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Neuro > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

Focal Seizure

A

Unilateral with local onset usually originates from cortical tissue

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2
Q

Generalized Seizure

A

Bilateral and originates from subortical or deeper brain focus.

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3
Q

Prodroma

A

early clinical manifestations of malaise, headache, and sense of depression
hours-few days before seizure onset

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4
Q

Aura

A

peculiar sensation preceding onset of focal seizure; gustatory (taste), visual or auditory experience; feeling of dizziness or numbness

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5
Q

Absence Seizure

A

sudden onset of interruption of activities, blank stare that lasts 20-30 seconds. No aura, prodroma, or postictal state

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6
Q

Myoclonic jerks

A

brief shock-like muscular contractions; single jerk or series of jerks. Synchronous and bilateral of the whole body. No alteration in concsiousness.

electric shock

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7
Q

Clonic

A

state of alternating contraction and relaxation of muscles; bilateral and more sustained/rhythmic than myoclonic

contract + relax

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8
Q

Tonic phase

A

state of muscle contraction with excessive tone (stiffening)

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9
Q

Tonic-clonic

A

initial tonic phase followed by clonic phase

stiff, contract, relax

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10
Q

Atonic

A

sudden loss of muscle tone

head drop, limb drop, or slumping

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11
Q

Post-ictal state

A

time period immediately following cessation of a seizure

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12
Q

Epilepsy

A

condition in which a person has recurrent seizures due to a chronic, underlying process

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13
Q

Seizures

Genetic causes

A

Juvenile Myoclonic Epilepsy (JME), Dravet Syndrome, Childhood Absence Epilepsy (CAE)
most common in childhood

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14
Q

Dravet Syndrome

A

mutations of voltage-gated Na+ channel type 1 alpha subunit (SCN1A)

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15
Q

Childhood Absence Epilepsy (CAE)

A

mutations in T-type Ca2+ channels and GABA receptor subunits

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16
Q

Seizures

Structural Causes

A
  • Mesial temporal lobe form occurs with sclerosis/glial scarring in hippocampus
  • Traumatic brain injury from blunt force or stroke
  • common in older adults
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17
Q

seizures

Infectious causes

A

the most common cause worldwide
development of epilepsy as sequele of infection
common in children

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18
Q

seizures

Metabolic and Immune forms

A
  • less common
  • metabolic: altered glycogen metabolism causes insoluble glycogen inclusion bodies
  • immune: anti-NMDA receptor encephalitis
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19
Q

Epilepsy risk factors

A

premature birth/low birth weight, family history, sleep deprivation, sensory stimuli, stress, hormonal changes can be associated with frequency

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20
Q

Drugs that Cause Seizures

A

theophylline, alcohol, phenothiazines, antidepressants, street drugs, or antiseizure drugs at toxic levels

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21
Q

Glutamate causes

A

excitation!

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22
Q

GABA causes

A

inhibition!

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23
Q

Status Epilepticus (SE)

A

a seizure lasting longer than 30 minnutes (now worry at 5 min) with/without impairment of consciousness or, occurence of recurrent seizures without intervening periods of consciousness

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24
Q

Status Epilepticus Causes

A

results from initiation mechanism or failure of termination mechanisms leading to abnormally prolonged seizures
high incidence in children < 1 and elderly >60

25
Q

Generalized Convulsive Status Epilepticus

A

most common and severe - repeated generalized seizures involving both hemispheres

26
Q

Nonconvulsive Status Epilepticus

A

“epileptic twilight”
altered consciousness and/or behavior

27
Q

4 stages of generalized convulsive status epilepticus

A
  1. impending (0-20 min)
  2. established (20-40 min)
  3. refractory (greater than 40-60)
  4. super refractory (greater than 24h)
28
Q

Status Epilepticus Phase 1

A

First 30 minutes
- increase in NE, Epi, steroids (HTN, tachycardia)
- increased insulin and glucagon due to initial hyperglycemia, then glucose decrease
- muscle contractions/hypoxia lead to lactic acid release
- muscle breakdown leads to secondary hyperkalemia

29
Q

Status Epilepticus Phase 2

A

decompensation: hypotension, decrease in cerebral blood flow, excess oxygen, and glucose consumption
not sustainable so respiratory and metabolic acidosis

30
Q

Pharmacology MOA

Modulation of cation channels (Na+, K+, Ca2+)

A
  1. prolongation of inactivated state of voltage gated Na+ channels
  2. positive modulation of K+ channels
  3. inhibition of Ca2+ channels
31
Q

Pharmacology MOA

Modulation of GABA A and it’s receptor

A
  1. stimulation of GABA A receptors to enhance GABA neurotransmitters
  2. modulation of GABA metabolism
  3. inhibition of GABA reuptake
32
Q

Pharmacology MOA

Acting on ________ to modulate synaptic release of neurotransmitter or on Ca2+ channels with the ____ subunit

A

SV2A protein, alpha2delta

33
Q

Pharmacology MOA

________ (decreasing, increasing) activation of ionotropic glutamate receptors: ____ and ____

A

decreasing, AMPA and NMDA

34
Q

Benzodiazepine MOA

A

Clobazam, Clonazepam, Diazepam, Lorazepam
enhance GABA-mediated synaptic inhibition
BZD receptor is integral part of GABA A, it increases the frequency of the opening of GABA activated Cl- channels and leads to hyperpolarization/increased seizure threshold

35
Q

What benzodiazepines used for status epilepticus?

A

Diazepam and Lorazepam at higher doses

36
Q

Barbiturates MOA

A

phenobarbital and primidone
increases synaptic inhibition via GABA A receptor
increases duration of bursts of the Cl- current

37
Q

Which barbiturate is a prodrug?

A

Primidone is rapidly metabolized to phenobarbital

38
Q

Hydrantoins MOA

A

Phenytoin and Fosphenytoin (prodrug)
decreases repetitive firing of APs – selectively slows rate of recovery of voltage-activated Na+ channels from inactivation
narrow therapeutic index, and 20% of patients develop Gingival hyperplasia

39
Q

Iminostilbenes MOA

A

carbamazepine, oxcarbazepine, eslicarbazepine
slows rate of recovery of Na+ channels from inactivation

40
Q

What is carbamazepines black box warning?

A

hepatotoxicity and aplastic anemia

41
Q

Oxcarbazepine is converted to

A

Eslicarbazepine which is then further converted to S-licarbazepine (faster than oxcarbazepine)

42
Q

Oxcarbazepine/Carbamazepine HLA variant

A

HLA-B15:02 variant is associated with SJS, TEN ADRS
-start low go slow-

43
Q

Succinimides: Ethosuximide MOA

A

** inhibition of (post-synaptic) T-type Ca2+ channels to reduce Ca2+ current**
significant effects in the thalamus, which exhibits large-amplitude T-type currents that underlie the APs

44
Q

Gabapentin and Pregabalin MOA

A

involves binding to a protein in cortical cell membranes that has an amino acid sequence identical to the Ca2+ channel subunit alpha2delta-1 and also binds to voltage-gated K+ channels
(inhibit Ca2+ and activate K+)

45
Q

Lacosamide MOA

A

first agent to prolong the slow inactivation of voltage-gated Na+ channels and limit sustained repetitive firing
also binds the phosphoprotein collapsin response mediator protein

46
Q

Topiramate MOA

A

reduces voltage-gated Na+ current with MOA similar to phenytoin
also activates hyperpolarizing K+ currents, enhances postsynaptic GABA A receptor currents, and decreases activation of AMPA-kainate glutamate receptors

47
Q

Valproate MOA

A

slows rate of recovery of Na+ channels from inactivation
also produces small reductions in T-type Ca2+ currents

48
Q

Ezogabine MOA

A

K+ channel opener - enhances outward K+ current mediated by KCNQ ion channel family - stabilizing resting membrane potential - reducing excitability
may also enhance GABA-mediated currents
A/E: blue skin and lips

49
Q

Felbamate MOA

A

MIGHT: inhibit NMDA-evoked responses and potentiates GABA-evoked responses
no longer uses - life threatening adverse effects

50
Q

Lamotrigine MOA

A

slows rate of recovery of Na+ channels from inactivation
may inhibit synaptic release of glutamate

51
Q

Perampel MOA

A

first in class selective noncompetitive antagonist of AMPA-type ionotropic glutamate receptor
prevents repetitive firing and reduces excitory signaling needed for seizures

52
Q

Levetiracetam and Brivaracetam MOA

A

involves SV2A (blocks and blocks release of glutamate) mutation in SV2A associated with disruption in action potential invoked GABA release
- Levetiracetam: also inhibits N-type Ca2+ channels and release of Ca2+
- Brivaracetam: binds with high affinity to SV2A and inhibits voltage-gated Na channels

53
Q

Rufinamide MOA

A

prolongs slow inactivation of voltage-gated Na+ channels limiting sustained repetitive firing

54
Q

Tiagabine MOA

A

Inhibits GAT-1 GABA transporter, reducing GABA uptake into neurons and glia, prolonging time GABA in the synapse
- can induce seizures in patients without epilepsy

55
Q

Vigabatran MOA

A

irreversible inhibitor of GABA transaminase resulting in increase GABA at receptor to enhance neurotransmission

transaminase breaks down GABA

56
Q

Zonisamide MOA

A

slows rate of recovery of Na+ channels from inactivation
also inhibits T-type Ca2+ currents

57
Q

Cannabidiol MOA

A

not mediated via cannabinoid receptors:
1. activation of the vanilloid receptor TRPV1
2. anatgonism of the orpha GPR55 and GPR55-mediated elevation of presynaptic Ca2+
3. activation of 5HT1A receptors
4. competitive inhibition of the equilibrative nucleoside transporter 1 (ENT-1) to regulate adenosine tone

for Dravet, Lennox-Gastaut and drug resistant epilepsy

58
Q

Cenobamate MOA

A

Na+ channel inhibitor and non-BZD-type positive modulator of GABA A receptor (enhances GABA current)

59
Q

Fenfluramine (amphetamine derivative) MOA

A

increase EC serotonin levels by inhibiting reuptake transporter SERT. Acts as agonists at 5HT2, 5HT1D, and 5HT2C receptors
dravet, lennox-gastaut, and drug-resistance epilepsy

Neuro (4 decks)

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