Seizures and Epilepsy Flashcards
Benign Epilepsy with Centrotemporal/Rolandic spikes
• **Most common
• Age - 5-12 y, normal development
• Aetiology - FHx 25%, 10-20% of all epilepsy
• Presentation - Sleep related, 3/4 at night or on waking, partial upper (face/arms), facial twitching, guttural sounds, drooling, dysphagia, speech arrest. Secondary GTCS in sleep
• EEG - Centrotemporal spikes (in Rolandic area), biphasic in repetitive bursts, increased in NREM sleep, normal background
• Treatment - usually don’t treat, valproate
• Prognosis - full remission by 15 years old, normal development
Benign occipital epilepsy
• Age - 8-9
• Aetiology- Idiopathic
• Presentation- Visual Sx, vomiting, post-ictal headache
• Early onset type - Panayiotopoulous - vomiting
• Late onset type - Gastuat - visual hallucinations, blindness
• EEG - Spikes in occipital areas, activated on eye closure
• Treatment - most AED effective, valproate, carbamaz
Prognosis - 1/3 remission before adulthood
Juvenile Myoclonic epilepsy
• Age - teenager 15 y.o
• Aetiology- presumed genetic, 10% of all epilepsy
• Presentation- myoclonic jerks (100%)- one arm or both arms, in morning, absence seizures (20-40%), GTCs tend to be on waking, no focal neuro
• EEG - 4-6Hz bilateral polyspike and slow wave discharges with frontal dominance, normal background
• Treatment - valproate
Prognosis - Quick and complete response to AED, lifelong AED
Childhood Absence epilepsy
• Age - 4-10
• Aetiology- Presumed genetic, 12% of all childhood epilepsy
• Presentation- 10s profound impairment, abrupt onset/offset, +/- eyelid movements, automatisms
• EEG - classic 3Hz spike wave discharges, provoked by hyperventilation
• Treatment - Ethosuximide, valproate, lamotrogine
Prognosis - most respond to 1st line AED
Seizure locations
Occipital
• Eye movements, loss of vision
• Contralateral side
• Assoc with benign occipital epilepsy of childhood
Frontal (contains motor)
• Motor - face and eyes
• Contralateral side
Temporal (most common focal)
• Complex partial (impaired awareness)
• Autonomic
Parietal
• Poorly understood
Numbness, paraesthesia
AEDs - Teratogenesis
- Which highest risk
- Specific causes
• Highest risk with VPA
• Specific:
• VPA - NTD
• Phenytoin - orofacial cleft, cardiac malformations, GUT defects
• CBZ - spina bifida
Phenobarbitone - cardiac, orofacial, gut
AED - therapeutic monitoring
• Barbiturates - phenobarbitone - level 3-4 weeks post
• Phenytoin - often, 5-7 days after dose change
CBZ - when at high doses
Seizure types
- Types of generalised and focal
Generalised
• Originating in one part and spreading rapidly
Motor
• Generalised tonic clonic - tonic phase (stiffening), followed by clonic phase
• Tonic - suddent stiffening, eyelid opening, eye deviation
• Myoclonic - sudden involuntary shock like contraction-
• Atonic - sudden loss of muscle tone without falling
Non motor
• Absence - impaired consciousness
Focal/Partial
• Originating limited to one hemisphere
• Localised
• Aura present - must be focal
Examples: focal clonic, focal impaired awareness seizure focal sensory, hyperkinetic, focal to bilateral tonic clonic
Causes of epilepsy
• Structural –> focal epileptogenic lesions in brain, major cerebral malformations
• Epilepsy genetics –> chromosomal etc
• Metabolic conditions
• Infections –> neurocysticercosis (parasite larva)
Immune –> limbic encephalitis, ADEM
Approach to further investigations for epilepsy - 2 x 2 table
Idiopathic - Focal
Eg
• Benign rolandic
• Benign occipital
No imaging
Idiopathic - Generalised
• Eg Childhood absence
• Juvenile absence
• Juvenile myoclonic
No imaging
Symptomatic - Focal - structural, localisation related
• Localisation related
Eg non idiopathic focal epilepsies
Imaging
Symptomatic - Generalised
• Eg Infantile spasms (West syndrome)
Lennox Gastaut
- All Ix - imaging, metabolic, chromosome
Phenytoin
- Indication, interactions, main SEs
Action
• Blocks Na channel
Indications
• Status- Partial or generalised
Metabolism
• Liver
Interactions
• Zero order kinetics
• Induces CYP450
• Reduces VPA
• Decreases effect of OCP and steroid
• Levels increased by macrolidses, alohol, amiodarone
• Levels decreased by rifampicin
Side effects
• Megaloblastic anaemia (decrease folate absorption)
• Rash
• Hirsuitism
• Gum hypertrophy
• Ataxia, dizziness, nystagmus
• Osteoprosis
• Periph neuropathy
• Hepatic dysfunction
• Worsens absence
Levels
• Check within 5-7 days
• Target 10-20
AED
- Monitoring tests
• CBZ - baseline LFT and FBE prior to starting and in 6 weeks
• VPA - baseline LFT and FBE prior to starting and in 6 weeks
• Topiramate - bicarb within a month, renal US and urine
VBG -visual field defect
Topiramate
Action
• Blocks Na channels
• AMPA
Indications
• Partial and generalised
Interactions
• Decreases OCP
Side effects
• Nephrolithiasis
• Metabolic acidosis
• Weight loss
• 70% renal excretion - impaired with renal impairment
• Mood
• Behavioural
• Cognitive
Monitoring + Levels
• Bicarb within a month
Renal US and urine
Sodium valproate/Valproic acid (Epilum)
Action
• Block Na channels and GABA
Indications
• Generalised, partial and absence
Metabolism
• Induces CYP
Interactions
• Blocks liver enzymes
• Increases levels of AEDs
Side effects
• Teratogenic - NTD (don’t put teenage girls on Epilium)
• Weight gain, insulin resistance
• Alopecia
• Pancreatitis
• Thrombocytopenia
• Tremor and CNS
• Liver failure
• Avoid in mitochondrial/metabolics - increases ammonia
Monitoring + Levels
Baseline LFT and FBE prior to starting and in 6 weeks
Lamotrogine
Action
• Block Na channels
Indications
• Generalised and partial
• Avoid - Dravets
• Least teratogenic
Metabolism
• Glucoronidation In liver
Interactions
• Valproate sig increases levels (diffferent dosing)
Drug inducers - decrease half life
• Carbamazepine
• Phenytoin
• OCP
• Rifampacin
Side effects
• SJS
• Hypersensitivity
• Hepatic
• CNS - tremor
Monitoring + Levels
Nil significant
West Syndrome/Infantile Spasms
Triad
• Epileptic spasms (seizure type), hypsarrythmia (EEG) and arrest of psychomotor development (clinical)
Background
• Peak onset 3-7 months, > 95% before age 2
Cause
• ~65% have identifiable cause
• CNS malformation
• Most common/important cause - focal cortical dysplasia
• Tuberous sclerosis, neurocutaneous, genetic
Clin Pres
• Epileptic spasms
• Clusters (5-30 secs apart), frequenty just after waking
• Flexor (salaam), extensor (cruciate) or mixed
• Asymmetric, have focal features
EEG
• Hypsarrythmia, high amplitude abnormal rhythym, electrical chaos
• MRI - structual brain abnormalities
• Metabolic work up
Mx
• ACTH
• Corticosteroid high dose (Pred)
• Vigabatrin - first line with TS (assoc with vision loss)
Febrile convulsions
- Simple vs complex
- Future risk of febrile seizures and future risk of afebrile seizures
Key 3
• Simple febrile convulsion - <15 min GTCS, once in illness, nil focal, otherwise neurodevelopment child - risk of future afebrile 1% (same as population)
• Complex febrile convulsion - >15 mins, focal features, not back to baseline 1 in hour, more than 1 seizure in same illness
• Risk factors for future afebrile seizures - Fhx epilepsy, complex - focal features or prolonged, any neurodevelopment problems
• Occur in 3% of children
• Normally assoc with simple viral infection
• Benign
• Afebrile febrile convulsion - viral illness eg gastro without documented fever at time
Mx
• As per normal seizure Mx
Epilepsy
What is risk of epilepsy after febrile convulsion?
What is risk of epilepsy after febrile convulsion?
• Simple febrile seizure - 1% (same as population)
• Recurrent febrile seizure - 4%
• Complex febrile seizure (more than 15 min duration or recurrent within 24 hours) - 6%
• Fever < 1 hour before febrile seizure - 11%
• FHx of epilepsy - 18%
• Complex febrile seizure (focal) - 29%
Neurodevelopmental abnormalities - 33%
