EPILEPSY & SEIZURES
def Seizure – clinical event caused by an
abnormal synchronised electrical discharge in the brain.
Epilepsy – neurological disorder characterised recurrent and unprovoked seizures.
pathophysiology Normal cortex – recurrent and collateral inhibitory
circuits that limit synchronised discharge
GABA – inhibitory neurotransmitter, GABA receptor drugs cause seizures
Acetylcholine, glutamate & aspartate – excitatory neurotransmitters
Epileptic cortex – reduced inhibitory signals or increased excitatory signals
classificationPhysiological classification: Partial/focal Generalised (primary)
Clinical seizure description: Pre-ictal Ictal Post-ictal
partial/focal seizures Limited to one part of cortex
Sx depend on part of the cortex involved: Simple partial seizures – consciousness
preserved Complex partial seizures – consciousness
impaired (involving centres of awareness – frontal/temporal)
Partial seizures with secondary generalisation – focal origin spreading to rest of the brain
partial/focal seizures Focal motor (Jacksonian)
Motor cortex origin - Speech arrest, involuntary turning of eyes or head etc
Rare – jacksonian march, focal clonus spread from distal to proximal in limbs
Temporal lobe Affective and/or cognitive fx. Feelings of unreality, deja vu,
vertigo, visual hallucinations etc Parietal lobe
Sensory fx – visual, auditory, somatosensory, vertiginous, olfactory etc
Frontal lobe Autonomic fx. Pallor, sweating, pupillary dilation, epigastric
sensation, piloerection, flushing
primary generalised seizures Electrical disturbance originates and spreads
from the diencephalon activating pathway (controls cortical activation).
Simultaneous bilateral cerebral discharge with LOC.
Types: Absence Myoclonic Tonic – clonic Atonic Tonic
absence seizure Almost always begins in children; tends to develop into
tonic-clonic Generalised absence seizure in children known as petit-mal Characterised by unconscious sudden behaviour arrest and
unresponsiveness Discharge doesn't spread out of the hemispheres hence
doesn't affect posture Possible eyelid and/or facial clonus, muscle spasms but
rarely lasting >10s Normal activity is resumed after attack Atypical presentations – with tonic, clonic and atonic
features with above signs.
tonic-clonic seizures Often preceded by an aura/prodome. Tonic phase
patient goes rigid (flexes), unconscious and falls heavily. respiration is arrested and central cyanosis may be seen. Tongue biting, incontinence occurs. A period of generalised
extension follows. Clonic phase
Generalised convulsions with frothing at mouth Tonic contractions alternate with atonia with increasing
duration of atonia between spasms till event ceases May last a few minutes
Post ictal – drowsiness, confusion or coma for several hrs after seizure.
Myoclonic Consciousness maintained Single or repetitive rapid muscle contractions (bilaterally
synchronous and symmetric) – shock like jerks. Tonic
Intense hypertonia not followed by clonic jerks Usually <10s, maybe up to 1 minute Usually occurs during non REM sleep, and periods of
drowsiness Less consciousness impairment than tonic-clonic
Atonic – ‘drop attacks’ Sudden loss of postural tone for 1-2s Brief LOC but quick recovery
aetiology Any cerebral pathology causing sustained
synchronised discharge of a group of neurons.Potential precipitating factors
• infection & inflammatory conditions • vascular (15%)• intracranial mass lesions (tumours, abscesses)Medications:• Monoamine oxidase inhibitors• Tricyclic antidepressants• Amphetamines• Lignocaine + othersMetabolic:• hypo –glycaemia/natraemia /calcaemia
• genetic• pyrexia (esp in children)• developmentalSensitivities:• flashing lights, loud noise, hymns, sleep deprivation, foods.• trauma & surgery (2%)• degenerative disorders (MS, Alzheimer's)• drugs/ETOH use and withdrawal (6%)
DDx Syncope TIA Narcolepsy (sleep disorder) Pseudo-seizures (resemble epileptic seizures
but not caused by electrical discharge in the brain).
Metabolic
Epilepsy is essentially a clinical Dx – Hx from witness important.
investigations EEG +/- video monitoring
Performed soon after event or during one Help to characterise the type of seizure Seizure activity is generally shown as either
focal cortical spikes or by generalised spikes and wave activity
EEG not a sensitive test for epilepsy – an abnormal EEG doesn't prove epilepsy
investigations Brain imaging – CT/MRI indications:
Epilepsy starts after age of 20 Seizures with focal clinical features EEG showing focal source Control of seizures is difficult or deteriorates
General tests: Glucose, Na, Ca, Mg Serum prolactin (increased, DDx pseudo-seizures) ECG (DDx syncope) Urine drug screen (amphetamines)
management Non pharmacological:
Diet + nutrition esp. in young people Stress and anxiety Counselling/psychotherapy – higher risk of depression Passion flower fusion – natural anticonvulsant Massage Rx Support groups
Epilepsy implications Driving Avoid solitary/dangerous sports (or hymns!) Jobs – machines In women – decreased fertility, 1/3 of women with epilepsy
have ovarian abnormalities
management Pharmacological
Control fits in 70-80% with tonic-clonic seizures, 30-40% of absence seizures
Patient monitoring essential after commencing drug Anti-epileptics induce liver enzymes:
Pregnancy – reduced OCP efficacy Patients on warfarin – increased risk of bleeding
Anti-epileptics also highly protein bound – decreased Alb.
SEs: hepatotoxicity, ataxia, diploplia, nystagmus + cognitive fx decline.
pharmacological Rx Rule of thumb:
Valproate Lamotrigine Absence – ethosuximide /vaproate Partial – carbamazepine
Partial seizures +/- secondary generalisation: 1st line – carbamazepine 2nd line – lamotrigine, gabapentin, vaproate, levetiracetam,
oxcarbazepine. Primary generalised:
1st line – vaproate 2nd line – lamotrigine, topiramate, carbamazepine Ethosuximide – more effective in absence seizures.
Mode of action of drugs Increase inhibitory transmission Alter sodium channels to prevent transmission
Na channel blockers – carbamazepine, valproate, phenytoin. Valproate also seems to increase GABAergin inhibition. Valproate and carbamazepine considered 1st line
because of least SEs. Phenytoin – pure Na channel blocker, primarily affects
the motor cortex (prevents seizure spreading), can cause cerebellar signs (nystagmus, chorea, ataxia), cognitive fx & other SEs. A lot of SEs.
Ca channel blockers Ethosuximide SE – abnormal LFTs, liver and renal imparment
Inhibits release of glutamate Lamotrigine – also blocks Na channels Fewer SE: CNS Sx, skin rxn esp. in children
Potentiate effects of GABA – gabapentin, benzodiazepines, phenobarbital Gabapentin – used as a ‘add-on drug’ when epilepsy is not being
controlled, also used in neuropathic pain. Well tolerated. Benzodiazepine - ^ GABA effects, used in ER situations – status
epilepticus, prolonged seizures. SE- withdrawal syndrome, cognitive fx. Levetiracetam & topiramate – unknown mech of action, powerful
new AEDs for secondary generalisation.
surgical Temporal lobectomy
Amputation of non dominant anterior temporal lobe
must have hippocampal sclerosis (imaging and EEG confirmation)
These cases represent < 1% of all cases bt cure rates are > 50 %
status epilepticus Def – two or more continuous seizures
where the patient has incomplete recovery of consciousness btw seizures.
Medical ER – up to 30% mortality from cardio respiratory arrest
>50% have no PHx of epilepsy Rx:
Benzodiazepines Phenytoin
Mednote share. Davidsons