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. Atonic – ‘drop attacks’
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. Potential precipitating factors
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 + others
Metabolic:
hypo –glycaemia/natraemia /calcaemia
genetic
pyrexia (esp in children)
developmental
Sensitivities:
flashing lights, loud noise, hymns, sleep deprivation, foods.
trauma & surgery (2%)
degenerative disorders (MS, Alzheimer's)
drugs/ETOH use and withdrawal (6%)

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: General tests:
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: Epilepsy implications
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, % 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. Na channel blockers – carbamazepine, valproate, phenytoin.
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. Inhibits release of glutamate
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