Clinical Epileptology Flashcards
What is epilepsy
- chronic brain disorder characterised by enduring predisposition to generate epileptic seizures
- defined by recurrent unprovoked (= spontaneously occurring) seizures
Frequency of seizures in epilepsy
10-20/month, each epilepsy lasting a minute
Interictal state
between seizures; important for EEG as epilepsy occasion is rarely recorded
Epileptogenesis
process by which a normal brain becomes epileptic potentially due to accidents/brain injury etc
Epileptic seizure
symptoms of paroxysmal change in behaviour due to synchronised rhythmic firing of populations of CNS neurons
Ictogenesis
process of induction, propagation and termination of seizures against the background of an interictal (time in between seizures) state in established epilepsy
Classification/level of epilepsy
- Symptom (focalised or generalised)
- Syndrome (focalised or generalised): collection of symptoms
- Disease (symptomatic/genetic or idiopathic/secondary)
Epileptic seizure is diagnosed
electroclinically = recording and behavioural symptoms
Level of focal seizures
origination from one side of hemisphere
- focal aware: preserved (no loss) of consciousness
- focal impaired awareness: impaired consciousness
- focal to bilateral tonic-clonic: loss of consciousness
Types of generalised seizures
origination from both side of hemisphere
- absence
- myoclonic: brief, shock-like jerks of a muscle or a group of muscles upon waking up; conscious but have no control over your body
- tonic: muscle stiffness & loss of consciousness
- clonic: jerking of the body
- tonic-clonic
- atonic: loss of muscle tone
How often is each type of seizures
focal aware: 15%
focal impaired: 25%
focal to bilateral: 35%
generalised:25%
Difficulty of absence seizures
Especially for young kid, it is hard to recognise the seizure but rather see it as a “slow/unresponsive” child
New type of epileptic seizure classification
- Onset (focal/generalised/unknown)
- awareness (intact/impaired)
- Symptom (motor or nonmotor)
nonmotor can include autonomic, cognitive, emotional, sensory, typical (5-10s), atypical (10-15s)
Localisation of focal aware non-motor seizures
e.g. aura
It can be used to assess how the symptom is progressing within the brain
-seizure in occipital lobes 5%
-parietal lobe 5%: paraestheia知覚異常 and/or vertigo
Jacksonian seizure-phenomenon where a simple partial seizure spreads from the distal part of the limb toward the ipsilateral face
-frontal lobe 25%: tonic/clonic movement
-temporal lobe 65%
lateral temporal lobe 10% (auditory symptoms)
mesial TL 90% (psychic/depressed or autonomic
symptoms)
Hyperkinetic symptoms
Where the limbs/body parts are swinging; patients fully aware but cannot control
Do not misdiagnose epileptic seizure with
- syncope/fainting
- psychogenic non-epileptic seizure
Generalised epilepsy
Easier to treat with drugs and can go drug free after some years
Most common type of epilepsy
focal, unknown etiology
history/clinical data of focal epilepsy vs generalised
focal
• partial or partial onsetseizures
• seizures during sleep
general
• generalised seizures
• 30 min after awakening
• positive family history
EEG of focal epilepsy vs generalised
focal
• focal slowing or hyperexcitability
general
• generalised hyperexcitability
cMRIof focal epilepsy vs generalised
focal
• structural lesion
generalised
• not helpful, always negative
Etiology of epilepsy
Most of the time unknown but it could be... structural genetic metabolic infectious immune
Importance of knowing the etiology of epilepsy
It is a common initial symptoms of a brain tumour
Testing for etiology
spinal fluid examination (for CNS inflammation or infection)
Febrile seizures
convulsions (痙攣) that is common for a kid to have upon high fever and the result is epileptic seizure. If lasted for too long, can lead to hippocampal damage
Structural epilepsy etiology (congenital and postnatal)
Congenital:
• hippocampal sclerosis
• malformation of cortical development (MCD)
• vascular malformations
postnatally acquired CNS lesions:
- infectious/inflammatory causes
- neoplasia
- cerebro-vascular accidents
- traumatic brain injury
- neurodegeneration - e.g. Alzheimer increase the risk
hippocampal sclerosis
congenital epilepsy etiology
pathology • neuronal loss: CA1 und CA4 • relative resistence to neuronal loss: CA2 und CA3 • gliosis: change in glial cells • axonal and synaptic reorganisation
steps of cortical development
- neuronal proliferation
- neuronal migration
- cortical organisation
malformation of cortical development @ neuronal proliferation
- cortical dysplasia with “balloon cells”
- Hemimegalencephaly (half brain larger than the other)
malformation of cortical development @ neuronal migration
- heterotopias (symptoms include gray matter not being in the outer layer)
- lissencephaly (smooth brain with no gyrus)
malformation of cortical development @ cortical organisation
- polymicrogyria (many small gyrus)
- cortical dysplasia w/out „balloon cells“
etiology of genetic/idiopathic epilepsy
Unknown
Some malfunctioning of ion channel mutation - Na+ channel - K+ channel - Cl- channel receptor mutation - GABA-receptor - acetyl-cholin-receptor ion transporter mutation - Na+K+ -ATPase
Epilepsy’s aetiology can be
- idiopathic/genetic
e. g. single gene epilepsies, epilepsies with complex inheritance - symptomatic
genetic could put some predisposition enhancing the risk of epilepsy
What is the risk of a child having epilepsy?
Epilepsies with complex inheritance is so complex that the risk will decrease to 6-8%
Why is epilepsy more prevalent is developing countries?
Because they have more risk of getting CNS infection
Types of differential diagnosis for epilepsy
- transient ischaemic attack (TIA)
- syncope
- migraine with aura
- hypoglycaemic episode
- psychogenic non-epileptic seizure
Syncope vs tonic/clonic seizure
Trigger: 50%/none Duration: <30s/1-2min Convulsion: 70-90% and rhythmic/ 100%rhythmical Eyes: both open Reorienting self: <30s/4-5min
epilepsy vs psychogenic non-epileptic seizures
- 15-25 years old
- more women
- have physical trauma/abuse history etc
on average takes 7 years of misdiagnosis as epilepsy, realise due to drug not working etc
keys to differentiate is…
- duration >10min
- motor convulsion fluctuates; attention from medical stuff intense the seizure; distraction from psychatric trigger can stop the seizure
- ictal EEG is unchanged
- eyes CLOSED
Epilepsy prevalence
0.7%
Life time tisk of one-time epileptic seizure
5%
Age dependency for epileptic seizure
Youth (congenital) and older (idiopathic)
Patients with first epileptic seizure
and have low risk of having second one, do not need to take medication but cannot drive for 6 months
Antileptic drugs should be taken
- after 2 epileptic seizures
- after 1 unprovoked seizure with either causative CNS disease and/or pathological EEG alterations
Treatment goal in chronic epilepsy
maintenance of normal life style = complete seizure
freedom and no or minimal substance adverse effects
How to decide drug
Not the efficacy (as it is fairly similar for all) but with tolerance/less side effects
Depends largely on sex, age, comorbidity, co-medication
Therapeutical approach
Not technically anti”epileptic” but rather anti”seizure”
- secondary prophylaxis予防
- „antiictogenic“ pharmacostrategy
- chronic disorder epilepsy cannot be modified or treated
Pathophysiological concepts of ictogenesis
„ionic channel hypothesis“: disturbance of
transmembranous ion transport
„GABA hypothesis“: disturbance of GABAergic inhibtion
„glutamate hypothesis“: increased glutamate-mediated neurotransmision
A drug which targets all components is
not necessary the best due to the adverse effects
all components (interact with Na and Ca channel, GABA and Glu system)
Most popular antiepileptic drug in Germany
lamotrigine (Na and Ca channel targeted), levetiracetam (Ca channel and GABA system targeted)
How successful are epileptic drugs?
60% good prognosis with monotherapy (one-drug); commonly seizure free with AntiEpilepticDrug termination
30% pharmacoresistant with polytherapy
10% seizure free with poly therapy
Who are the candidates for epilepsy surgery?
• pharmacoresistance • identification of one epileptic focus with EEG • suitable MRI lesion • resection possible without persistent neurological/neuropsychological deficits
Q: Which of the following statements is correct?
(A) Epilepsy is a rare neurological disorder
(B) An aura characterised by fear is a simple partial seizure
(C) Motor convulsions of the right upper extremity without loss of
consciousness indicate a temporal lobe onset
(D) Visual symptoms at seizure onset indicate a parietal lobe seizure
focus
(E) Complex partial seizures always originate in the temporal lobe
(B) An aura characterised by fear is a simple partial seizure
Q: Which of the following statements is correct?
(A) Hyperexcitability in the EEG indicates epilepsy and the need for antiepileptic drug treatment
(B) Patients with a first epileptic seizure four weeks after middle
cerebral artery stroke should be recommended antiepileptics
(C) Benzodiazepines are a good treatment option in epilepsy
(D) Hippocampal sclerosis indicates idiopathic generalised epilepsy
(E) Closed eyes are typical feature of an epileptic seizure
(B) Patients with a first epileptic seizure four weeks after middle cerebral artery stroke should be recommended antiepileptics
Which of the following statements is not correct?
(A) Prevalence of epilepsy is independent of gender
(B) Middle-aged patients have the highest risk to develop epilepsy
(C) Generalised epilepsies commonly are idiopathic
(D) Absence seizures indicate generalised epilepsy
(E) Patients with idiopathic generalised epilepsies need cMRI for work-up
(B) Middle-aged patients have the highest risk to develop epilepsy
Epilepsy and death
It is rare for epilepsy to be the direct cause
The common death is drowning or from cardiac arrhythmia
