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

classification

Physiological 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