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PRESENTED BY:
CHALLA.ANITHA, Pharm-D student
Vignan Pharmacy College, Vadlamudi, Guntur
1
CONTENTS
 INTRODUCTION
 ETIOLOGY
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 CLINICAL MANIFESTATIONS
 DIAGNOSIS
 FIRST AID FOR SEIZURES
 TREATMENT
 REFERENCES
2
INTRODUCTION:
Epilepsy is a common chronic neurological condition characterised by:
• Recurrent seizures
• Loss of consciousness
• With or with out body movements
 It is derived from a greek word Epi – upon, Leptos – seizures.
 It is also known as seizure disorder.
 Seizures are nothing but sudden, excessive, abnormal discharges of cerebral neurons.
 It is usually controlled but not cured.
 World epilepsy day is celebrated on MARCH 26th
every year.
 It is also known as purple day & it was designed to raise awareness on epilepsy.
FIG NO 1: LOGO OF PURPLE DAY
ETIOLOGY:
In 28% cases cause can be determined, rest 72% are idiopathic ( of unknown cause)
3
CATEGORIES DETERMINED CAUSES
Inherited / genetic Single gene mutation (< 2%), multiple genes + environmental factors,
genetic disorders ( down, dravet, etc ), > 200 genes have the
capability of causing epilepsy.
Acquired Head trauma, neurosurgery, cerebrovascular disease, infections
(meningitis, influenza, toxoplasmosis, mumps, measles, syphilis),
metabolic disorders (such as hypoglycemia and hypocalcemia),
Intracranial neoplasms
Congenital Inborn error of metabolism
Withdrawal of drugs Alcohol, benzodiazepines, barbiturates, antiepileptics
Drugs that induce
seizures
Some of the antibiotics, antidiabetics, anesthetics, antimalarials,
antispastics, antidepressants, antipsychotics, mood satbilisers
4
TABLE NO: 1 DETERMINED CAUSES
AGE AT SEIZURE ONSET PROBABLE CAUSE OF SEIZURE
Birth to 1 month
1–6 months
6 months to 2 years
3–10 years
10–18 years
18–25 years
35–60 years
> 60 years
Birth injury or anoxia, congenital hereditary diseases,
and metabolic disorders
As above, plus infantile spasms
Infantile spasms, febrile convulsions, birth injury or
anoxia, meningitis, and head trauma
Birth injury or anoxia, meningitis, cerebral vessel
thrombosis, and idiopathic epilepsy
Idiopathic epilepsy and head trauma
Idiopathic epilepsy, trauma, neoplasm, and
withdrawal from alcohol or drugs
Trauma, neoplasm, vascular disease, and withdrawal
from alcohol or drugs
Vascular disease, neoplasm, degenerative disease,
and trauma
5
TABLE NO: 2 PROBABLE CAUSES OF SEIZURE IN DIFFERENT AGE GROUPS
EPIDEMIOLOGY:
Incidence of epileptic seizures is around 50 cases per 100,000 of the population.
PATHOPHYSIOLOGY:
6
Abnormalities in ion channel ( Na+, K+, Ca+ )
(or)
Decreased INT activity / inactivation of INT activity
Rhythmic & repetitive hypersynchronus discharge of neurons
Seizures focus
Seizures
Repeated seizures
Epilepsy
Increased ENT activity
FIGURE NO 2: PATHOPHYSIOLOGY OF EPILEPSY
7
FIG NO:3 NEURO HUMORAL TRANMISSION, MOA OF ANTIEPILEPTIC DRUGS
INTERNATIONAL CLASSIFICATION OF EPILEPTIC SEIZURES
I.) Partial / Focal seizures (seizures begin locally)
A. Simple (without impairment of consciousness)
B. Complex (with impairment of consciousness)
C. Secondarily generalized (partial onset evolving to generalized tonic-clonic
seizures)
II.) Generalized seizures (bilaterally symmetrical and without local onset)
A. Absence
B. Myoclonic
C. Clonic
D. Tonic
E. Tonic-clonic
F. Atonic
G. Infantile spasms
III.) Unclassified seizures
IV.) Status epilepticus
8
CLINICAL MANIFESTATIONS
TYPE OF GENERALISED SEIZURE CLINICAL MANIFESTATIONS
Absence / petit mal Happen exclusively in childhood and early adolescence
The child goes blank & stares; fluttering of the eyelids and
flopping of the head may occur.
The attacks last only few seconds & often go un recognized.
Myoclonic Involuntary shock-like jerks, which may involve the whole body,
or the arms or the head.
Tonic-clonic / grand mal Commonest of all epileptic seizures.
Without warning the patient suddenly goes stiff, falls and
convulses
Laboured breathing and salivation, cyanosis, incontinence and
tongue biting may also occur.
The convulsion ceases after a few minutes and may often be
followed by a period of drowsiness, confusion, headache and sleep.
Atonic / falling out The patient looses consciousness, muscle tone. No muscle
movements are typically noted, & the patient will fall when they
are not lying down or sitting in chair.
9
TABLE NO 3:GENERALIZED SEIZURES (BILATERALLY SYMMETRICAL AND WITHOUT LOCAL ONSET):
TYPE OF PARTIAL SEIZURE CLINICAL MANIFESTATIONS
Simple partial seizures The patient will have a sensation of uncontrolled
muscle movement of a portion of their body
without an alteration in consciousness
Complex partial seizures Alteration in the patients level of consciousness
Secondarily generalized Partial onset evolving to generalized tonic-clonic
seizures
10
TABLE NO 4: PARTIAL / FOCAL SEIZURES (SEIZURES BEGIN LOCALLY)
Status epilepticus: If it lasts ≥ 5 min ongoing / without returning to normal
DIAGNOSIS:
 Neurological examination / neuropsychological tests - Doctor tests for behavior, motor
abilities, mental function & other symptoms.
 Medical history
 Electroencephalogram (EEG) – Tracks electrical signals from the brain.
 CT scan, MRI scan – Used to detect abnormalities in brain ( tumors, bleeding, cysts)
 fMRI – Used to measure the changes in blood flow
 PET ( Positron Emission Tomography) – Used to visualize active areas of brain & detect
abnormalities
 SPECT ( Single Photon Emission Computerized Tomography) – Used when MRI & EEG
didn’t pinpoint the location in brain where the seizures are originating.
 SISCOM ( Substraction Ictal SPECT Coregistered to MRI ) – A form of SPECT test
which may provide even more detailed results.
 Genetic testing
11
FIG NO 4: EEG OF PARTIAL SEIZURES FIG NO 5: EEG OF GENERALISED SEIZURES
12
VIDEO NO : 1 FIRST AID FOR SEIZURES
13
TREATMENT
Pharmacological / drug
therapy.
Non pharmacological
treatment / non drug therapy.
1.) MODULATION OF VOLTAGE GATED ION
CHANNELS:
a.) Na+ channel blockers:
Phenytoin, Carbamazepine,Valproicacid, Lamotrigine,
Topiramate, Zonisamide.
b.) Calcium channel blockers:
Ethosuximide, Topiramate, Gabapentin
2.) ENHANCEMENT OF SYNAPTIC INHIBITION:
a.) Increased GABA activity:
•Barbiturates , Benzodiazepines
•Vigabatrin – GABA transaminase inhibitor
•Tigabine – GABA reuptake inhibitor
3.) INHIBITION OF SYNAPTIC EXCITEMENT:
a.) Decreased glutamate activity
4.) Levitriacetam
a) Ketogenic diet
b) Surgery
1) Lobe resection
2) Lesionectomy
3) Corpus callosotomy/ split brain surgery
4) Functional hemispherectomy
5) Multiple subpial transection (MST)
6) Vagus nerve stimulation (VNS)
7) Responsive neurostimulation device (RNS)
c) Avoiding of precipitating factors:
1) Stress
2) Sleep deprivation
3) Ingestion of excessive amount of
caeffine (or) alcohol
d) Promotion of emotional wellbeing
( yoga)
e) Reduction of psychiatric
co-morbidities (anxiety or depression)
Seizure type First line drugs Alternative drugs
Partial seizures Carbamazepine, phenytoin,
lamotrigine, valproic acid,
oxcarbazepine
Gabapentin, Topiramate,
levetriacetam, zonisamide,
tigabine, primidone,
phenobarbital,
felbamate
Generalised seizures
Absence
Myoclonic
Tonic- clonic seizures
Valproicacid,
Ethosuximide
Valproicacid,
Clonazepam
Phenytoin,
Valproic acid
Lamotrigine,
Levetriacetam
Lamotrigine,
Levetriacetam
Topiramate, zonisamide
Lamotrigine, Topiramate ,
Oxacarbazepine
Levetriacetam,
oxcarbazepine
14
TABLE NO: 5 CHOICE OF TREATMENT
15
DRUGS BRAND NAME DOSE ADVERSE EFFECTS
Phenobarbitone GARDENAL 1-3 mg/kg/day Hyperactivity, sedation, behavior
changes, metabolic bone disorders,
ataxia, blood dyscrasias,
unsteadiness.
Phenytoin DILANTIN 3-5 mg/kg Ataxia, nystagmus, behavior
changes, hirsutism, gingival
hyperplasia, visual blurring, blood
dyscrasias
Carbamazepine TEGRETOL 400mg/day Hyponatremia, rash, drowsiness,
unsteadiness, blood dyscrasias
( diseased state in which there are
abnormal blood components)
Ethosuximide ZARONTIN 500mg/day Drowsiness, unsteadiness, ataxia,
behavioral changes, blood
dyscrasias, hiccoughs.
Valproic acid DEPAKENE
DEPAKOTE
DEPACON
15 mg/kg Thrombocytopenia, GI upset, tremor,
acute hepatic failure, acute
pancreatitis, alopecia
TABLE NO: 6 TREATMENT
16
DRUG BRAND NAME DOSE ADVERSE EFFECTS
Clonazepam KLONOPIN 1.5 mg/day Drowsiness, loss of appetite,
constipation
Lamotrigine LAMICTAL 25 mg qod if on
VPA
25-50mg/day if not
on VPA
Ataxia ( inability to coordinate
voluntary muscle movements),
diplopia, unsteadiness, skin
rash ( Steven Johnson
Syndrome)
Gabapentin NEURONTIN 900mg/day Pedal edema, weight gain,
dizziness, ataxia, Somnolence (
state of being drowsy), fatigue
Tigabine GABITRIL 4-8 mg/day Dizziness, fatigue, difficulty in
concentrating, spike wave
stupor, blurred vision, tremor.
Topiramate TOPAMAX 25-50mg/day Psychomotor slowing , Acute
angle, glaucoma , Weight loss
Oligohydrosis, Somnolence
( state of being drowsy),
kidney stones
TABLE NO: 7 TREATMENT
17
DRUG BRAND NAME DOSE ADVERSE EFFECTS
Diazepam VALIUM PO - 4-40 mg
IV - 5-10 mg
Shakiness, unsteady walk,
unsteadiness
Vigabatrin SABRIL 250 mg twice daily Drowsiness, dizziness,
tremor
Lorazepam ATIVAN PO - 10 mg/day
IV – 0.044 mg/kg/day
Sleepiness,
abdominal/stomach pain,
aggressive black tarry stools
etc
Levitriacetam KEPPRA 3000 – 4000 mg Sedation, behavioral
disturbances
Zonisamide ZONEGRAN 600 mg Sedation, Kidney stones
Dizziness, Rash, Weight
loss, Cognitive impairment
Oligohydrosis
TABLE NO: 8 TREATMENT
STATUS EPILEPTICUS:
1.) Initial management of status epilepticus is supportive and may include:
 Positioning the person to avoid injury
 Supporting respiration
 Maintaining blood pressure
 Correcting hypoglycaemia
2.) First line agents Intravenous lorazepam or diazepam.
3.) Alternative medicines Midazolam
NON PHARMACOLOGICAL TREATMENT:
KETOGENIC DIET:
Ketogenic diet containing high content of fats, followed by proteins, cabohydrates
was found to reduce seizures in some children
FIG NO 6: KETOGENIC DIET
18
Side effects: Constipation, slow growth because of nutritional deficiencies, build
up of uric acid in blood , kidney stones
SURGERIES:
 Medications can control seizures in most people with epilepsy, but they don’t
work for everyone.
 About 30% of people taking the drugs can’t tolerate the side effects. In such
cases, brain surgery may be an option.
1) Lobe resection
2) Lesionectomy
3) Corpus callosotomy/ split brain surgery
4) Functional hemispherectomy
5) Multiple subpial transection (MST)
6) Vagus nerve stimulation (VNS)
7) Responsive neurostimulation device (RNS)
19
VAGUS NERVE STIMULATION (VNS):
A device implanted under your skin sends an electronic jolt to the vagus nerve,
which
controls activity between your brain & major internal organs.
FIG NO 7: VAGUS NERVE STIMULATOR
20
GOALS
Remove the area of
the brain that causes
seizures.
Disrupt the nerve
pathways that seizure
impulses take through
your brain.
Implant a device to
treat epilepsy.
REFERENCES:
 RODGER WALKER, CATE WHITTLESEA; Epilepsy ; Clinical pharmacy &
Therapeutics; 5th
Edition; p.g.no: 489 - 506
 ERIC. T. HERFINDAL, DICK R. GOURLEY, HART; Epilepsy ; Clinical
pharmacy & Therapeutics; 8h
Edition; p.g.no: 1608 - 1645
 JOSEPH T. DIPIRO et.al; Epilepsy ; Pharmacotherapy A Pathophysiologic
approach; 6th
edition; p.g.no: 1023 – 1048
 Comprehensive pharmacy review for NAPLEX, Leon shargel, Alan H.
Mutnick etal; hepatic disorders; 8th
edition pg.no:- 743 - 773
 www. medicinet. com
 www. healthline. com
 www. emedicinehealth.com
 www. medical newstoday. com
21
22
 ppt on epilepsy
 ppt on epilepsy

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ppt on epilepsy

  • 1. PRESENTED BY: CHALLA.ANITHA, Pharm-D student Vignan Pharmacy College, Vadlamudi, Guntur 1
  • 2. CONTENTS  INTRODUCTION  ETIOLOGY  EPIDEMIOLOGY  PATHOPHYSIOLOGY  CLINICAL MANIFESTATIONS  DIAGNOSIS  FIRST AID FOR SEIZURES  TREATMENT  REFERENCES 2
  • 3. INTRODUCTION: Epilepsy is a common chronic neurological condition characterised by: • Recurrent seizures • Loss of consciousness • With or with out body movements  It is derived from a greek word Epi – upon, Leptos – seizures.  It is also known as seizure disorder.  Seizures are nothing but sudden, excessive, abnormal discharges of cerebral neurons.  It is usually controlled but not cured.  World epilepsy day is celebrated on MARCH 26th every year.  It is also known as purple day & it was designed to raise awareness on epilepsy. FIG NO 1: LOGO OF PURPLE DAY ETIOLOGY: In 28% cases cause can be determined, rest 72% are idiopathic ( of unknown cause) 3
  • 4. CATEGORIES DETERMINED CAUSES Inherited / genetic Single gene mutation (< 2%), multiple genes + environmental factors, genetic disorders ( down, dravet, etc ), > 200 genes have the capability of causing epilepsy. Acquired Head trauma, neurosurgery, cerebrovascular disease, infections (meningitis, influenza, toxoplasmosis, mumps, measles, syphilis), metabolic disorders (such as hypoglycemia and hypocalcemia), Intracranial neoplasms Congenital Inborn error of metabolism Withdrawal of drugs Alcohol, benzodiazepines, barbiturates, antiepileptics Drugs that induce seizures Some of the antibiotics, antidiabetics, anesthetics, antimalarials, antispastics, antidepressants, antipsychotics, mood satbilisers 4 TABLE NO: 1 DETERMINED CAUSES
  • 5. AGE AT SEIZURE ONSET PROBABLE CAUSE OF SEIZURE Birth to 1 month 1–6 months 6 months to 2 years 3–10 years 10–18 years 18–25 years 35–60 years > 60 years Birth injury or anoxia, congenital hereditary diseases, and metabolic disorders As above, plus infantile spasms Infantile spasms, febrile convulsions, birth injury or anoxia, meningitis, and head trauma Birth injury or anoxia, meningitis, cerebral vessel thrombosis, and idiopathic epilepsy Idiopathic epilepsy and head trauma Idiopathic epilepsy, trauma, neoplasm, and withdrawal from alcohol or drugs Trauma, neoplasm, vascular disease, and withdrawal from alcohol or drugs Vascular disease, neoplasm, degenerative disease, and trauma 5 TABLE NO: 2 PROBABLE CAUSES OF SEIZURE IN DIFFERENT AGE GROUPS
  • 6. EPIDEMIOLOGY: Incidence of epileptic seizures is around 50 cases per 100,000 of the population. PATHOPHYSIOLOGY: 6 Abnormalities in ion channel ( Na+, K+, Ca+ ) (or) Decreased INT activity / inactivation of INT activity Rhythmic & repetitive hypersynchronus discharge of neurons Seizures focus Seizures Repeated seizures Epilepsy Increased ENT activity FIGURE NO 2: PATHOPHYSIOLOGY OF EPILEPSY
  • 7. 7 FIG NO:3 NEURO HUMORAL TRANMISSION, MOA OF ANTIEPILEPTIC DRUGS
  • 8. INTERNATIONAL CLASSIFICATION OF EPILEPTIC SEIZURES I.) Partial / Focal seizures (seizures begin locally) A. Simple (without impairment of consciousness) B. Complex (with impairment of consciousness) C. Secondarily generalized (partial onset evolving to generalized tonic-clonic seizures) II.) Generalized seizures (bilaterally symmetrical and without local onset) A. Absence B. Myoclonic C. Clonic D. Tonic E. Tonic-clonic F. Atonic G. Infantile spasms III.) Unclassified seizures IV.) Status epilepticus 8 CLINICAL MANIFESTATIONS
  • 9. TYPE OF GENERALISED SEIZURE CLINICAL MANIFESTATIONS Absence / petit mal Happen exclusively in childhood and early adolescence The child goes blank & stares; fluttering of the eyelids and flopping of the head may occur. The attacks last only few seconds & often go un recognized. Myoclonic Involuntary shock-like jerks, which may involve the whole body, or the arms or the head. Tonic-clonic / grand mal Commonest of all epileptic seizures. Without warning the patient suddenly goes stiff, falls and convulses Laboured breathing and salivation, cyanosis, incontinence and tongue biting may also occur. The convulsion ceases after a few minutes and may often be followed by a period of drowsiness, confusion, headache and sleep. Atonic / falling out The patient looses consciousness, muscle tone. No muscle movements are typically noted, & the patient will fall when they are not lying down or sitting in chair. 9 TABLE NO 3:GENERALIZED SEIZURES (BILATERALLY SYMMETRICAL AND WITHOUT LOCAL ONSET):
  • 10. TYPE OF PARTIAL SEIZURE CLINICAL MANIFESTATIONS Simple partial seizures The patient will have a sensation of uncontrolled muscle movement of a portion of their body without an alteration in consciousness Complex partial seizures Alteration in the patients level of consciousness Secondarily generalized Partial onset evolving to generalized tonic-clonic seizures 10 TABLE NO 4: PARTIAL / FOCAL SEIZURES (SEIZURES BEGIN LOCALLY) Status epilepticus: If it lasts ≥ 5 min ongoing / without returning to normal
  • 11. DIAGNOSIS:  Neurological examination / neuropsychological tests - Doctor tests for behavior, motor abilities, mental function & other symptoms.  Medical history  Electroencephalogram (EEG) – Tracks electrical signals from the brain.  CT scan, MRI scan – Used to detect abnormalities in brain ( tumors, bleeding, cysts)  fMRI – Used to measure the changes in blood flow  PET ( Positron Emission Tomography) – Used to visualize active areas of brain & detect abnormalities  SPECT ( Single Photon Emission Computerized Tomography) – Used when MRI & EEG didn’t pinpoint the location in brain where the seizures are originating.  SISCOM ( Substraction Ictal SPECT Coregistered to MRI ) – A form of SPECT test which may provide even more detailed results.  Genetic testing 11 FIG NO 4: EEG OF PARTIAL SEIZURES FIG NO 5: EEG OF GENERALISED SEIZURES
  • 12. 12 VIDEO NO : 1 FIRST AID FOR SEIZURES
  • 13. 13 TREATMENT Pharmacological / drug therapy. Non pharmacological treatment / non drug therapy. 1.) MODULATION OF VOLTAGE GATED ION CHANNELS: a.) Na+ channel blockers: Phenytoin, Carbamazepine,Valproicacid, Lamotrigine, Topiramate, Zonisamide. b.) Calcium channel blockers: Ethosuximide, Topiramate, Gabapentin 2.) ENHANCEMENT OF SYNAPTIC INHIBITION: a.) Increased GABA activity: •Barbiturates , Benzodiazepines •Vigabatrin – GABA transaminase inhibitor •Tigabine – GABA reuptake inhibitor 3.) INHIBITION OF SYNAPTIC EXCITEMENT: a.) Decreased glutamate activity 4.) Levitriacetam a) Ketogenic diet b) Surgery 1) Lobe resection 2) Lesionectomy 3) Corpus callosotomy/ split brain surgery 4) Functional hemispherectomy 5) Multiple subpial transection (MST) 6) Vagus nerve stimulation (VNS) 7) Responsive neurostimulation device (RNS) c) Avoiding of precipitating factors: 1) Stress 2) Sleep deprivation 3) Ingestion of excessive amount of caeffine (or) alcohol d) Promotion of emotional wellbeing ( yoga) e) Reduction of psychiatric co-morbidities (anxiety or depression)
  • 14. Seizure type First line drugs Alternative drugs Partial seizures Carbamazepine, phenytoin, lamotrigine, valproic acid, oxcarbazepine Gabapentin, Topiramate, levetriacetam, zonisamide, tigabine, primidone, phenobarbital, felbamate Generalised seizures Absence Myoclonic Tonic- clonic seizures Valproicacid, Ethosuximide Valproicacid, Clonazepam Phenytoin, Valproic acid Lamotrigine, Levetriacetam Lamotrigine, Levetriacetam Topiramate, zonisamide Lamotrigine, Topiramate , Oxacarbazepine Levetriacetam, oxcarbazepine 14 TABLE NO: 5 CHOICE OF TREATMENT
  • 15. 15 DRUGS BRAND NAME DOSE ADVERSE EFFECTS Phenobarbitone GARDENAL 1-3 mg/kg/day Hyperactivity, sedation, behavior changes, metabolic bone disorders, ataxia, blood dyscrasias, unsteadiness. Phenytoin DILANTIN 3-5 mg/kg Ataxia, nystagmus, behavior changes, hirsutism, gingival hyperplasia, visual blurring, blood dyscrasias Carbamazepine TEGRETOL 400mg/day Hyponatremia, rash, drowsiness, unsteadiness, blood dyscrasias ( diseased state in which there are abnormal blood components) Ethosuximide ZARONTIN 500mg/day Drowsiness, unsteadiness, ataxia, behavioral changes, blood dyscrasias, hiccoughs. Valproic acid DEPAKENE DEPAKOTE DEPACON 15 mg/kg Thrombocytopenia, GI upset, tremor, acute hepatic failure, acute pancreatitis, alopecia TABLE NO: 6 TREATMENT
  • 16. 16 DRUG BRAND NAME DOSE ADVERSE EFFECTS Clonazepam KLONOPIN 1.5 mg/day Drowsiness, loss of appetite, constipation Lamotrigine LAMICTAL 25 mg qod if on VPA 25-50mg/day if not on VPA Ataxia ( inability to coordinate voluntary muscle movements), diplopia, unsteadiness, skin rash ( Steven Johnson Syndrome) Gabapentin NEURONTIN 900mg/day Pedal edema, weight gain, dizziness, ataxia, Somnolence ( state of being drowsy), fatigue Tigabine GABITRIL 4-8 mg/day Dizziness, fatigue, difficulty in concentrating, spike wave stupor, blurred vision, tremor. Topiramate TOPAMAX 25-50mg/day Psychomotor slowing , Acute angle, glaucoma , Weight loss Oligohydrosis, Somnolence ( state of being drowsy), kidney stones TABLE NO: 7 TREATMENT
  • 17. 17 DRUG BRAND NAME DOSE ADVERSE EFFECTS Diazepam VALIUM PO - 4-40 mg IV - 5-10 mg Shakiness, unsteady walk, unsteadiness Vigabatrin SABRIL 250 mg twice daily Drowsiness, dizziness, tremor Lorazepam ATIVAN PO - 10 mg/day IV – 0.044 mg/kg/day Sleepiness, abdominal/stomach pain, aggressive black tarry stools etc Levitriacetam KEPPRA 3000 – 4000 mg Sedation, behavioral disturbances Zonisamide ZONEGRAN 600 mg Sedation, Kidney stones Dizziness, Rash, Weight loss, Cognitive impairment Oligohydrosis TABLE NO: 8 TREATMENT
  • 18. STATUS EPILEPTICUS: 1.) Initial management of status epilepticus is supportive and may include:  Positioning the person to avoid injury  Supporting respiration  Maintaining blood pressure  Correcting hypoglycaemia 2.) First line agents Intravenous lorazepam or diazepam. 3.) Alternative medicines Midazolam NON PHARMACOLOGICAL TREATMENT: KETOGENIC DIET: Ketogenic diet containing high content of fats, followed by proteins, cabohydrates was found to reduce seizures in some children FIG NO 6: KETOGENIC DIET 18
  • 19. Side effects: Constipation, slow growth because of nutritional deficiencies, build up of uric acid in blood , kidney stones SURGERIES:  Medications can control seizures in most people with epilepsy, but they don’t work for everyone.  About 30% of people taking the drugs can’t tolerate the side effects. In such cases, brain surgery may be an option. 1) Lobe resection 2) Lesionectomy 3) Corpus callosotomy/ split brain surgery 4) Functional hemispherectomy 5) Multiple subpial transection (MST) 6) Vagus nerve stimulation (VNS) 7) Responsive neurostimulation device (RNS) 19
  • 20. VAGUS NERVE STIMULATION (VNS): A device implanted under your skin sends an electronic jolt to the vagus nerve, which controls activity between your brain & major internal organs. FIG NO 7: VAGUS NERVE STIMULATOR 20 GOALS Remove the area of the brain that causes seizures. Disrupt the nerve pathways that seizure impulses take through your brain. Implant a device to treat epilepsy.
  • 21. REFERENCES:  RODGER WALKER, CATE WHITTLESEA; Epilepsy ; Clinical pharmacy & Therapeutics; 5th Edition; p.g.no: 489 - 506  ERIC. T. HERFINDAL, DICK R. GOURLEY, HART; Epilepsy ; Clinical pharmacy & Therapeutics; 8h Edition; p.g.no: 1608 - 1645  JOSEPH T. DIPIRO et.al; Epilepsy ; Pharmacotherapy A Pathophysiologic approach; 6th edition; p.g.no: 1023 – 1048  Comprehensive pharmacy review for NAPLEX, Leon shargel, Alan H. Mutnick etal; hepatic disorders; 8th edition pg.no:- 743 - 773  www. medicinet. com  www. healthline. com  www. emedicinehealth.com  www. medical newstoday. com 21
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