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NMH: Module 2 > Epilepsy and its treatment > Flashcards

Epilepsy and its treatment Flashcards

1
Q

Define epilepsy

A

a disease characterized by a tendency to recurrent unprovoked seizures

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2
Q

Define seizure

A

abnormal, excessive synchronized discharge of cerebral neurons

NB: epileptic seizures are a clinical manifestation of epilepsy

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3
Q

Comment on the age of incidence of epilepsy

A

Huge variety in age of incidence of epilepsy
2 peaks:
- childhood adolescence (20 ish)]- genetic predesposition?
- later in life (75)]- secondary to brain injury e.g. Alzheimer’s, stroke etc

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4
Q

What is SUDEP?

A

Sudden Unexpected Death in Epilepsy (SUDEP)

It is a primary brain disorder (“short circuited” brain that fails to reboot)

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5
Q

Best way to prevent SUDEP?

A

Control the seizures

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6
Q

How to categorise the causes of epilepsy?

A
  • Idiopathic (70%) i.e. genetic: mendelian-2% risk or non-mendelian-47% risk (“complex”)
  • Symptomatic (30%) i.e. secondary to brain injury: acquired or inherited
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7
Q

Mechanism of innate immunity in environmentally-acquired epilepsy

A

HMGB1 is released in chronic epilepsy -> binds to Toll-like receptors -> inflammatory cascade (cytokine release) -> cytokines interact w/ NMDA receptors -> hyperexcitability -> chronic seizures -> more HMGB1 released

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8
Q

Mechanism of adaptive immunity in environmentally-acquired epilepsy?

A

Autoantibodies against VGKC, NMDA, AMPA, GABA-a, GAD etc

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9
Q

Mechanism of inherited brain injury causing epilepsy?

A

Malformation of Cortical Development (MCD)

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10
Q

How do we classify epilepsy?

A

According to anatomical location of seizure onset

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12
Q

Loci identified by GWAS

A
  • SCN1a (VGSC)
  • PCDH7
  • FANCL
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13
Q

How does a seizure in the latero-temporal cortex manifest?

A

Auditory hallucination

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14
Q

How does a seizure in the medial temporal lobe manifest?

A

Memory disturbance

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15
Q

How does a seizure in the occipital lobe manifest?

A

Visual hallucination

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16
Q

How does a seizure in the occipital pole manifest?

A

Seeing “lights”

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17
Q

Standardise Recording convention on EEG for epilepsy?

A

10-20 convention:

Distance between electrodes within 10-20% of AP and lateral dimensions of skukk

18
Q

Describe why a deflection appears on an EEG

A

Synchronised discharge from a set of neurons -> Na+ influx -> sudden depletion of Na+ ions -> EEG -ve deflection

19
Q

What appearance does epilepsy have on EEG?

A

Spike and slow wave

20
Q

Limitations of using EEG for epilepsy?

A
  • many layers of scalp diminish signal
  • Bell’s reflex (blinking causes artefact)
  • scalp muscles give artefact
21
Q

How to categorise seizures?

A

Generalised epilepsy:
- absence, tonic, tonic-clonic, myoclonic, atonic

Focal epilepsy:
simple partial, complex partial, secondary generalised

22
Q

Main causes of death from epilepsy in the UK?

A
  • SUDEP
  • status epilepticus -> can’t breathe -> hypoxia
  • LOC -> drowning
23
Q

What is generalised epilepsy?

A
  • `Extensive, synchronised discharge in both cerebral hemispheres + LOC
  • Global ictal discharge
24
Q

What is focal (partial) epilepsy?

A

Localised, synchronised discharge in one part of the brain

25
Q

Describe tonic seizure

A

Contraction

26
Q

Describe tonic-clonic seizure

A

Tense, jerk, repeat

27
Q

Describe myoclonic seizure

A

Fasciculation

28
Q

Describe atonic seizure

A

No muscle tone

29
Q

Describe absence seizure

A

Brief LOC

30
Q

Describe simple-partial seizure

A

No LOC

31
Q

Describe complex-partial seizure

A

LOC

32
Q

Describe secondary-generalised seizure

A

Partial -> Generalised

33
Q

What factors influence the decision to treat epilepsy?

A
  • Benefits vs Harm
  • No. of seizure at presentation (more seizures = more risk)
  • Seizure type, severity, cause
34
Q

Mechanisms of action to treat seizures?

A
  • Increase GABA inhibition
  • Decrease glutamate
  • Decrease VGSC (voltage-gated sodium channel_
  • Decrease calcium channels
35
Q

E.g.s of drugs that increase GABA inhibition w/ mechanism?

A

Benzodiazepine: allosteric modification of GABAr -> increased GABA influx

Barbituates: allosteric modification of GABAr -> increased GABA influx

Vitabatrin: inhibits GABA transaminase -> decreased GABA degradation -> increased synaptic GABA ]- NOT USED AS BLINDNESS IN 1/3

Tiagabine: inhibits GAT1 (GABA transporter 1) -> decreased reuptake -> increased synaptic GABA

36
Q

E.g. of drugs that decrease glutamate w/ mechanism?

A

Pre-synaptic
- Levetiracetam: binds to pre-synaptic vesicle protein SV2A -> decreased exocytosis

Post-synaptic

  • Parampanel: AMPAr antagonist
  • Felbamate: NMDAr antagonist
37
Q

E.g. of drugs that decrease calcium channels w/ mechanism

A

Gabapentin: inhibits alpha-2-delta subunit of channel -> decreased Ca2+ influx -> decreased exocytosis

38
Q

E.g. of drugs that decrease VGSCs

A
  • Phentoin
  • Carbamazepine
  • Valproate

NMH: Module 2 (33 decks)

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