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C&M Neuroanatomy > Week 8: Epilepsy > Flashcards

Week 8: Epilepsy Flashcards

1
Q

What is a seizure?

A
  • the clinical manifestation of an abnormally excessive and hypersynchronous activity of neurones located predominantly in the cerebral cortex
  • too much neuronal activity = a seizure
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2
Q

What are the two basic mechanisms underlying seizures?

A
  1. Too much excitation
    - inward Na+ and Ca2+ currents
    - increased release of neurotransmitter - glutamate, aspartate
  2. Too little inhibition
    - insufficient K+ current, inward Cl-
    - decreased release of neurotransmitter - GABA
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3
Q

What do inhibitory interneurones do?

A

allow brain activity to spread in one direction, but not to spread out sideways

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4
Q

What might occur if localised hyperexcitability is not counterbalanced by inhibitory neurones?

A
  • starts to spread out, involving more and more neurones
  • activity spreads out sideways
  • too many cells become active at once
  • a visible seizure is the result
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5
Q

What do intracellular calcium levels tell us?

A

measures excitation

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6
Q

What is an antiepileptic drug?

A
  • a drug which decreases the frequency and/or severity of seizures in people with epilepsy
  • treats the symptom of seizures, not the underlying epileptic condition
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7
Q

What are the 3 potential modes of action of AEDs?

A
  1. Supress action potential
    - Na+ channel blocker
    - K+ channel opener
  2. Enhance GABA transmission
    - GABA uptake inhibitor
  3. Suppression of excitatory transmission
    - glutamate receptor antagonist
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8
Q

What would be the top 3 drugs of choice for partial simple, partial complex and generalised tonic clonic seizure?

A
  1. valproic acid
  2. phenytoin
  3. carbamazepine
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9
Q

What drug could you give for both absence and atypical absence seizures?

A

valproic acid

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10
Q

What drug would you give for febrile seizures?

A

diazepam, rectal

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11
Q

How do we detect absent seizures?

A

can only be detected by ECGs as there are no signs other than a blank expression

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12
Q

What is the most widely used AED in the world?

A

valproic acid

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13
Q

Who is influenced by feibrile seizures?

A

infants

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14
Q

What is GABA and how does it act?

A
  • major inhibitory neurotransmitter

- acts via GABAa or GABAb receptors

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15
Q

What type of receptor is a GABAa receptor and how does this work?

A

ligand-gated chloride channel receptor
When the GABAa receptor is activated through the binding of GABA, the GABAa receptor forms a chloride channel so chloride ions can enter the cell

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16
Q

How can we enhance GABA action (and increase Cl- influx)

A
  • barbiturates e.g phenobarbital
  • benxodiazepines e.g clonazepam
  • inhibit GABA transaminase
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17
Q

What is chlonazepam and what seizures is it effective in?

A
  • benzodiazepine

- generalised tonic-clonic, absence and partial seizures

18
Q

What is status epilepticus?

A
  • a life threatening condition in which the brain is in a state of persistant seizure
  • more than 30 minutes continous seizure activity
  • two or more sequential seizures spanning this period without full recovery between seizures
  • medical emergency
19
Q

What drug is used to counter SE?

A

Diazepam - a GABAa receptor antagonist

20
Q

List all the actions of benzodiazepines?

A
  • sedative (calming)
  • hypnotic (initiates or prolongs sleep)
  • anxiolytic (reduces anxiety)
  • anticonvulsant (reduce epileptiform activity)
  • muscle relaxant
  • amnesic
21
Q

How do benzodiazepines work?

A
  • increase affinity of GABA for its receptor
  • increases Cl- current
  • suppresses seizure focus by raising action potential threshhold
  • strengthens surround inhibition - prevents spread
22
Q

When are benzodiazepines toxic?

A

if than with other CNS depressants or with ethanol (as this can cause respiratory depression)

23
Q

What are the unwanted effects of benzodiazepines?

A

drowsiness, confusion, amnesia, poor co-ordination

24
Q

What drug should be administered in case of a BZ overdose?

A

a BZ-site antagonist - flumazenil

25
Q

What is the main problem with BZs?

A

dependence –> marked withdrawel syndrome so should only be used for short term treatment

26
Q

Which anti-epileptic drugs work by inhibition of Na+ chanels?

A
  • phenytoin

- carbamazepine

27
Q

Explain the 3 possible states that a voltage-dependent Na+ chanel can exist in during an action potential

A
  1. closed - before activation
  2. open - during depolarisation
  3. inactivated - shortly after the peak of depolarisation (channel doesn’t open in response to a new signal until the membrane has repolarised)
28
Q

How does phenytoin work??

A

binds to Na+ channel in an inactivated state and slows down its recovery (takes longer to go back to the closed state where it can be activated again)

29
Q

Why is phenytoin known as a ‘use-dependant block’?

A
  • phenytoin only binds to Na+ channels that have been recently opened
  • the more channels that have been opened, the more will be in the inactivated state and therefore be accessed by phenytoin
  • only rapid firing neurones are blocked so does not interfere with normally firing neurones
30
Q

How is phenytoin taken and what does it bind to?

A

taken orally - well absorbed

binds to the inside of the inner pore of the Na+ channel (NaV1.2)

31
Q

what is meant by ‘free’ phenytoin?

A
  • if taken with another drug that has the same binding site e.g valproate, this produces more ‘free’ phenytoin (because binding sites are occupied)
  • the ‘free phenytoin’ is not bound to plasma protein
  • this tends to increase hepatic clearance of the drug so effects can be unpredictable
32
Q

Explain how phenytoin is metabolised?

A
  • highly metabolised in the liver to an inactive metabolite
  • metabolism is saturable –> liver cannot metabolise further
  • small increase in dose caan lead to large increase in plasma concentration, as elimination becomes saturated
33
Q

In phenytoin, what is the relationship between dose and plasma concentration?

A

non linear –> highly variable concentrations even with minor dosage changes

34
Q

What are some minor unwanted effects of phenytoin? e.g at 100umol/L

A

vertigo, ataxia, headache and nystagmus (uncontrollable eye movements)

35
Q

What are some severe unwanted effects of phenytoin? e.g at 150 umol/L

A
  • confusion, intellectual deterioration
  • hyperplasia of the gums, hirsutism
  • hypersensitivity and rashes
  • hepatatis
  • foetal malformations
36
Q

What is foetal hydantoin syndrome?

A

up to 30% of children whose mothers are taking pheytoin during pregnancy typically have:

  • growth restruction
  • microcephaly
  • craniofacial and limb defects
  • developmental delay, mental retardation
  • heart defects

so it is a group of defects caused to the developing foetus by exposure to the teratogenic effects of phenytoin, or more rarely, carbamazepine

37
Q

Which AEDs have mixed actions?

A
  1. valproate
  2. gabapentin
  3. levetiracetman
38
Q

What is valproate used for and how is it taken?

A
  • valproic acid
  • effective against tonic-clonic and absence seizures
  • can also be used in bipolar
  • taken orally and well absorbed
39
Q

Explain the mechanism of action of valproate?

A
  • inhibits Na+ channels
  • decrease GABA turnover
  • inhibit GABA transaminase
  • blocks neurotransmitter release
40
Q

What is foetal valproate sydrome?

A

there is a 6-9% risk of congenital malformations in infants exposed to the VPA pre-natally

41
Q

How beneficial is using drugs to treat epilepsy?

A
  • 70% will be seizure free with one drug –> careful monitoring and adjustment
  • 5-10% seizure free with two or more drugs
  • 20% still have seizures (refractory epilepsy) –> because the seizures cannot be controlled by currently available drugs

C&M Neuroanatomy (44 decks)

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