The approach to someone with the first seizure

Epidem

 8-10% lifetime risk of one seizure

 3% of epilepsy
 Note that a first seizure that is caused by an acute disturbance of brain function (acute
symptomatic or provoked) is unlikely to recur (3-10%)
 If the first seizure is unprovoked, there will be a 30-50% chance of recurrence in the next 2 eyars
and after the second a 70-80% risk of recurrence
 This justifies the dx of epilepsy
 Many people presenting for the first time with a convulsive seizure have had prior unrecognised
seizures. They may have had simple or complex partial seizures (e.g. intense dea vu, sudden
feeling of fear, bad smell or taste or brief language difficulties), absence seizures and spileptic
myoclonus
 25-30% of first seizures are acute symptomatic or provoked by a brain insult or metabolic/toxic
disturbance of brain function
 These provoking factors include
 Fever
 Withdrawl or intoxication from drugs incl. EtOH
 Proconvulsive drugs
 Clozapine
 Maprotiline
 Tramadol
 Theophylline
 Baclofen
 Reflexes can also cause seizures eg. Reading or strobing lights
 Pregnancy -eclampsia
 Acute neurological insult
 Stroke – ischaemic stroke and intracranial haemorrhage
 Trauma – head injury
 Infection - brain
 Inflammation
 Biochemical derangement
 Hypo or hyper glycaemia
 Hypo or hyper natraemia
 Hypomagnesaemia
 Hypo or hyper calcaemia
 Those that are provoked by a disorder that cause permanent damage to the brain e.g. abscess,
have a high risk of recurrence >10% compared to <3%
 Seizures due to severe psychological stress or sleep deprivation are not considered to be acute
symptomatic. Instead they are triggered in susceptivle individuals with underlying epilepsy
disorder
 The risk of recurrence after the first unprovked seizure was 42%; 60-70% of which are in the first
6mths
 Note that 2 seizures in 24hrs is considered a single event;
 epilepsy is classified as 2 unprovoked seizures >24hrs apart or after one seizure if EEG or
neuroimaging indicate a genetic or structural basis for a seizure tendinacy. Epilepsy is still a
clinical diagnosis and normal EEG and imaging do not exclude the dx; rather the findings assist in
classifying the syndrome
 The risk factors of recurrence
 Aetiology e.g. pre existing brian abnormalities indicate remote symptomatic epilepsy
 EEG abnormalities esp focal spikes
 Focal neurological findings
 Focal seizure phenomonogy e.g. Todd’s paresis
 Focal or generalised epileptiform activity on EEG
 Tumours or other lesions
 Status epilepticus
 Fx
 Previous febrile seizures

Ddx
 Syncope
 Breath holding
 Pallid syncope
 TIA
 Metabolic encephalopathy
 Hypoglycaemia
 Electrolyte disturbance
 Sleep walking
 Night terrors
 Complex migranes
 Arrhythmias
 Psychogenic non-epileptic seizures
 Migrane
 Proxsymal dyskinesia
 parasomnia
 Pseudosiezuresconvulsive syncope
 When syncope provokes a post-anoxic convulsion

Hx
 A hx from both the patient and other witnesses is needed
 Tongue biting is not common but specific for convulsive siezures
 Post-ictal confsion suggests a seizure

NOTE
 The first seizure mandates individual counselling about the risks fo recurrence and the pros and
cons of drug treatment and the impact on lifestyle. Most do not choose anti-epileptics after the
first seizure.
 Note the limitations on driving

Ix
 Prompt EEG
 Usually MRI
 Need to assess seizuresemiology
 Lab tests depending on the clinical circumstances
 CSF if encephalitis or SAH suspected
 Drug and toxic screening
 Early standard EEG if possible within 24 hrs
 Sleep deprived EEG within 1 week
 High resolution MRI if possible
 There is little justification for routine investigations of blood, urine and CSF in children
 The circumstances of a first seizure should direct investigations
 E.g. someone with DM  Ix hypoglycaemia
 Fever and headache  LP for encephalitis
 If the first seizure is unprovoked, there is value for EEG and often MRI
 The dx is actually a clinical dx
 EEG is to point to focal lesions especially localised slow waves; predict recurrence and
indicate a specific epileptic syndrome (spike pattern)
 EEGs show abnormalities in 70% of cases if in 24-48hrs
 If the EEG is negative then try sleep deprived EEG as it will dectect an additional 13-31% of
cases and any
 MRI is the best method for structural imaging. This is better than CT scans as the CT may not
detect small tumours
 The ability for MRI to detect structural abnormalities more in adults than children

Dx
 While the diagnosis of epilepsy requires more than one seizure, an epileptic syndrome can be
diagnosed just after one
 Epileptic syndrome
 This is a broader concept rather than the dx of epilepsy (recurrence risk) and incorporates
age of onset, aetiology, prognosis and response to tx

Mx
 Non medical
 Educate the patient to avoid provokgin factors e.g. sleep deprivation
 Restrictions to recreational activity limited to 2-3months
 Suspension from dangerous machines 6mths
 Driving
 Reproductive health issues  enzyme inducing AEDs reduce the efficacy of the combined
OCP by increasing the clearance of oestrogen and progestogen. Can prescribe a high dose
oestrogen forumaltion or doubling the dose; using pills continuously rather than 21 days on
7 days off; alternative methods of contraceptive or changing AEDs
 1st trimester is most important to avoid risk of congenital malformations. Precnceptional
folate is recommended for valproate?
 Bone health  long term use of AED is associated with low BMD, increase risk of fracture
 Optimise exercise
  Ca
 Correct vit D deficicney
 Smoking cessation
 Medical
 Treatment after the first seizure does not have an effect on long term remission
 Most say wait until the next seizure
 If drug treatment is considered
 Things to consider
 Efficacy
 Long term safety
 Tolerance
 Low interaction potential
 QoL – esp as 50% won’t even get another seizure
 Dose -start low
 Drug options
 Phenytoin and barbiturates should be avoided

For focal seizures

 Carbamazepine
 Clobazam – esp for children
 Gabapentin
 Lamotrigine
 Oxcarbazepine
 Topiramate
 Valproate

For generalised seizures

 Lamotrigine
 Toporamate
 Valproate

Generalised tonic clonic

In the initial phase of stiffening, consciousness is lost for a few seconds, causing falls, often with a
forced scream (ictal cry). All-limb jerking then occurs, lasting for up to 2 minutes. Cyanosis,
tongue-biting and urinary incontinence are common during these seizures. Post-ictal stertor,
confusion and amnesia typically persist for several minutes.

Generaloised absence
frequent (>daily), brief (<30 seconds) episodes of behavioural arrest without prominent motor features
and with immediate recovery of alertness when the seizure ends. They occur in some forms of
genetic generalised epilepsies (primary/idiopathic generalised epilepsies) with onset in childhood
or adolescence.

Myoclonic seizures
single jerks of muscles, usually generalised, occurring during wakefulness, but otherwise similar to
hypnic jerks. Specific inquiry is necessary as most patients do not recognise these as seizures.

Focal seizures
confined to one cerebral hemisphere, but may evolve to become bilateral convulsive seizures
(secondary generalisation)
features are myriad, spanning motor, somatosensory, autonomic, visual, auditory and
experiential/psychic disturbances. In the individual patient, seizures show a high degree of
stereotypy. Focal seizures without and with impairment of consciousness (simple or complex
partial seizures, respectively), are often (mis)labelled by patients and doctors as petit mal
seizures as distinct from grand mal seizures. Typically, complex partial seizures are less frequent
and more prolonged than absence seizures, and post-ictal recovery of full alertness is delayed.

Juvenile myoclonic epilepsy

It is a common, under-recognised genetic generalised epilepsy syndrome in which myoclonic
seizures, GTCS and sometimes absence seizures commence around adolescence.7Typically,
excellent seizure control is achieved with low doses of some medications (eg. valproate,
levetiracetam). Some other AEDs may control GTCS in this condition but can potentiate absence
or myoclonic seizures. Most patients require lifelong treatment
Drugs
All AED have dose dependent neurotoxic SE e.g. somnolence, cognitive impairment and ataxia
Newer AED have similar efficacy but fewer SE and interactions
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1363913/
http://www.racgp.org.au/afp/2014/march/epilepsy/