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Neuro - Week 2 > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

the clinical manifestation of an abnormal and excessive excitations of a population of brain cells (cortical neurons)

A

Seizure

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2
Q

sudden, violent, irregular movement of the limb or body, caused by involuntary contraction of muscles, associated with brain disorders e.g. epilepsy

A

Convulsions

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3
Q

Hyperventilation triggers this type of seizure

A

Absence

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4
Q

Are seizures caused by identified provocations (alcohol/drugs) considered epilespy?

A

NO

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5
Q

What is the typical age of patients with seizures?

A

Bimodal peak = infancy and elderly

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6
Q

Etiology of epilepsy that arises spontaneous, cause is unknown but likely related to genetic cause

A

Idiopathic etiology

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7
Q

Etiology of epilepsy that is uncertain origin, no obvious cause

A

Cryptogenic etiology

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8
Q

Etiology of epilepsy where there is evidence of underlying brain damage or cause

A

Symptomatic etiology

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9
Q

site in the CNS from which the repetitive discharge originates

A

Focus

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10
Q

This describes when with time, nerves near the focus are ‘recruited’ and begin the repetitive discharge (kindling)

A

Recruitment or spread

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11
Q

the period after the seizure characterized by fatigue, amnesia, and difficulty focusing

A

Postictal depression

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12
Q

What drug is used to treat Lennox-Gastaut syndrome?

A

Benzodiazepines

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13
Q

Form of epilepsy with onset common between 1-6 years of age and in males
Characterized by intellectual disability, mixed seizures (tonic, atonic, atypical, etc), abnormal EEG activity of less than 2.5 Hz, and difficult management

A

Lennox-Gastaut syndrome

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14
Q

Classification of seizures that begin locally and may have asymmetric manifestations
Types include simple and complex

A

Partial (focal) seizures

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15
Q

Type of partial seizure that is without impairment of consciousness

A

Simple

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16
Q

Type of partial seizure that is with impairment of consciousness

A

Complex

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17
Q

This describes when partial seizures evolve over time to generalized seizures
Mechanism of evolution may be similar to the process of kindling

A

Secondarily generalized seizures

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18
Q

Classification of seizures that originates in one part of one of the cerebral hemispheres; highly localized

A

Focal (partial)

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19
Q

Classification of seizures that is diffuse and often involves both cerebral hemispheres

A

Generalized

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20
Q

Is there loss of consciousness with generalized seizures?

A

is expected

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21
Q

Is there loss of consciousness with simple partial seizures?

A

No

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22
Q

Is there loss of consciousness with complex partial seizures?

A

yes

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23
Q

Generalized non-motor seizures are primarily this type, and corresponds to the old term “petit mal”

A

Absence seizure

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24
Q

Petit mal is a term corresponding to this type of seizure

A

Absence seizure

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25
Q

Characteristic 3-Hz spike-and-wave EEG pattern indicates this type of seizure

A

Absence seizures

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26
Q

What is the characteristic EEG pattern of absence seizures?

A

3-Hz spike-and-wave pattern

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27
Q

Type of generalized seizure with Lapse of consciousness, Cessation of purposeful behavior, and Motionless stare, may show brief upward roll of eyes

A

Absence seizure

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28
Q

Type of generalized seizure with stiffening and jerking
Loosely corresponds to “grand mal”

A

Tonic-clonic

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29
Q

Type of generalized seizure with stiffening and jerking

A

Tonic-clonic

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30
Q

Type of generalized seizure that loosely corresponds to “grand mal” seizure

A

Tonic-clonic

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31
Q

Type of generalized seizure with sudden, brief shock-like muscle contractions
Often triggered by strobing light and sound

A

Myoclonic

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32
Q

In tonic-clonic seizures, is the tonic or clonic phase first?

A

Tonic - tonic muscle contractions with arm and legs becoming extended
(clonic phase follows where tonic rigidity is interrupted by brief intermittent muscle relaxation)

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33
Q

Amnesia incontinence, headache, fatigue, and disorientation can occur in the postictal period after this type of generalized seizure

A

Tonic-clonic

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34
Q

Type of generalized seizure with sudden loss of tone in postural muscles
May be localized to head drop, limb drop, or slumping to ground
Sometimes called drop attacks or astatic seizures

A

Atonic

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35
Q

Type of generalized seizure that may present in clusters of up to 100 per episode and several clusters per day

A

Infantile spasms

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36
Q

Convulsion pattern of this type of generalized seizure includes sudden bending forward of body with stiffening of arms and legs

A

Infantile spasms

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37
Q

This type of diet may be helpful in epilepsy management

A

Ketogenic diet
(high in fats and low in carbs and protein)

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38
Q

Acidosis and ketosis are expected with this diet that may be helpful for epilepsy management

A

Ketogenic diet

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39
Q

Vagal nerve stimulator is most beneficial in this type of seizure

A

Absence
(also depression)

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40
Q

What are the 3 requirements for surgical treatment for epilepsy?

A

Absolute diagnosis of epilepsy
Failure on drug therapy trials
Clear identification of the electro-clinical syndrome

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41
Q

With epilepsy drugs, Never abruptly discontinue a drug after a patient has been taking it more than this long

A

2 weeks

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42
Q

What is the leading cause of treatment failure in epilepsy?

A

Noncompliance

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43
Q

If a patient misses a dose of their epilepsy drug, what should they do?

A

Take dose asap
Resume normal schedule with next dose
Do NOT double dose

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44
Q

This antigen is common in patients of Southeast Asia heritage, and predicts Stevens-Johnson risk of carbamazepine and phenytoin

A

HLA-B*1502

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45
Q

HLA-B*1502 antigen is common in patients this heritage, and predicts Stevens-Johnson risk of carbamazepine and phenytoin

A

Southeast Asia

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46
Q

HLA-B*1502 antigen is common in patients of Southeast Asia heritage, and predicts risk of this with use of carbamazepine and phenytoin

A

Stevens-Johnson syndrome

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47
Q

HLA-B*1502 antigen is common in patients of Southeast Asia heritage, and predicts Stevens-Johnson risk with use of either of these epilepsy drugs

A

Carbamazepine and Phenytoin

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48
Q

Is weight loss or gain a chronic effect of epilepsy drugs?

A

Weight gain

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49
Q

Is hypernatremia or hyponatremia a chronic effect of epilepsy drugs?

A

Hyponatremia

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50
Q

Interactions with other CNS depressants, Oral contraceptives may be less effective because of enzyme induction, Teratogenic effects and Coagulation disorders are shared toxicities of this type of drug

A

Epilepsy drugs

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51
Q

Antiepileptics may induce metabolism of these in oral contraceptives making them ineffective

A

Hormones

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52
Q

Do epilepsy drugs appear in breast milk?

A

Most do

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53
Q

3 epilepsy drugs that increase sperm abnormalities

A

Carbamazepine
Oxcarbazepine
Valproic acid

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54
Q

Epilepsy drug that may cause testicular atrophy and reduced testosterone

A

Valproic acid

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55
Q

Process by which a seizure or other brain event is both initiated and its recurrence made more likely
(Seizures that are not fully treated will generally become more intense)
If you can fully control seizures, you may be able to stop medications

A

Kindling

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56
Q

MOA of this antiepileptic drug is central inhibition of carbonic anhydrase that increases central CO2 levels that inhibit neuronal activity

A

Acetazolamide

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57
Q

MOA of Acetazolamide is central inhibition of this enzyme that increases central CO2 levels that inhibit neuronal activity

A

Carbonic anhydrase

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58
Q

MOA of Acetazolamide is central inhibition of carbonic anhydrase that increases central levels of this, which inhibits neuronal activity

A

CO2

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59
Q

Does the MOA of Acetazolamide involve central or peripheral inhibition of carbonic anhydrase?

A

Central

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60
Q

What is the MOA of Acetazolamide?

A

Central inhibition of carbonic anhydrase
(increases central CO2 levels that inhibit neuronal activity)

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61
Q

Does Acetazolamide have short or long duration of action?

A

Short

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62
Q

What limits the use of Acetazolamide use in epilepsy?

A

Rapid development of tolerance

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63
Q

Antiepileptic drug with use limited to epilepsy of periodic and predictable occurrence

A

Acetazolamide

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64
Q

What is the MOA of Benzodiazepines?

A

Allosteric enhancement of GABA inhibition

65
Q

The MOA of Benzodiazepines involves allosteric enhancement of this

A

GABA inhibition

66
Q

Antiepileptic drug that allosterically enhances GABA inhibition

A

Benzodiazepines

67
Q

Tolerance may develop abruptly after long-term use, so avoid using this class of drugs to chronically treat most seizures

A

Benzodiazepines

68
Q

What is the MOA of Carbamazepine?

A

Blocks sodium channels

69
Q

Carbamazepine blocks these channels

70
Q

2 anti-epileptic drugs with bone marrow depression, hepatotoxicity, and teratogenicity as adverse effects

A

Carbamazepine
Valproic acid / Divalproex sodium

71
Q

What is the first line drug for partial and generalized seizures?

A

Carbamazepine

72
Q

Anti-epileptic drug that is an auto-inducer with active metabolite

A

Carbamazepine

73
Q

These are adverse effects of this anti-epileptic drug:
Bone marrow depression (black box warning)
Asian patients (black box warning for life threatening rash, screen for HLA-B 1502 variant)
Hepatotoxicity
Teratogenicity (1% spinal bifida)

A

Carbamazepine

74
Q

Hyponatremia limits use of this anti-epileptic in elderly

A

Oxcarbazepine

75
Q

This adverse effect of Oxcarbazepine limits use in the elderly

A

Hyponatremia

76
Q

Anti-epileptic drug with MOA of inhibiting T-type calcium channels

A

Ethosuximide

77
Q

What is the MOA of Ethosuximide?

A

Inhibition of T-type calcium channels

78
Q

Ethosuximide inhibits this type of channel

A

T-type calcium channels

79
Q

Ethosuximide is the first line drug for this type of seizure

80
Q

First line drug for absence seizures

A

Ethosuximide

81
Q

Anti-epileptic drug that blocks N-methyl-D-aspartate receptors at the glycine binding site

82
Q

Felbamate blocks this receptor

A

N-methyl-D-aspartate receptors

83
Q

What is the MOA of Felbamate?

A

Blocks NMDA receptors at the glycine binding site

84
Q

Aplastic anemia (1/3k) and liver failure (1/10k) are black box warnings of this anti-epileptic
Typically within 1st year of therapy

85
Q

What are two black box warnings of Felbamate?

A

Aplastic anemia (1/3k)
Liver failure (1/10k)

86
Q

Anti-epileptic that is reserved for patients not responding to other less dangerous drugs

87
Q

Anti-epileptic that binds to a specific receptor to inhibit calcium channels

A

Gabapentin

88
Q

What is the MOA of Gabapentin?

A

Binds to a specific receptor to inhibit calcium channels

89
Q

Gabapentin binds to a specific receptor to inhibit this type of channel

A

Calcium channels

90
Q

Withdrawal from this anti-epileptic is characterized by anxiety, insomnia, sweating and pain

A

Gabapentin

91
Q

Anti-epileptic that is also indicated for chronic pain, migraines, spasticity, bipolar disorder, psychosis, and restless leg syndrome

A

Gabapentin

92
Q

Anti-epileptic that blocks Na+ channels suppressing the release of glutamate and aspartate, thus decreasing seizure frequency

A

Lamotrigine

93
Q

Lamotrigine blocks these channels, suppressing the release of glutamate and aspartate

A

sodium channels

94
Q

Lamotrigine blocks sodium channels, suppressing the release of these 2 compounds

A

Glutamate and Aspartate

95
Q

What is the MOA of Lamotrigine?

A

Blocks Na+ channels suppressing the release of glutamate and aspartate

96
Q

Rash early in therapy that may become severe (life threatening) and dose limiting is a black box warning for this anti-epileptic

A

Lamotrigine

97
Q

Anti-epileptic that has additive toxicity with other antiepileptic drugs

A

Lamotrigine

98
Q

Anti-epileptic drug that binds synaptic vesicle protein 2A to modulate neurotransmitter release

A

Levetiracetam
(and Brivaracetam)

99
Q

Levetiracetam (and Brivaracetam) bind to this to modulate neurotransmitter release

A

Synaptic vesicle protein 2A

100
Q

Levetiracetam (and Brivaracetam) bind to synaptic vesicle protein 2A to modulate this

A

Neurotransmitter release

101
Q

What is the MOA of Levetiracetam (and Brivaracetam)?

A

Bind synaptic vesicle protein 2A to modulate neurotransmitter release

102
Q

Cognitive disruption in adults and Behavioral disruption in children are adverse effects of this anti-epileptic

A

Levetiracetam
(and Brivaracetam)

103
Q

High levels of this anti-epileptic appear in breast milk

A

Levetiracetam
(and Brivaracetam)

104
Q

This antiepileptic drug antagonizes post-synaptic AMPA receptors, reducing glutamate-mediated neuronal activation

A

Perampanel

105
Q

Perampanel antagonizes post-synaptic receptors of this type, reducing glutamate-mediated neuronal activation

106
Q

Perampanel antagonizes or agonizes post-synaptic AMPA receptors?

A

Antagonizes

107
Q

Perampanel antagonizes post-synaptic AMPA receptors, reducing neuronal activation that is mediated by this

108
Q

What is the MOA of Perampanel?

A

Antagonizes post-synaptic AMPA receptors, reducing glutamate-mediated neuronal activation

109
Q

What is the most important MOA of Phenobarbital?

A

Enhancement of GABA inhibition
(also blocks calcium channels)

110
Q

Anti-epileptic that enhances GABA inhibition, and blocks calcium channels, blocking excitatory processes (glutamate release)

A

Phenobarbital

111
Q

Serious rash and other hypersensitivity disorders are adverse effects of this anti-epileptic

A

Phenobarbital

112
Q

Anti-epileptic that may cause:
Sedation, respiratory and cardiac depression
Cognitive disruption and hyperactivity in children

A

Phenobarbital

113
Q

Phenobarbital can not be used in patients with this condition

114
Q

This anti-epileptic cannot be used in patients with porphyria

A

Phenobarbital

115
Q

This anti-epileptic is oxidized to phenylethylmalonamide (PEMA) and phenobarbital, which are all active

116
Q

Which of the following has the longest duration: Primidone, PEMA, or phenobarbital?

A

Phenobarbital
(its blood level is 2x that of primidone)

117
Q

Primidone is oxidized to these 2 compounds

A

Phenylethylmalonamide (PEMA)
Phenobarbital

118
Q

Anti-epileptic that disrupts sodium channel activation and mainly blocks spread of seizure

119
Q

This anti-epileptic follows zero order kinetics at therapeutic levels

120
Q

Gingival hyperplasia is an adverse effect of this anti-epileptic

121
Q

Elevated cardiac toxicity when used intravenously is a black box warning of this anti-epileptic

122
Q

Dermatological toxicity in Asian patients with HLA-B*1502 variant is an adverse effect of this anti-epileptic

123
Q

What is the MOA of phenytoin?

A

Disruption of Na+ channel activation and mainly blocks spread of seizure

124
Q

Phenytoin disrupts this type of channel

125
Q

Pregabalin disruption of this appear most important in its MOA

126
Q

Anti-epileptic that has risk of respiratory depression when in combination with opioids

A

Pregabalin

127
Q

Pregabalin has risk of respiratory depression when in combination with these drugs

128
Q

Pregabalin has risk of this when used in combination with opioids

A

Respiratory depression

129
Q

Anti-epileptic that:
Slows Na+ channel reactivation
Enhances GABA inhibition
Modules Ca++ channels
Blocks glutamate receptors

A

Topiramate

130
Q

Topiramate slows reactivation of these channels

131
Q

Topiramate blocks these receptors

132
Q

Anti-epileptic that shows saturable binding to RBC

A

Topiramate

133
Q

Topiramate shows saturable binding to this

134
Q

Impaired concentration, memory difficulties, attentional deficits, confusion, and Nephrolithiasis are adverse effects of this anti-epileptic

A

Topiramate

135
Q

First line drug for partial and generalized seizures that is also used in migraines and pain management

A

Topiramate

136
Q

Anti-epileptic drug that:
Slows Na+ channel reactivation
Enhances GABA inhibition
Modulates Ca++ channels
Direct membrane stabilizer

A

Valproic acid / Divalproex sodium

137
Q

Pancreatitis is a black box warning of this anti-epileptic

A

Valproic acid / Divalproex sodium

138
Q

Valproic acid / Divalproex sodium use should be avoided in patients with this type of disease (black box)

A

Mitochondrial disease

139
Q

Anti-epileptic with black box warning against use in patients with mitochondrial disease

A

Valproic acid / Divalproex sodium

140
Q

Pancreatitis, weight gain, hepatotoxicity, teratogenicity and bone marrow suppression are adverse effects of this anti-epileptic

A

Valproic acid / Divalproex sodium

141
Q

This anti-epileptic is generally considered as the drug of choice for patients with generalized and unclassified epilepsies – but safety is a powerful consideration

A

Valproic acid / Divalproex sodium

142
Q

Anti-epileptic that should not be used with clonazepam due to intense depression and absence epilepsy side effects

A

Valproic acid / Divalproex sodium

143
Q

Valproic acid / Divalproex sodium should not be used with this drug, due to intense depression and absence epilepsy with concurrent use

A

Clonazepam

144
Q

Valproic acid / Divalproex sodium should not be used with clonazepam due to side effects of intense depression and this type of epilepsy

A

Absence
(even in cases where a patient has never had it before)

145
Q

Anti-epileptic that is an irreversible inhibitor of GABA-transaminase, a primary GABA degradation enzyme

A

Vigabatrin

146
Q

Vigabatrin is an irreversible inhibitor of this enzyme

A

GABA-transaminase
(a primary GABA degradation enzyme)

147
Q

What is the MOA of Vigabatrin?

A

Irreversible inhibitor of GABA-transaminase
(a primary GABA degradation enzyme)

148
Q

Anti-epileptic that may cause permanent visual disturbance and vision loss (black box warning)

A

Vigabatrin

149
Q

Anti-epileptic that may aggravate absence and myoclonic seizures in patients with generalized seizures

A

Vigabatrin

150
Q

Anti-epileptic that may aggravate absence and myoclonic seizures in patients with generalized seizures, and also may intensify depression, psychosis or behavioral disturbances

A

Vigabatrin

151
Q

A black box warning of Vigabatrin is that is may cause loss of this

152
Q

Anti-epileptic indicated for seizures associated with CDKL5 deficiency disorder in patients >2 years age

A

Ganaxolone

153
Q

Anti-epileptic that enhances the inhibitor effects of GABAa receptors, stabilizing neuronal activity and reducing seizure frequency

A

Ganaxolone

154
Q

Life-threatening neurological condition characterized by 5 or more minutes of either continuous seizure activity or repetitive seizures without regaining consciousness

A

Status epilepticus

155
Q

Propofol anesthetic is an alternative drug used to treat this condition

A

Status epilepticus

156
Q

This drug is an alternative used to treat Status epilepticus

157
Q

Spina bifida may occur from use of this drug’s teratogenicity

A

Carbamazepine

158
Q

Anti-epileptic that is a powerful inducer and should not be used in porphryia

A

Phenobarbital

159
Q

This drug is the most teratogenic of all anti-seizure compounds

A

Valproic acid / Divalproex sodium

Neuro - Week 2 (10 decks)

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