Epilepsy Symposium Flashcards
1
Q
What is epilepsy?
A
- a recurring unprovoked (spontaneous) seizures
- acute symptomatic seizures are provoked by acute insults such as
- stroke, infection, alcohol withdrawal, or a metabolic disturbance
2
Q
What types of seizures are there?
A
- Primary generalized onset: electrical discharges appear to start over the whole brain at the same time on EEG
- Partial/focal onset: electrical discharge appears to start in one cortical region and then may remain localized or may spread over the whole brain - secondary generalized
3
Q
What are the classifications of Idiopathic (Primary) Generalized seizures?
A
- Limited repertoire of seizures
- Tonic-clonic seizures (“grand mal”)
- Absences (“petit mal”)
- Tonic seizures
- Atonic seizures
- Myoclonic seizures
4
Q
Give an overview of what Idiopathic Generalized Seizures are?
A
- Onset in childhood or adolescence
- Usually no focal symptoms/signs
- Often a number of seizure types cluster
- A polygenic cause is presumed with no identifiable structural lesion on imaging
- Generalized (all leads) spike and wave discharges on EEG may be induced by hyperventilation, and on photosensitivity testing
- Provoked by sleep deprivation
5
Q
What is Juvenile Myoclonic Epilepsy (JME? - give an overview
A
- Commonest form of primary generalized epilepsy 3-12% all epilepsy
- Juvenile onset, probably lifelong
- Early morning myoclonic jerks (ask)
- Photosensitive, sleep deprivation triggers
- +/- absences
- generalized tonic-clonic seizures – occur without warning
6
Q
Give an overview of the presentation of Generalised Tonic-Clonic Seizures “grand mal”
A
- sudden onset without warning in primary generalised epilepsy
- Tonic phase
- continuous muscle spasm, fall, cyanosis, tongue biting, incontinence
- Clonic phase
- rhythmic jerking slows and gets larger in amplitude as the attack progresses
- Ends; the duration is typically 1-3 minutes
- Post-ictal (post-seizure) phase
- coma, drowsiness, confusion, headache
- muscle aching
- red/blue, wakes in ambulance/A&E
7
Q
Give an overview of Absences “petit mal”
A
- Abrupt, short, 5-20 seconds
- Multiple times/day, can lead to learning difficulties
- Unresponsive, amnesia for the gap, rapid recovery
- Tone preserved (or mildly reduced)
- If absences only, tend to remit in adulthood (childhood absence epilepsy)
8
Q
What ways are there Focal Onset Seizure?
A
- a simple partial seizure where the patient is aware (used to be an aura)
- focal seizure with awareness
- a complex partial seizure- aura/warning with a level of reduced awareness
- focal seizure with reduced awareness
9
Q
Where d partial seizures frequently present themselves in the lobe?
A
- Temporal lobe - 70%
- Frontal lobe - 25%
- Occipital lobe - 4%
- Parietal lobe - 1%
10
Q
Give temporal lobe seizures by aetiology
A
- Hippocampal sclerosis: 50%
- have a history of febrile convulsion
- Tumour: 18%
- Birth Hypoxia: 10%
- Vascular: 10%
- Post Traumatic: 8%
- Other: 4%
11
Q
What are the symptoms and signs of temporal lobe epilepsy?
A
- hallucinations of taste, speech and /or smell, visual distortion; memory déjà vu and jamais vu
- epigastric rising sensation (over humpback bridge)
- fear, elation, low mood
- pallor/ flushing/ heart rate changes (can mimic panic/hyperventilation attacks)
- automatisms- semi-purposeful limb movements
- Oral automatisms- lip-smacking, chewing movements
- dystonic posturing (limb rises)
- speech disturbance (dominant hemisphere onset) last 1-3 minutes typically
12
Q
What are the symptoms of a frontal lobe seizure?
A
- brief 10-30 seconds, rapid recovery, frequent
- predominantly nocturnal
- forced head /eye deviation to the contralateral side
- motor activity often bizarre, thrashing
- often misdiagnosed as non-epileptic
- ictal EEG (during the seizure) is often normal
- Jacksonian spread with Todd’s paresis
- automatisms, dystonic posturing for example
- a fencing posture (overlap TLE)
13
Q
What are Parietal lobe epilepsy symptoms?
A
- positive sensory symptoms (unlike TIA/stroke)
- tingling, pain
- distortion of body shape/image
- Jacksonian march of positive sensory symptoms
14
Q
What are Occipital lobe epilepsy symptoms?
A
- typically simple visual hallucinations -balls of coloured or flashing lights
- amaurosis (blackout or whiteout) at onset -25%
15
Q
What anti-epileptic drugs make myoclonic jerks and absences worse?
A
- Phenytoin
- treats tonic-clonic seizures
- safe to use in status epilepticus (when a seizure lasts more than 5 minutes or are close together)
- Carbamazepine,
- Gabapentin,
- Pregabalin
21
Q
Explain the development of Focal (partial) seizures
A
- synchronized ‘paroxysmal depolarizing shift’ (PDS, 20 to 40 mV, lasting 50 to 200 ms) overcomes inhibition
- increased extracellular K+ due to neuronal damage or reduced uptake by the astrocytes as well as glutamate release from neurons or astrocytes contribute to PDS
- during the PDS trains of action, potentials occur
- hippocampal neurons have similar responses under normal conditions, making the hippocampus more prone to seizures than the neocortex
- Focal seizures may spread to other brain regions along the normal neuronal pathways and may also show secondary generalization if the activity spreads to the thalamus (tonic clonic seizure)
22
Q
Explain the development of Primary Generalized seizures.
A
- Primary generalized seizures reach the cerebral cortex via normal neuronal pathways from the thalamus
- e.g. tonic clonic seizure; absence; juvenile myoclonic epilepsy
- pathways originate in the brainstem and are normally involved in regulating the sleep/wake cycle and arousal of the cerebral cortex
- Ca2+ channels and inhibitory GABA receptors in thalamic neurons have been implicated in ‘spike and wave’ seizures, showing that inhibition (the wave) is preserved
24
Q
What AEDs work by inhibiting the excitatory process in neurons?
A
- Phenytoin, Carbama/ Oxcarba-zepine, Eslicarbazepine acetate, Lamotrigine, Lacos/ Zonis-amide
- inhibits voltage-gated Na+ ion channel
- Ethosuximide
- inhibits Ca2++ entry into postsynaptic neuron
- Retigabine
- increases excite of K+ from the postsynaptic neuron
- Perampanel
- inhibits the AMPA receptor which glutamate binds to and allows NA+ into the postsynaptic neuron
25
Q
What AEDs work by increasing the activity of the inhibitory process in neurons?
A
- Levetiracetam
- increases activity of SV2A- regulates action potential-dependent neurotransmitter release
- Retigabine
- increases the activity of KCNQ K+ channels in the pre and postsynaptic neuron
- Gabapentin, Pregabalin
- inhibit alpha-2-beta-subunit of Ca2+ channels in the presynaptic neuron
- Tiagabine
- Inhibits GAT-1 in presynaptic neurons and on glial cells
- Benzodiazepines, Barbiturates
- increases activity of GABAA more Cl- moved into the postsynaptic neuron
