Neurology Flashcards
What is epilepsy?
What are seizures and how can they be classified?
Disease characterised by the enduring predisposition to generate epileptic seizures and the neurobiological, cognitive, psychological and social consequences of the condition
Seizures are a transient occurrence of signs and symptoms resulting from abnormal excessive or asynchronous brain activity
May be focal (partial) - start in 1 part of the brain
Or may be generalised - more distributed affecting both brain hemispheres
What are the RF for epilepsy ?
- Genetic predisposition
- Trauma
- Perinatal asphyxia
- Structural CNS abnormalities
- Metabolic disorders
- Complex febrile seizures
How can epileptic seizures be categorised? [International League against Epilepsy 2017]
- Where they begin in the brain:
- Focal
- Generalised
- Unknown
- Focal to Bilateral (AKA secondary generalised - where starts focally then becomes generalised) - Level of awareness:
- Focal aware
- Focal impaired
- Awareness unknown (unwitnessed)
- Generalised (presumed to affect awareness) - Other features of the seizure (motor vs non-motor):
- IF Focal onset: MOTOR onset (jerking, twitching, stiffening) or NON-MOTOR (cognitive, emotional, sensory)
- IF Generalised onset: MOTOR (tonic/stiffenining and clonic/jerkining) or NON-MOTOR (absence, brief changes in awareness +/- automatic/repeated movements)
What are the signs and symptoms of:
- Absence/generalised non-motor seizure?
Absence/generalised non-motor:
- Brief impairment of consciousness (5-10 secs)
- Behavioural arrest or staring, interrupting normal activity
What are the signs and symptoms of a:
- Tonic-clonic seizure?
Tonic-clonic/’Grand Mal’:
- Patient falls unconscious and may have a preceding aura
- Violent muscle contractions and shaking
- Eyes may roll back, tongue biting, incontinence
- Post-ictal phenomena (confusion, drowsiness, headache, nausea)
What are the signs and symptoms of a:
- Myoclonic seizure?
- Different types (BRE, JME, PME)
Myoclonic:
- Brief, arrhythmic muscular jerking movements
- Last a few seconds, sudden jerking or twitching
Benign Rolandic Epilepsy (BRE):
- Most common childhood epilepsy affecting 3-12yo, but outgrow by puberty
- Seizures of face/upper limbs DURING SLEEP with hyper salivation and speech arrest (AKA sylvan seizures)
Juvenile myoclonic epilepsy (AKA ‘fly in cornflakes’):
- Begin around puberty (12-18yo)
- Usually involve neck, shoulders, upper arms occurring mostly AFTER WAKING up)
Progressive myoclonic epilepsy:
- Rare syndromes
- Combination of myoclonic and tonic-clonic
- Pt deteriorates over time
How would you manage a patient with epilepsy (Ix/Mx)?
note: think about AEDs + SEs/CI
[EEGs are not that useful so mainly clinical?/Mx]
- MDT based –> paediatrician, neurologist, epilepsy nurse, GP, schools
- Urgent referral to neurologist if 1st fit; whilst waiting for a referral then advise:
- -> how to recognise a seizure + what to do
- -> avoiding dangerous activities e.g. swimming
- -> video other seizures
- -> seek help if another event before referral
Treatment:
- Not all children require AEDs as weight vs risk of drug SE and severity/freq/type of seizures (i.e. BRE is not usually treated pharmacologically)
Appropriate AED choices:
Generalised:
–>TC - Valproate > Lamotrigine (or carbemapzepine/ oxcarbazepine)
–>Absence - Ethosuximide (girls) or Valproate, > lamotrigine (note: carbamazepine exacerbates absence seizures!)
–>Myoclonic - Valproate > levetiracetam, topimerate (note: lamotrigine + carbemazepine exacerbates myoclonic seizures!)
Focal seizures:
–> Carbemazepine, Lamotrigine (or consider adjuncts of valproate, topimerate or alternatives like levetirectam)
note:
- AEDs may be discontinued after 2y free of seizures
- monotherapy at lowest possible dose; can use adjuncts but try to limit dose
- ++ rescue therapy for status epilepticus >5 mins (buccal midozalam)
- monitoring only for carbamazepine
SE of drugs:
- Valproate (weight gain, hair loss, idiosyncratic liver failure)
- Carbemazepine - hyponatremia (SIADH), rash, neutropenia, drug-inducer
- Lamotrigine (severe skin rash - Steven Johnson syndrome)
What other treatments may be available for intractable epilepsies?
- Ketogenic diets
- Vagal nerve stimulation
- Surgery (if well localised structural cause)
What is Status Epilepticus?
1 epileptic seizure lasting >5 minutes OR at least 2/+ seizures within a 5 minute period without the person returning back to normal in-between OR 1 febrile seizure lasting >30 mins
How would you manage a child with status epilepticus?
A to E assessment:
Airway - high flow oxygen and don’t ever forget glucose
Circulation - if vascular access/can get quickly then IV/IO Lorazepam - if not then Buccal Midozalam (or rectal Diazepam) - in first 5 mins!
Then if not, try I/IO Lorazepam again and call for senior help
- reconfirm it is an epileptic seizure
- prepare phenytoin (IV/IO over 20 min)
- alert ICU and anaesthetist
- consider rectal paraldehyde
- if already on phenytoin, then give phenobarbitone IV/IO over 5mins
Final step - Anaesthetist must be present; rapid sequence induction of anaesthesia with thiopental
What are infantile spasms and who do they affect?
Epilepsy syndrome presenting in infancy (<1y, 3-8mo peak incidence)
- Characteristically part of West Syndrome (infantile spasms, developmental plateau and hypsarrhythmia - characteristic disordered brain activity on EEG)
- more common in males
Causes of infantile spasms?
- Any disorder causing brain damage
- Genetic syndromes
- Congenital infections
- Prenatal conditions
- HIE/Trauma
- Idiopathic
How would a child with infantile spasms present?
- Spasms: sudden, rapid, tonic contractions of trunk and limb muscles with gradual relaxation over 0.5-2 seconds
- ‘Salaam attacks’ - head goes down and arms up [looks like colic]
- Contractions last 5-10 seconds
- Can be gentle nodding of head –> powerful body movements
- Occurs in clusters; usually when WAKING or BEFORE sleeping
- Psychomotor delay
- Hypopigmented skin lesions (tuberous sclerosis)
- Growth restriction
How would you manage (Ix+Mx) a child with infantile spasms?
Ix:
- EEG - characteristic hypsarrhythmia (“random high-voltage spike and slow waves of varying amplitude, arising from multiple foci that vary over time. The background is asynchronous and generally chaotic” - BMJ)
- Others (glucose, Mg, Ca) to rule out other aetiology
Mx:
- Vigabatrin or corticosteriods
[Poor prognosis]
note: vigabatrin associated with visual field defects
What are Muscular Dystrophies and what is the most common one?
Progressive generalised diseases of muscles, often caused by defective/absent glycoproteins e.g. dystrophin in the muscle membrane.
–> Duchenne is the most common (DMD)
When does Duchennes normally present + continue and how is it inherited/acquired?
EXTRA: What is the pathophysiology of this mutation?
1:3000-6000 infants
X-linked recessive (males mainly affected) but 1/3 have denovo mutations (must check FHx!!)
- [dystrophin gene deletion means no connection of muscle fibre cytoskeleton to ECM through cell membrane and so Ca influx –> calmodulin breakdown + excess free radicals –> myofibre necrosis
Presents around 1-3yo with symptoms and diagnosed at 5; no longer walking by~10 with median LE ~35yo but on increase now
How may a child with DMD present?
Presents 1-3yo:
- Developmental delay (persistent waddling gait, some language delay)
- toe-walking
- decreased tone and power (flexors stronger > extensors therefore may also have lumbar lordosis, scoliosis also)
- Gower’s sign - need to turn prone to rise
- Pseudohypertrophy of calves due to fat+fibrous tissue replacing muscle
- Primary dilated cardiomyopathy
- Risk of aspiration pneumonia with infections also
What Ix would you do in a child with suspected DMD?/MD
- Plasma CK (creatine kinase) - elevated (~50-100x normal) due to myofibre necrosis
- genetic testing (Xp21),
- other: EMG, biopsy
How would you manage a child with DMD?
Note: no cure, just symptomatic treatment
- Physiotherapy (to clear lungs) + exercise (to reduce contractures)
- Psychological support
- Dietician for gastric feeding if indicated + VitD + Ca supplements
- Medical
- -> CPAP overnight for respiratory support (weakness of intercostal muscles may cause nocturnal hypoxia)
- -> Glucocorticoids to delay need for wheelchair
- -> Ataluren - drug that restores dystrophin synthesis and may be used if 5/+yo
- -> Cardio protective drugs e.g. carvedilol for preservation of LVEF
Surgery if needed (tendoachilles lengthening, scoliosis surgery)
What happens in Becker MD?
Same signs and symptoms as DMD but often LESS SEVERE and progresses SLOWER (also X-linked)
- learn to walk later than usual
- muscle cramps after exercise, struggle with sport at school
- as age increases, struggle with lifting objects
- can walk into their 40-50s but then need wheelchair
What happens in Myotonic MD? Inheritance mode + how they present?
Autosomal dominant trinucleotide repeat disorder (CTG)
- most common adult onset (20-30s) MD
- exhibits genetic anticipation (gets worse/earlier onset as gene passed down generations)
- variable LE (neonatal death-normal)
Sx:
- muscles contract but unable relax
- progressive muscle loss + weakness in smaller muscles>larger muscles (opposite to DMD)
- heart problems, cataracts, abnormal intellectual functional, myotonia
What are the indications for CT scanning in children after head injury? Why are these important?
Children are at high risk for contusion + intracerebral haemorrhage after head injury BUT also at risk from CT radiation to the head causing cancer
Therefore:
Head injury + 2/+ of:
- LOC>5mins
- Abnormal drowsiness
- 3/+ vomiting episodes
- Dangerous mechanism/high impact injury
- Amnesia>5 mins (anterograde and retrograde)
= CT SCAN <1h, if just 1 of those listed then observe for minimum 4h
Head injury with 1/+ of:
- NAI
- Post-traumatic seizure (no epilepsy Hx)
- GCS<14
- GCS <15 2h+ post injury
-Suspected open/depressed skull fracture/tense fontanelle
- Basal skull fracture signs (racoon eyes, battle sign [postauricular bruising], CSF rhinorrhoea)
- Focal neurological deficit
- Child <1y and bruise/swelling/laceration >5cm on head
= CT SCAN <1h
What are the 4 main TBI classifications and how may they present (not IVH)? How would you Ix + Mx these patients?
Extradural:
- Usually following direct trauma
- May have skull fracture (pterion, MMA tear) - battle sign and racoon eyes for basal fracture
- LUCID interval followed by deterioration of consciousness + seizures
- May have focal signs (dilation of ipsilateral pupil, paresis of contralateral limb, shock and anaemia)
- Ix: CT head (lemon sign)
- Mx: Fluid resus to correct hypvolaemia + neurosurgery to evacuate the haematoma and stop the bleeding
Subdural
- Results from tear of vein crossing the subdural space
- GCS GRADUALLY decreases i.e. no lucid interval like EDH
- Characteristically NAI e.g. shaken baby syndrome (triad of subdural haematoma, retinal haemorrhages and brainswelling/encephalopathy) or direct trauma
Ix: CT Head (banana sign)
Subarachnoid
- rare in children, often caused by aneurysm or arteriovenous malformation
- acute onset head pain, neck stiffness, fever +/or seizures/coma
- CT head, avoid LP due to risk of increased ICP
- Mx = neurosurgery or IR
Intraventricular (see other flashcard)
How may a patient with intraventricular haemorrhage present (note: grading + risks)? How would you Ix + Mx them? What is the aetiology and epidemiology? What are the risks?
Intraventricular haemorrhage:
- bleeding into ventricles
- occurs more in premature babies (LBW + VLBW)
- caused by changes in perfusion to growing brain, e.g. from ECMO in premature babies with severe RDS or congenital CMV infection
Graded:
o Grade I – bleeding just in germinal matrix
o Grade II – intraventricular bleeding (but no enlargement)
o Grade III – intraventricular bleeding with enlargement ventricles
o Grade IV – bleeding extends into brain tissue around ventricles
[I+II –> most common; no further complication
III+IV –> Can lead to long-term brain injury; also after GIII/IV, clots can form leading to secondary hydrocephalus
note: 50% of those with progressive post haemorrhage ventricular dilation go on to develop cerebral palsy
If there is bilateral multiple cysts then = PVL (periventricular leukomalacia) - 80-90% risk of spastic CP
(can only potentially see cystic lesions 2-4w later on USS)
presents - sleepiness, lethargy, apnoea, low tone, no moro reflex, tense fontanelle
Ix - trans-fontanelle USS
Mx - fluid replacement, anticonvulsants, acetazolamide (reduce CSF) +/- LP
- ventriculo-peritoneal shunt if hydrocephalus
Outline the criteria for each part in GCS scoring?
Score ranges from 3 - 15
this is the adult one below but differences, mainly in verbal response, for paediatric criteria
Eyes: 4 - spontaneously open 3 - open to verbal 2 - open to pain 1 - no opening of eyes
Verbal: 5 - orientated to TPP 4 - confused 3 - inappropriate words 2 - incomprehensible sounds 1 - no response
Motor:
6 - obeys/spontaneous
5 - moves to localised pain
4 - withdrawal to pain (flexion)
3 - abnormal flexion (decorticate - arms up)
2 - extension response (decerebrate - arms down)
1 - no response
What is vasovagal syncope - how does it present, how would you investigate and manage it?
LOC which is caused by either emotional trigger (fear/shock/pain/sudden sounds or sights) or orthostatic (prolonged standing, crows, hot)
Sx:
-> Brief LOC with spontaneous recovery, no signs of seizure activity and link to trigger
Ix:
- > Lying and standing BP
- > FBC (rule out anaemia and bleeding)
- > ECG if indicated/cardiac cause queried
Mx:
- > Avoid triggers
- > Lie down flat to avoid fainting (when feel sensation close to occurring)
What is a febrile convulsion? In who and how does it present? Simple vs Complex?
Seizure and fever in the absence of an intracranial infection
- > Occurs in children 6m to 3y
- > Genetic predisposition (30% get further seizures)
Sx:
-> Brief, generalised tonic-clonic seizure
-> fever
NOTE: simple febrile seizure = cause no brain damage and no increased risk of epilepsy
complex febrile seizure = focal, >15 mins, repeated in same illness and associated with a 4-12% increased risk of epilepsy
What investigations would you do after a febrile seizure?
Ix:
- > Identify and manage the cause of fever (check ears, throat, listen to chest)
- > Consider screening for meningitis/encephalitis, urine MC&S, blood glucose
How would you manage a febrile seizure?
Mx:
- During a seizure:
- > protect from injury (cushion head, remove nearby objects and don’t restrain)
- > if <5 mins, do nothing UNLESS 1st seizure, severe cause, breathing problems
- > if >5 mins - call ambulance OR rescue meds: buccal midozalam or PR diazepam (repeat PR after 5 mins if still not stopped). IF >10 mins after 1st dose then call an ambulance
- > IF ongoing seizure in hospital then status epileptics guidelines (IV Lorazepam)
- > Midozalam = 2.5mg 6m-11m, 5mg 1-4y and 7.5mg 5-9y
- > Diazepam = 5mg 6m-1y and 10mg 2-11y
AFTER the seizure:
- > Immediately after check ABCs and place in recovery position
- > Admission + immediate assessment by paeds only if 1st febrile seizure, <18m old, uncertain diagnoses of cause, currently on Abx and complex febrile seizure
- > Check blood glucose if child can’t be roused/convulsing
- > Otherwise managed at home with advice:
- 33-50% may have another FC, not same as epilepsy just due to fever and they are common in children but nonetheless worrying for parents
- safety net (>5 mins and don’t have meds etc)
- don’t try to cool the child, ensure adequate fluids, regular paracetamol and ibuprofen, seek advice if fever lasting a long time
- keep getting immunisations
What is hydrocephalus? What are the 2 types and causes?
Hydrocephalus is an increased volume of CSF occupying the ventricles. Can be differentiated into:
-> Communicating = flow of CSF is obstructed AFTER it exists the ventricles i.e. a failure to resorb CSF due to e.g. Meningitis (TB, pneumococcal) and SAH
-> Non-communicating = flow of CSF is obstructed WITHIN the ventricles. May be due to a congenital cause:
- Aqueduct stenosis
- Dandy-Walker malformation (enlarged 4th ventricle with no outlets)
- Chiari malformation (Cerebellar tonsils displaced down through foramen magnum)
Acquired causes:
- Aqueduct stenosis from IVH (preterm infants) or tumours
How does hydrocephalus present?
Sx -
Acute = vomiting, irritable, impaired consciousness
Chronic = FTT, developmental delay
Other = increased head circumference, tense fontanelle, increased tone, papillodema and sunset sign (eyes driven down bilaterally), ataxic gait, 6th nerve palsy
How would you Ix and Mx hydrocephalus?
Ix:
- Measure head circumference
- Cranial USS
Mx:
- 1st line = Ventriculoperitoneal shunt (may fail due to blockage or infection and require replacement/removal of blockage)
- Medical tx = furosemide to inhibit CSF production
What are Tics? What is Tourette’s? Who does it affect?
Fast, repetitive muscle movement that result in sudden, difficult to control body jolts/sounds
- appear around 5yo, most disappear by adulthood
- 1/3 rules (1/3 won’t have it as an adult, 1/3 have mild tics and 1/3 have severe tics)
- genetic component - can occur alongside OCD and ADHD
Tourette’s = chronic and multiple tics
- No cure, same Tx as tics
- Tics must begin before 18y and persist for >1y
- Exclude any other cause
How may someone with tic disorder present?
Sx:
- brought about by triggers, focussing on them can make it worse
- Types of tic = blinking, coughing/grunting, clicking fingers, repeating sound or phrase
How would you manage a patient with tic disorder?
Mx: (+Ix)
- Self-help - stress and sleep management, don’t draw attention to it or tell child off for it
- If very debilitating:
- -> HABIT REVERSAL THERAPY (learn movements to ‘compete’ with tics so tic’s can’t occur at the same time)
- -> EXPOSURE WITH RESPONSE PREVENTION (ERP) (help the child get used to the unpleasant pre-tic sensation which can stop the tic from occurring)
- Medications:
- -> 1st line = antipsychotics (risperidone - SE include weight gain, blurry vision, constipation, dry mouth)
- -> 2nd line = Clonidine (treats ticks and ADHD simultaneously), Clonazepam, Botulinum toxin into certain muscle (last 3m only) and Tetrabenazine (for tics caused by an underlying condition such as Huntington’s)
- > Surgery (e.g. severe Tourette’s) - deep brain stimulation therapy
What is developmental delay and how may it present? What are some causes?
Developmental delay is where a child takes longer to reach developmental milestones that would be expected for their age
Causes:
Sx:
- > Isolated DD in 1 domain i.e. gross motor, fine motor and hearing, speech and language and social
- > Global DD
- > FHx of delay or syndromes
- > Dysmorphic features or PMH of syndrome
What are some Ix and Mx of developmental delay?
Ix:
- [Would’ve done a full developmental assessment +/- hearing + sight tests]
- Metabolic, genetic, infection screening
- ASD/ADHD testing
- IQ test
Mx:
- Referral + MDT based with SALT, OT, PT, family counselling, behavioural intervention and educational assistance
- Manage social issues
- Isolated has a better prognosis; global has a high association with poor prognosis syndromes
What is somatisation? What are some common ways it may present?
Somatisation = manifestation/communication of emotional distress, troubled relationships and personal predicaments through bodily symptoms
Sx:
- > Recurrent abdominal pain (peak at 9yo) - affects 10% school age children, around umbilicus (Apley’s rule)
- > Recurrent headaches (peak at 12yo)
- > Limb pain, aching muscles, neurological symptoms (>12yo)
How would you Ix and Mx somatisation?
Ix:
- Dx of exclusion so must exclude other cuases
- Full physical examination
- Full detailed history, collateral from school and family if possible
Mx:
- 1st line = promote communication between child and family (+school if needed) and pain coping techniques like relaxation for headaches
- 2nd line = if fails/family or general dysfunction then referral to CAMHS
State some neurocutaneous syndromes?
- Neurofibramatosis type 1
- Tuberous Sclerosis
- Sturge Weber syndrome
What is NF1, how does it present and what are some associations with it? What is NF2?
NF1 - autosomal dominant and has variable expression
- > mutation in the NF1 gene, 50% are de novo mutations
- > Associated with MEN2, Pulmonary HTN, pheochromocytoma and RAS with HTN
NOTE: NF2 is like NF1 but less common, seen in adolescence with bilateral acoustic neuromas + deafness, and other cerebellar symptoms
Sx: [requires at least 2/+ of the following for Dx]
- at least 6/+ cafe au last spots (>5mm pre-puberty, >15mm post puberty)
- > 1 neurofibroma (firm nodular overgrowth of nerve)
- axillary freckles
- optic glioma +/- visual impairment
- Hamartoma of iris (Lisch nodule - brown dots in iris)
- First degree relative with NF1
- Bony lesions +/- eye protrusion
What is Tuberous Sclerosis? How does it present and how would you Ix it?
TS is also AD with 70% cases from new mutations. Causes mainly benign tumours to develop in the body
Sx:
-> Cutaneous features - Shagreen patches (rough skin on lumbar spine). ‘Ash leaf’ hypo pigmented patches under Wood’s lamp, angiofibromata (butterfly facial distribution)
-> Neurological - infantile spasms, focal epilepsy, intellectual disability-often with ASD
-> Other - angiomyolipoma (kidney tumour), dense white areas on retina, sublingual fibromata
-> NC Hydrocephalus if a nodule in brain (subependymal giant cell astrocytoma)
[ASHLEAFS] - ash leaf spots, shagreen patches, heart rhabdomyomas, lung lymphangioleiomyomatosis, epilepsy due to tubers (+DD/InfSpasms/ASD), angiomyolipoma in kidney, facial angiofibromas and subependymal giant cell astrocytoma–>NC hydrocephalus
Ix:
- CT scan (can see calcified subependymal nodules and tubers from 2+ years)
- MRI scan (more sensitive and clearly identify other lesions/tubers)
What is Sturge-Weber syndrome and how does it present? What is an investigation necessary?
Sporadic disorder + not inherited
- -> Haemangiomatous facial lesion (port-wine stain) in the distribution of the TRIGEMINAL NERVE
- Lesion may be intracranial (ipsilateral leptomeningeal angioma)
- Ophthalmic branch of trigeminal nerve always involved
Sx:
- Epilepsy
- Contralateral hemiplegia
- Pheochromocytoma
- Intellectual disability
- Glaucoma in 50%
- Port wine stain
Ix -> MRI; assess depths of lesions
What are 4 types of headaches?
Primary
- Migraine = main
- Tension type
- Cluster
Secondary - due to underlying pathology e.g. SOL, raised ICP, alcohol
How would tension headaches present?
Symmetrical
Gradual onset
Feels like tight band
How would migraine present?
90% without aura, 10% with aura
- Aura may be visual (or less often sensory/motor)
- Uni or bilateral throbbing pain, pulsatile temporal, GI sx, worse with physical activity
- Photophobia
- FHx of migraine
- Vomiting/pallor
- Triggers e.g. certain foods, stress
How would a cluster headache present?
Unilateral, near the eye or side of face
Sharp/burning/throbbing pain
Watery/swollen eye
Occurs in clusters
How would a secondary headache present?
Focal neurological signs - gait/CN etc
Visual field defects
Growth failure
Papillodema
Early morning headache
How would you Dx migraines (criteria)?
Migraines must:
- 5 or more headache attacks lasting 4-72h
- Lasts 4-72h
- At least 2 of the following: bilateral/unilateral location, pulsating, moderate-severe intensity, aggravated by routine physical activity
- At least 1 of: N+/vomiting, photophobia or phonophobia
How would you Ix and manage headaches in children?
Good history and examination
- -> If suspect meningitis then bloods/LP etc
- -> Imaging if red flag Sx e.g. early morning headache
- -> Consider headache diary for trigger identification
Mx:
- Medical education that they are common and no long-term harm
- analgesia = ibuprofen > paracetamol
- anti-emetics (anti-histamines) = prochlorperazine
- Triptans in 12+ (nasal sumatriptan)
How would you specifically manage migraines in children?
Mx:
- Medical education on safety and common
- Obviouly causes distress however - assess this impact and patterns noted
- Identify cause (emotional problems) –> consider psychiatry referral, headache diary for 8w, optician referral, weight, height and BP
Acute Mx: in 12-17yo
- -> 1st = Simple analgesia (paracetamol and ibuprofen but not aspirin, unless 16+, due to risk of Reye’s syndrome = liver and brain swelling)
- -> 2nd = nasal sumatriptan (oral not licensed for <18yo)
- -> 3rd = Combined nasal triptan and NSAID/paracetamol; consider anti emetics and f/u in 1m or if Sx worsen
- -> Prophylaxis = Topiramate (no pregnancy), propanalol (not in asthma) BUT requires specialist referral
