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PR3136 CA2 > L13-14 Epilepsy > Flashcards

L13-14 Epilepsy Flashcards

1
Q

seizure vs epilepsy

A
  • transient occurrence of signs and/or sx due to abnormal excessive or synchronous neuronal activity in the brain
    vs
  • brain disorder, characterised by an enduring predisposition to generate epleptic seizures
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2
Q

key concept for the pathophysiolgy of seizure

A

hyperexcitability and hypersynchronisation

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3
Q

hyperexcitability

A

enhanced predispostion of a neuron to depolarise

  • voltage or ligand-gated K+, Na+, Ca2+, Cl- ion channels: abnormalities in intra- and extracellular substances eg. Na+, K+, O2, glucose, etc.
  • excessive excitatory neurotransmitters eg. glutamine, acetylcholine, histamine, cytokines, etc.
  • insufficient inhibitory neurotransmitters eg GABA, dopamine
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4
Q

hypersynchronisation

A

(network disorder)
intrinsic organisation of local circuits: hippocampus, the neocortex and the thalamus
- contribute to synchronisation and promote generation of epileptiform activity
- reorganisation: new, sprouting fibers that intrude self-perpetuating excitatory circuits

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5
Q

simple partial seizures

A

focal onset seizures (without dyscognitive features) seizures

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6
Q

difference between absence seizures and complex partial seizures (4)

A
  1. absence seizures are never preceded by auras
  2. ’’ lasts seconds, rather than minutes
  3. ’’ begin frequently and end abruptly
  4. produce characteristic EEG pattern: 3Hz waves (specific for absence seizures)
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7
Q

epileptiform discharges on EEG ______ diagnosis

A

if diagnosis of seizures or epilepsy is considered

- a normal eeg does not excl possibility of epilepsy

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8
Q

investigations

A

scalp EEG, MRI with gadolinium, biochemical/toxicology

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9
Q

risk factors for seizure recurrence

A
  • epileptiform abnormalities on EEG
  • prior brain insult eg stroke, brain trauma
  • structural abnormality in the brain imaging
  • nocturnal seizure
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10
Q

do you start ASM after 1st seizure?

A

unlikely, unless there is a presence of risk factors

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11
Q

after a single unprovoked seizure, recurrence is

A

approx 30%

- 80-90% of which had a second seizure within 2 years

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12
Q

with 2 unprovoked nonfebrile seizures, the risk of recurrence is

A

approx 70%

- initiate tx

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13
Q

non pharmaco tx

A
  • keto diet
  • vagus nerve stimulation
  • responsive neurostimulator system
  • surgery
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14
Q

general principles of pharmaco tx

A

monotherapy preferred

  • likely lower incidence of AE
  • absence of DDI
  • reduced risk of birth defects
  • lower cost
  • easier to correlate response and AE
  • better adherance
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15
Q

drug resistant epilepsy

A

failure of adequate trials of 2 tolerated, appropriately chosen and used ASM drug schedule to achieve sustained seizure freedom
- whether as monotherapy or in combi

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16
Q

seizure triggers (9)

A
  • hyperventilation
  • photostimulation
  • physical and emotional stress
  • sleep deprivation
  • electrolytes imbalance: hypoglycemia, hypo/hyperNa, hypoCa, hypoMg
  • sensory stimuli
  • infection
  • hormonal changes: time of menses, puberty, or pregnancy
  • drugs (decr seizure threshold) eg. theophylline, alc, high-dose phenothiazines, antidepressants esp bupropion, tramadol, carbapenems
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17
Q

appropriate seizure first aid: for generalised grand mal

A
  • ease the person to the floor
  • turn the person gently onto one side, help the person breathe
  • clear the area around the person of anything hard or sharp, prevent injury
  • put something soft and flat, like a folded jacket, under his or her head
  • remove eyeglasses
  • loosen ties or anything around the neck that may make it hard to breathe
  • time the seizure, call 911 if the seizure lasts longer than 5 mins
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18
Q

migraine

A

consider topiramate, valproate

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19
Q

dep/anx

A

use levetiracetam with caution

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20
Q

women w child-bearing potential

A

avoid valproate, consider levetiracetam/lamotrigine

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21
Q

NICE 1st line agents for new onset, focal onset epilepsy

A

carbamazepine, levetiracetam, valproate, lamotrigine, oxcarbazepine

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22
Q

NICE 1st line agents for new onset, generalised tonic-clonic epilepsy

A

lamotrigine, valproate, carbamazepine, oxc?

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23
Q

tx option: refractory, focal onset epilepsy

A

clobazam, lacosamide, pregabalin, perampanel

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24
Q

tx option: refractory, generalised tonic clonic epilepsy

A

clobazam, levetiracetam

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25
Q

topiramate

A

possible cognitive adverse effect, possible teratogenicity

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26
Q

What ASMs are preferentially avoided for use in pregnancy?

A

valproate, topiramate, phenytoin

27
Q

phenytoin

A

possible teratogenicity

28
Q

1st ASM is predominantly cleared via the _____ route?

A

hepatic

29
Q

Does 1st gen or 2nd gen ASM have more ddi?

A

1st gen, significant protein binding

30
Q

which of the 2nd gen ASMs experience DDI?

A

LEV (few, 55%), TPM (dose dependent, 15%), CLB (80-90%)

31
Q

Are 2nd gen ASMs usually cleared renally/hepatically?

A

renally

32
Q

Which of the 2nd gen ASMs are eliminated hepatically?

A

LTG (100%)

33
Q

for patients who require >200mg/day of TPM

A

potentially significant DDI

34
Q

what kind of interaction is easily overlooked, since it is not captured by most CPOE platforms or pharmacy system?

A

deinduction interactions

  • when enzyme-inducing ASM is discontinued, activity of affected enzymes will return to baseline
  • drugs that are metabolised by the affected enzymes may required dose adjustment
35
Q

what is usually the main limiting factor in the tx of epilepsy?

A

adverse effects

36
Q

Chronic adverse effect of gingival hyperplasia is usually observed in patients receiving what therapy?

A

phenytoin

37
Q

Chronic adverse effect of hirsutism is usually observed in patients receiving what therapy?

A

phenytoin

38
Q

Chronic adverse effect of alopecia is usually observed in patients receiving what therapy?

A

valproate

39
Q

Chronic adverse effect of encephalopathy is usually observed in patients receiving what therapy?

A

phenytoin at high doses, or phenobarbitone

40
Q

Chronic adverse effect of peripheral neuropathy is usually observed in patients receiving what therapy?

A

phenytoin at high doses, also a/w cbz and pb

41
Q

How to reverse chronic adverse effect peripheral neuropathy?

A

May or may not improve with decrease in ASM doses

42
Q

How can peripheral neuropathy be reversed?

A

May respond to folate supplementation

43
Q

Is chronic adverse effect increased weight gain reversible?

A

Gradually reverses spontaneously with discontinuation of treatment

44
Q

Which ASM is indicated as a possible pharmacological agent for weight loss?

A

Topiramate

45
Q

Chronic adverse effect of increased weight gain is usually observed in patients receiving what therapy?

A

val

46
Q

Chronic adverse effect of anorexia and weight loss is usually observed in patients receiving what therapy?

A

topiramate and felbamate

47
Q

Is chronic adverse effect increased weight loss and anorexia reversible?

A

reversible with discontinuation of drug

48
Q

Chronic adverse effect of osteomalaccia is usually observed in patients receiving what therapy?

A

phenytoin, phenobarbitone, cbz, maybe val

49
Q

Chronic adverse effect of blood dyscrasis is usually observed in patients receiving what therapy?

A

isolated cases associated with nearly all ASMs

50
Q

Chronic adverse effect of megaloblastic anaemia is usually observed in patients receiving what therapy?

A

phenytoin (predominantly), also a/w cbz and phenobarbitone

51
Q

Chronic adverse effect of neonatal congenital defects is usually observed in patients receiving what therapy?

A
  • a/w phenytoin, pb, tpm (malformation risks)

- val (cognition)

52
Q

What is the main hypothesis for the mechanism by which ASM induce skin reactions?

A

Unclear: ASM with an aromatic ring can form an arene-oxide intermediate
- become immunogenic through interactions with proteins or cellular macromolecules

53
Q

indications for ASM TDM

A
  1. To establish an individual’s ‘therapeutic range’
  2. To assess lack of efficacy
  3. To assess potential toxicity
  4. To assess loss of efficacy (breakthrough seizures)
54
Q

ref range of phenytoin

A

10-20mg/L

55
Q

ref range of val

A

50-100mg/L

56
Q

ref range of cbz

A

4-12mg/L

57
Q

ref range of pb

A

15-40mg/L

58
Q

epilepsy is considred to be resolved for

A

indiv who had an age-dependent epilepsy syndrome
- but now part the applicable age

who have remained seizure-free for the last 10 years
- w no seizure meds for the last 5 years

59
Q

status epilepticus

A

condition resulting either from

  • failure of the mech responsible for seizure termination
  • from the initiation of mech which lead to abnormally prolonged seizures
60
Q

tonic clonic SE: operational dimension 1

A

5 min

- when a seizure is likely to be prolonged leading to continuous seizure activity

61
Q

tonic clonic SE: operational dimension 2

A

30 mins
- when a seizure may cause LT consequences (incl neuronal injury, neuronal death, alteration of neuronal networks and functional deficits)

62
Q

5-20 mins: initial therapy phase

A

benzodiazepine, first line:

  • im midazolam
  • iv lorazepam
  • iv diazepam

others: iv pb, rectal diazepam, intranasal midazolam (not avail in sg)

63
Q

20-40 min: sec therapy phase

A

single dose:

  • iv fosphenytoin
  • iv valproic acid
  • iv levetiracetam

otherwise, iv pb

64
Q

40-60min: third therapy phase

A

no clear evidence to guide therapy in this phase

- repeat second line therapy or anesthetic doses of: thiopental, midazolam, pb, profolol (all w cont EEG monitoring)

PR3136 CA2 (5 decks)

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