Antiepileptics Flashcards

1
Q

_____ people experience a seizure during their lifetime

A

11%

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2
Q

_____ of people that have a seizure are diagnosed with epilepsy

A

3%

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3
Q

seizure activity reports ___ of emergency department visits

A

1%

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4
Q

recurrent seizures are associated with a ____ fold increased risk of sudden death

A

2.5

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5
Q

what are the impacts of epilepsy on quality of life

A
  • education: inadequate schooling
  • employment: unemployment levels are higher
  • independence: physical disability, fear of future seizures, cognitive consequences of disease and treatment, ineffective treatments, inability to obtain a drivers license
  • social isolation: depression
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6
Q

what is a seizure

A

a discrete clinical event that results in the abnormal discharge of a set of neurons in the brain

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7
Q

epilepsy is at least:

A

2 unprovoked seizures

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8
Q

what are acute repetitive seizures

A

seizure clusters over 1-2 days, usually less than 5 minutes, differs from normal pattern, recover consciousness between seizures

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9
Q

what is convulsive status epilepticus

A

failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms which lead to abnormally prolonged seizures
- length of seizures beyond 5 minutes
- second seizure without recovery from the first
- repeated seizures lasting 30 mins or longer

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10
Q

what is the pathophysiology of seizures

A

excessive excitation of cortical neurons (hyperexcitable/hypersynchronization)
- neuronal hyperexcitability
- alterations in the properties of ion channels in the neuronal membrane
- defects in ion transport across neuronal membranes
- abnormal synaptic vesicle protein 2-A
- biochemical modification of receptors
- modulation of second messaging systems and gene expression
- changes in extracellular ion concentrations
- alterations in neuroransmitter uptake and metabolism in glial cells
- modifications in the ratio and function of inhibitory circuits
- transitory imbalance in NTs

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11
Q

what is neuronal hyperexcitability

A

enhanced predisposition of neuronal depolarization and discharge when stimulated

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12
Q

what ion channels in the neuronal membrane are altered

A

Na+, Ca2+ and Cl-

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13
Q

what is synaptic vesicle protein 2-A responsible for

A

fusion of vesicles to membrane but get upregulated in some epilepsies

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14
Q

what are the imbalances in NTs

A

ehanced excitatory neurotransmission
- glutamate/aspartate
- NMDA/AMPA receptors

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15
Q

what are the epilepsy etiologies

A
  • genetic
  • structural
  • infectious
  • metabolic
  • immune
  • unknown
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16
Q

describe the genetic epilepsy etiology

A
  • usually present at a young age
  • dravet syndrome: mutations in sodium channel, type I alpha subunit
  • childhood absence epilepsy- mutations in T-type Ca2+ channels and GABA receptor subunits
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17
Q

what are the structural epilepsy etiologies

A
  • abnormalities found with neuronal imaging- cortical dysplasia, post traumatic epilepsy
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18
Q

what are the infectious etiologies of epilepsy

A

neurocysticercosis (parasite), meningitis, encephalitis

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19
Q

what are the metabolic epilepsy etiologies

A

abnormal glycogen metabolism (LaFora Disease)

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20
Q

what is the immune etiology of epilepsy

A

anti_NMDA receptor encephalitis (autoimmune)

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21
Q

what are the additional seizure etiological considerations

A
  • cerebrovascular abnormality
  • tumors
  • head trauma
  • infection
  • hypoxia
  • fever
  • medications and seizure meds: clozapine (dose), bupropion (dose), carbamazepine (SIADH), TCAs, phenothiazines
  • drug intoxication: cocaine, ephedrine
  • metabolic distrurbance: high or low
  • electrolyte disturbance: calcium, sodium, magnesium
  • alcohol withdrawal
  • sleep deprivation
  • hormonal changes
  • stress
  • prenatal or birth injury
  • congenital malformation
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22
Q

what are the seizure recurrence risk factors

A
  • abnormal EEG
  • seizure occurs during sleep
  • positive fam history (sibling)
  • prior acute seizure
  • downs syndrome and cerebral palsy
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23
Q

with downs syndrome and cerebral palsy:

A

there is no clear associate with seizure type, seizure length or age of onset

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24
Q

what are the seizure types

A
  • focal onset
  • generalized onset
  • unknown onset
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25
Q

describe generalized seizures

A
  • originate at some point within and rapidly engage bilaterally distributed networks
  • can include cortical and subcortical structures but not necessarily the entire cortex
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26
Q

describe focal seizures

A
  • originate within networks limited to one hemisphere
  • may be discretely localized or more widely distributed
27
Q

when a seizure type begins with “focal, generalized or absence” then the word ____ can be presumed

28
Q

what are the classifications of focal onset

A
  • aware
  • impaired awareness
  • focal to bilateral tonic clonic
  • motor onset:
  • automatisms
  • atonic
  • clonic
  • epileptic spasms
  • hyperkinetic
  • myoclonic
  • tonic
  • Nonmotor onset:
  • autonomic
  • behavior arrest
  • cognitive
  • emotional
  • sensory
29
Q

what are the classifications for generalized onset

A
  • motor:
  • tonic-clonic
  • clonic
  • tonic
  • myoclonic
  • myoclonic-tonic-clonic
  • myoclonic- atonic
  • atonic
  • epileptic spasms
  • nonmotor (absence):
    -typical
  • atypical
  • myoclonic
  • eyelid myoclonia
30
Q

what are the classifications for unknown onset

A
  • motor:
  • tonic-clonic
  • epileptic spasms
  • nonmotor:
  • behavior arrest
31
Q

focal seizures occur in:

A

one hemisphere

32
Q

what are the types of focal seizures

A
  • focal aware
  • focal impaired awareness
  • focal to bilateral tonic-clonic
33
Q

what are the focal seizure subgroups

A

motor onset:
- automatisms: lip smacking, rubbing hands, clothes picking
- atonic
- clonic
- spasms
- myoclonic
- tonic
nonmotor onset
- autonomic
- behavioral
- cognitive
- emotional
- sensory

34
Q

what are the types of generalized seizures

A
  • absence (5-20 seconds)
  • myoclonic
  • clonic
  • tonic
  • tonic-clonic
  • atonic
  • infantile spasms
35
Q

what does tonic mean

A

muscles in the body become stiff

36
Q

what are the words used to describe generalized seizures

A
  • tonic
  • atonic
  • myoclonic
  • clonic
37
Q

what is atonic

A

muscle in the body relax

38
Q

what is myoclonic

A

short jerking in parts of the body

39
Q

what is clonic

A

periods of shaking or jerking parts on the body

40
Q

describe childhood epilepsy

A
  • many children become seizure free
  • most seizures are brief
  • rarely do seizures cause long term brain damage without neurologic insult- hypoxia in first 24-48 hours increases risk
  • medications may cause long term side effects
  • children with idiopathic first seizure and normal EEG have favorable prognosis
41
Q

rule out_______ in childhood epilepsy

A

fever, infection, trauma

42
Q

what do EEGs tell us

A
  • graphical representation of cortical electrical activity
  • provides high temporal resolution, poor spatial resolution or cortical disorder
  • most important neuropsychological assessment tool for dx and tx
43
Q

what is taken in a seizure disorder history

A
  • identifiable source
  • precipitating event (stress)
  • age of onset/frequency
  • EEG patterns
  • severity
  • family hx
  • current meds
  • observe and note the before, during and after
44
Q

what can be the sources in a seizure hx

A
  • phenothiazines, TCAs, clozapine, bupropion
  • unmasking: CBZ, phenytoin, phnobarbital (absence)
45
Q

what might labs show in precipitating event

A
  • strss
  • hypoglycemia
  • hyponatremia
  • infection
46
Q

what are the medications associated with lowering the seizure threshold

A
  • theopylline
  • carbapenems
  • flouroquinolones
  • isoniazid
  • antidepressants
  • lithium
  • chlorpromazine
  • clozapine
  • cyclosporine
47
Q

what is phase 1 of physiologic effects of continued seizure activity

A
  • continued seizure activity
  • increased autonomic hyperactivity
  • hypertension
  • hyperglycemia
  • hyperpyrexia
  • sweating
  • salivation
48
Q

what is phase 2 of seizure activity

A
  • minor twitching
  • failure of cerebral circulation
  • decreased cerebral blood flow
  • increased intracranial hypertension
  • systemic hypotension
49
Q

what are the considerations for starting therapy

A
  • what is the risk for recurrent seizures
  • what is the expected benefit
  • tolerability of medications
  • patient values and preferences
  • unprovoked 1st seizure recurrence risk is 21-45% in following 2 years
  • after two or more unprovoked seizures
50
Q

consider treating after first seizure if:

A
  • idiopathic and abnormal EEG
  • symptomatic and abnormal EEG
  • prior neurologic or brain imaging abnormality
  • positive family history
  • nocturnal seizures
51
Q

what are the treatment goals

A
  • prevent occurrence of seizure: decrease frequency and severity
  • prevent or reduce drug side effects and drug interactions (no side effects)
  • prevent the development of neurologic changes
  • improve the patients quality of life
52
Q

longer or repeated seizures =

A

more ischemia, increased risk of cognitive decline secondary to neuronal damage

53
Q

how does treatment improve patients quality of life

A
  • provide cost effective care
  • ensure patient satisfaction
  • prevent toxicity
54
Q

what are the targets for treatment and the effect

A
  • sodium channels: decrease AP frequency
  • calcium T type channel: decrease thalamocortical reverbs
  • calcium L type channel: decrease cortical excitation
  • calcium N type channel: decrease NT release
  • enhanced GABA transmission: increased inhibition
  • decreased glutamate transmission: decreased excitation
55
Q

how is GABA transmission enhanced

A
  • increased GABAa receptor activity
  • increased GABA synthesis
  • decreased GABA reuptake
  • increased serotonin release
56
Q

how is glutamate transmission decreased

A

inhibit receptor/decrease release

57
Q

what are the reasons treatments dont work

A
  • inappropriate treatment: choose wrong drug
  • inappropriate dose
  • poor compliance/lack of education
  • drug storage issues - CBZ
  • drug administration issues - phenytoin suspension
  • drug interactions: cytochrome P450 and p-glycoprotein
  • seizure refractoriness
58
Q

when can you consider trying to stop AED medications

A
  • seizure free for 2-4 years
  • 2 years for absence
  • 4 years for focal and generalized tonic-clonic
  • normal neuro exam/ normal IQ
  • normal EEG with treatment
  • epilepsy of single seizure type
  • history of control within one year
  • no juvenile or myoclonic epilepsy
59
Q

what are the seizure disorder meds

A
  • dilantin (phenytoin)
  • luminal (phenobarbital)
  • tegretol (carbamazepine)
  • depakote (divalproex)
  • keppra (levetiracetam)
  • zonegran (zonidamide)
  • gabitril (tiagabine)
  • banzel (rufinamide)
  • briviact (brivaracetam)
  • onfi (clobazam)
  • cenobamate (Xcopri)
  • fenfluramine (Fintepla)
  • topamax (topiramate)
  • trileptal (felbamate)
  • lamictal (lamotrigine)
  • neurotonin (gabapentin)
  • lyrica (pregabalin)
  • zarontim (ethosuximide)
  • vimpat (lacosamide)
  • fyocompa (perampanel)
  • aptiom (aslicarbazepine)
  • epidiolex (cannabidiol)
  • valtoco (diazepam NS)
  • diacomit (stiripentol)
60
Q

what are the FDA approved treatments for focal onset new dx

A
  • carbamazepine
  • lacosamide
  • phenobarbital
  • phenytoin
  • topiramate
  • valproic acid
  • brivaracetam
  • cenmobamate
61
Q

what are the FDA approved treatments for focal onset refractory adjunct

A
  • carbamazepine
  • gabapentin
  • lamotrigine
  • levetiracetam
  • oxcarbazepine
  • phenobarbital
  • phenytoin
  • pregabalin
  • tiagabine
  • valproic acid
  • vigabatrin
  • zonisamide
62
Q

what are the treatments for generalized absene

A
  • lamotrigine
  • ethosuzimide
  • valproic acid
63
Q

what are the FDA approved treatments for generalized tonic clonic

A
  • lamotrigine
  • levetiracetam
  • topiramate
  • perampanel