Epilepsy & Seizures

1. Epilepsy & Seizures

2. def • Seizure – clinical event caused by an abnormal synchronised electrical discharge in the brain. • Epilepsy – neurological disorder characterised recurrent and unprovoked seizures.

3. 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

4. classification Physiological classification: • Partial/focal • Generalised (primary) Clinical seizure description: • Pre-ictal • Ictal • Post-ictal

5. 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

6. 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

7. 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

8. 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.

9. 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.

10. 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

11. aetiology • Any cerebral pathology causing sustained synchronised discharge of a group of neurons.

12. 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.

13. 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

14. 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)

15. 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

16. 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.

17. 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.

18. 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.

19. 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.

20. 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 %

21. 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

22. Mednote share. • Davidsons