Diagnosis and management
Clinical features of seizures
It is important to elicit features before, during, and after the episode being reported. Premorbid state and any prodromal illness are also key features and may guide towards identification of a precipitant, as well as helping to differentiate a true seizure from an alternative explanation. Collateral history is, once again, essential.
| Focal | Generalised | |
|---|---|---|
| Clinical features | Aura
Automatism: lip smacking, chewing, fidgeting Sensory disturbance (e.g. visual) Speech difficulty Post-ictal period |
Aura
Absence Motor features: tonic-clonic, myoclonic Tongue biting Incontinence Post-ictal period |
| Important syndromes | Jacksonian march: focal epilepsy syndrome affecting primary motor cortex (PMC) resulting in progression of focal features as abnormal activity spreads through PMC
Todd’s paresis: post-ictal weakness classically seen in contralateral limb to focus of seizure; also associated with generalised seizures |
Juvenile myoclonic epilepsy: manifests in teenage years with myoclonus (which can be confused with clumsiness) and progresses to generalised epilepsy in most
May be associated with developmental and inherited syndromes, particularly errors of metabolism and mitochondrial disease |
Investigation of seizures
The approach should be as per that to a patient with altered conscious level. It is important to rule out potential precipitants with bedside investigations (e.g. glucose, electrolytes). Potential effects of existing illnesses or medication must be considered, e.g. hypertension, immunosuppression or renal failure may suggest PRES; disturbance to sodium and/or magnesium as a result of PPI use etc.
As with all acute neurological presentations, first-line imaging is CT brain. This may demonstrate a precipitating lesion (e.g. tumour, haemorrhage), but MRI provides the best resolution to demonstrate epileptogenic foci (e.g. in mesial temporal lobe or hippocampus).
EEG is an important facet in the diagnosis of epilepsy. It may be normal but can demonstrate abnormalities or epileptogenic discharges if taken during an event so should be combined with imaging studies. In cases where a precipitating factor is suspected, EEG can be carried out with provocation, e.g. for photosensitive epilepsy.
Management of seizures
Anti-epileptic drugs are not usually indicated after a first seizure unless there is thought to be a high risk of recurrence, e.g. if a precipitating lesion is identified.
Be aware of drug-drug interactions impairing the effectiveness of AEDs – many are metabolised via the cytochrome P450 pathway. This should be considered carefully when a patient with previously well-controlled epilepsy presents with a new seizure.
| Focal | Generalised |
|---|---|
| First line if male or woman beyond childbearing years: lamotrigine or carbamazepine
If woman of childbearing age: lamotrigine Second line: levetiracetam, oxcarbazepine |
Benzodiazepines to terminate seizure with later consideration of anti-epileptic drugs
Cause specific, e.g. MgSO₄ for eclampsia, correction of Na⁺ (hypertonic saline if causing seizures)/Ca²⁺/Mg²⁺/glucose First line if male or woman beyond childbearing years: sodium valproate If woman of childbearing age: lamotrigine Second line: carbamazepine, oxcarbazepine |
It is important to be aware of the impact of a seizure on a patient’s eligibility to drive following the event. In broad summary: patients must not drive a car or motorcycle for 6 months after an isolated or provoked seizure (unless there is a factor that is likely to drive recurrence, i.e. a precipitating lesion) or for 12 months after the most recent recurrent seizure. This is much more stringent for bus and lorry driving: patients must not drive for 5 and 10 years for isolated and recurrent seizures respectively, and may not be reliant on anti-epileptic drugs.
Take your subscriptions with you
Our mobile app allows you to access your interview and exam question banks wherever you are.