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Epilepsies of Childhood (i) - Coggle Diagram
Epilepsies of Childhood (i)
Intro
prevalence = 0.5%
chronic neuro disorder, recurrent unprovoked seizures
abnormal, excessive, synchronous neuronal activity in the brain
most idiopathic
Seizure types
generalised
from both hemispheres
absence, myoclonic, tonic, tonic-clonic, atonic
always LOC
no warning
symm seizures
bilat synchronous seizure discharge on EEG
focal
depends on part of brain where discharge originates
frontal: motor/premotor cortex, hyperkinetic, clonic movements e.g. Jacksonian march
temporal lobe: most common focal epilepsy, aura, taste/smell abnormalities, distorted sounds + shapes, automatisms (lip smacking, hand movements), deja vu, jamais vu, consciousness can be impaired, lasts longer than typical absence seizure
occipital: distorted vision
parietal: contralat dysaesthesia
conciousness may be lost/retained
secondary generalisation may occur
absence: precipitated by hyperventilation, unaccompanied by motor phenomena
tonic: increased tone
tonic-clonic: may fall + injure themselves, cyanosis, saliva in mouth, tongue biting, incontinence, deep sleep after for several hrs
atonic: transient loss of muscle tone, sudden fall/head drop
small group of dysfunctional neurons
can be hard to classify in children esp under 5s
Dx
detailed hx
eyewitnesses/video
ask about triggers, educational/psych/social impact
check skin for neurocut syndromes
Investigations
EEG
indicated whenever epilepsy suspected
neuronal hyperexcitability (sharp waves, spike wave complexes)
unless seizure actually captured, only provides supportive evidence
sleep/sleep-deprived/24 hr ambulatory/video telemetry helpful
subdural electrodes for preop assessment
MRI/CTs not required for childhood generalised epilepsies
indicated if neuro signs, focal seizures, tumour, vasc lesion, sclerosis
MRI FLAIR better to detect mesial temporal sclerosis in TLE
PET / SPECT
detect areas of abnormal metabolism suggestive of seizure foci
isotopes taken up by metabolically active cells
hyper/hypometabolism
Psych testing + memory assessment
metabolic investigations
genetic studies
e.g. SCN1A mutations in severe myoclonic epilepsy of infancy (Dravet syndrome)
Management
explanation + advice, promote confidence + independence
specialist epilepsy nurse
AEDs
not all seizures need AEDs
inappropriate AEDs may be detrimental (e.g. carbamazepine can make absence + myoclonic seizures worse)
goal = monotx @ min dosage
SEs should be discussed with child + parents
drug levels not measured routinely, but useful to check for adherence
can be discontinued after 2yrs seizure free
for tonic clonic: valproate (SEs = weight gain, hair loss, liver failure) / carbamazepine (SEs = rash, neutropenia, hyponatraemia, ataxia)
for absence: valproate / ethosuximide (SEs = N+V)
myoclonic: valproate
focal: carbamazepine / valproate
all can cause drowsiness + rashes
rescue tx for children with hx of prolonged seizures (rectal diazepam + buccal midazolam)
for intractable seizures...
ketogenic diet (MOA poorly understood)
vagal N stim
surgery
for well localised foci demonstrated by concordance between EEG + MRI
temporal lobectomy for mesial temporal sclerosis
hemispherectomy
hemispherotomy (isolate abnormal brain activity in 1 half of brain)
psych support
educate teacher on seizure tx
avoid baths, swimming alone, triggering TV shows if photosensitive, alcohol + sleep deprivation (can be triggers)
considerations for driving (if seizure free for 1yr), contraception, pregnancy
counsel on SUDEP
Prognosis
do less well educationally, socially, in employment