause drowsiness in morning
caution for driving and machinery use
what is giant cell arthritis/temporal arthritis
arteries at the temples become inflamed
serious form of vasculitis
typical history of giant cell arthritis/temporal arthritis
over 55
malaise
sweats
proximal muscle aching
causes of raised intracranial pressure
space occupying lesion
intracranial bleeding
CSF flow obstruction
brain swelling
venous sinus thrombosis
signs and symptoms of raised ICP
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
what is the most common cause of subarachnoid haemorrhage
trauma
other causes of subarachnoid haemorrhage
aneurysmal
perimesencephalic (where no aneurysm can be found- milder and have better prognosis)
vasculitis
typical presentation of subarachnoid haemorrhage
thunderclap headache (sudden and severe- maximal intensity within 1-5mins)
photophobia and vomiting (due to meningeal irritation)
reduced GCS
focal symptoms
management of subarachnoid haemorrhage
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
role of nimodipine in subarachnoid haemorrhage
prevents secondary complication of vasospasm
what is meningitis
inflammation of the meningeal tissue
caused by infectious or non-infectious triggers
most severe meningitis type
bacterial
mortality of bacterial meningitis
20-30%
requires prompt recognition and treatment
the bacterias which most commonly cause community acquired bacterial meningitis
streptococcus pneumoniae and neisseria meningitides
most common cause of bacterial meningitis in immunocompromised over 50s
listeria monocytogenes
what other infection can cause meningitis
TB can disseminate and cause meningitis
most common causes of bacterial meningitis in neonates
group B streptococcus, E.coli and less commonly listeria monocytogenes
what are the most common causes of bacterial health-care associated meningitis
after neurosurgery or cranial trauma, where there is internal or external ventricular drains
staphylococci or aerobic gram -ve bacilli are most common causes
most common bacterial cause of meningitis in returning travellers
penicillin-resistant streptococcus pneumoniae
viral causes of meningitis
enteroviruses
mumps (and other paramyxoviruses)
herpes simplex virus (primary HSV infection or disseminated HSV)
most common fungal cause of meningitis
cryptococcus neoformans
in which patients does fungal meningitis typically occur
in those with severe deficiencies in cell-mediated immunity (such as HIV patients)
clinical features of meningitis
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
in what type of meningitis is meningococcal rash or petechial inflammation typically seen
neisseria meningitides (meningococcal disease)
what protocol should be followed in meningitis patients
surviving sepsis protocol
how can you check for the clinical signs of meningitis
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)
differentials for meningism
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
lumbar puncture and meningitis management
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
what to do if you suspect sepsis with meningitis
in those with sepsis or rapidly evolving rash- commence SEPSIS 6
LP when patient is stabilised
what vertebral level would you do LP
between L3 and L4 or L4 and L5 (this is below the level at which the spinal cord terminates)
precautions to rule of before doing LP
make sure not on anticoagulants and doesnt have clotting disorder
rule out raised ICP with risk of herination or suspected spinal epidural abscess
risk factors which would make you do CT head before performing lumbar puncture
immunocompromised
history of CNS infection, masses or stroke
new-onset seizure
papilloedema
altered consciousness
focal neurologic deficit
what are you looking for in the CSF
cell count and differential
glucose concentration
protein concentration
gram stain, bacterial culture and PCR
viral PCR
how many specimen pots do you need for the CSF
minimum of 4 samples
treatment of bacterial meningitis
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
treatment of viral meningitis
once confirmed it is viral, stop antibiotics if they have already been administered
no treatment necessary
can give supportive IV fluids if needed
what can be seen on fundoscopy with papilloedema
blurred edges of the optic disc (due to swelling)
haemorrhagic changes around the disc margins
what does pronator drift mean
means there is subtle pyramidal tract dysfunction (issue is in contralateral hemisphere)
is there is pronator drift is the issue unilateral or contralateral
contralateral
what type of rays do CT scans use
X-rays
which artery is most commonly compromised with extra-dural haematomas
middle meningeal artery (is at the temporoparietal area)
typical presentation of extra-dural haematomas
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
the difference between sub-dural and extra-dural haematoma
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
typical presentation of sub-dural haematoma
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
do primary brain tumours metastasise
no
classification of brain tumours
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
growth speed of miningeomas vs gliomas
meningeomas= slow growth
gliomas= range of growth (multiforme is the worst)
what is the treatment given for brain oedema
steroids (dexamethasone)
questions to ask about before attack (potentially seizure)
what they were doing before
position
feeling unwell (warning signs)
light headedness, nausea, altered vision, pale/clammy
twitching/jerking
questions to ask about during attack (potentially seizure)
memory of event
hearing anyone talking
body stiffness
floppy body
shaking
breathing
blue around lips
eyes open/closed
length of attack
questions to ask about after attack (potentially seizure)
feeling when came round
injury (tongue bite)
incontinence
did you know where you were
how long did you take to come round
management after first seizure
neurological and cardiovascular examination
routine bloods
12 lead ECG
refer to first fit clinic
stop driving until definitive diagnosis and treatment
features of temporal lobe seizures
limbic- deja vu and memory loss
abdominal rising sensation (from epigastric region)
vomiting, flushing, pallor, altered HR
altered language
features of frontal lobe seizures
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)
features of parietal lobe seizures
may begin with odd sensations (tingling/numbness)
may have complex visual hallucinations
features of occipital lobe seizures
visual symptoms (shapes and/or flashes)
shapes are often more colourful and circular than migraine
focal vs generalised seizures
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
focal seizures classification
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)
what is aura
warning sign- symptoms before the main seizure
symptoms= flashing lights, strange gut feeling, deja vu, sensing smells
aura is most common in seizures affecting which lobe
temporal
what is benign rolandic epilepsy
commonest epilepsy in children (5-10)
nocturnal seizures- facial twitches, eye flickering, lip smacking
what types of primary generalised seizures are there
absense seizures (aka petit mal, nonmotor)
generalised tonic-clonic seizures (GTCS, aka grand mal, motor)
atonic seizures (aka akinetic)
myoclonic seizures
absence seizures features
behavioural pause (usually less than 10 secs)
starts in childhood
Hz spike and slow-wave complexes on ECG
generalised tonic-clonic seizures features
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
atonic seizures features
sudden brief loss of tone and consciousness
will fall or regain consciousness and catch themselves
myoclonic seizures features
sudden jerk of bilateral limbs (usually arms) face, or trunk which may lead to fall
single/multiple
may occur on waking
triggers for seizures (especially generalised)
lack of sleep
alcohol
fever
flickering light
drugs/drug withdrawal
causes for seizures which isn’t epilepsy
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
types of focal seizures and types of generalised seizures
focal= focal aware seizure, focal unaware seizure, focal to bilateral tonic clonic seizure
generalised= primary generalised tonic clonic seizure, absence seizure, generalised myoclonic seizure
what are function seizures
they are non-epileptic dissociative seizures
aka psychogenic non epileptic seizures (PNES) or non epileptic attach disorder (NEAD)
what do function seizures typically look like
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
risk factors for epileptic seizures
alcohol misuse
febrile convulsions in childhood
perinatal brain injury
family history of epilepsy
traumatic brain injury
previous CNS infection
recreational drug use
management of epilepsy once diagnosis has been made
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
what effects need to be discussed with a patient when starting them on lamotrigine
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
what may be observed in cariogenic syncope
collapse in floppy manner
myoclonic jerking may occur, especially if in upright position
features of epileptic seizures (length, initial movements, nature of jerking and eyes)
2-5mins
whole body stiffening
there is rhythmic jerking, then reducing amplitude and frequency
eyes are open
features of non-epileptic seizures (length, initial movements, nature of jerking and eyes)
over 10mins
back arching movements
asynchronous limb movements
eyes may be tightly closed
features of syncope (length, initial movements, nature of jerking and eyes)
less than 1min
floppy collapse
brief jerking of low amplitude
eyes closed
what is syncope
transient loss of consciousness due to temporary reduction in cerebral blood flow
2 types of syncope
vaso-vagal (fainting)
cariogenic syncope
features of vasodilation-vagal syncope
symptoms before- dizziness, light-headedness, clamminess, visual blurring
there is postural correction on falling
consciousness regained in 30-60secs
well orientated on recovery
what could cause cardiogenic syncope
underlying cardiac arrhythmia/structural heart disease
does cariogenic syncope have preceding warning symptoms
typically no
what would you do when finding out someone had complete heart block
refer urgently to cardiology
consider permanent pacemaker
vital initial test when someone presents with altered conscious level
blood glucose
