2. LEARNING OBJECTIVES
Define terminology related to epilepsy, including seizure,
convulsion, and epilepsy.
Describe the basic pathophysiology of seizures and
epilepsy
Differentiate and classify seizure types when provided a
description of the clinical presentation of the seizure and
electroencephalogram
Recommend an appropriate pharmacological treatments
Analyse potential drug interactions with antiepileptic drugs
(AEDs)
Select appropriate monitoring parameters for a
pharmacotherapeutic regimen for AEDs
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3. SEIZURE VS. EPILEPSY
A seizure :a paroxysmal event due to abnormal
excessive or synchronous neuronal activity in the
brain.
Epilepsy :a chronic neurologic disorder
manifested by repeated seizures resulted from
paroxysmal uncontrolled discharges of neurons
within the central nervous system
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4. SEIZURE VS. EPILEPSY
Seizure: A sudden, explosive and transient
disturbance in cerebral function caused by abnormal
neuronal discharge (EEG-definition)
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5. SEIZURE VS. EPILEPSY
Epilepsy is defined by the occurrence of at least
two unprovoked/unconfirmed seizures separated
by 24 hours
A cording to Ethiopian STG….2014
A paroxysmal neurologic disorder characterized
by a sudden onset of sensory perception or
motor activity with or without loss of
consciousness due to aberrant cortical electrical
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6. EPIDEMIOLOGY
Approximately 5–10% of the population will have
at least one seizure attack in life.
Epilepsy usually presents in childhood or
adolescence but may occur for the first time at
any age
The largest number of patients suffering from
epilepsy is between the ages of(early childhood,
<15) and (late adulthood, >64 years) and affects
45million world wide
While the basic, underlying risk of developing
epilepsy is about 1%, individuals in certain
populations are at higher risk
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7. EPIDEMIOLOGY
10% of children with
mental retardation
10% of children with
cerebral palsy
(inability to move)
50% of children with
both disabilities
10% of patients with
Alzheimer’s disease
7% of ischemic stroke
patients
15% of hemorrhagic
cortical stroke patients
8.7% of children of
mothers with epilepsy
2.4% of children of
fathers with epilepsy
33% of people who have
had a single, unprovoked
seizure
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8. SOCIAL IMPACT
Epilepsy is a disorder with profound impact on a
patient’s lifestyle
Driving
Persistent seizure- poor school attendance and
therefore poor grades
Increase unemployment rate
Cognitive difficult
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9. ETIOLOGIES
In 80% of cases, the underlying etiology is unknown.
(cryptogenic/idiophatic)
The most common recognized causes of epilepsy are
head trauma and stroke.
Developmental and genetic defects are the cause of
about 5% of cases of epilepsy
Metabolic disturbance (Hypoglycemia or hyperglycemia)
Electrolyte imbalance (hyponatremia, hypokalemia,
hypomagenesaemia, hypocalcaemia )
Kidney failure with uremia
Infection of NS (meningitis, encephalatis, HIV and related
infections)
Neurodegenerative disease like Alzheimer's disease
Febrile seizure
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10. ETIOLOGIES
Isolated seizures that are not epilepsy can be
caused by stroke, central nervous system
trauma, central nervous system infections,
metabolic disturbances (e.g., hyponatremia and
hypoglycemia), and hypoxia.
If these underlying causes of seizures are not
corrected, they may lead to the development of
recurrent seizures or epilepsy
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11. MEDICATIONS
bupropion
tramadol
theophylline
Some
antidepressants
Some antipsychotics,
Sympathomimetics or
stimulants
(amphetamines,
cocaine)
imipenem
lithium,
excessive doses of
penicillins (antagonize the
activity of GABA)or
Cephalosporins
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12. PATHOPHYSIOLOGY
The 19th century neurologist Hughlings Jackson
suggested “a sudden excessive disorderly discharge of
cerebral neurons“ as the causation of epileptic seizures.
Cellular definition: excessive or over synchronized
discharges of cortical neurons
GABA receptor mediates inhibition responsible for
normal termination of a seizure
NMDA (N-methyl-D-aspartate) (Glutamate)
receptor activation required for propagation of
seizure activity
Alterations of ion channels in neuronal membranes
A shift in the normal balance of excitation and inhibition
with in the CNS or
Imbalance between Glutamate & GABA
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14. PATHOPHYSIOLOGY
GLUTAMATE: Major excitatory neurotransmitter in cerebral
cortex
Presynaptic neuron released……opening of membrane
channels to allow sodium or calcium to flow into the
postsynaptic neuron…depolarization…neuronal excitation
Many antiepileptic drugs (e.g., phenytoin,
carbamazepine, and lamotrigine) work by interfering
with this mechanism, either by blocking the release of
glutamate or by blocking the sodium or calcium
channels, thus preventing excessive excitation
These drugs typically do not block normal neuronal
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15. PATHOPHYSIOLOGY
GABA: Major inhibitory neurotransmitter
Presynaptic release….open chloride
channel…chloride in flow and hyperpolarization
….less excitable
When chloride flows into the neuron, it becomes
hyperpolarized and less excitable. This mechanism is
probably critical for shutting off seizure activity by
controlling the excessive neuronal firing
Some antiepileptic drugs, primarily barbiturates and
benzodiazepines, work by enhancing the action of
GABA
Nearly all seizures stop spontaneously, because after
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16. PRESENTATION
General Principles
Careful diagnosis and identification of seizure types
is essential to proper treatment of epilepsy
Classification of epileptic seizures is based upon
electroencephalographic (EEG) findings
combined with the
clinical findings of the seizure events.
Clinical presentations of seizures vary widely,
depending on the region and amount of brain
involved in the seizure.
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17. SEIZURE CLASSIFICATION AND PRESENTATION
Motor symptoms: abnormal movements of the
hand synchronous with movement of the face
Sensory /somatic sensory symptoms:
Paresthesias/tingling/burning sensation
Vision (flashing lights or formed hallucinations)
Equilibrium (sensation of falling or vertigo)
Autonomic function (flushing, sweating,
alterations in hearing, olfaction)
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18. SEIZURE CLASSIFICATION AND PRESENTATION
Psychic symptoms:
Sensation of unusual
Intense odors or highly complex sounds
Fear
A sense of impending change
Detachment/disinterest
Depersonalization
Illusions that objects are growing smaller
(micropsia) or larger (macropsia).
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20. PRIMARY GENERALIZED SEIZURES
Entire cerebral cortex is involved in the seizure from
the onset of the seizure
Tonic-clonic
Generally lasts 1 to 3 minutes
Begin with a short tonic contraction of muscles and a
period of rigidity
Clonic phase of repetitive jerking
Patient may lose sphincter control, bite the tongue, or
become cyanotic (skin bluish color)
The episode may be followed by unconsciousness,
and frequently the patient goes into a deep sleep
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21. PRIMARY GENERALIZED SEIZURES
Absence seizures
Sudden and brief (duration 10-30se) losses of
consciousness without muscle movements.
Primarily in children
Sudden onset
Usually accompanied by subtle/faint, bilateral
motor signs (rapid blinking of the eyelids,
chewing movements, clonic movements of the
hands)
Precipitated by hyperventilation/too much lose of
co2
These seizures are often described as
daydreaming or blanking out episodes.
A common term for these seizures is “petit mal.”
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22. PRIMARY GENERALIZED SEIZURES
Myoclonic jerks
Brief shock-like muscular contractions of the face,
trunk, and extremities
This may be isolated events or rapidly repetitive
Single and very brief jerks of all major muscle
groups
Patients with these may not lose
consciousness, due to the seizure lasting less
than 3 - 4 seconds.
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23. PRIMARY GENERALIZED SEIZURES
Atonic seizures
Sudden loss of muscle tone that may be
described as a head drop, dropping of a limb, or
slumping to the ground
Loses consciousness and muscle tone.
No muscle movements are typically noted
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24. PARTIAL SEIZURES
Begins in a localized area of the brain
Simple
The patient will have a sensation or uncontrolled
muscle movement of a portion of their body
without an alteration in consciousness.
The type of sensation or movement is dependent
on the location of seizure in the brain
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25. PARTIAL SEIZURES
Complex
Although the seizure is localized in a specific
area of the brain, like a simple partial seizure,
this seizure causes an alteration in the
patient’s level of consciousness.
Secondarily generalized
Seizures that start as a simple or complex partial
seizure and spread to involve the entire brain.
Patients may report a warning or aura, and
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29. NEUROIMAGING
All patients should receive neuroimaging.
MRI preferred over CT to identify small lesions
such as cortical dysplasias (unusual growth),
infarcts (dead tissue), or tumors.
CT scan is suitable in emergency situations to
exclude a mass lesion, hemorrhage, or large
stroke.
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30. TREATMENT
Goals of treatment
Decreasing the frequency of seizures to
seizure-free state
Minimizing side effects
Improving functionality & QOL
Treating neuropsychiatric comorbidities such as
depression, anxiety, and sleep disturbances
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31. TREATMENT
Management principles
Treatment of underlying causes
Avoidance of precipitating factors
Prophylactic therapy with antiepileptic
medications or surgery
Addressing psychological and social issues
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32. NON-DRUG MANAGEMENT
Adequate sleep
Avoidance of alcohol, stimulants, etc.
Avoidance of known precipitants
Stress reduction
Avoidance of risky conditions: swimming,
firework, machine work, climbing
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33. ACUTE MANAGEMENT/FIRST AIDS
• Place the patient in semiprone position with head to
the side to avoid aspiration
• Support the head to avoid head injury
• Protect from nearby hazards
• Tongue blades or other objects should not be forced
between clenched teeth
• Don’t put any object in mouth
• Transfer to hospital needed if
• Multiple seizure or status epilepticus
• Person is pregnant, injured, diabetic
• New onset seizure
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34. ACUTE MGT (HOSPITAL)
Oxygen should be given via face mask
Reversible metabolic disorders should be
promptly corrected.
Give parentral anticonvulsant therapy (diazepam,
lorazepam) and consider prophylactic AED
therapy.
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36. EPILEPSY: DRUG THERAPY
Choice of AED based on
Seizure type
Efficacy
Adverse effect
Pharmacokinetic profile
Cost
Patient preferences
Co-morbid conditions
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37. THERAPY
1) Two or more seizures
2) Single seizure secondary to identified CNS
lesion with an epileptogenic focus
3) Consider if significant occupational risk if
patient suffers a second event.
4) Consider if single seizure event with one or
more risk factors for recurrent seizures
5) Consider in the elderly patient with increased
risk of seizure related morbidity
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38. AN APPARENTLY UNPROVOKED OR IDIOPATHIC
SEIZURE
31 to 71% risk in the first 12 months after the
initial seizure.
Risk factors associated with recurrent seizures
include the following:
(1) evidence of a structural lesion
(2) EEG abnormalities
(3) partial type seizure
(4) family history of seizures
(5) focal abnormalities on exam
Most patients with one or more of these risk
factors should be treated
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39. PRINCIPLES OF TREATMENT
Start with an average dose of a first line drug
Poor control? Address compliance, maximize drug
dose, confirm right diagnosis (partial complex v.s
generalized)
Majority of patients are controlled with single
antiepileptic drug.
This drug can be gradually withdrawn if seizure free
for two years.
The drug can be reduced by 25% every two to four
weeks
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40. PRINCIPLES OF TREATMENT
20-35% of patients with epilepsy have persistent
seizures despite medical therapy.
If poor control with maximal dose then start with
monotherapy with second drug.
Continue to administer first drug until a full
dose of second drug reached, then gradually
withdraw first drug.
If monotherapy with two drugs fail, patient may
need re-evaluation (repeat MRI/EEG) before
polytherapy commenced
Polytherapy:
Maximize the doses & serum concentrations
of the first anticonvulsant
Add an anticonvulsant with a different
mechanism of action
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41. WHEN TO SWITCH THERAPY
If seizures continue despite gradual increases to the
maximum tolerated dose and documented
compliance or
Intolerable side effects
Maintaining the patient on the first drug while a
second drug is added,
Then the first drug can be gradually withdrawn
(usually over weeks unless there is significant
toxicity).
The dose of the second drug is then further
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42. STOPPING THERAPY
Epilepsy is generally considered to be a lifelong disorder
that requires ongoing treatment
Five criteria must be met before considering the
discontinuation of AED
No seizures for 2 to 5 years
Normal neurologic examination
Normal intelligence quotient
Single type of partial or generalized seizure
Normal EEG with treatment
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43. STOPPING THERAPY
Individuals who fulfill all of these criteria have a
61% chance of remaining seizure-free after AEDs
are discontinued.
Additionally, there is a direct relationship between
the duration of seizure freedom while taking
medications and the chance of being seizure-free
after medications are withdrawn.
Withdrawal of AEDs is done slowly, usually
with a tapering dose over at least 3 months
The drug can be reduced by 25% every two to four
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44. DRUG INTERACTIONS
AEDs are associated with many different drug
interactions
These interactions are primarily in relation to
absorption, metabolism, and protein binding.
Tube feedings and antacids are known to reduce
the absorption of phenytoin and carbamazepine
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46. SPECIAL POPULATIONS
Children and women present special challenges in
the management of epilepsy and use of AEDs
In children, developmental changes occur rapidly,
and metabolic rates are greater than those seen in
adults.
When treating a child it is imperative/necessary to
control seizures as quickly as possible to avoid
interference with development of the brain and
cognition
For women, the treatment of epilepsy poses
challenges, including
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48. AEDS AND PREGNANCY
Seizure is very harmful for pregnant women
plus most of AEDs available are harmful to
the fetus.
Monotherapy usually better than drugs
combination
Use divided doses or ER formulations to even
out fluctuations
Folic acid is recommended to be given for
every pregnant women with epilepsy
Phenytoin & sodium valproate are absolutely
contraindicated
Lamotrigine and Oxcarbamazepine is better
than carbamazepine
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49. OTHER MANAGEMENT ISSUES
Impact on independence, self-esteem,
employment.
Driving regulations:
Private drivers cannot drive for 3 months after
a single seizure.
Private drivers can resume driving after being
seizure free for 12 months on medication
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53. OUTCOME EVALUATION
Efficacy
• Seizure counts are the only reasonable and
standard way to evaluate efficacy of treatment.
• Encourage patients to keep a seizure calendar
that notes the time and day seizures occur and
the type of seizure.
Comparisons can then be made on a monthly
basis to determine the level of seizure control.
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54. OUTCOME EVALUATION
Toxicity
Monitor toxicity of AEDs at every clinic visit.
Question patients about common adverse effects of the
AEDs they are receiving.
Weigh the impact of acute adverse effects against the
extent of seizure control achieved
If it is determined that the adverse effects negatively
impact a patient more than the extent of seizure control
obtained benefits the patient, adjust the therapeutic
regimen.
Continuously monitor chronic adverse effects of AEDs.
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55. REASONS FOR TREATMENT FAILURE
Incorrect diagnosis
Wrong anticonvulsant selected
Inappropriate dose, route, or formulation
Altered pharmacokinetics that require a dosage
alteration
Poor patient adherence (60% nonadherence)
Seizures refractory to medical therapy (20–30%)
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56. SPECIFIC DRUG INFORMATION
Carbamazepine
MOA: decrease synaptic transmission in the CNS by
inhibiting voltage gated sodium channels in neurons
First line for partial seizures especially complex
partial seizure and GTC
Other uses: bipolar disorder & trigeminal neuralgia
Ineffective in the treatment of absence seizure
Dose: 200mg BID increase by 200mg/d every
7days until therapeutic levels are reached
Therapeutic plasma concentration: 6-12 µg/ml
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57. PHARMACOKINETICS
Available only in oral form & absorption is erratic but
complete because of its low water solubility
Food especially fat may enhance the bioavailability
Available as control release and sustained release
better seizure control and fewer side effects
Highly protein bound-80%
Metabolized by the liver to:
CBZ-10.11-epioxide(active) &
CBZ -10,11-dihydroxide (inactive)
Induce its own metabolism-Autoinduction
Drugs that increase its concentration includes: Cimetidine,
isoniazid, Erythromycin…
Drugs that decrease its plasma concentration
Oral contraceptives, Warfarin
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58. SIDE EFFECTS OF CPZ
Osteomalacia (Treat with vitamin D)
Folate deficiency may cause megaloblastic
anemia
Leukopenia (10%)
Teratogenic: spina bifida in 1% if taken
in first trimester.
Use a supplementalbirth control method to
prevent pregnancy.
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59. COUNSELING TIPS
Tip 1: If rash, blister or fever develops contact
physician
CPZ can cause serious form of skin reaction
such as Stevens-Johnson syndrome (SJS) or
toxic epidermal necrolysis (TEN)
Tip 2: Sore throat, fever, chills, or other signs of
infection; unusual bleeding or bruising; tiny
purple dots or spots on the skin; mouth
sores; or rash
Cause decrease number of blood cells
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60. PHENYTOIN
MOA: limit seizure propagation by inhibiting
voltage dependant sodium channel
Clinical use:
Any generalized seizure type except
absence seizure(may worsen it)
Partial seizure
Dose: Loading-15 to 20 mg/kg PO or IV(1 g)
Maintenance-300-400mg/day
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62. SIDE EFFECTS OF PTH
Non-dose related:
Gingival hyperplasia
Hirsutism(hypertrichosis)
Agranulocytosis, Aplastic anemia
Hypersensitivity reactions
mainly skin rashes but in sever cases result in stevens-
johnson syndrome
Hepatitis –rare
Fetal malformations- esp. cleft plate
Bleeding disorders (infants)
Osteomalacia due to abnormalities in Vit D
metabolism
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63. SIDE EFFECTS OF PTH
Folate deficiency
Peripheral neuropathy
Encephalopathy
Dose related
G.I. upset
Neurological problems
Headache, vertigo, diplopia
Ataxia (>30µg/L): gross lack of
coordination of muscle movements
Diminished mental capacity (>40µg/L)
Sedation
At level >50µg/L may exacerbate seizure
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64. COUNSELING TIPS
Tip 1: Care for your mouth properly to decrease
the risk of gum damage caused by
phenytoin
Tip 2: Do not drive a car or operate machinery
until you know how this medication
affects you.
Phenytoin may cause dizziness and
problems with coordination
Tip 3: Caution pregnancy and breast feeding
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65. VALPROIC ACID/DIVALPROEX SODIUM
MOA: increase the level of GABA
May potentiate postsynaptic GABA
responses, direct membrane stabilizing effect,
and affect Na channels
Clinical use:
First line for most generalized seizure
including absence & myoclonic
First choice for combination of absence
and either generalized or partial seizure
Partial seizure
In this regard CPZ is more effective
Also have a place for status epilepticus &
neonatal seizures
Other use: Bipolar disorder
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66. PHARMACOKINETICS
DEPAKOTE tablet (divalproex sodium),
DEPAKENE syrup & capsule(valproic acid) and
injectionsodium valproate
Well absorbed after oral administration on empty
stomach
Highly protein bound: 90 – 95%
Diurnal variation in absorption:
Night times plasma concentration was lower than the day
time
Metabolized by liver: 4-ene-vpa
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67. SIDE EFFECTS
Nausea, vomiting and GIT disturbances
Start with low doses, enteric coated formulation or take with
food
Increased appetite & weight gain
Transient hair loss.
Hepatotoxicity -Most serious
Thrombocytopenia
Neural tube defect to the fetus
Contraindicated in pregnancy: category D
Note: VA is associated with less cognitive deficit than phenytoin and
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68. COUNSELING TIPS
Tip 1: if any of the symptoms below develop
contact physician
Excessive tiredness, lack of energy,
weakness, stomach pain, loss of appetite,
nausea, vomiting, or swelling of the face
VA can damage to liver and pancreas
Tip 2: Take caution during pregnancy and
breast feeding
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69. OXCARBAZEPINE
Clinical & safety profile similar to
carbamazepine
Potential 1st line for partial & generalized
seizure
Hyponatremia is a major problem
Less rash than carbamazepine
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71. NEWER ANTIEPILEPTIC DRUGS
( SECOND- GENERATION )
Newer agents differ from older drugs by
Relatively lack of drug-drug interaction
Simple pharmacokinetic profile
Improved tolerability
HOWEVER THEY ARE…………
Costly with limited clinical experience
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72. LAMOTRIGINE
MOA-Inhibits excitatory amino acid release (glutamate &
aspartate ) by blockade of Na channels.
Clinical use:
Adjunct or monotherapy for partial seizure
Alternative for generalized seizure such as absence
seizure
Pharmacokinetics
Well absorbed from GIT
Metabolized primarily by glucuronidation
Does NOT induce or inhibit ………CYP-450
However its metabolism is inhibited by valproate
which require to decrease dose by 50%
Side effects
N/V, ataxia, headaches, diplopia
SKIN RASH
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73. GABAPENTIN
MOA: May increase the activity of GABA or
inhibits its re-uptake
Clinical use:
Adjunctive for partial seizure
Other use-neuropatic pain
Pharmacokinetics
Not bound to proteins, Not metabolized
and Excreted unchanged in urine
Does not induce or inhibit hepatic
enzymes
Side effects
fatigue, somnolence, dizziness , ataxia,
nystagmus
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74. TOPIRAMATE
MOA-Blocks sodium channels (membrane
stabilization) and also potentiates the
inhibitory effect of GABA
Clinical use:
Present-adjunctive for partial seizure
Its role as a primary agent is being
evaluated
Pharmacokinetics
Well absorbed orally ( 80 % )
Food has no effect on its absorption & it
does not affect liver enzymes
Minimal protein bound: 9-17%
Mostly excreted unchanged in urine
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75. SIDE EFFECTS
Psychological or cognitive dysfunction
Impaired concentration, memory difficulty,
attention deficits
Weight loss
Nephrolithiasis
Sedation, Dizziness, Fatigue, metabolic
acidosis
Paresthesias (abnormal sensation )
Suicide attempt
Cases of secondary angle closure glaucoma
have been reported in pediatric and adult
populations
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76. ZONISAMIDE
Clinical indication:
Add-on therapy for partial seizures
Pharmacokinetics
Well absorbed from GI (100 %)
Protein binding -40%
Extensively metabolized in the liver
No effect on ………….liver enzymes
Side effects
Dizziness, fatigue, anorexia, agitation/irritability
Hypersensitivity rxn- sulfa allergy
Metabolic acidosis
Note-Topiramate & Zonisamide cause metabolic acidosis
Carbonic anhydrase inhibitors increase biocarb
excretion
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77. TIAGABINE
Clinical use:
Adjunctive therapy in partial seizure
Pharmacokinetics
Bioavailability > 90 %
Highly protein bound ( 96% )
Metabolized in the liver
Side effects:
Asthenia, Sedation, Dizziness, Mild
memory impairment, Abdominal pain
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78. ROLE OF PHARMACIST
To ensure that patients are compliant with their
medications.
To advise patients on the proper use of
medications and side effects.
Monitor for any drug interactions &/or adverse
drug reactions.
Monitor drug levels of medications and ensure
the drugs are not subtherapeutic
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79. PATIENT COUNSELING
Keep a seizure diary and keep regular appointments with
the doctor/pharmacist
Counsel patients that full effects may not be seen for
several weeks
Continue to take medication unless directed otherwise by
your physician/pharmacist
Take with food or milk if upset stomach occurs
Do not drink alcohol or take CNS depressants or illegal
drugs with these medications
If this medication causes blurred vision or drowsiness, do
not drive or operate heavy machinery (exception:
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80. PATIENT COUNSELING
Consult your physician/pharmacist if you anticipate
pregnancy, become pregnant or plan to breast-feed while
on this medication
Some anticonvulsants decrease the effectiveness of birth
control pills. Therefore use a back-up birth control method
to prevent pregnancy
If woman of childbearing age, then take 1mg of folic acid
daily
Do not stop taking this medication unless your
doctor/pharmacist advises you to do so.
Check with your pharmacist or doctor before taking or
starting any new medication
Missed dose: if you missed a dose take it as soon as you
remember. Do not take extra or double up doses. If it is
almost time for the next dose resume normal schedule
Contact your doctor/pharmacist if any skin rash occurs
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81. STATUS EPILEPTICUS
A more practical definition to guide treatment
would be:
Continuous seizures lasting more than 5
minutes or
Two or more seizures without complete
recovery of consciousness
SE can present as non-convulsive status
epilepticus (NCSE) or generalized convulsive
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84. EPILEPTICUS
Seizure activity that does not respond to
benzodiazepines (first-line) and antiepileptics
(second-line) or persists beyond 60 minutes in
duration can be considered refractory status
epilepticus (RSE).
It can occur in up to 30% of patients with SE and has
a mortality rate approaching 50%.
Treatment of RSE consists of continuous
intravenous infusions of benzodiazepines
(midazolam), anesthetic agents (propofol), or
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