07 Epileptic Seizures & Epilepsy Flashcards
definition epileptic seizure
paroxysmal (sudden, krampfartig) change in behavior due to synchronized rhythmic firing of populations of CNS neurons
definition epilepsy
defined by recurrent unprovoked (= spontaneously occurring) seizures
epilepsy - epidemiology
- prevalence: 70 mio. worldwide
- in Germany: 5,5 / 1000
- lifetime risk of one epileptic seizure: 5%
- age-dependent incidence: more likely in childhood and after 50
epileptic seizures - unprovoked vs. provoked
unprovoked
acute - symptomatic (“provoked”)
- acute brain lesion (e.g. intracranial bleeding, stroke, head trauma, infection)
- alcohol withdrawal
- metabolic disturbances (e.g. hypoglycemia)
- intoxication
- in children: fever > 35,8°C
non-epileptic seizures
- syncope
- dissociative seizure
- migraine
- sleep disorder
- paroxysmal movement disorder
diagnostic criteria for epilepsy
- 2 unprovoked seizures occurring more than 24 hours apart
- one unprovoked seizure and a probability of further seizures similar to general recurrence risk after two unprovoked seizures (at least 60%) over next 10 years
- causative CNS disease
- pathological EEG alterations
- diagnosis of an epilepsy syndrome
classification of epileptic seizures
focal onset:
- initial symptoms/signs (clinical and EEG) indicate origination of seizure activity within an area of one hemisphere
- aware vs. impaired awareness
- motor onset vs. nonmotor onset
- focal to bilateral tonic-clonic
generalized onset:
- seizure activity simultaneously in both hemispheres
- motor vs- nonmotor
localisation of focal aware seizures (auras)
temporal lobe (65%)
- mesial (90%): psychic or autonomic symptoms
- lateral (10%): auditory symptoms
frontal lobe (25%)
- tonic/clonic movements
parietal lobe (5%)
- paraesthesia
- vertigo
occipital lobe (5%)
- visual symptoms
focal epilepsy - causes
- hippocampal sclerosis
- malformation of cortical development (MCD)
- vascular malformations
- (postnatal) acquired CNS lesions: infectious/inflammatory causes, neoplasia, cerebro-vascular accidents, traumatic brain injury, neurodegeneration
generalized epilepsy - causes
genetic causes
- ion channel mutations (Na+-, K+-, Cl–channel)
- receptor mutation (GABA-, Acetylcholin-receptor
- ion transporter mutation (Na+-K+-ATPase)
epilepsy imitators
- syncope
- transient ischaemic attack (TIA)
- migraine with aura
- hypoglycaemic episode
- psychogenic non-epileptic seizure
syncope vs. tonic-clonic seizure
- 50% of syncopes are triggered (seizures almost never)
- syncope mostly lasts less than 30s (seizure 1-2min)
- convulsions in syncope are arrhythmic (in seizure always rhythmical)
- tongue biting rare in syncope (frequent in seizure)
- incontinence possible in syncope (frequent in seizure)
- reorientation takes not more than 30s in syncope (4-45 minutes in seizure)
- creatine kinase normal - slightly increased (2-3-fold increased in seizure)
duration and reorientation main difference
psychogenic non-epileptic seizure
- duration: more than 10min
- motor convulsions fluctuating
- put on, deflectable
- tip of the tongue biting
- never out of sleep
- injuries rare
- ictal EEG unchanged
- eyes closed (strong indicator)
treatment via antiseizure medication (ASM)
- pharmacotherapy suppresses the symptom
- chronic disorder epilepsy cannot be modified or treated
- no antiepileptogenic effects have been shown for currently available ASM
- new ASMs are as efficient as old ASMs and have better tolerability
pathophysiological concepts
- ionic channel hypothesis: disturbance of transmembranous ion transport
- GABA hypothesis: disturbance of GABAergic inhibition
- glutamate hypothesis: increased glutamate-mediated neurotransmission
