Epilepsy: Factsheet
27/11/2007
- Epilepsy is the continuing tendency to have seizures: this propensity can
arise from many aetiologies. Thus epilepsy is considered a symptom of
underlying brain disorder.
- Affects 0.5% of the population
Epileptic seizure = synchronous, paroxysmal and excessive discharge of
neurones in cerebral cortex, causing a clinically discernable event.
• Clinical manifestations depend on region of cortex affected.
• Frequently – sudden onset and cease spontaneously
-Brief, lasting seconds to minutes.
• Seizures are usually followed by post-ictal drowsiness and confusion
Mechanisms
• Spread of electrical activity between neurones is normally restricted –
synchronous discharge produces normal EEG.
• Seizure: large groups of neurones are activated repetitively, unrestrictedly
and hypersynchronously.
• This produces high voltage, spike-and-wave EEG activity (hallmark!)
• Seizures are facilitated by lack of neuronal inhibition hence one
anticonvulsant strategy is to increase GABA levels in the brain and spinal
cord.
Aetiology
Trauma perinatal insults (contusion and haemorrhage) fetal
anoxia
depressed skull fracture/ penetrating brain injury
Cerebrovascular disease AVM, Cavernoma, Vasculitis , Post stroke
(15%)
Cerebral tumours (6%) 1y, particularly slow growing (e.g. meningioma,
oligodendrocytoma)
Alcohol-related (6%) Withdrawal: 5-15% chronic alcoholic have seizures1
Drugs Recreational – cocaine, amphetamines2; Therapeutic -
isoniazid
Infection Acute bacterial meningitis, encephalitis, abscess, prion
(CJD), AIDS
Degenerative Alzheimer’s disease, multiple sclerosis
Genetic (<2%) 30% epileptic pts have 1st degree relatives w/ epilepsy.
Metabolic abnormalities Hypoglycaemia, hypocalcaemia, hypoxia, mitochondrial
disease
Classification
1. Generalised seizure types
a. Absence – typical (3Hz spike and wave) or atypical
b. Myoclonic
c. Tonic – stiffening of body not followed by jerking
d. Clonic
e. Tonic-clonic
1
Alcohol-induced hypoglycaemia may provoke seizures
2
Phenothiazines, monoamine oxidase inhibitors, TCAs, propofol provoke if low seizure threshold
f. Atonic (Akinetic) seizures -rare: sudden loss of tone pt falls to ground
2. Partial seizure types
a. Simple partial – e.g. Jacksonian march (consciousness preserved)
b. Complex partial (loss of consciousness)
c. Secondarily generalised
3. Unclassifiable Seizure Types
Generalised Seizures
• Tonic Clonic (grand mal)
o patient has vague warning (prodrome) of malaise
o Initial TONIC phase – body becomes rigid, patient utters cry and
falls
o Tongue usually bitten
o Next CLONIC phase – generalised convulsion, 4 limbs rhythmic
jerking
o Followed by muscle relaxation, drowsiness and confusion
o Incontinence can occur at end of clonic phase
o Abrupt, isolated muscle jerking
• Absence seizures (petit mal)
o Occur almost exclusively in childhood/adolescence
o Each attack accompanied by 3Hz spike and wave EEG
o Child appears suddenly blank and pales slightly for a few seconds
o May be precipitated by hyperventilation
o Eyelids twitch; a few muscle jerks may occur
o Children w/ AS tend to develop GTCS in adulthood
o Clinically similar absence attacks also caused by partial seizures of
temporal lobes
Partial Seizures
• A partial (focal) seizure = localised epileptic activity. This activity either
remains focal or spreads to involve both hemispheres (generalised
seizure).
• Most common sites are temporal lobes (60-70%), frontal lobes (30%)
• FRONTAL: Jacksonian/focal motor seizures
o Simple partial seizures originating in motor cortex
o Clonic Jerking movements begin in hand and spread to involve
contiguous muscle groups contralateral to epileptic focus.
o If frontal lesion, conjugate gaze and head deviate away from focus
o Weakness of convulsing limbs several hours afterwards = Todd’s
paralysis
• TEMPORAL: can be complex or simple partial seizures
o Commonly derive from hippocampus Hippocampal sclerosis
o Structural lesion in temporal cortex e.g. glioma, angioma
o Feelings of unreality (jamais vu) or undue familiarity (déjà vu)
o Vertigo, visual hallucinations
• Can get other types of partial seizures e.g.
o Autonomic disturbances: flushing, sweating, piloerection,
hyperventilation
o Frotnal cortex: strange smells
o Parietal cortex: sensory disturbances
o Occipital cortex: crude visual shapes
o Auditory cortex: strange sounds.
Diagnosis
• Collateral Hx from witness is crucial
• Examine onset, setting and stages of attacks
• Neurological Examination to exclude differential diagnosis¨- e.g.
hemiparesis /papilloedema
in tumour.
• FBC (e.g. serum Ca2+)and EEG should be carried out
• Imaging: CT/MRI
Treatment
• One general measure is to avoid precipitating factors e.g. alcohol, lack of
sleep, lights
• Emergency
o Ensure patient comes to as little harm as possible
o Airway should be maintained during attack and post-ictal coma
o Prolonged seizure – rectal or i.v. diazepam
o If hypoglycaemia – give i.v. glucose
• Status Epilepticus
o Seizure or series of seizures lasting > 30 minutes without regaining
consciousness
GENERAL: Secure airway and resuscitate: Oxygen, BP, routine bloods
MEDICATION:
o Exclude hypoglycaemia and treat if present -> i.v. glucose
o Immediate i.v. lorazepam or diazepam (or rectally)
o If alcohol abuse suspected give i.v. thiamine
o Anticonvulsants: lorazepam, i.v. fosphenytoin Phenobarbital if
necessary!
o If nothing else works thiopental or i.v. propofol general
anaesthesia!
• Anticonvulsant drugs:
o Indicated when a firm clinical diagnosis of epilepsy is made –
substantial risk of recurrence
o Monotherapy w/ established anticonvulsant is best
o Dose is increased until control is achieved or tolerance exceeded
o Second drug added if control is not achieved
Drug Type of epilepsy Side effects
Carbamazepine Partial, 2y gen, GTCS Rashes,
Blood dyscrasias
-leucopaenia
Phenytoin Partial, 2y gen, GTCS Rashes, SLE ,
lymphadenopathy,
Blood dyscrasias
Sodium valproate3 Partial, 2y gen, GTCS, Anorexia, hair loss, liver
Absence damage
Ethosuxamide Absence
Gabapentin Partial, 2y gen, GTCS
(?)
Lamotrigine Partial, 2y gen, GTCS, Toxic epidermal necrolysis
Myoclonic
Vigabatrin (Infantile Partial, 2y gen, GTCS Retinal damage,
spasm) (?) psychological
Tiagabine Partial, 2y gen
Notes from Dr Mifsud tutorial
Complex Partial Seizures
• Complex partial seizure does not necessarily imply loss of consciousness –
more accurate to say ALTERED level of consciousness
e.g. patient might not fall to the floor – to a witness a CPS may look
rather like an absence seizure
• Most CPS originate in the temporal lobe
• Focal Symptoms
o Visual images (same one over and over)
o Speech (altered awareness)
o Olfactory (foul rubber burning)
o Dysmnestic: Déjà vu and jamais vu, recall of former lives
o Affective : fear, anger, depression, dreamy states
• A typical account from a witness may be of the patient staring and not
being able to respond to questions/ functions of daily life (e.g. brushing
hair, making tea).
• Reactive automatisms before the seizure e.g. blinking, smacking lips,
pulling at buttons
• Individual may not remember what had happened during the aura or the
seizure
• Treat with CARBAMAZEPINE – to find out if seizures are fully controlled
afterwards, the best thing to ask is “ do you still experience auras” –
because in this case the auras ARE the seizures.
Juvenile Myoclonic Epilepsy
• Begins at 8-18 years of age –family history is common
3
Valproate does not reduce efficacy of contraceptives (inhibits GABA transaminase)
• Present with triad of absences, morning Myoclonus and GS. Absences
• Seizures consist of unilateral or bilateral myoclonic jerks
usually affecting the upper limbs
• Tonic clonic seizures and absences may occur also.
• Seizures occur in the morning, precipitated by alcohol
• EEG shows irregular spike and wave, and high frequency spikes
• Seizures respond well to VALPROATE Generalised Seizures
Morning Myoclonus
• Some drugs make myoclonus worse : Carbamazepine,
vigabatrin, barbituates
ABSENCE SEIZURES COMPLEX PARTIAL SEIZURES
No aura Aura
Shorter duration Longer duration
No post-ictal phase Post-ictal phase common
Absences seizures
• Primary generalised seizures - begin at 7-11 years
• Natural course is to grow out of them although a small proportion of
children go on to develop GTCS
Diagnosing Epilepsy
• When diagnosing epilepsy: think is this generalised o focal?
• ONSET matters because this is a guide fo treatment e.g. Carbamazepine
can make 1y generalised seizures WORSE!
• If you think seizures are of focal onset:
o Carbamazepine – side effects of dizziness and diplopia
o Levitiracetam (Kepra)
o Lamotrigine
o Valproate (Epilim)
o Gabapentin (pain)
o Vigabatrin – not used due to risk of severe visual defects (only in
West syndrome)
• NB. Levitiracetam can be used for both focal onset and 1y generalised
seizures
o Efficacious at low doses
o May cause behavioural disturbances
• Gabapentin –not useful
• Pregabalin – efficacious at low doses (used in refractory epilepsy)
• If seizures are 1y generalised:
o give phenytoin 300mg/day – risk of rashes, blood dyscrasias and
lymphadenopathy
o Phenytoin has complex pharmacokinetics
o As for any drug: 5 half-lives to reach steady state
o Each half life for phenytoin is 24 hours (hence measuring blood
levels after 24 hours is useless – must check after 5 days)
o Aesthetic side effects of phenytoin: gum hypertrophy, acne,
hirsutism
• Toxicity:
o Nausea/vomiting
o Dizziness and ataxia (balance totally off)
o Nystagmus
o Drowsiness
o Diplopia
• NB. Can get liver damage sue to drug interactions e.g. with antibiotics (so
always check the BNF before prescribing drugs)
• Scenario: 22 year old man brought into A/E: 4 fits in one day and still has
not woken up
o Secure airway, intubate and give oxygen
o Monitor routine bloods and BP
o Secure venous access – many anticonvulsants cause phlebitis so
choose large vein
o U&Es – check glucose, calcium, sodium + DRUGS: alcohol, cocaine,
amphetamines
o Give glucose/thiamine to treat any underlying hypoglycaemia/
nutritional deficiency
o Imaging to check for head injury
o Check temperature for febrile convulsions -encephalitis/meningitis
