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Neurology > Seizure Management and Treatment > Flashcards

Seizure Management and Treatment Flashcards

1
Q

Seizure

A

Disorder viewed as a symptom of disturbed electrical activity in the brain
* A disruption of homeostasis of neurons and their stability, which may trigger hyperexcitability

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2
Q

Epilepsy

A

A chronic disorder of recurrent, unprovoked seizures

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3
Q

What are some medications that may cause seizures?

A
  • Sub-therapeutic anti-epileptic drug (AED) levels
  • Withdrawal of CNS depressants
  • Antibiotics
  • Bupropion
  • SSRIs
  • Theophylline
  • Meperidine (especially with renal dysfunction)
  • Overdose
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4
Q

What medications can you overdose to cause seizures?

A
  • Effexor
  • Tri-cyclic antidepressants
  • Salicylates
  • Tramadol
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5
Q

Partial (focal) seizures

A
  • Begin in one hemisphere and result in asymmetric motor manifestation
  • Can manifest as changes in motor function, sensory, or somatosensory symptoms, or automatisms
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6
Q

Generalized seizures

A

Clinical manifestaions tha indicate involvement of both hemisphere
* Loss of consciousness
* There are 6 types

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7
Q

Automatism

A

A set of brief unconscious behaviors (lip smacking or finger rubbing)

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8
Q

Simple partial seizure

A

Without loss or change of consciousness

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9
Q

Complex partial seizure

A

With loss or change of consciousness

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10
Q

Secondary generalization

A

Partial onset which evolves into generalized tonic-clonic seizure

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11
Q

Absence (Generalized) seizure

A
  • Sudden onset, interruption of ongoing activities, blank stare, possibly brief upward rotation of the eyes
  • Commonly occurs in young children through adolescence
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12
Q

Myoclonic (Generalized) seizure

A

Brief shock-like contractions of the face, trunk, and extremities

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13
Q

Clonic (Generalized) Seizure

A

Rhythmic contractions

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14
Q

Tonic (Generalized) Seizure

A

Contraction of muscles into a rigid position

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15
Q

Tonic-clonic (Generalized) Seizure

A
  • Sudden sharp contractions followed by a period of rigidity
  • Patients may moan, cry, lose sphincter control, bite the tongue, develop cyanosis
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16
Q

Atonic (Generalized) Seizure

A
  • Sudden loss of muscle tone
  • Patients often wear protective head gear
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17
Q

Status Epilepticus (SE)

A
  • A neurologic emergency that can be associated with brain damage and death
  • ≥ 5 minutes of continuous seizures, or
  • ≥ 2 discrete seizures between which there is incomplete recovery of consciousness
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18
Q

Febrile Seizures

A
  • Occurs primarily in children between 6 months and 6 years (majority between 12-18 months)
  • Seizures often develop as the temperature is increasing rapidly but may develop as the fever is declining
  • Can occur during both viral and bacterial infections
  • Majority have febrile seizures on 1st day of illness
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19
Q

What are the four factors in a prospective cohort study that INCREASE the recurrence risk?

A
  • Young age at onset
  • History of febrile seizures in a first-degree relative
  • Low degree of fever while in the emergency department
  • Brief duration between the onset of fever & initial seizure
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20
Q

Traumatic Brain Injury (TBI)

A
  • Seizures are a complication of TBI
  • The more severe the head injury, the longer the patient is at risk for late seizures
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21
Q

Electroencephalogram (EEG)

A
  • Can be an important diagnostic test in evaluating a patient with possible epilepsy/seizures
  • Measures the electrical activity of the brain
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22
Q

What is the pathophysiology of seizures?

A
  • From excessive excitation of a large population of cortical neurons (reflects as a sharp wave or spike on the EEG)
  • Normal membrane conductance & inhibitory synaptic currents break down
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23
Q

What do the clinical manifestations of seizures depend on?

A
  • Site of focus
  • Degree of surrounding brain area irritability
  • Intensity of the impulse
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24
Q

What are the mechanisms that may contribute to synchronous hyperexcitability?

A
  • Alterations in the distribution, number, type, and biophysical properties of ion channels in the neuronal membranes
  • Biochemical modifications of receptors
  • Modulation of second messaging systems and gene expression
  • Changes in extracellular ion concentrations
  • Alterations in neurotransmitter uptake and metabolism
  • Modifications in the ratio and function of inhibitory circuits
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25
Q

What are the mechanisms of control of abnormal neuronal activity by AEDs?

A
  • Elevating the threshold of neurons to electrical or chemical stimuli
    • Involves stabilization of neuronal membranes
  • Limiting the propagation of the seizure discharge from the origin
    • Depression of synaptic transmission and reduction of nerve conductance
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26
Q

Why should you initiate AED after a 1st seizure?

A
  • Epileptiform abnormalities on EEG
  • Remote symptomatic cause, as identified by clinical history or neuroimaging
  • Abnormal neurologic examination, including focal findings
  • Treatment is generally started after 2nd seizure
  • Seizure recurrence indicates on INCREASE risk for additional seizures
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27
Q

How should you discontinue AEDs?

A
  • May be considered by a neurologist after a 2-4 year seizure free interval
  • Recommend tapering at 25% of the dose monthly
  • If patient is one more than one AED, stop the medication that is less appropriate for the seizure type or the agent responsible for ADE
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28
Q

What are some factors that increase the risk of seizure recurrence?

A
  • History of high frequency seizures
  • Repeated episodes of status epilepticus
  • A combination of seizure types
  • Development of abnormal mental functioning
  • Identifiable brain disease (e.g., brain tumor, congenital malformation, encephalomalacia)
  • Abnormal neurologic examination
  • Seizure onset after the first decade
  • Poor initial response to treatment
  • Combination therapy at the time of withdrawal
  • Selected epilepsy syndromes (especially juvenile myoclonic epilepsy)
  • Abnormal electroencephalogram (EEG)
  • Family history of epilepsy
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29
Q

What are some considerations for the Elderly?

A
  • Drug interactions
  • Hypoalbuminemia is common
    • Some AEDs (phenytoin, valproic acid, tiagabine) bound to albumin which makes monitor difficult
  • Increase in fat, decrease in total body water
  • Affect volume of distribution of drugs
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30
Q

What are some considerations for the Neonates/infants?

A
  • Increase in total body water to fat ratio
  • DECREASE in serum albumin and alpha-glycoprotein (results in volume of distribution changes)
  • Newborn up to 2-3 years have decreased renal elimination and hepatic function
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31
Q

What are some considerations for the Women?

A
  • Highest seizure vulnerability b/c estrogen is a seizure activating effect
    • Just before and during the menstruation
    • At ovulation
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32
Q

What are some Pregnancy category D medications?

A
  • Phenytoin
  • Carbamazepine
  • Valproic acid
  • Phenobarbital
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33
Q

What drugs affect hormonal contraception?

Enzyme inducing AEDs

A

Older AEDs:
* Phenytoin, phenobarbital, carbamazepine
Newer agents:
* Felbamate, topiramate, oxcarbazepine

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34
Q

What are some drug inducers?

A
  • Carbamazepine
  • Phenytoin
  • Phenobarbital
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35
Q

What are some drug inhibitors?

A

Valproic acid

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36
Q

What are some drug inhibitors and inducers?

A
  • Felbamate
  • Oxcarbamazepine
  • Topiramate
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37
Q

Clobazam MOA

A

Benzodiazepine
-Involves potentiation of GABAergic neurotransmission from binding at the benzodiazepine site of the GABA receptor

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38
Q

What is the place of therapy Clobazam?

A

Adjunctive treatment of seizures associated with Lennox-Gastaut syndrome (LGS) in patients 2 years of age or older

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39
Q

What are the adverse effects of Clobazam?

A
  • Somnolence and/or sedation
  • WARNING: Abrupt withdrawal should be avoided
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40
Q

What are the counseling points of Clobazam?

A
  • Controlled substance Category IV
  • Pregnancy Category C
  • Need medication guide
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41
Q

What is the place of therapy of Ethosuximibe?

A

First line treatment for absence of seizures

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42
Q

What is the therapeutic level of Ethosuximibe?

A

40-100 mg/dL

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43
Q

What is the adverse effect of Ethosuximibe?

A

Cutaneous Reaction:
-Urticaria, rash, Stevens-Johnson syndrome, systemic lupus erythematosus

-N/V/D/weight loss
-Aplastic anemia
-Drowsiness, fatigue, ataxia

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44
Q

What is the place of therapy of Ezogabine?

A

-Adjunctive agent for partial seizures
-Known internationally as Retigabine

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45
Q

What is the adverse effect of Ezogabine?

A

-Dizziness (32%), somnolence (27%), urinary retention (2%)

Warnings:
-QT-interval prolongation has been reported within 3 hours of administration; monitoring recommended

46
Q

What are some counseling points of Ezogabine?

A
  • REMS for urinary retention and symptoms of acute urinary retention
  • Medication Guide
47
Q

What is the placeof therapy of Felbamate?

A

Reserved for patients not responding to other AEDs

48
Q

What is the adverse effect of Felbamate?

A

-Aplastic anemia and acute liver failure
* Patient or guardian must sign a consent form

49
Q

What is the place of therapy of Gabapentin?

A

-Second line agent for partial seizures +/- generalizations
-Possibly a role in the treatment of less severe seizure disorders such as new onset partial epilepsy
-Highly used for off-label indications: Neuropathic pain, migraines, & bipolar disorder

50
Q

What is the adverse effect of Gabapentin?

A

-Fatigue, somnolence
-Weight gain
-Behavior changes (hostility in children)

51
Q

What is the place of therapy of Lacosamide?

A

FDA approved for adjunctive treatment of partial seizures

52
Q

What are the adverse effects of Lacosamide?

A

-Dizziness (31%)
-Headache (13%)
-Fatigue (9%)

53
Q

What are the counseling points of Lacosamide?

A

Schedule V controlled substance

Warning:
-Prolongation of the PR interval may occur. Use caution in patients with conductance problems (second degree heart block or greater)

Medication Guide must be dispensed with each prescription

54
Q

What is the place of therapy of Lamotrigine?

A

-Monotherapy after trying other AEDs & adjunctive treatment in patients with partial seizures
-Alternatives agent for myoclonic or absence seizures to avoid VPA use (weight gain, polycystic ovary syndrome)
-Adjunctive therapy in patients with generalized tonic-clonic seizures

55
Q

What are the adverse effect of Lamotrigine?

A

-Diplopia, drowsiness, ataxia
-Rash in 5-10% (due to Stevens-Johnson Syndrome)
* Often at 3-4 weeks
* High initial dose, concurrent valproic acid use, rapid escalation
* Can be potentially life-threatening in 1% of patients

56
Q

What are some counseling points of Lamotrigine?

A

Drug Interactions:
-Valproic acid INCREASE serum concentration by 200%
* Due to interference with lamotrigine’s metabolic clearance
-Enzyme inducing drugs (Phenytoin, carbamazepine) accelerates metabolism

57
Q

What is the place of therapy of Levetiracetam?

A

-For patients with partial seizures who have failed previous therapy; Role as monotherapy is NOT clear
-Adjunctive treatment for myoclonic seizures in patients with juvenile myoclonic epilepsy

58
Q

What are the adverse effects of Levetiracetam?

A

Overall best safety profile

Minimal ADEs:
-Somnolence, asthenia, headache, agitation, anxiety
-Behavioral effects in young children (anxiety, agitation, irritability)

59
Q

What is the place of therapy of Rufinamide?

A

Adjunctive treatment of generalized seizures of Lennox-Gastaut Syndrome

60
Q

What are the adverse effect of Rufinamide?

A

-QT shortening (46-65%)
-Headache (16-27%)
-Dizziness (3-19%)
-Fatigue (9-16%)

Contraindicated in pts with familial short QT syndrome

61
Q

What are the counseling points of Rufinamide?

A

Medication Guide for each prescription

62
Q

What is the place of therapy of Oxcarbazepine?

A

-Monotherapy or adjunctive therapy in the treatment of partial seizures in adults and children as young as 4 yrs old
-Potential 1st line agent for primary generalized convulsive seizures

63
Q

How to get the dose from carbamazepine to oxcarbazepine?

A

CBZ dose per day x 1.5

64
Q

What are the adverse effects of Oxcarbazepine?

A
  • Dizziness, nausea, headache, ataxia
  • CNS effects are more common at doses > 1200 mg/day
  • 25-30% carbamazepine cross-sensitivity with rash
    • Less rash than carbamazepine
  • Hyponatremia in 2.5%
    • More common than carbamazepine
    • Reduce dose, d/c diuretics, fluid restrict, Na+ replace
65
Q

What are the counseling points of Oxcarbazepine?

A

Pregnancy Category C

Drug Interaction:
* DECREASE bioavailability of oral contraceptives
* Less potent inducer than carbamazepine and phenytoin
- Transition from carbamazepine to oxcarbamazepine can lead to toxicity of certain drugs (less enzyme induction)
- Valproic acid, phenytoin, warfarin

66
Q

What is the place of therapy of Tiagabine?

A

2nd line agent for partial seizures in patients who failed initial therapy

67
Q

What are the counseling points of Tiagabine?

A

Drug Interactions:
* No inhibition or induction of hepatic enzymes
* CYP3A4 substrate
- Phenytoin, carbamazepine, phenobarbital DECREASE serum concentrations

68
Q

What is the place of therapy of Topiramate?

A

-First line AED for partial seizures
-Also approved for treatment of tonic-clonic seizures in primary generalized epilepsy and migraine prophylaxis
-Migraine prophylaxis

69
Q

What are the adverse effects of Topiramate?

A
  • CNS effects: psychomotor slowing, somnolence, irritability, slurred speech, confusion
    • Seen with rapid dose titration and higher dose
  • Kidney stones (1.5%) 2-4x normal
  • Counsel to maintain good fluid intake
  • Weight loss
  • Glaucoma
70
Q

What are the counseling points of Topiramate?

A

Drug Interactions:
* Metabolism INCREASE by 50% when given with enzyme-inducing AEDs
- Drug levels reduced
* Topiramate may DECREASE the levels of oral contraceptives, digoxin

71
Q

What are the counseling points of Vigabatrin?

A
  • Black Box Warning: Permanent vision loss
  • Available only through the SHARE program
  • REMS program for permanent vision loss
72
Q

What is the place of therapy of Zonisamide?

A

Adjunctive treatment of partial seizures

73
Q

What are the adverse effect of Zonisamide?

A
  • Most common: fatigue, dizziness, ataxia, anorexia
  • Idiosyncratic severe skin rash, Steven Johnson Syndrome
    • D/C zonisamide immediately
  • Weight loss
  • Nephrolithiasis

Contraindication: Sulfa allergy

74
Q

What is the place of therapy of Medical Marijuana?

A

Potential alternative for refractory epilepsy in adults and children who do not respond to current medications

75
Q

What are some advantages of newer AED?

A
  • Lower side-effects rates
  • Little or no need for serum monitoring
  • Once or twice daily dosing for some agents
  • Fewer drug interactions
  • Pregnancy category C
76
Q

What is the FDA alert in 2008?

A
  • Increased suicidality of 11 AED drugs
77
Q

What is the place of therapy of Phenytoin?

A

First-line for primary generalized convulsive & partial seizures

78
Q

What is the PK of Phenytoin?

A
  • Absorption:
    • Differences in salt products
    • Tube feedings decrease absorption
    • Oral absorption is 100%
  • Distribution:
  • 90% bound to albumin
  • Severe burn patients have INCREASE free phenytoin concentrations
  • Obesity increases volume of distribution: BWAdj = IBW + ((ACT-IBW) * 0.4)
  • Metabolism:
  • Zero order kinetics
  • Saturates at doses
  • Renally eliminated
79
Q

What is the dosing of Phenytoin?

A

Loading dose: 15-20 mg/kg IV at rate of ≤ 50 mg/min
* Administer IV slow to avoid venous irritation, pain, and thrombophlebitis
* Administration related hypotension and cardiac arrhythmias may also occur with fast administration

Maintenance: 300 mg/day (5-6 mg/kg/day in 1-3 divided doses)

For oral: 20 mg/kg then divide by 3 & administer divided doses q 2-4 hours

Use adjusted body weight if obese
BWAdj = IBW + ((ACT-IBW)*0.4)

80
Q

What are some concentration dependent adverse effects of Phenytoin?

A
  • Lethargy
  • fatigue
  • in-coordination
  • blurred vision
  • dizziness
  • ataxia
  • nystagmus
81
Q

What are some concentration independent adverse effects of Phenytoin?

A
  • Hypertrichosis
  • Gingival hypertrophy (50%)
  • Thickening of facial features
  • Osteomalacia (long term effect)
  • Folate deficiency (long term effect)
  • Hypersensitivity reactions
82
Q

Purple Glove Syndrome

A
  • A rare complication of intravenous phenytoin use that typically presents with pain, edema, and discoloration at the injection site that spreads to the distal limb
  • Phenytoin
83
Q

What are some monitoring parameters of Phenytoin?

A
  • BP
  • Vital signs with IV use
  • Plasma phenytoin levels
  • CBC
  • Liver function
84
Q

What is the therapeutic range of Phenytoin?

A

Total 10-20 mg/L
* Free 1-2 mg/L
Obtain trough levels 2-3 weeks after initiation or change of dose

85
Q

What is the recommended dose increase if normal renal function?

A

Steady state PHT Increase by
< 7 mg/L 100 mg/day
7 to < 12 mg/L 50 mg/day
≥ 12 mg/L 30 mg/day

86
Q

What are the calculations of Phenytoin?

A
  • Correction for Hypoalbuminemia
    • C corrected = C observed/ 0.2(Alb + 0.1)
  • Correction for renal failure (CrCl < 10mL/min)
    • C corrected = C observed/ 0.1(Alb + 0.1)
      -Extra LD to achieve desired serum levels; then use table if normal renal function to change maintenance dose
  • IV dose(mg/kg) = (C desired – C actual) 0.7
    (add extra 10% to oral dose)
87
Q

Fosphenytoin dose

A
  • LD 10-20 mg/kg PE
88
Q

What is the advantage of Fosphenytoin?

A
  • More advantageous for peripheral IV administration
  • Can give IM for those w/o IV access
89
Q

MOA of Carbamazepine?

A

-Thought to be due to inhibition of voltage-dependent sodium channels
-Interaction with voltage-gated calcium and potassium channels

90
Q

What is the place of therapy of Carbamazepine?

A

First line AED for partial and primary generalized convulsive seizures who are not in an emergent situation

Pregnancy Category D

91
Q

What is the PK of Carbamazepine?

A
  • Auto-induction of its own metabolism
    • Max auto-induction 2-4 weeks after initiation or dose change
    • Re-adjust dose at 3-4 weeks due to auto-induction
92
Q

What is the dose of Carbamazepine?

A

Starting dose: 200 mg BID
* Weekly increase: 200 mg/day
* Usual dose: 800-1200 mg/day given in 2-4 divided doses (max: 1.6-2.4 g/day)

93
Q

What is the therapeutic level of Carbamazepine?

A

4-12 mg/L

94
Q

What is the concentration dependent ADE of carbamazepine?

A
  • Nystagmus
  • Ataxia
  • Blurred vision
  • Diplopia
  • Vomiting
  • Sedation
  • Dizziness
95
Q

What is the concentration independent ADE of carbamazepine?

A
  • Leukopenia (10%)
    • Hold drug if WBC < 2500 cell/mm^3 and absolute neutrophil count < 1000/mm3.
    • Hypersensitivity (rash in 10% SJS)
96
Q

What do you monitor for carbamazepine?

A

CBC with platelet count, serum iron at baseline and periodically during therapy

97
Q

What are the counseling point of Carbamazepine?

A

FDA Alert:
* Screening of patients for HLA B * 1502 allele
* Strong correlation with the presence of the HLA-B * 1502 allele & serious dermatologic reactions with carbamazepine
- Including Stevens-Johnson syndrome & toxic epidermal necrolysis
- Characterized by skin lesions, blisters, fever, itching
* Patients testing positive for the HLA-B*1502 allele should not be treated with carbamazepine

98
Q

What are some drug interactions of Carbamazepine?

A
  • Macrolide antibiotics DECREASE the metabolism of carbamazepine which may result in toxicity
  • Serum concentrations of warfarin may be DECREASE by carbamazepine resulting in subtherapeutic warfarin
99
Q

What is the place of therapy of Valproic acid?

A

-First line AED for primary generalized seizures such as myoclonic, atonic, and absence seizures
-Can be used as monotherapy or adjunctive therapy for partial seizures
-Useful in patients with mixed seizure disorders

100
Q

What is the dosage of Valproic acid?

A

LD: 15-20 mg/kg IV
Maintenance:
* Initial 10-15 mg/kg/day in 2-3 divided doses
* Weekly increases 10mg/kg/day
* Target maintenance: 30-60 mg/kg/day in 2-3 divided doses

101
Q

What is the therapeutic dose of Valproic acid?

A

Total 50-100 mg/L

102
Q

What are some dose dependent ADE of Valproic acid?

A
  • GI complaints (20%)
  • Alopecia (temporary)
  • Thrombocytopenia, platelet dysfunction
103
Q

What is the dose independent ADE of Valproic acid?

A

-Hepatotoxicity
* Unpredictable/fatal
* Most common in young children < 2yrs, on polytherapy, within 1st 6-12 months of therapy
* Patients complaining of nausea, vomiting, lethargy, anorexia, and edema early in the therapy course should have liver function tests done

104
Q

What are some drug interactions of Valproic acid?

A
  • INCREASE carbamazepine metabolite, 10,11 epoxide
  • Ethosuximide INCREASE or DECREASE
  • INCREASE lamotrigine
  • Phenytoin INCREASE free, DECREASE total
  • Aspirin INCREASE Valproic free concentration levels (displacement of drug from albumin)
  • Carbamazepine, phenytoin, phenobarbital DECREASE valproic acid levels
105
Q

What are some monitoring parameters for Valproic acid?

A

-Baseline & periodically throughout therapy: Liver enzymes, CBC w/ platelets
-Serum valproate levels

106
Q

What is the place of therapy of Phenobarbital?

A

-Drug of choice for neonatal seizures, but is reserved in other situations for patients who have failed therapy with other AEDs
-May be useful given IV in refractory status epilepticus

107
Q

What is the dose of Phenobarbital?

A

LD: 15-20 mg/kg IV
* Avoid rapid administration due to hypotension

Maintenance Dose IV/PO: 50-100 mg 2-3 times daily (1-3 mg/kg/d in 1-2 doses)

108
Q

What is the therapeutic level of Phenobarbital?

A

15-40 mg/L (trough)

109
Q

What are the concentration dependent ADE of Phenobarbital?

A
  • Sedation
  • Respiratory depression
  • Hypotension
110
Q

What is the concentration independent ADE of Phenobarbital?

A
  • Hypersensitivity reactions
  • Hyperactivity
  • Altered concentration
  • Altered learning
  • Depression

Neurology (21 decks)

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