Seizures Flashcards
What is a seizure?
a seizure is a transient occurrence of signs and/or symptoms due to abnormal excessive neuronal activity in the brain
[esp vs blackouts which is a transient LOC due to global cerebral hypoperfusion]
(key part is presence of symptoms/signs is key to definition as only occur in whole organsims)
What is a focal seizure?
a focal seizure has a discrete cortical origin
–> strange sensations or jerking movements
what types of focal seizure did there used to be/what have they become now according to Prof. H. Cock?
- FOCAL AWARE: (previously: simple)
- maintain consciousness
- FOCAL UNAWARE (previously: complex)
- altered awareness or LOC
-
+/- emotional disturbance and automatism -
- fried reticular formation –> e.g. the neuronal pathways in the brainstem connecting the spinal cord, cerebrum and cerebellum, mediating the overall level of consciousness
What is a primary generalised seizure?
primary generalised seizure:
- usually involves both hemispheres upon onset
- & usually loss of consciousness
What is a secondary generalised seizure?
- a type of focal/partial seizure that spreads to both hemispheres
- thus develops into a generalised seizure
What are the types of partial/focal seizure?
they are split to the parts of the brain they can be localised to, TF the types of focal seizures are:
- temporal lobe
- frontal lobe
- parietal lobe
- occipital lobe
*
Carbamazepine or lamotrigine are most commonly used for which seizure type: partial or generalised?
carbamazepine or lamotrigine are used for partial/focal seizures
e.g. ones in temporal, frontal, parietal, occipital lobes
sodium valproate is an AEDs used in which type of seizure: focal or generalised?
sodium valproate is an AED used in generalised seizure types
e.g. tonic, atonic, clonic, tonic-clonic, myoclonic or absence
Temporal lobe focal seizures show particular symptoms due to where in the brain is experiencing abnormal excessive neuronal activity.
The acronym for temporal lobe seizures is ADDFAT, what does this stand for?
- A - Aura
- [intense emotional, memory, epigastric rising (rising sensations in abdomen)
- D - Deja Vu / Dysphagia
- ictal or post ictal (/foaming at mouth TF?)
- D - Delusional behaviour
- [hallucinations- complex sensory experiences - can be auditory, gustatory, olfactory]
- F - Fear
- (often hippocampal involvement –> sudden terror, panic, anger or elation, derealisation)
- A - Automatisms
- (lip smacking/grabbing etc)
- T - Taste/smell
- (uncal involvement - hallucinations of smell or taste or dreamlike state)
Frontal lobe focal seizures show particular symptoms due to where in the brain is experiencing abnormal excessive neuronal activity.
The acronym for frontal lobe seizures is JAM, what does this stand for?
J - Jacksonian march
- seizure starts in one muscle group and spreads ro other groups often starting at thumb of face
A = pAlsy e.g. todds palsy, typically limbs/but can be all body wekness on just L or R sides etc - post ictal, lasts minutes to hours - usual resolution e/i 48hrs
M - motor features including motor arrest; posturing, versive head movements, peddling movements of legs,
+ dysphagia or speech arrest, subtle behavioural differences
(NB: frontal lobe contians the 1o motor cortex while temporal contains 1o sensory)
PARIETAL lobe focal seizures show particular symptoms due to where in the brain is experiencing abnormal excessive neuronal activity.
What are the symptoms of parietal lobe seizure?
- sensory disturbances - tingling, numbness and rarely pain
- motor symptoms - spread to pre-central gyrus
- aura - motor, simple sensory
*
Occipital lobe focal seizures show particular symptoms due to where in the brain is experiencing abnormal excessive neuronal activity.
What are the symptoms of occipital lobe seizure?
visual hallucinations aura (coloured)
visual pohenomena e.g. spots lines, flashes
What are the different types of generalised seizure?
- Tonic: stiff/flexed - fall BACKWARDS
- Atonic: muscles relaxed - fall TOWARDS
- Clonic: convulsions
- Tonic-Clonic: tonic phase followed by convulsions - often produce an epileptic cry ~30s
- Myoclonic: short muscle twitches
- Absence: impaired awareness & responsiveness - only outward sign is person looking spaced out
- This type of seizure presents between 3-10y/o
- commoner in Girls > Boys
- can be provoked by hyperventilation or stress
- they are normally unaware of the seizure
- they may occur many times in a day
- it lasts a few seconds and is associated with a quick recovery
What would the EEG show of this seizure type?
this is an absence seizure
EEG: bilateral, symmetrical 3Hz spike and wave pattern
What are the classic signs of a seizure/ seizure markers?
- Duration LoC/Amnesia >5 mins
- prodromal focal features
- seizure activity (tonic/clonic/automatisms etc)
- motor features: head turning, ususual posturinig, prolonged
- tongue biting (lateral)
- incontinence
- injury
- post-ictal confusion [THIS IS PATHOGNOMONIC, you dont get confusion with syncope…]
What can cause a seziure?
Almost any brain injury if severe enough, causes seizures (- useful for animal models)
- acute symptomatic seizures occur within hours/days of insult
- Metabolic upset (low Na or Ca)
- Traumatic brain injury – concussive seizure
- Stroke/haemorrhage – at time of the stroke
- Alcohol & recreational drugs - Alcohol withdrawal peak timing is ~36hrs (~1.5d)
- Infection (encephalitis)
- Febrile seizures (infants)
- Structural
- Epilepsy: unprovoked, remote symptoms
- Psychogenic non-epileptic seizures
- Neoplasm
- Tuberous sclerosis, sarcoidosis, PAN, SLE
- Uraemia
What is the typical age group of febrile seizures?
- 6 months - 5 yrs
- ~3% of children will have at least 1x febrile convulsion & these usually occur early in a viral infection due to the temperature rising rapidly
- seizures are typically brief and generalised tonic/tonic-clonic in nature
- A febrile convulsion cay cause hippocampal sclerosis –> structural causes of seizures
What are the structural causes of seizures?
cortical scarring
developmental
DOL
hippocampal sclerosis (after a febrile convulsion)
vascular malformations
What do you ask in a seizures history?
- Before = aura, trauma, screen for other pathologies - headache?
- Previous risk factors, circumstances, posture, prodrome
- During = can you act out what they were doing, urinary incontinence, trauma?
- Witness account where possible, duration, LOC
- After =
- post-ictal state (5-30mins - strong seizure marker)
- how long to return to usual self?
- confusion?
- blood in mouth (tongue biting)
- tired (use up lots of glucose doing tonic clonic)
What investigations are done for seizures?
- ABCDE, blood glucose, GCS
- Vitals, bloods, imaging for Traumatic brain imaging–>
- CTH/MRI
- EEG
- RAISED PROLACTIN IN SEIZURES
What are the differentials for a drop attack?
- CVS problems
- acute brain disturbance
- metabolic cataplexy
What are the differentials for a loss of awareness?
- syncope
- panic attack
- hypotension
- hypoglycaemia
- sleep
What are the differentials for convulsions?
- Movement disorders
- dissociative non-epileptic seizures
What are the differentials for transient focal symptoms?
- TIA
- demyelinating disease
- vestibular
- migraine NB: can get vestibular migraines etc…
- psychiatric
What are the differentials for attacks in sleep?
- hypnic jerks,
- restless legs,
- sleep apnoea,
- parasomnias…
What is the first aid Rx for any seizure?
the acronym is ACTION
A - assess ?safe place / dont touoch mouth
C - cushion head
T - time the fit/seizure
I - identify - red brarcelet/ID
O - over –> on recovery position
N - never restrain!
get IV access; O2 - not co-ordinating breathing; anti-epileptics if known epilepsy
What is epilepsy?
what is epilepsy vs a seizure
epilepsy = recurrent unprovoked seizures
[e.g. a provoked seizure is something that if it happened to anyone would give a seizure e.g. trauma/infection]
Epilepsy = a disorder of the brain characterised by enduring predisposition to generate epileptic seizures and by the neurobiological, cognitive, psychological & social consequences of this condition
a seizure = pathologic neuronal activation leading to abnormal brain function
What is required for a diagnosis of epilepsy (recurrent, unprovoked seizures)?
- 2 or > unprovoked or reflex seizures >24h apart
OR
- 1x unprovoked or reflex seizure but increased risk e.g.
probability of further seizures to general recurrence risk >60% after 2 unprovoked seizures occuring over the next 10 years
OR
- Dx of an epilepsy syndrome
What are some RF for babies to have epilepsy?
- Babies small for their age,
- Babies who have seizures in the first month of life
- Babies who are born with abnormal areas in the brain
Using vitamin CDEF surgical seive what are the RF for epilepsy?
- Vascular - bleeding into the brain, abnormal BV in the brain, stroke from arteries blockage
- Infective/inflam - infections of brain abscess, meningitis or encephalitis
- Trauma - serious brain injury or lack of O2 to brain, early post-traumatic seizures (e.g. occur within days of head injury NB: unlikely to get epilepsy from a mild head injury)
- Autoimmune
- Metabolic - illegal drugs e.g. cocaine
- Iatrogenic/ Idiopathic - 2/3rds of epilpepsy cause is idiopathic
- Neoplastic - brain tumours
- Congenital - cerebral palsy, Autism
- Degenerative - conditions with intellectual and developmental disabilities,
- Endocrine
- Functional - Fhx of fever related seizures or fever seizures that are very long / status epilepticus
What are the structural caues of epilepsy?
- cortical scarring - post-traumatic / stroke / encephalic
- developmental abnormalities
- SOL (tumours)
- stroke
- hippocampal sclerosis
- vascular malformation
What conditions can cause epilepsy?
- tuberous sclerosis
- sarcoidosis
- SLE
- PAN (early onset childhood occipital epilepsy)
- Dementia
- Genetic abnormalities
- NB: sleep deprivation and pregnancy are also ictogenic
What is the (hypotheses of the) pathophysiology of epilepsy?
- that sudden excitatory signals occur in epilepsy over and over
- called - “paroxysmal (sudden) electrical discharges”
- these can be caused by
-
changes in inhibition
- network problem
- (normally GABA on GABA receptors –> Cl- into cells)
-
increased excitation
- (glutamate on NMDA receptors means Ca2+ comes into cells = excites it)
-
“epileptic neuron”
- __rather than a network problem is just individual neuronal problems then when enough of them = a seizure?
-
changes in inhibition
What should you check on examination of a pt with a seizure (after hx)?
- vital sign abnormalities
- nuchal rigidity
- head trauma
- tongue laceration
- shoulder dislocation
- neuro exam
What bloods do you take for seizures / ?epilepsy by ruling out provoking seizure causes?
- FBC, U&E,
- LFT (hepatic dysfunction, alcoholic hepatitis
- lactate, glucose
- anti-epileptic drug levels
- b-hCG (preg & pre E!)
- CSF
- PROLACTIN (raised in seizures!)
Why is brain imaging importatnt in seizures?
Using CT or MRI to look for malicious abnormalities underlying seizures e.g. tumours
is there a diagnostic test for epilepsy?
no diagnostic test
- 10-20% chronic epilepsy cases referred to 3o care and >50% diagnosed in 1o dont have epilepsy
Regarding EEG =
- abnormal findings are found in 50% of patients with clinically defined epilepsy - rising to 80% of provocation e.g. sleep deprivation, hyperventilation or photic stimulation (flickering light)
- EEG/these things help classify & prognosticate but 10% of pts never show epileptiform discharges
What is the epileptiform activity identifiable on EEG to help determine seizure type & epilepsy syndrome?
NB: EEGs are specific not sensitive e.g. if it shows you have it its likely you have it but you may have the condition without it showing up on EEG
epileptiform activity includes:
- generalised discharges = “spike & wave”
- they are:
- synchronous (all channels at the same time)
- symmetrical - however focal abnormalities may have quick spread & can be seen to look like pts with generalised epilepsy
-
focal discharges
- localised, may appear in mutiple areas or remain localised throughout recording
- NB: focal abnormalities can be seen in pts with generalised epilepsy
When is hyperventilation a useful activation procedure in epilepsy/EEG Dx?
hyperventilation for 3 mins is useful in dx childhood absence epilepsy because of the changes in EEG shown, thought to be caused by low CO2 in blood
Why is photic stimulation useful as an EEG activation procedure in epilepsy?
Photic stimulation a.k.a. a range of flash frequencies with eyes open and closed
- useful in Dx juvenile myoclonic epilepsy
–> shows generalised discharges associated with photic stimulation have a strong association with epilepsy
What does this describe?
trying & capturing seizure/epileptic attack on EEG & video – useful for diagnosis & pre-surgical evaluation (decrease meds & use activation procedures)
Long term monitoring
Video telometry
What Ix for epilepsy does this describe?
electrodes inserted during surgery
- –> used to determine region to be removed or leave in
- & monitor on the ward*
to accurately identify location of seizure (& onset )
intracranial readings
What is the general management (C, M & S?) for epilepsy?
- Conservative:
- ketogenic diet
- forces body to burn fat instead of carbs; produces ketone body used by brain instead of glucose - mechanism unclear
-
counselling: “fit” advice about dangers e.g. swimming, driving, employment, insurance
- avoid driving until seizure free for >1 year “must contact DVLA”
-
neuromodulation/nerve stimulation
- stimulates vagus nerve - influences NT release
- Medical
- daily medications - anticonvulsants
- Surgical
- epilepsy surgery (remove cause, use intracranial readings)
When is neuromodulation used as an epilepsy Rx?
neuromodulation is not curative: it is used in drug resistant patients who are unsuitable for surgery
- Vagal nerve stimulation: non-invasive, good evidence, not sure of mechanism, ?influences NT release
- Deep Brain Stimulation (DBS - on anterior thalamic nuclei e.g. where all the M&S info is relayed to cerebral cortex)
-
Responsive neurostimulation (seizure foci) - EEG picks up that the seizure is about to happen and delivers the shock to area to stop it
- used in brain areas that cannot be removed surgically e.g. for speech
When is epileptic surgery indicated?
is an option for drug resistant patients
protocol: MDT assessment –> MRI –> functional & multi-modal imaging –> neuropsychiatric assessment, video EEG & seizure capture
With surgeries there is risk of death/stroke but these = that of living with CHRONIC SEIZURES
What conditions causing epilepsy does neurosurgery “fix”?
- indolent (painless) glioma - 80% chance of being seizure free (vs 1:20 for drugs)
- small vascular lesions
- hippocampal sclerosis
- larvge AVMs (as oxygen/blood is shunted away)
- Trauma
- Cortical dysplasia = 50% chance of being seizure free - dont do if odds <50%
What counselling should a patient be given after an epilepsy diagnosis?
- After any fit, advise about dangers (e.g. swimming, driving, heights) until diagnosis is known
- Then consider employment, sport, insurance & contraception advice
Must contact DVLA,
- cannot drive until seizure free for >1yr
- = 6 months if first unprovoked/ isolated seizure & normal CT Head + EEG
- NB: [lorry drivers after 1 seizure cant drive for 5 yrs and if after 2 seizures = not for 10 years, & ?doesnt count unless seizure free for 1 yr w/o anti-convulsants]
When are AEDs prescribed regarding seizures?
- AEDs suppress seizures but dont modify the underlying cause of epilepsy - there is no effect once you stop taking them
- Treatment typically initiated upon diagnosis (>1 seizure) ONLY if risk of recurrence is high
- e.g. structural brain lesion, focal CNS deficit, or unequivocal epileptiform EEG;
- otherwise discuss after a 2nd fit
- “Start low, go slow” approach to seizure control
- Monotherapy is effective in 2/3rds patients
- Some people with minor seizures choose not to take: SEs, willing to live without driving, risk vs benefit
- MDT involved in decision: shared decision making
What are the aims of AED treatment?
Goals:
- seizure freedom,
- decreased seizure frequency/severity,
- good tolerability/low risk adverse effects
What is the first and 2nd line AED for tonic-clonic seizures?
- sodium valproate
- second line: lamotrigine, carbamazepine
What is the AED Rx for absence seizures?
- sodium valproate or ethosuximide
- sodium valproate particularly effective if co-existent tonic-clonic seizures in primary generalised epilepsy (e.g. seizure involves both hemispheres upon onset and consciousness is usually lost)
What is the AED medication and 2nd line for myoclonic seizures?
- sodium valproate
- second line: clonazepam, lamotrigine
What is the AED treatment for focal seizures and the 2nd line?
- carbamazepine or lamotrigine
- second line: levetiracetam, oxcarbazepine or sodium valproate
Phenytoin, carbamazepine, sodium valproate and lamotrigine all work by what mecahanism?
they are all Na+ channel antagonists
Name 4 x Na+ channel antagonists e.g. AEDs?
- phenytoin
- carbamazepine
- sodium valproate
- lamotrigine
What mechanism of action does ethosuxamide (RX: for asbence seizures, this or Valproate) have?
Ca2+ channel antagonist
Name a Ca2+ channel antagonist (an AED)
ethosuxamide
used to treat absence seizures
Benzodiazepines, barbiturates and sodium valproate & gabapentin all have what MoA?
they all are GABAA and GABAB potentiators
Benzos = increase GABAA channel opening FREQUENCY
barbs: increase GABAA channel opening DURATION
SV: modifies GABA synthesis
gabapentin: modifies GABA release
Some people with minor seizures choose not to take: SEs, willing to live without driving, risk vs benefit
What are common AED SE’s?
- (less neuronal firing:)
- Drowsiness/sedation,
- fatigue,
- unsteadiness,
- constipation/diarrhoea,
- double vision (most AEDs)
AEDs can cause from simple rash to steven jonson syndrome (idiosynchratic rxn)
what makes carbamazepine induced steven johnston more likely?
in Han Chinesee (east asian, worlds largest ethnic group)
w/ HLA-b*1502 allele
Which AED causes bone marrow suppression and skin rash?
carbamazepine
can also cause steven jonson syndrome (skin & MM fall off) - idiosyncratic rxn though
Which AED gives risk of birth defects?
Sodium valproate
- its the best drug for genetic generalised epilepsied but increased risk of teratogencicity, neurodevelopmental risk, lower IQ in babies…
What side effect of lamotrigine give (this one the best for focal epilepsy with carbamazepine)?
skin rash
Which AED causes gingival hypertrophy (gums cover teeth) & peripheral neuropathy?
phenytoin
a Na+ channel antagnoist used for status epilepticus
Side effects of sodium valproate can be remembered by the acronym VALPROATE - the V stands for valproate. What are the side effects?
- Valproate
- Appetite gain
- Liver failure
- Pancreatitis
- Reversible hair loss
- Oedema
- Ataxia
- Teratogenicity/tremor/thrombocytopenia
- Encephalopathy (ammonia)
AED drug interactions can be caused by being enzyme inducer AEDs, what drug interactions does this mean you need to look out for?
Oral contraceptive pill
warfarin
AED drug interactions can be caused by being enzyme INBHIBITOR AEDs, what drug interactions does this mean you need to look out for?
e.g. valproate is an enzyme inhibitor AED
need to check warfarin, other liver drugs
Which type of AEDs are good for patients with comobidities?
newer AEDs
becucase they tend to have less interactions
How can you monitor AEDs?
- Apps can be used as an objective measure
- show epilepsy is inherently variable with good & bad spells, shows the importance of long term studies
- Pill reminders
- Therapeutic drug monitoring (TDM)
- –> measuring drug concentration in body fluid as aid to optimising therapy
Therapeutic drug monitoring is used with AEDs to measure drug concentration in body fluid as an aid to optimising therapy. - which patient groups is this done it?
- pregnancy
- polypharmacy
- children
- elderly
- renal & hepatic disease
Which drug of phenytoin, lamotrigine and leviteracetam does this describe:
- long ½ life, saturation kinetics, hepatic oxidation (faster in children w/ ethanol & carbamazepine, slowed by enzyme inducers)
- Target range: 10-20mg/L but WIDE VARIATION
- Neurotoxicity: ~30mg/L
phenytoin
Which drug of phenytoin, lamotrigine and leviteracetam does this describe:
rapid absorption,
hydrolysis in whole blood,
renal clearance (higher in children, decrease in pregnancy)
leviteracetam
Which drug of phenytoin, lamotrigine and leviteracetam does this describe:
rapid absorption, heptic glucoronidation (faster in pregnancy)
Need monitoring for polypharmacy
Adverse effects: rash, CNS effects
lamotrigine
What is status epilepticus?
- Continuous seizure activity that fails to self-terminate >5mins or recurs without complete recovery between
- RISK NEUROLOGICAL DAMAGE
What is the Rx for status epilepticus?
ABCDE, cannulate, O2, suction, vitals, IV access & take bloods inc toxicology, Ca2+, Mg2+ etc
- IV lorazepam (or buccal midazolam)
- Wait 10mins
- IV lorazepam (or buccal midazolam)
- Wait 10mins (20 min total); notify anaesthetist
- IV Phenytoin
- Wait 10mins (30m total)–>
- Rapid sequence induction (RSI) with propofol, thiopental sodium or midazolam
ONCE UNDER CONTROL GIVE BASELINE ELVEL OF BENZO & WEAN OFF
What should be given in management of status epilepticus except lorazepams (benzos) & phenytoin (Na+ channel antagonist)
- give thiamine/pabrinex (250mg IV ove 30m) if suspect ALCOHOLISM or MALNOURISHMENT
- Give glucose (5omL 50% IV) if hypoglycaemia unless glucose known to be normal
- treat acidosis if severe
- correct hypotension with fluids
- -> give dexamethasome if suspect cerebral oedema/vasculitis
What do 40% of epilepsy pts also have?
At least 1 mood disorder e.g. depression & anxiety
- independent of seizure control
- Multifactorial: biological factors (frontal/temporal lobe), personality, sociological factors (driving, work, family), perceived stigma & prejudice
also neuropsychological deficits form the sizures/drugs/epilepsy causes and also memory and cognitive complaints are very common
