EPILEPSY Flashcards
define seizure
signs or symptoms due to abnormal excessive or synchronous neuronal activity in the brain
define epilepsy
neurological disorder in which a person experiences recurring seizures
At least two unprovoked seizures occurring more than 24 hours apart
define status epilepticus
prolonged convulsive seizure lasting for 5 minutes or longer, or recurrent seizures one after the other without recovery in between
causes of epilepsy
structural - stroke, trauma, malformation
genetic - ie Dravet syndrome
infectious - meningitis, TB, cerebral malaria, HIV and Zika virus
Metabolic - porphyria, pryridoxine deficiency
immune
risk factors for epilepsy
Premature birth.
Complicated febrile seizures.
A genetic condition that is known to be associated with epilepsy, such as tuberous sclerosis or neurofibromatosis.
Brain development malformations
A family history of epilepsy or neurologic illness.
Head trauma, infections (for example meningitis, encephalitis), or tumours
Comorbid conditions such as cerebrovascular disease or stroke — more common in older people.
Dementia and neurodegenerative disorders (people with Alzheimer’s disease are up to ten times more likely to develop epilepsy than the general population).
complications of epilepsy
sudden unexpected death in epilepsy
injuries
depression and anxiety disorders
absence from school or work
how to assess a patient with seizure
Any subjective symptoms at the start of the seizure (aura) — suggestive of focal epilepsy; these may provide information on where the seizure might arise.
Any potential triggers, for example sleep deprivation, stress, light sensitivity, or alcohol use.
specific features about the seizure
Residual symptoms after the attack (post-ictal phenomena), such as drowsiness, headaches, amnesia, or confusion (usually occur only after generalised tonic and/or clonic seizures).
what are the specific features of the seizure
Short-lived (less than 1 minute), abrupt, generalised muscle stiffening (may cause a fall) with rapid recovery — suggestive of tonic seizure.
Generalised stiffening and subsequent rhythmic jerking of the limbs, urinary incontinence, tongue biting —suggestive of a generalised tonic-clonic seizure.
Behavioural arrest — indicative of absence seizure.
Sudden onset of loss of muscle tone — suggestive of atonic seizure.
Brief, ‘shock-like’ involuntary single or multiple jerks —suggestive of myoclonic seizure
what physical examination will one do for a patient who experienced a seizure
Cardiac, neurological, and mental state, and a developmental assessment if appropriate.
Examination of the oral mucosa to identify lateral tongue bites.
Identification of any injuries sustained during the seizure.
what blood tests will be done is you suspect epilepsy
- FBC
- U&Es
- LFTs
- glucose
- calcium
- (ECG).
- blood gases
- set up cardiac monitor and pulse oximetry
DD for epilepsy
- Vasovagal syncope.
- Cardiac arrhythmias.
- Panic attacks with hyperventilation.
- Non-epileptic attack disorders (psychogenic non-epileptic seizures, dissociative seizures, or pseudoseizures).
- Transient ischaemic attack.
- Migraine.
- Medication, alcohol, or drug intoxication.
- Sleep disorders.
- Movement disorders.
- Hypoglycaemia and metabolic disorders.
- Transient global amnesia.
- Delerium or dementia — altered awareness may be mistaken for seizure activity.
DD for epilepsy in children
- Febrile convulsions.
- Breath-holding attacks.
- Night terrors.
- Stereotyped/ritulistic behaviour — especially in those with a learning disability.
how do you manage someone with sus epilepsy
1) urgently refer if its first epileptic seizure
2) give info sheet - record future seizures
3) stop driving until confrim of diagnosis, dont do heaby machinery
what do you do if someone has a tonic clonic seizure less than 5 minutes
Look for an epilepsy identity card or jewellery.
Protect them from injury by:
Cushioning their head, for example with a pillow.
Removing glasses if they are wearing them.
Removing harmful objects from nearby, or if this is not possible, moving the person away from immediate danger.
Do not restrain them or put anything in their mouth.
When the seizure stops, check their airway and place them in the recovery position.
Observe them until they have recovered.
Examine for, and manage, any injuries.
what do you do if someone has tonic clonic seizure lasting more than 5 mins or 3 seizures within an hour
Treat with one of the following:
- Buccal midazolam as first-line treatment in the community.
- Rectal diazepam if preferred, or if buccal midazolam is not available.
- Intravenous lorazepam if intravenous access is already established and resuscitation facilities are available.
features of temporal lobe epilepsy (partial epilpesy)
frontal
parietal
occipital
Hallucinations (auditory/gustatory/olfactory)
Epigastric rising/Emotional
Automatisms (lip smacking/grabbing/plucking)
Deja vu/Dysphasia post-ictal)
Head/leg movements, posturing, post-ictal weakness, Jacksonian march
Paraesthesia
Floaters/flashes
what is jacksonian epilepsy
starts in one place and spreads
begin in the corner of mouth, the thumb, index finger or the great toe
then movements spreads on the face or ascend the limb (Jacksonian march)
the affected limb may remain temporarily weak (Todd’s paralysis)
what is epilpesia partialis continua
children under 3 months or adults over 18 years of age
rare condition involving recurrent and sometimes intractable focal onset seizures associated with retained awareness. EPC seizures can occur over hours, days, or even years. The disease can manifest in a variety of ways, a few of which include myoclonic epilepsy, localized myoclonus, Jacksonian epilepsy, or sensorimotor clonic seizures.
what is febrile convulsions
with fever
less than 15 mins
what is infantile spasms (West’s syndrome)
features
Ix
Mx
typically present in the 3-12 months of life
- more common in males
TRIAD
- shock-like flexion of arms, head and neck with drawing up of the knees (salaam attaack)
- multiple bursts of violent flexor spasms last 1/2 s but repeated maybe upto 50 times - baby cry
- progressive learning dfifficulties
most undergo neurodegenerative neuro-encephelatic process.
Ix
EEG abnormality - hypsarrhythmia and burst suppression
CT - diffuse or localised brain disease
Mx
corticosteroids and vigabatrin PERIPHERAL VISUAL LOSS (first line if tuberous sclerosis)
- poor prognosis
name of inhibitory neurotransmitter and receptor
GABA
types of generalised seizures
tonic - stiff flexed atonic - relaxed clonic - convulsions tonic-clonic - stiff and they fit myoclonic - short muscle twitches absence - spaced out
what is generalised seizures
lose consciousness and involves both hemispheres
diagnosis of seizures
MRI
CT
EEG
management for west’s syndrome/ infantile spasms
corticosteroids or vigabatrin PERIPHERAL VISUAL LOSS (first line if tuberous sclerosis)
absence epilepsy in children
stare blank into space - eyes may flutter or roll up
characteristic EEG abnormalities - 3-Hz generalised, symmetrical spike-wave abnormalities
juvenile myoclonic epilepsy (Janz syndrome)
age of onset - 10-20 occurs after eaking - myoclonic - tonic-clonic - absence
polyspike waves
causes of refractory epilepsy
non compliance
pseudoseizures/non epileptic attaks
ass structural brain disease - dev abnormlaitits
alcohol and lifestyle
when to stat antiepileptics after first seizure
after the first seizure if any of the following are present:
- the patient has a neurological deficit
- brain imaging shows a structural abnormality
- the EEG shows unequivocal epileptic activity
- the patient or their family or carers consider the risk of having a further seizure unacceptable
first line treatment for patients with tonic clonic generalised seizure
sodium valporate boys
lamotrigine women childbearing age
first treatment used for focal seizures
carbamzepine
second line treatment for patients with generalised seizure
lamotrigine or carbamazepine
management for myoclonic seizures
sodium valproate
second line: clonazepam, lamotrigine
what type of seizures can carbamazepine exarcerbate
myoclonic
absence
how to differentiate between a pseudo seizure and general seizure
Elevated serum prolactin 10 to 20 minutes after an episode in an actual seizure
factors precipitating pseudoseizures
- pelvic thrusting
- family member with epilepsy
- much more common in females
- crying after seizure
- don’t occur when alone
- gradual onset
what is lennox-gastaut syndrome
Difficult to treat - 1-3 years
Multiple seizure types
- most common atonic - mistaken for falls
- atypical (subtle) absences lasting 10s to several minutes - head nodding/rapid blinking
- tonic seizure may happen only at night
Poor prognosis e neurodevelopmental arrest or regression
slow generalised spike and wave (1-3Hz)
Mx - ketogenic diet
what is benign rolandic epilepsy
common in children M>F -> 4-10yrs
outgrow it by puberty ‘benign’
seizures originate in the ‘rolandic’ region called centerotemporal
often start during sleep or when just about to wake up with:
- feeling if tingling on one side of the mouth
- may involve throat - speech inlcear/throaty/gurgling noises
- can cause clonic or tonic to one side of mouth or face
- can spread and affect the whole body
Ix
EEG - posterior sharp waves or occipital discharges
features of absence seizures
absences last a few seconds and are associated with a quick recovery
seizures may be provoked by hyperventilation or stress
the child is usually
unaware of the seizure
they may occur many times a day
EEG: bilateral, symmetrical 3Hz spike and wave pattern
Mx for absence seizures
sodium valproate and ethosuximide are first-line treatment
good prognosis - 90-95% become seizure free in adolescence
causes of secondary epilepsy
tuberous sclerosis neurofibroamtosis brain tumor stroke hypoglycaemia cerebral palsy mitochondrial diseases
what is secondary epilepsy
when it starts off as a focal seizure then it becomes generalised
other causes of seizures
febrile convulsions
alcohol withdrawal seizures
psychogenic non-epileptic seizures
what is Psychogenic non-epileptic seizures
previously termed pseudoseizures, this term describes patients who present with epileptic-like seizures but do not have characteristic electrical discharges
REMAIN CONSCIOUS
NO POST ICTAL STATE
PSYCHIATRIC COMORBIDITIES
patients may have a history of mental health problems or a personality disorder
features of alochol withdrawal seizures
ccur in patients with a history of alcohol excess who suddenly stop drinking, for example following admission to hospital
chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors.Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)
the peak incidence of seizures is at around 36 hours following cessation of drinking
patients are often given benzodiazepines following cessation of drinking to reduce the risk
when do you start antiepileptics
second epileptic seizure
the patient has a neurological deficit
brain imaging shows a structural abnormality
the EEG shows unequivocal epileptic activity
the patient or their family or carers consider the risk of having a further seizure unacceptable
epilepsy and driving
generally patients cannot drive for 6 months following a seizure. For patients with established epilepsy they must be fit free for 12 months before being able to drive
MOA of sodium valoprate
Increases GABA activity
adverse effects of sodium valoprate
ncreased appetite and weight gain alopecia: regrowth may be curly P450 enzyme inhibitor ataxia tremor hepatitis pancreatitis thrombocytopaenia teratogenic (neural tube defects)
MOA of carbamazepine
Binds to sodium channels increasing their refractory period
SE of carbamazepine
P450 enzyme inducer dizziness and ataxia drowsiness leucopenia and agranulocytosis syndrome of inappropriate ADH secretion visual disturbances (especially diplopia) skin rash N/V inactivates the OCP
MOA of lamotrigine
Sodium channel blocker
SE of lamotrigine
- SJS
- risk of interacting with other medications such as OCP
- risk of rash
- risk of harm to fetus if she falls pregnant
MON of phenytoin
increase sodium uptake increasing refracotry period
SE of phenytoin
Acute
- initially: dizziness, diplopia, nystagmus, slurred speech, ataxia
- later: confusion, seizures
Chronic
common: gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness
megaloblastic anaemia (secondary to altered folate metabolism)
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia
non epileptic seizures
EEG normal
patients look like they having seizures
more frequent
no tongue biting or incontinence
status epilepticus treatment
- secure the airway, administer O2, support respiration if necessary
- assess CVS status
- obtain IV access
- check glucose - if hypoglycaemic administer IV 50ml of 50% glucose
- administer IV pabrinex - if alcoholism or malnutrition is suspected
- bloods
- IV lorazepam 4mg, rate = 2mg/minute; repeat once after 15 minutes
- IV lorazepam - 10mg at a rate of 2-5mg/minute
after 10 minutes
- IV phenytoin 20mg/kg by slow IV infusion at a max rate 50 mg/min with ECG monitoring
- measure serum levels at 2h/4h
If no response (‘refractory status’) within 45 minutes from onset, then the best way to achieve rapid control of seizure activity is induction of general anaesthesia.
PR diaszepam IM midazolam
twice
ITU
ABG on seizure
resp arrest - not much oxygen getting into body
lactate high
acidosis
factors favouring pseudoseizures
- pelvic thrusting
- family member with epilepsy
- much more common in females
- crying after seizure
- don’t occur when alone
- gradual onset
generalised tonic-clonic seizures Mx
sodium valproate
second line: lamotrigine, carbamazepine
Myoclonic seizures**
MX
sodium valproate
second line: clonazepam, lamotrigine
Focal seizures
MX
Focal seizures
1st line carbamazepine or lamotrigine
second line: levetiracetam, oxcarbazepine or sodium valproate
which drug exacerbates absence and myoclonic seizures
carbamzepine
what is idiopathic generalised epilepsy
A group of epileptic disorders that are believed to have a strong underlying genetic basis and so often have a family history of epilepsy.
Patients with IGE are typically otherwise normal and have no structural brain abnormalities.
IGE tends to manifest itself between early childhood and adolescence although it can be diagnosed later.
Seizure types include absence, myoclonus and primary generalized tonic-clonic.
what increases the risk of fits in juvenile myoclonic/idiopathic generalised epilepsy
sleep deprivation and alcohol significantly increase the risk of fits
First line Mx for Childhood absence epilepsy, juvenile absence epilepsy or other absence epilepsy syndromes
ethosuximide to girls
sodium valpoate for boys
first line Mx of dravet syndrome
topiramate for girls
sodium valporate for boys
apart from pharm Mx what other interventions are available
- psychological intervention
- vagus nerve stimualtion
- > reduce frequency of seizures
if someone is continually fitting a CT is needed what do u do
liase with anaesthetist to do CT under intubation
Mx of cerebral mets causing fits
liase w oncologist/radiotherapist
administer IV dexamethasone and start oral steroid course to reduce cerebral oedema around lesions
introduce anti-convulsant meds
consider restaging of pt via CT or FDG PET
Analgesia as needed
what is traumatic tap adn what is seen
when u do LP and than pt moves vigorously
shows raised CSF protein
causes of status epilepticus
epilepsy
recent medication reduction/with- drawal
intercurrent illness metabolic derangement
progressive disease
complications of status epilepticus
Cerebral oedema + i ICP
Cerebral damage secondary to hypoxia, seizure, or metabolic derangement
Cerebral venous thrombosis
Cerebral haemorrhage and infarction
Hyper/hypotension Cardiac arrhythmias Cardiogenic shock Cardiac arrest Hypoxia (often severe) Aspiration pneumonia Pulmonary oedema Pulmonary embolism Respiratory failure
Dehydration Electrolyte derangement (especially d glucose, d Na, d Mg, i K) Metabolic acidosis Hyperthermia Rhabdomyolysis Pancreatitis Acute renal failure (often acute tubular necrosis) Acute hepatic failure Disseminated intravascular coagulation Fractures
what bloods are done for status epilepticus
U&Es Calcium glucose Mg2+ FBC clotting and blood cultures
Adverse effects of sodium valproate
teratogenic P450 inhibitor gastrointestinal: nausea increased appetite and weight gain alopecia: regrowth may be curly ataxia tremor hepatotoxicity pancreatitis thrombocytopaenia hyponatraemia hyperammonemic encephalopathy: L-carnitine may be used as treatment if this develops
Causes of seizures
epilepsy alcohol intoxication infections head trauma drugs -MAOI, illicit hypoxia degenerative disease sickle cell crisis metabolic disturbance intracranial tumours toxins - CO
