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Year 2 - Theme 1 > Seizures and epilepsy symposium > Flashcards

Seizures and epilepsy symposium Flashcards

1
Q

Definition of epilepsy

A
  • Is defined as recurring, unprovoked(spontaneous) seizures
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2
Q

What are acute symptomatic seizures provoked by

A

Acute insults such as

  • Stroke
  • alcohol withdrawal
  • Metabolic disturbance
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3
Q

What are most cases of epilepsy caused by?

A
  • Idiopathic causes
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4
Q

What is a generalised onset seizure?

A
  • Electrical discharges appear to start over the whole brain at the same time on EEG
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5
Q

What is a partial/focal onset seizure

A
  • Electrical discharge appears to start in one cortical region and then may remain localised or spread over the whole brain - secondary generalised
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6
Q

How are seizures classified

A 
- Idiopathic (Primary) Generalized Seizures
• limited repertoire of seizures
• tonic-clonic seizures (“grand mal”)
• absences (“petit mal”)
• tonic seizures
• atonic seizures
myoclonic seizures
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7
Q

Features of an idiopathic generalised seizure

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, photosensitivity may be present
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8
Q

Features of a juvenile myoclonic epilepsy

A
  • 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
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9
Q

Features of tonic clonic seizures ‘grand mal’

A 
occurs without warning –risk of injury
tonic phase
• continuous muscle spasm, fall, cyanosis, tongue biting, incontinence
clonic phase
• rhythmic jerking slows and gets larger in amplitude as attack ends
post-ictal (post-seizure) phase
• coma, drowsiness, confusion, headache
• muscle aching
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10
Q

Features 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)
  • eyelid flickering
  • absences only, tend to remit in adulthood (childhood absence epilepsy)
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11
Q

What are absences characterised by on an EEG

A
  • A 3 Hz spike and wave
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12
Q

What are the different types of partial seizures - focal onset seizures

A
  • simple partial seizure (SPS)– patient aware - aura
  • complex partial seizure (CPS) – aura/warning with a level of reduced awareness
  • (patients may call these “absences”, “blanks” – this is medically inaccurate terminology)
  • can be secondary generalized- patient may experience a prior warning, either SPS, CPS, or both, before the tonic clonic seizure
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13
Q

Features of secondary generalised tonic clonic seizures(GTCS)

A
  • warning/aura –eg epigastric rising sensation, altered smell, déjà vu, fear
  • cannot abort attack
  • onset sudden
  • duration 1-3 minutes
  • then falls , loses consciousness as seizure generalizes
  • rigidity/ convulsive jerks/ excess salivation
  • incontinence/tongue bite common
  • red/blue, wakes in ambulance/A&E
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14
Q

Where do most partial seizures occur and what percentage approx

A
  • Temporal 70%

second most frequent frontal at 25%

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15
Q

What are the psychological symptoms of temporal lobe epilepsy

A
  • Deja vu
  • speech arrest(dominant hemisphere)
  • formed words during the seizure implies non-dominant hemisphere focus
  • Fear, elation, depression, anger
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16
Q

Physical symptoms of temporal lobe epilepsy

A
  • hallucination of taste, speech and/or smell, visual distortion
  • Epigastric rising sensation
  • Pallor/flushing/heart rate changes(can mimic panic/hyperventilation attacks)
  • Automatisms - semi-purposeful movements
  • Oral - lip smacking, chewing movements
  • Dystonic posturing(limb rises)
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17
Q

How long do frontal lobe seizures last for on avg

A

10-30 secs

- Rapid recovery, frequent predominantly nocturnal

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18
Q

Features of a frontal lobe seizure

A
  • Forced head/eye deviation to contralateral side
  • Motor activity often bizarre, thrashing
  • Often misdiagnosed as non-epileptic
  • EEG(during the seizure) is often normal
  • Jacksonian spread with todd’s paresis
  • Automatisms, dystonic posturing(overlap TLE)
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19
Q

Symptoms of parietal epilepsy

A
  • Positive sensory symptoms(unlike TIA/stroke)
  • Tingling, pain
  • Distortion of body shape/image
  • Jacksonian march of positive sensory symptoms
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20
Q

What anti-epileptic drugs can make myoclonic jerks and absences worse

A

phenytoin, carbamazepine, gabapentin, pregabalin
• (although all treat tonic clonic seizures so safe to use in status epilepticus)
• some syndromes remit, and some don’t, correct advice to patient re medication

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21
Q

Which seizure patients should you prioritise scanning

A
  • Jacksonian motor or sensory seizure are priority as they have a focal neurological deficity
  • Alcohol withdrawal seizure should only be scanned if subdural hematoma suspected
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22
Q

What is epileptogenesis

A
  • Process by which parts of the normal brain are converted to a hyperexcitable brain
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23
Q

Physiological definition of a seizure

A
  • An explosion of synchronous activity by lots of neurons at once that has a tendency to spread throughout the cerebral cortex causing an ‘electrical brain-storm’
  • A brief change in behaviour caused by the synchronous and rhythmic firing of action potentials by populations of neurons in the CNS
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24
Q

What is epilepsy as a result of?

A
  • A single neuron can fire a train(or trains) of action potentials spontaneously, without any external stimulation(intrinsic excitability)
  • Stimulation of any one cell can lead to a chain reaction due to the progressive spread of activity over a large area
  • Epilepsy represents a failure of inhibitory regulation, either focally(eg motor cortex, temporal cortex) or generally(whole cortex at once)
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25
Q

Link between Na+ channel inactivation and epilepsy

A
  • Na+ channel inactivation too slow
  • eg generalised epilepsy with febrile seizures(fever-induced convulsions in infants or small children)
  • Point mutation in part of Na+ channel(beta subunit) –> abnormally slow inactivation
  • Action potential repolarization impaired
26
Q

Link between number of functional K+ channels and epilepsy

A

eg. benign familial neonatal convulsions
- defect in KCNQ2 or KCNQ3 k+ channel subunit(K+ channels are tetramers of 4 alpha subunits) –> impaired activation
- Action potential repolarization impaired

27
Q

When are the largest potentials recorded in an EEG

A
  • Paradoxically, the largest potentials are recorded when the brain is at rest
  • When left alone and without sensory inputs the various neural networks feedback upon themselves, leading to rhythmic oscillations
28
Q

What is seen in an EEG when aroused

A
  • Neuronal activity becomes desynchronised
  • The hyperexcitation of seizure again to synchronous activity on the EEG
  • EEG can help with determining the localization of a seizure
  • EEG can help with determining the localization of a seizure
29
Q

Where do focal(partial) seizures originate from

A
  • Originate from within a small group of about 1000 neurons: the seizure focus(temporal lobe seizures, focal motor convulsions)
30
Q

How do focal(partial) seizures start

A
  • Synchronised ‘paroxysmal depolarizing shift’(PDS, 20 to 40mV, 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 PDS, trains of action potentials occur
  • Hippocampal neurons have similar responses under normal conditions, making the hippocampus more prone to seizures than the neocortex
31
Q

When do focal seizures spread to other brain regions

A
  • 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)
32
Q

How do primary generalised seizures reach the cerebral cortex

A
  • Via normal neuronal pathways from the thalamus(eg tonic clonic seizure; absence; juvenile myoclonic epilepsy)
33
Q

What are pathways that originate in the brainstem normally involved in?

A
  • Regulation of the sleep/wake cycle and arousal of the cerebral cortex
34
Q

How do we know that inhibition is preserved in epilepsy

A
  • Ca2+ channels and inhibitory GABA receptors in thalamic neurons have been implicated in ‘spike and wave’ seizures, showing that inhibition(the wave) is preserved
35
Q

How do most antileptic drugs work generally

A
  • AEDs do NOT prevent the development of epilepsy
  • Most drugs work to prevent the spread of epileptic discharges
  • Thus, they control epilepsy’s major symptom: the seizure, not the cause ;;’
36
Q

What actions during epileptic seizures do antiepileptic drugs work to counter

A

Increased activity in the brain may be attributable to:
• Increased membrane excitability
• Increased efficiency of excitatory synaptic transmission - glutamate
• Decreased efficiency of inhibitory synaptic transmission – GABA
• Treatments are be aimed at opposing these actions;

37
Q

What were the first generation anti-epileptic drugs

A
  • Sodium channel blockers and GABA enhancers
38
Q

Give examples of anticonvulsant drugs - Na+ channel blockers(just try and remember .a few)

A
  • Phenytoin
  • ## LamotrogineCarbamazepine/oxcarbazepine/eslicarbazepine
  • Zonsiamide
  • Lacosamide
39
Q

How does lacosamide work as a sodium channel blocker

A
  • Lacosamide enhances slow inactivation of sodium channels
40
Q

How do drugs such as carbamazepine, oxcarbazepine and eslicarbazepine inhibit voltage gated sodium channels

A
  • Competitively inhibit the voltage gated sodium channel by binding with the receptor in its inactive state, prolonging the period between successive firings(prevents burst firing)
  • Blockade increases with repetitive firing
  • Drug has greater effect at partially depolarised channel, as a result of facilitated binding
41
Q

What receptors are targeted by anti-epileptic drugs

A
  • Glutamate receptors
42
Q

Give an example of a more recently licensed antiepileptic drug

A
  • Perampanel

- AMPA receptor antagonist

43
Q

How does perampanel work

A
  • non-competitive blockade of AMPA glutamate receptor
  • reduce spread / generalisation of seizure
  • well tolerated with improved alertness
  • role in LD with multiple seizure types not established for perampanel (or lacosamide)
44
Q

How is neurotransmitter release controlled

A
  • Calcium channels are voltage-gated and require strong membrane depolarization for gating
  • They are largely responsible for the regulation of calcium entry and neurotransmitter release from pre-synaptic nerve terminals
45
Q

Which anticonvulsant drugs work by affecting Ca2+ channels

A
  • Topiramate
  • Gabapentin/pregablin
  • Lamotrigine/zonisamide
46
Q

What are the type of calcium channels involved in action potentials

A
  • T-type calcium channels involved in bursting and intrinsic oscillations
47
Q

What part of the calcium channels are targeted by

A
  • Act at a1G subunits containing channels heavily represented in thalamic neurones
  • Thalamic neurones from knockout mice missing a1G fail to fire in burst mode and are resistant to chemical induction of absence-like events
  • A rat model of ‘absence’ increased expression of T-type channels
48
Q

Effect of ethosuximide

A
  • Highly effective in absence epilepsy, but not other seizure types blocks T-channels in thalamus
    (zonisamide also acts on T-type channels)
49
Q

How does GABA increase efficiency of inhibitory synaptic transmission?

A
  • Focal epilepsy characterised by intermittent high amplitude discharges at site of epileptic focus during inter-ictal (seizure) periods
  • Two phases, - synchronous depolarisation (caused by strong excitatory inputs to the region of the focus), followed by a period of hyperpolarisation, reflecting activation of GABA inhibition.
  • Transition from inter-ictal discharges to full-blown seizure is a decrease in the hyper-polarisation phase (failure of inhibition to kick in)
50
Q

Give examples of anticonvulsant drugs

A
  • Sodium valporate(sodium channels)
  • Benzodiazepines(clobazam, lorazepam)
  • Barbiturates/primidone
  • Tiagabine(inhibits re-uptake)
  • Vigabatrin(inhibits GABA-T)
51
Q

Features of levetiracetam

A 
• high-affinity synaptic vesicle protein-2A ligand
• modulates neurotransmitter release
• rapidly titrated and is effective
• Keeps patients alert but…
mood lowering/agitation side-effects
52
Q

Features of an ideal antieplieptic agent

A
  • good efficacy, easy and rapid to titrate
  • no drug-drug interactions/liver enzyme induction
  • no cognitive side-effects/low sodium
  • no bone marrow suppression
  • no affective (mood)/drowsy side-effects
  • different routes of administration
  • cost effective
53
Q

Features of established anti-epileptics

A
  • single mode of action
  • less selective effects
  • more side effects in cognition, sedation
  • more drug interactions
  • kinetics/narrow therapeutic range
  • much cheaper
54
Q

Features of modern anti-epileptics

A
  • Act in broad spectrum
  • More selective actions
  • Less sedating side effects but have many psychiatric/behavioural effects
  • Less long term toxicity
  • Fewer or no drug interactions
  • Easier titration
  • 10X expensive
55
Q

Drugs used to treat primary generalized epilepsy

A
  • Sodium valporate, lamotrigine first line
  • Also levetiracetam, topiramate, zonisamide)
  • Broad spectrum antiepileptic drugs
56
Q

Drugs used to treat partial(focal onset) epilepsy

A
  • carbamazepine, lamotrigine first line

* all other antiepileptic drugs have efficacy (all new antiepileptic drugs are tested first in partial epilepsy)

57
Q

Give examples of drugs that exacerbate generalized seizure types such as myoclonus and absences

A
  • Phenytoin
  • Carbamazepine
  • Gabapentin/pregablin
58
Q

What is a teratogen

A

A teratogen is an agent that can disturb the development of the embryo or fetus. Teratogens halt the pregnancy or produce a congenital malformation (a birth defect)

59
Q

What are the teratogenic effects that anticonvulsants can have

A
  • most anticonvulsants implicated in congenital
  • birth defects - less data for newer agents
  • sodium valproate –affects cognitive development; reduced IQ in infant by 9-10 points, and has a higher rate (3-4% vs 2% of major congenital malformations - dose related). Commoner in mums with a LD
  • epilepsy pregnancy register – voluntary, not randomised or controlled. Risk increased > 1 AED
60
Q

What percentage of patients remain refractory to pharmacological treatment(AEDs)

A
  • 30-40%
61
Q

What set of enzymes are most implicated in drug-drug interactions

A
  • CYP450 liver enzymes
62
Q

What is the most common type of generalised primary epilepsy

A
  • Juvenile myoclonic epilepsy

Year 2 - Theme 1 (30 decks)

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