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MODERATOR: PHARM AKPAN MFON
DISCUSSANT: PHARM OKOLO NZUBECHUKWU JULIUS
Outline
 Introduction
 Epidemiology
 Pathophysiology
 Classification of epilepsy
 Symptoms of epilepsy
 Risk factors of epilepsy
 Prevention of epilepsy
 Diagnosis
 Treatment option
 Pharmacist role
 Case presentation
 Conclusion
 Reference
INTRODUCTION
 Epilepsy is a chronic non communicable disease of the brain characterized by
an enduring (i.e., persisting) recurrent seizures.
 This is usually diagnosed when someone has two or more unprovoked episode
of seizure occurring at list 24 h apart.
 Epilepsy is one of the most common neurological diseases and affects people
of all ages, races, social classes, and geographical locations.
INTRODUCTION Cont
 Epileptic seizures can affect your feelings, awareness or
movement. Different types of seizures involve different things. These
may include confusion, strange feelings, repetitive movements, 'blank'
moments (where you are briefly unresponsive), muscle jerks, sudden
falls, or jerking movements (while unconscious).
 While all people with epilepsy experience seizures, not all individuals
with seizures have epilepsy.
EPIDEMIOLOGY
The prevalence of epilepsy differs significantly among countries
depending on the local distribution of risk and etiologic factors.
 According to WHO over 50 million people worldwide have epilepsy,
making it the most common neurological disease globally.
 According Hauser W et al, the incidence of epilepsy is higher in the
youngest and oldest age-groups, with estimates of 46 per 100,000
people diagnosed with epilepsy in high income countries, 139 per
100,000 people diagnosed with epilepsy in low and middle income
countries. This is likely due to increased risk in of endemic conditions
such as neurocysticercosis.
EPIDEMIOLOGY Cont
 Nearly 80% 0f people with epilepsy live in low and middle income countries.
(https://www.who.int/news-room/fact-sheets/detail/epilepsy)
 While 70% of people living with epilepsy could live seizure free if properly
diagnosed and treated. (https://www.who.int/news-room/fact-sheets/detail/epilepsy)
 In UBTH for the past three years, precisely children emergency an average of 168
patients are diagnosed of epilepsy annually.
 However, according to Bharucha N et al, Incidence and prevalence of epilepsy are
slightly higher in men than in women. The difference might be explained by the
different prevalence of the most common risk factors and the concealment of the
condition in women for sociocultural reasons in certain regions.
PATHOPYSIOLOGY
 Pathophysiology of epileptic diseases are caused by ion channel mutations.
Although epileptic syndromes differ pathophysiologically. Masuda H, et al
 In neurochemical mechanism of epilepsy, An imbalance between glutamate
and gamma-aminobutyric acid neurotransmitter systems can lead to
hyperexcitability but catecholaminergic neurotransmitter systems and opioid
peptides were shown to play a role in epileptogenesis as well.
PATHOPHYSIOLOGY Contd.
 During a seizure episode, the membrane potential of neurons is altered in a way that causes
neurons to be hypersensitive or overactive due to certain stimuli or triggering events. The
causes of seizures can be known or unknown.
 Environmental triggers can include loud noises, strobe lights, and rhythmic music Boro A et al.
Medical triggers include high fevers, infections, tumors, hypoglycemia, poor nutrition
(causing electrolyte imbalances), trauma, physical exhaustion and toxic substances, such as
medications, alcohol, and illicit drugs Boro A et al.
 Seizures can even have psychosocial triggers, including emotional stress and shock.
PATHOPHYSIOLOGY Cont
CLASSIFICATION OF EPILEPSY
FOCAL GENERALIZED UNKNOWN
Awareness / impaired awareness motor motor
Motor onset
• Automatism
• Atonic
• Clonic
• Tonic
• Epileptic spasm
• Hyperkinetic
• Myoclonic
• Tonic-clonic
• Clonic
• Tonic
• Myoclonic
• Myoclonic tonic-clonic
• Myoclonic atonic
• Atonic
• Epileptic spasm
• Tonic-clonic
• Epileptic spasm
Non motor onset
• Autonomic
• Behavior arrest
• Cognitive
• Emotional
• Sensory
Non motor (Absence)
• Typical
• Atypical
• Myoclonic
• Eyelid myoclonia
Non motor
• Behavior arrest
Focal to bilateral tonic-clonic Unclassified
SYMPTOMS OF EPILEPSY
 Temporary confusion
 A starring spell
 Stiff muscles
 Uncontrollable jerking movement of the arms and legs
 Loss of consciousness or awareness
 Psychological symptoms such as fear anxiety or deja vu
RISK FACTORS OF EPILEPSY
 Stroke and other vascular disease
 Brain tumor
 A severe head injury
 Drug abuse or alcohol misuse
 A brain infection
 Lack of oxygen during birth
 Congenital abnormalities or genetic condition with associated brain
malfunctions.
PREVENTION OF EPILEPSY
 Reduce your risk of traumatic brain injury.
 Reduce your risk of stroke and cardiovascular disease by eating a healthy
diet.
 Ensure physical exercise and quitting smoking
 Adequate vaccination lowers the chances of infection that can sometimes
predispose the individual to epilepsy.
 Stay healthy during your pregnancy.
 Maintaining good hygiene and prepare food safely. This is because an
infection called cysticercosis is the most common cause of epilepsy
worldwide and commonly caused by a parasite tenia solium
DIAGNOSES OF EPILEPSY
The diagnoses of epilepsy requires at least two or more unprovoked seizure
occurring greater than twenty four hours apart (>24 hrs).
This disorder can be diagnosed using the following system
 Neurological examination
 Blood testing
 Electroencephalogram (EEG)
 Magnetic resonance imaging (MRI)
 Computed tomography (CTs)
DIAGNOSES OF EPILEPSY cont
EEG brain activity
An EEG records the electrical activity of the brain via electrodes affixed to the scalp. EEG results show changes in brain activity that may be useful in
diagnosing brain conditions, especially epilepsy and other seizure disorders.
DIAGNOSES OF EPILEPSY cont
TREATMENT OF EPILEPSY
In treatment of epilepsy it is important to understand the mechanism of action
and the pharmacokinetics of antiepileptic drugs (AEDs) so that these agent can
be used effectively in clinical practice, especially in multidrug regimens
Molgaard-Nielsen D.
The different mechanism of action include the following
 Sodium channel blockers
 Calcium channel blockers
 Gamma amino butyric acid (GABA) enhancer
 Glutamate blockers
TREATMENT OF EPILEPSY cont
Ion
channel
Mechanism of
action (MOA)
Drugs Doses
(Adult)
Treatment Adverse effect
Sodium
channel
blockers
This works by
blocking the
activated gated
Na+ channel influx
into the neuronal
cell there by
inhibiting
repetitive firing of
presynaptic and
postsynaptic nerves
Carbamazepine
400mg, 200mg
Lamotrigine 100mg,
Valproate 500mg
phenytoin 200mg,
Fos-PHT 100mg/2ml
oxcarbamazepine
300mg, 600mg
Zonisamide 100mg,
lacosamide 50mg,
cenobamate 25mg
50mg 100mg 200mg
Tab 200mg b.d
Tab 50mg dly
Cap 250mg b.d
Cap 100mg tds
15-20mg/kg iv,
Tab 600mg dly
Cap 100mg dly
Tab 100mg b.d
Tab 12.5mg dly
Focal and generalized
tonic-clonic seizure
focal/secondary genlz
Focal/generalized
Focal and generalized
Status epileticus
Focal/secondary genlz
Focal/secondary genlz
Status epilepticus & F/s
Focal seizure
Dizziness,
hepatotoxicity
headache, nausea,
ataxia, anorexia,
allergic rashes,
growth deficit,
mental slowing,
tremor, insomnia,
osteoporosis
embrayofetal and
perinatal mortality
TREATMENT OF EPILEPSY cont
Ion
channels
Mechanism of action
(MOA)
Drugs Doses (Adult) Treatment Adverse effect
Calcium
channel
blockers
This channel exist as
L,N and T forms in
human brain, its MOA
is inhibition of T-type
channels responsible
for depolarization
necessary to generate
spike wave burst as
seen in absence seizure.
Ethosuximide Tab 250mg b.d Absence seizure headache, nausea,
ataxia, anorexia,
allergic rashes,
growth deficit,
mental slowing,
tremor, insomnia
confusion
TREATMENT OF EPILEPSY cont
Ion
channels
Mechanism of action
(MOA)
Drug examples Doses(Adult) Treatment Adverse
effect
GABA
enhancers
Comprises of two receptors
GABA A and GABA B.
when GABA binds to
GABA A receptor, it results
to influx of cl- into the
neuronal cell thereby
increasing the negativity of
the membrane and
returning it to a resting
potentials. Also the AEDs
works by blocking the
reuptake of GABA or by
inhibiting its metabolism
as mediated by GABA
transaminase
Benzodiazepine e.g
diazepam 10mg
clobazam 10mg
clonazepam 2mg
Barbiturates e.g
phenobarbital 100mg
primidone 50mg
200mg
GABAtransaminase
e.g vigabatrin 500mg
Tiagabine 4mg
GABA enhancers eg
Gabapentin 300mg
Tab 5-10mg bd
Tab 20-30mg dly
Tab 1.5mg dly
inj 3mg/kg/day IV
Tab 100-125mg b.d
Tab 500mg b.d
Tab 4mg dly
Tab 300mg tds
Status epilepticus
Focal epilepsy
Myoclonic seizure
and subcortical
myoclonus.
Status epilepticus.
Focal seizure
Refractory focal/s
Focal sec/ genlz
Focal/sec genlz
Dizziness,
sedation,
blurred
vision,
diplopia,
skin rash
depression,
muscle
fatigue,
somnolence,
headache
TREATMENT OF EPILEPSY cont
Ion
channels
Mechanism of action
(MOA)
Drug examples Doses
(Adult)
Treatment Adverse
effect
Glutamate
blockers
Comprises of different
binding sites
• Alpha –amino-3-hyroxy-5-
methylisozole-4-propionic
acid (AMPA)
• N-methyl-D-aspartate
(NMDA)
• Metabotropic site
This works by binding of the
AEDs to either of this
receptor sites and inhibits the
influx of Na+ and Ca2+ into
the neuronal cell while
retaining more of the Cl-
NMDA receptor
blocker eg
felbamate 400mg
AMPA receptors
eg topiramate
400mg
Metabotrophic
blocker eg still
under
experimental
studies
Tab 1200mg tds
Tab 400mg dly
Multiple
seizures, hypoxic
ischemic injuries.
Weight loss,
insomnia,
nausea,
decreased
appetite,
dizziness,
lethargy,
fatigue,
hepatic
failure,
TREATMENT OF EPILEPSY cont
Ion channels Mechanism of
action (MOA)
Drug
examples
doses(Adult) Treatment Adverse effect
Piracetam
derivatives
Inhibits Ca2+
released from
inositol-triphosphate
sensitive stores
without reducing
Ca2+ storage
Levetiracetam
250mg, 500mg
Brivaracetam
50mg, 100mg
Tab 500mg b.d
Tab 50mg b.d
Focal/generalized
seizure with tonic-
clonic symptoms.
Focal seizure
Somnolence,
asthenia,
dizziness,
headache,
fatigue, anorexia,
weakness.
PHARMACIST ROLE IN MANAGEMENT OF EPILEPSY
 Educating patients about epilepsy so they understand the disease condition and
take good precaution.
 Patient are advised on accurate dosing of there drugs as prescribed by the
physician.
 patient are advised on adherence to medication
 establishing a therapeutic drug monitoring protocol, adjusting doses and
monitoring of adverse drug reaction.
CASE PRESENTATION
 Demographic data
Patient SP is an 11 years old child, Benin by bribe, a Christian and a student, lives in
Benin city with her parents.
 Family history
Patient SP is the second child of family of three children.
 Social history
Patient SP doesn’t take alcohol or use tobacco in any form.
 Chief complaint
Patient SP complain of frequent headache and nausea.
CASE PRESENTATION cont
 Past medical history
 Patient did not cry after delivery
 Patient was admitted in hospital at birth
 The last time of seizure was three years ago
 Patient has undergone an operation (appendicitis)
 Past medication history
 Tab Ibuprofen 200mg B.D x 2/7
 Tab Paracetamol 500mg tds x 2/7
 Im Promethazine 25mg stat
 Tab Cefuroxime 250mg B.D x 5/7
CASE PRESENTATION cont
Vital signs
 Blood pressure 120/80mmHg
 weight 56kg
 Temp 36.1◦c
 PR 88 b/m
 Physical examination
 patient SP is calm adolescent, afebrile, not pale, acyanosed, not dehydrated , no
pedal oedema.
 Pupil is equal and bilateral reactive to light.
 Neck is supple.
CASE PRESENTATION cont
date Time Nature of seizure duration intervention
1/3/22 2 pm Generalized seizure 60 seconds Inj I.V diazepam 10mg given and iv
phenobarbitone 855mg start
‘’ 6 pm Nil seizure
‘’ 9 pm Nil seizure
7/3/22 6 am Nil seizure
7 am Generalized seizure 60 seconds Aborted by inj I.V diazepam 10mg given
7:10 am Generalized seizure 30 seconds
8:30 am Generalized seizure 40 seconds
10:00 am Nil seizure
12:30 pm Nil seizure
13/3/22 9:00pm Generalized seizure 60 seconds Aborted with I.V diazepam 10mg and I.V
phenytoin 500mg in 100mls IVF N/S
Patient SP seizure chart
CASE PRESENTATION cont
 Plan
 Iv diazepam 0.3mg stat
 iv phenytoin 145mg 12hrly in 30mls normal saline.
 Tab sodium valproate 700mg 12hrly
 Tab levetiracetam 250mg 12hrly.
• Diagnosis
• Focal to generalized seizure
GOAL OF THERAPY
 To prevention or minimise unwanted reoccurrence of episodes of seizure
 To improve patient quality of life
 To ensure safe and efficacious drug availability
 To ensure proper adherence to prescribed medication
DRUG THERAPY PROBLEM
Unnecessary drug therapy Nil
Wrong drug Nil
Dose too high Nil
Dose too low Nil
Adverse drug reaction yes
Inappropriate adherence yes
Needs additional drug therapy. Nil
DRUG THERAPY PROBLEM
 Actual Drug therapy problem.
Adverse drug Reaction:
 Cause- patient SP had an undesirable reaction to levetiracetam which was not
dose related
 Potential drug therapy problem
Inappropriate Adherence:
Cause- affordability and availability problems.
Inability to self administer drug appropriately.
PHARMACEUTICAL CARE PLAN
 Drug focused intervention
 Tab levetiracetam was withdrawn from her medication and was advice to
continue with sodium valproate 700mg twice daily.
Patient focused intervention
 Patient was educated on the use of his/her drugs and the possible side effects.
 Patient was counseled to strictly come for checkups and drug refills.
PHARMACEUTICAL CARE PLAN cont
 Clinical intervention
 The incidence of epileptic crises was greatly reduced.
 Strict management and proper follow up was carried out which reinforce
patient quick recovery.
 Economic outcome
 Patient could afford her medication.
 Humanistic outcome
 Patient was satisfied with the service rendered.
 Quality of life was improved.
 Patient has a better understanding about disease condition and management.
CONCLUSION
Epilepsy is a complex neurological and metabolic disorder characterized by two or more
unprovoked seizure occurring greater than 24 hours apart, which is as a result of
abnormal neuronal firing in the brain.
This disorder comes out with abnormal signs and symptoms, predisposing the patient to
injuries and harm. And a more reason for urgent attention and treatment.
Through patient education, counseling and collaboration with other health care
providers, pharmacist can play a key role in reducing the long term health risk
associated with epilepsy down to 70% in low income countries with adequate diagnostic
tools and medications. (https://www.who.int/news-room/fact-sheets/detail/epilepsy)
REFERENCE
 Jj, scheffer IE, fisher RS, falcon walter. The new definition and classification
seizure and epilepsy. Epilepsy Research.2018;139:73-79
 Fiest KM, Sauro KM, Wiebe S, Patten SB, Kwon CS, Dykeman J. Prevalence
and incidence of epilepsy: A systematic review and meta-analysis of
international studies. Neurology. 2017 Jan;88(3):296–303.
 Kaiboriboon K, Bakaki PM, Lhatoo SD, Koroukian S. Incidence and
prevalence of treated epilepsy among poor health and low-income
Americans. Neurology. 2013 May;80(21):1942–9.
 Masuda H, shariff E, Tohyama J. clinical patterns and pathophysiology of
hypermotor seizures: an ictal SPECT study. Epileptic disord. 2012;14:32-40
REFERENCE cont
 Bharucha NE, Bharucha EP, Bharucha AE, Bhise AV Schoenberg BS. Prevalence of
epilepsy in the Parsi community of Bombay. Epilepsia. 1988 Mar-Apr;29(2):111–115.
 Hauser WA, Annegers JF, Kurland LT. Incidence of epilepsy and unprovoked seizures
in Rochester, Epilepsia. 1993 May-Jun;34(3):453–68.
 Camfield P, Camfield C. Incidence, prevalence and aetiology of seizures and epilepsy
in children. Epileptic Disord. 2015 Jun;17(2):117–23.
 Berenguer B. pharmaceutical care: past present and future. Curr pharm Des 2004;
10;3931-3946.
 Boro A, Haut S. Medical comorbidities in the treatment of epilepsy. Epilepsy
Behavior.2003;4:2-12.
 Molgaard-Nielsen D, Haviid A, Newer generation antiepileptic drugs and the risk of
major birth defects. JAMA. 2011 May 18. 305(19):19916-2002.
Thanks for Listening

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MANAGEMENT OF EPILEPSY MODIFIED 2.pptx

  • 1. MODERATOR: PHARM AKPAN MFON DISCUSSANT: PHARM OKOLO NZUBECHUKWU JULIUS
  • 2. Outline  Introduction  Epidemiology  Pathophysiology  Classification of epilepsy  Symptoms of epilepsy  Risk factors of epilepsy  Prevention of epilepsy  Diagnosis  Treatment option  Pharmacist role  Case presentation  Conclusion  Reference
  • 3. INTRODUCTION  Epilepsy is a chronic non communicable disease of the brain characterized by an enduring (i.e., persisting) recurrent seizures.  This is usually diagnosed when someone has two or more unprovoked episode of seizure occurring at list 24 h apart.  Epilepsy is one of the most common neurological diseases and affects people of all ages, races, social classes, and geographical locations.
  • 4. INTRODUCTION Cont  Epileptic seizures can affect your feelings, awareness or movement. Different types of seizures involve different things. These may include confusion, strange feelings, repetitive movements, 'blank' moments (where you are briefly unresponsive), muscle jerks, sudden falls, or jerking movements (while unconscious).  While all people with epilepsy experience seizures, not all individuals with seizures have epilepsy.
  • 5. EPIDEMIOLOGY The prevalence of epilepsy differs significantly among countries depending on the local distribution of risk and etiologic factors.  According to WHO over 50 million people worldwide have epilepsy, making it the most common neurological disease globally.  According Hauser W et al, the incidence of epilepsy is higher in the youngest and oldest age-groups, with estimates of 46 per 100,000 people diagnosed with epilepsy in high income countries, 139 per 100,000 people diagnosed with epilepsy in low and middle income countries. This is likely due to increased risk in of endemic conditions such as neurocysticercosis.
  • 6. EPIDEMIOLOGY Cont  Nearly 80% 0f people with epilepsy live in low and middle income countries. (https://www.who.int/news-room/fact-sheets/detail/epilepsy)  While 70% of people living with epilepsy could live seizure free if properly diagnosed and treated. (https://www.who.int/news-room/fact-sheets/detail/epilepsy)  In UBTH for the past three years, precisely children emergency an average of 168 patients are diagnosed of epilepsy annually.  However, according to Bharucha N et al, Incidence and prevalence of epilepsy are slightly higher in men than in women. The difference might be explained by the different prevalence of the most common risk factors and the concealment of the condition in women for sociocultural reasons in certain regions.
  • 7. PATHOPYSIOLOGY  Pathophysiology of epileptic diseases are caused by ion channel mutations. Although epileptic syndromes differ pathophysiologically. Masuda H, et al  In neurochemical mechanism of epilepsy, An imbalance between glutamate and gamma-aminobutyric acid neurotransmitter systems can lead to hyperexcitability but catecholaminergic neurotransmitter systems and opioid peptides were shown to play a role in epileptogenesis as well.
  • 8. PATHOPHYSIOLOGY Contd.  During a seizure episode, the membrane potential of neurons is altered in a way that causes neurons to be hypersensitive or overactive due to certain stimuli or triggering events. The causes of seizures can be known or unknown.  Environmental triggers can include loud noises, strobe lights, and rhythmic music Boro A et al. Medical triggers include high fevers, infections, tumors, hypoglycemia, poor nutrition (causing electrolyte imbalances), trauma, physical exhaustion and toxic substances, such as medications, alcohol, and illicit drugs Boro A et al.  Seizures can even have psychosocial triggers, including emotional stress and shock.
  • 10. CLASSIFICATION OF EPILEPSY FOCAL GENERALIZED UNKNOWN Awareness / impaired awareness motor motor Motor onset • Automatism • Atonic • Clonic • Tonic • Epileptic spasm • Hyperkinetic • Myoclonic • Tonic-clonic • Clonic • Tonic • Myoclonic • Myoclonic tonic-clonic • Myoclonic atonic • Atonic • Epileptic spasm • Tonic-clonic • Epileptic spasm Non motor onset • Autonomic • Behavior arrest • Cognitive • Emotional • Sensory Non motor (Absence) • Typical • Atypical • Myoclonic • Eyelid myoclonia Non motor • Behavior arrest Focal to bilateral tonic-clonic Unclassified
  • 11. SYMPTOMS OF EPILEPSY  Temporary confusion  A starring spell  Stiff muscles  Uncontrollable jerking movement of the arms and legs  Loss of consciousness or awareness  Psychological symptoms such as fear anxiety or deja vu
  • 12. RISK FACTORS OF EPILEPSY  Stroke and other vascular disease  Brain tumor  A severe head injury  Drug abuse or alcohol misuse  A brain infection  Lack of oxygen during birth  Congenital abnormalities or genetic condition with associated brain malfunctions.
  • 13. PREVENTION OF EPILEPSY  Reduce your risk of traumatic brain injury.  Reduce your risk of stroke and cardiovascular disease by eating a healthy diet.  Ensure physical exercise and quitting smoking  Adequate vaccination lowers the chances of infection that can sometimes predispose the individual to epilepsy.  Stay healthy during your pregnancy.  Maintaining good hygiene and prepare food safely. This is because an infection called cysticercosis is the most common cause of epilepsy worldwide and commonly caused by a parasite tenia solium
  • 14. DIAGNOSES OF EPILEPSY The diagnoses of epilepsy requires at least two or more unprovoked seizure occurring greater than twenty four hours apart (>24 hrs). This disorder can be diagnosed using the following system  Neurological examination  Blood testing  Electroencephalogram (EEG)  Magnetic resonance imaging (MRI)  Computed tomography (CTs)
  • 15. DIAGNOSES OF EPILEPSY cont EEG brain activity An EEG records the electrical activity of the brain via electrodes affixed to the scalp. EEG results show changes in brain activity that may be useful in diagnosing brain conditions, especially epilepsy and other seizure disorders.
  • 17. TREATMENT OF EPILEPSY In treatment of epilepsy it is important to understand the mechanism of action and the pharmacokinetics of antiepileptic drugs (AEDs) so that these agent can be used effectively in clinical practice, especially in multidrug regimens Molgaard-Nielsen D. The different mechanism of action include the following  Sodium channel blockers  Calcium channel blockers  Gamma amino butyric acid (GABA) enhancer  Glutamate blockers
  • 18. TREATMENT OF EPILEPSY cont Ion channel Mechanism of action (MOA) Drugs Doses (Adult) Treatment Adverse effect Sodium channel blockers This works by blocking the activated gated Na+ channel influx into the neuronal cell there by inhibiting repetitive firing of presynaptic and postsynaptic nerves Carbamazepine 400mg, 200mg Lamotrigine 100mg, Valproate 500mg phenytoin 200mg, Fos-PHT 100mg/2ml oxcarbamazepine 300mg, 600mg Zonisamide 100mg, lacosamide 50mg, cenobamate 25mg 50mg 100mg 200mg Tab 200mg b.d Tab 50mg dly Cap 250mg b.d Cap 100mg tds 15-20mg/kg iv, Tab 600mg dly Cap 100mg dly Tab 100mg b.d Tab 12.5mg dly Focal and generalized tonic-clonic seizure focal/secondary genlz Focal/generalized Focal and generalized Status epileticus Focal/secondary genlz Focal/secondary genlz Status epilepticus & F/s Focal seizure Dizziness, hepatotoxicity headache, nausea, ataxia, anorexia, allergic rashes, growth deficit, mental slowing, tremor, insomnia, osteoporosis embrayofetal and perinatal mortality
  • 19. TREATMENT OF EPILEPSY cont Ion channels Mechanism of action (MOA) Drugs Doses (Adult) Treatment Adverse effect Calcium channel blockers This channel exist as L,N and T forms in human brain, its MOA is inhibition of T-type channels responsible for depolarization necessary to generate spike wave burst as seen in absence seizure. Ethosuximide Tab 250mg b.d Absence seizure headache, nausea, ataxia, anorexia, allergic rashes, growth deficit, mental slowing, tremor, insomnia confusion
  • 20. TREATMENT OF EPILEPSY cont Ion channels Mechanism of action (MOA) Drug examples Doses(Adult) Treatment Adverse effect GABA enhancers Comprises of two receptors GABA A and GABA B. when GABA binds to GABA A receptor, it results to influx of cl- into the neuronal cell thereby increasing the negativity of the membrane and returning it to a resting potentials. Also the AEDs works by blocking the reuptake of GABA or by inhibiting its metabolism as mediated by GABA transaminase Benzodiazepine e.g diazepam 10mg clobazam 10mg clonazepam 2mg Barbiturates e.g phenobarbital 100mg primidone 50mg 200mg GABAtransaminase e.g vigabatrin 500mg Tiagabine 4mg GABA enhancers eg Gabapentin 300mg Tab 5-10mg bd Tab 20-30mg dly Tab 1.5mg dly inj 3mg/kg/day IV Tab 100-125mg b.d Tab 500mg b.d Tab 4mg dly Tab 300mg tds Status epilepticus Focal epilepsy Myoclonic seizure and subcortical myoclonus. Status epilepticus. Focal seizure Refractory focal/s Focal sec/ genlz Focal/sec genlz Dizziness, sedation, blurred vision, diplopia, skin rash depression, muscle fatigue, somnolence, headache
  • 21. TREATMENT OF EPILEPSY cont Ion channels Mechanism of action (MOA) Drug examples Doses (Adult) Treatment Adverse effect Glutamate blockers Comprises of different binding sites • Alpha –amino-3-hyroxy-5- methylisozole-4-propionic acid (AMPA) • N-methyl-D-aspartate (NMDA) • Metabotropic site This works by binding of the AEDs to either of this receptor sites and inhibits the influx of Na+ and Ca2+ into the neuronal cell while retaining more of the Cl- NMDA receptor blocker eg felbamate 400mg AMPA receptors eg topiramate 400mg Metabotrophic blocker eg still under experimental studies Tab 1200mg tds Tab 400mg dly Multiple seizures, hypoxic ischemic injuries. Weight loss, insomnia, nausea, decreased appetite, dizziness, lethargy, fatigue, hepatic failure,
  • 22. TREATMENT OF EPILEPSY cont Ion channels Mechanism of action (MOA) Drug examples doses(Adult) Treatment Adverse effect Piracetam derivatives Inhibits Ca2+ released from inositol-triphosphate sensitive stores without reducing Ca2+ storage Levetiracetam 250mg, 500mg Brivaracetam 50mg, 100mg Tab 500mg b.d Tab 50mg b.d Focal/generalized seizure with tonic- clonic symptoms. Focal seizure Somnolence, asthenia, dizziness, headache, fatigue, anorexia, weakness.
  • 23. PHARMACIST ROLE IN MANAGEMENT OF EPILEPSY  Educating patients about epilepsy so they understand the disease condition and take good precaution.  Patient are advised on accurate dosing of there drugs as prescribed by the physician.  patient are advised on adherence to medication  establishing a therapeutic drug monitoring protocol, adjusting doses and monitoring of adverse drug reaction.
  • 24. CASE PRESENTATION  Demographic data Patient SP is an 11 years old child, Benin by bribe, a Christian and a student, lives in Benin city with her parents.  Family history Patient SP is the second child of family of three children.  Social history Patient SP doesn’t take alcohol or use tobacco in any form.  Chief complaint Patient SP complain of frequent headache and nausea.
  • 25. CASE PRESENTATION cont  Past medical history  Patient did not cry after delivery  Patient was admitted in hospital at birth  The last time of seizure was three years ago  Patient has undergone an operation (appendicitis)  Past medication history  Tab Ibuprofen 200mg B.D x 2/7  Tab Paracetamol 500mg tds x 2/7  Im Promethazine 25mg stat  Tab Cefuroxime 250mg B.D x 5/7
  • 26. CASE PRESENTATION cont Vital signs  Blood pressure 120/80mmHg  weight 56kg  Temp 36.1◦c  PR 88 b/m  Physical examination  patient SP is calm adolescent, afebrile, not pale, acyanosed, not dehydrated , no pedal oedema.  Pupil is equal and bilateral reactive to light.  Neck is supple.
  • 27. CASE PRESENTATION cont date Time Nature of seizure duration intervention 1/3/22 2 pm Generalized seizure 60 seconds Inj I.V diazepam 10mg given and iv phenobarbitone 855mg start ‘’ 6 pm Nil seizure ‘’ 9 pm Nil seizure 7/3/22 6 am Nil seizure 7 am Generalized seizure 60 seconds Aborted by inj I.V diazepam 10mg given 7:10 am Generalized seizure 30 seconds 8:30 am Generalized seizure 40 seconds 10:00 am Nil seizure 12:30 pm Nil seizure 13/3/22 9:00pm Generalized seizure 60 seconds Aborted with I.V diazepam 10mg and I.V phenytoin 500mg in 100mls IVF N/S Patient SP seizure chart
  • 28. CASE PRESENTATION cont  Plan  Iv diazepam 0.3mg stat  iv phenytoin 145mg 12hrly in 30mls normal saline.  Tab sodium valproate 700mg 12hrly  Tab levetiracetam 250mg 12hrly. • Diagnosis • Focal to generalized seizure
  • 29. GOAL OF THERAPY  To prevention or minimise unwanted reoccurrence of episodes of seizure  To improve patient quality of life  To ensure safe and efficacious drug availability  To ensure proper adherence to prescribed medication
  • 30. DRUG THERAPY PROBLEM Unnecessary drug therapy Nil Wrong drug Nil Dose too high Nil Dose too low Nil Adverse drug reaction yes Inappropriate adherence yes Needs additional drug therapy. Nil
  • 31. DRUG THERAPY PROBLEM  Actual Drug therapy problem. Adverse drug Reaction:  Cause- patient SP had an undesirable reaction to levetiracetam which was not dose related  Potential drug therapy problem Inappropriate Adherence: Cause- affordability and availability problems. Inability to self administer drug appropriately.
  • 32. PHARMACEUTICAL CARE PLAN  Drug focused intervention  Tab levetiracetam was withdrawn from her medication and was advice to continue with sodium valproate 700mg twice daily. Patient focused intervention  Patient was educated on the use of his/her drugs and the possible side effects.  Patient was counseled to strictly come for checkups and drug refills.
  • 33. PHARMACEUTICAL CARE PLAN cont  Clinical intervention  The incidence of epileptic crises was greatly reduced.  Strict management and proper follow up was carried out which reinforce patient quick recovery.  Economic outcome  Patient could afford her medication.  Humanistic outcome  Patient was satisfied with the service rendered.  Quality of life was improved.  Patient has a better understanding about disease condition and management.
  • 34. CONCLUSION Epilepsy is a complex neurological and metabolic disorder characterized by two or more unprovoked seizure occurring greater than 24 hours apart, which is as a result of abnormal neuronal firing in the brain. This disorder comes out with abnormal signs and symptoms, predisposing the patient to injuries and harm. And a more reason for urgent attention and treatment. Through patient education, counseling and collaboration with other health care providers, pharmacist can play a key role in reducing the long term health risk associated with epilepsy down to 70% in low income countries with adequate diagnostic tools and medications. (https://www.who.int/news-room/fact-sheets/detail/epilepsy)
  • 35. REFERENCE  Jj, scheffer IE, fisher RS, falcon walter. The new definition and classification seizure and epilepsy. Epilepsy Research.2018;139:73-79  Fiest KM, Sauro KM, Wiebe S, Patten SB, Kwon CS, Dykeman J. Prevalence and incidence of epilepsy: A systematic review and meta-analysis of international studies. Neurology. 2017 Jan;88(3):296–303.  Kaiboriboon K, Bakaki PM, Lhatoo SD, Koroukian S. Incidence and prevalence of treated epilepsy among poor health and low-income Americans. Neurology. 2013 May;80(21):1942–9.  Masuda H, shariff E, Tohyama J. clinical patterns and pathophysiology of hypermotor seizures: an ictal SPECT study. Epileptic disord. 2012;14:32-40
  • 36. REFERENCE cont  Bharucha NE, Bharucha EP, Bharucha AE, Bhise AV Schoenberg BS. Prevalence of epilepsy in the Parsi community of Bombay. Epilepsia. 1988 Mar-Apr;29(2):111–115.  Hauser WA, Annegers JF, Kurland LT. Incidence of epilepsy and unprovoked seizures in Rochester, Epilepsia. 1993 May-Jun;34(3):453–68.  Camfield P, Camfield C. Incidence, prevalence and aetiology of seizures and epilepsy in children. Epileptic Disord. 2015 Jun;17(2):117–23.  Berenguer B. pharmaceutical care: past present and future. Curr pharm Des 2004; 10;3931-3946.  Boro A, Haut S. Medical comorbidities in the treatment of epilepsy. Epilepsy Behavior.2003;4:2-12.  Molgaard-Nielsen D, Haviid A, Newer generation antiepileptic drugs and the risk of major birth defects. JAMA. 2011 May 18. 305(19):19916-2002.