seminar on neonatal seizure

seminar on neonatal seizure

1. SEMINAR
on
Seizure Disorder in Newborn
Presented by
Dr. Md. MoklesurRahman
Resident (PHO) Year -2
Dr. SarbariSaha
Resident (Neonatology) Year -5

2. Case scenario 1
•S/OSanta,term(38weeks),weighing3200grams,
admittedattheageof20hourswiththeH/O
convulsionat12hoursofage.Hewasdeliveredat
home.DeliverywasconductedbyTBA.Resuscitation
effortscouldn’tbeelicited.Liquorwasclear.Baby
didn’tcryimmediatelyafterbirth.O/E-Lethargic,
hypotonic,mororeflex-weak,vitals–normal,pupil-
constricted.
•Whatmaybethecauseofconvulsion?

3. Case scenario 2
•S/OHalima,Term(37weeks),LGA(5200grams),IDM
developedconvulsionattheageof3hour.Mother
hadh/ogestationalDMandtreatedwithinsulin.
HbA1c-7.1.O/E-Babyisplumpy,plethoric,CBG-1.6
mmol/l.
•Whatmaybethecauseofconvulsion?

4. Case scenario 3
•S/OMaksuda,Term(37weeks),AGA(3400gram)
admittedonday3withthecomplaintsofless
activity,reluctanttofeed,convulsion.Seizurewas
difficulttomanage,requiredmultipleanti-convulsive
drugs(PHB,FosphenandMidazolam).Onquery,
historyrevealedconsanguineousmarriage,H/O1
abortion.O/E-babyislethargic,reflexandactivity-
poor,hepato-splenomegalypresent.Bloodgasreport
showsseveremetabolicacidosis.
•Whatmaybethecauseofconvulsion?

5. Outline
•Introduction
•Definition
•Incidence
•Pathophysiology
•Etiology
•Classification
•Diagnostic approach to
a newborn with seizure
•Management
•Prognosis
•Follow up

6. Introduction
CommonmanifestationofaseriousCNSdisease
Mostcommonneurologicalemergencyinneonatal
period.
Powerfulpredictoroflongtermcognitiveand
developmentalimpairment
Diagnosticandtherapeuticchallengetoclinicians
worldwide

7. Seizure
A seizure is defined clinically as paroxysmal alteration
in neurological function ( i.e. motor, behavioral and/or
autonomic)

8. Incidence
-Preciseincidenceisdifficulttodelineateanddepends
onstudypopulationandcriteriausedfordiagnosisof
seizure.
-Incidenceof10.3per1000live-births.
-Incidenceincreasewithdecreasinggestationandbirth
weight.
-PreterminfantsvsTerminfants=20.8vs8.4per1000
live-births.
-Verylowbirthweightinfants=36.1per1000livebirth
The National Neonatal Perinatal Database
(NNPD; 2002-03)

9. Pathophysiology
Neurons in CNS undergo –
Depolarization-Inward migration of Na
Repolarization-Efflux of K
A seizure occurs when there is excessive
depolarization.

11. Possible reasons for excessive depolarization
FailureofNa-Kpumpduetodisturbanceinenergy
production-Hypoxemia,ischemia,andhypoglycemia
Arelativeexcessofexcitatoryneurotransmitter
-Hypoxemia,ischemia,andhypoglycemia
Arelativedeficiencyofinhibitoryneurotransmitter
-Pyridoxinedependency
Alterationofneuronalmembrane(increaseNa+
permeability)-Hypocalcemia,hypomagnesemia

12. Neonates are more prone to seizure
•Overdevelopment of excitatory systems
•Decreased efficacy of inhibitory neurotransmission
•Ion channel configuration favors depolarization
•Role for neuropeptides in the hyperexcitability

13. •Overdevelopment of excitatory systems:
Glutamate receptors are transiently over expressed in
developing brain
NMDA-N-methyl-D-aspartate
AMPA-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic
acid
Kainate

14. Decreased efficacy of inhibitory neurotransmission:
GABAionchannelsarerelativelyunderexpressedin
theimmaturebrain.
Incertainareasofthedevelopingbrainthese
immatureGABAmaybedepolarizing(excitatory)rather
thanhyperpolarizing(inhibitory)
Cl−gradientisreversedintheimmaturebrain-
UnderexpressionoftheCl−exporterKCC2
OverexpressionCl−importerNKCC1
**GABAreceptorislesssensitivetobenzodiazepinesandseizures
intheimmaturebrainrespondpoorlytobenzodiazepines

17. Ion channel configuration favors depolarization:
Mutations in the K+ channels KCNQ2 and KCNQ3 are
associated with benign familial neonatal convulsions
Interfere with the normal hyperpolarizing K+ current
that prevents repetitive action potential firing

18. Role for neuropeptides in the hyperexcitability:
CRH-is a potent neuronal excitator
CRH and its receptors are expressed at higher levels in
the perinatal period
ACTH-in infantile spasm

19. Neonatal seizures differ in many ways from those in
older patients:
Due to neuroanatomic and neurophysiological developmental
status-
Immature state of brain development
Underdeveloped organization of the cortex
Undermyelination of axons
These factor leads to unique pattern of seizure.
Seizures in the newborn may be very subtle
The motor manifestations are often disorganized and an
orderly progression of convulsive activity is very uncommon
Primary generalized seizures are very rare in the newborn

20. Causes of neonatal seizures
Metabolic abnormalities:
Transient disturbances
Hypoglycemia
Hypocalcemia
Hypomagnesemia
Hyponatremia
Hypernatremia
Inborn errors of metabolism
Pyridoxin dependency
Folinicacid-responsive seizures
Urea cycle defects
Maple syrup urine disease
Propionicaciduria
Methylmalonicaciduria
Mitochondrial diseases
Glucose transporter deficiency
Perinatalasphyxia
Intracranial hemorrhage
Subarachnoid
Subdural
Intraventricular
hemorrhage
Infection :
Meningitis
Sepsis
Cerebral abscess
TORCH infections
Cerebral Infarction

21. Developmental brain defects
Cerebral dysgenesis
Neoronal migration disorders
Maternal anesthetic agents
Drug toxicity-theophylline
Syndromic Neonatal Seizure
Others-Polycythemia
Drug withdrawl
Tuberous sclerosis
Sturge Weber Syndrome
Bilirubin encephalopathy
Causes of neonatal seizures

22. •AstudyconductedintheNeonatology
DepartmentofBSMMUandNICUofCentral
HospitalLimitedshowed–
Perinatal asphyxia -56.86%,
Septicemia -15.67% ,
Meningitis -11.76%,
Hypoglycemia -19.6%,
Hypocalcemia -15.7%,
Acidosis -29.4%

23. Causes of neonatal seizures

24. Hypoxic Ischemic Encephalopathy
–Contributes50%ormoreofneonatalseizures.
–mostseizuresduetoHIE(about50-65%)start
withinthefirst12hoursoflifewhiletherest
manifestby24-48hoursofage.
–Mostsevereinfirst72hoursthensubside
irrespectiveoftreatment.
–Subtle,generalizedtonic,myoclonicseizuresmost
common

25. Intracranial hemorrhage
•Seizuresduetosubarachnoid,intraparenchymalor
subduralhemorrhageoccurmoreofteninterm
neonateswhileseizuressecondarytointraventricular
hemorrhage(IVH)occurinpreterminfants.
•Mostseizuresduetointracranialhemorrhageoccur
between2and7daysofage.
•Adiagnosisofintracranialbleedinginatermbaby
shouldleadtosearchforcoagulationdisorder
includingvitaminKdeficiencyandtestingfor
hemophiliainboys.

26. Focal cerebral infarction
•Patientswitharterialstrokesorvenoussinus
thrombosiscanpresentwithseizure.
•Perinatalstrokemostcommonlyoccurinleftmiddle
cerebralarterydistributionandpresentwithin1
st
two
days.
•Accounts10-15%ofseizureinterm.
•Diagnosedbyneuroimaging.Venoussinusthrombosis
couldbemissedunlessMRorCTvenographystudies
arerequested.
•Diagnosisshouldtriggerinvestigationstoruleout
underlyingthrombotictendency.

27. Infection
•Bacterialandnonbacterialinfectionsaccountfor5-
10%ofthecasesofneonatalseizuresandinclude
bacterialmeningitis,TORCH(toxoplasmosis,other
infections,rubella,cytomegalovirus,herpessimplex
virus)infections,particularlyherpessimplex
encephalitis.
•Seizureusuallyoccurafter1
st
weekoflife.

28. Metabolic cause
•Hypoglycemia-
-cancauseneurologicdisturbancesandisvery
commoninIUGRandneonateswhosemothersare
diabeticorprediabetic.
-Thedurationofhypoglycemiaisverycriticalin
determiningtheincidenceofneurologicsymptoms.

29. Metabolic cause(cont..)
•Hypocalcemia–riskfactorforLBW,asphyxiated
infant,infantwithDigeorgesyndrome,infantbornto
motherwithhyperparathyroidism
•Hypomagnesemia-isoftenassociatedwith
hypocalcemia.
•Hyponatremia-isoftensecondarytoinappropriate
antidiuretichormonesecretion.
•Hypernatremia-Inadequatebreastmilk,excessive
useofsodiumbicarbonate

30. Pyridoxine Dependency seizure
Impaired binding of the active form of pyridoxine to
the enzyme glutamic acid decarboxylase.
This enzyme is responsible for the conversion of the
glutamate to GABA.
DecreasedGABAandincreasedglutamateproduction
leadstointractableseizuresinfirstdaysoflife.
Thediagnosisisusuallymadebyatherapeutictrialof
intravenouspyridoxinewithsimultaneousEEG
monitoring.
Seizuresceaseafterappropriatedosesofpyridoxine.

31. Folinicacid-responsive seizures
Maypresentwithinthefirstfewhoursasasevere
neonatalepilepticencephalopathywithmyoclonic,
clonicorapneicspells
Neonatalseizuresofunknownetiologythatpersist
afteranadequatetrialofanticonvulsantdrugsand
pyridoxine,warranta24to48hourtrialofenteral
folinicacid
Seizuresusuallyceasewithin24hoursoftreatment.
DiagnosedbyCSFlevelof5-methyltetrahydrofolate
assay.

32. Neonatal Seizure Syndromes
Benign epileptic syndromes
Benign familial neonatal seizures
Benign idiopathic neonatal seizures -Fifth day fits
Malignant epileptic syndromes
Neonatal myoclonic encephalopathy
Early infantile epileptic encephalopathy (Ohtahara's
syndrome)

33. Benign Familial Neonatal seizures
Autosomal dominant
Impairment of potassium dependent neuronal
repolarization
Onset around the second to third day of life.
May recur for days to weeks before gradually resolving.
Most cases have a normal long-term neuro-
developmental outcome.
Aggressive anticonvulsant therapy may not be indicated.
Less than 10% of cases later develop epilepsy.

34. Benign Idiopathic Neonatal seizure
(Fifth day fits)
Approximately5%ofseizuresinterminfants
Thecausefortheseseizuresremainsunknownbut
mayberelatedtoatransientzincdeficiency
Seizureonsetbetweendays4and6oflife(5
th
day)
Usuallyclonicandapneaiscommon.
Neurologicalstateisusuallynormalattheonsetand
nofamilyhistoryofseizure.
Anormalinter-ictalEEG.
Seizuresseldompersistinglongerthan2weeks.
Thelong-termoutcomeisinvariablyfavorableand
laterepilepsydoesnotoccur.

35. Neonatal Myoclonic encephalopathy
These seizures typically start as focal motor seizures
and later evolve into typical infantile spasms.
The most common etiologies associated with this
condition are metabolic disorders (nonketotic
hyperglycinemia)
The interictal EEG shows a burst suppression pattern
The long-term outcome is universally poor with a high
mortality in the first year and severe retardation in all
survivors.

36. Ohtaharasyndrome
Usually presents within the first 10 days of life but may
present as late as 3 months
The seizures are typically numerous brief tonic spasms
The causes tend to be structural-dysgenetic
Prognosis is universally grim with early death , among
survivors, severe handicap

37. Classification
According to EEG activitiesAccording to seizure types
•Epileptic seizures
•Non-epileptic seizures
•EEG seizures
•Subtle
•Tonic
•Clonic
•Myoclonic

38. Classification(cont..)
•Epilepticseizures:phenomenaassociated
withcorrespondingEEGseizureactivitye.g.
clonicseizures.
•Non-epilepticseizures:clinicalseizures
withoutcorrespondingEEGcorrelatee.g.
subtleandgeneralizedtonicseizures
•EEGseizures:abnormalEEGactivitywithno
clinicalcorrelation.

39. Subtle seizures
Commonest type-50% of all seizures
More common in preterm than full term infant
Ocular-Tonic horizontal deviation of eyes ,Sustained
eye opening with ocular fixation , Cycled fluttering
Oral-facial-lingual movements -Chewing, Tongue
thrusting , Lip-smacking
Limb movement -Cycling, Paddling, swimming
movement of limbs
Autonomic phenomena-Tachycardia , Bradycardia
Apnea-rare manifestation as seizure

41. Clonicseizures(25-30%)
Primarily in term
Focal or multifocal
Characterized by rhythmic jerking movements of
muscle groups
Fast and slow components
Consciousness may be preserved

43. Tonic seizures(20%)
Primarily in Preterm
refers to a sustained flexion or extension of axial or
appendicular muscle groups.
May be generalized or focal
may be decerebrate or decorticate

45. Myoclonicseizures
Rare(about 5%)
Focal, multifocal or generalized
Lightning-like jerks of extremities (upper > lower)
Myoclonic seizures are usually associated with poor
long-term outcome.

46. Early onset seizures
•Perinatal asphyxia
•Hypoglycaemia
•Intraventricular haemorrage
•Structural defect/congenital cerebral malformation
•Inborn error of metabolism.

47. Late onset seizure
•Meningitis
•Hypocalcemia, Hypomagnesemia
•Benign familial neonatal seizure
•Benign idipathic neonatal seizure (Fifth day fits)
•Bilirubin encephalopathy

48. Causes of intractable or prolonged seizure
•Perinatal asphyxia
•Intraventricular hemorrhage (IVH)
•Structural defect/Cerebral malformation
•Inborn error of metabolism (eg. pyridoxine
dependency)
•Ohtahara syndrome

49. First 24 hours
•Hypoxic Ischemic Encephalopathy
•CNS & Intrauterine infections + Sepsis
•Drug withdrawal
•Vascular
•Birth Trauma
•Pyridoxine dependency
•Inadvertent local anesthetic Toxicity

50. 24 to 72 hours
•Cerebral dysgenesis
•Vascular
•Metabolic
•Urea cycle disorders
•Drug withdrawal
•Pyridoxine dependency
•Incontinentia pigmenti
•Tuberous sclerosis

51. 72 hours to 1 week
•Familial neonatal seizure
•Cerebral malformations
•Cerebral infarction
•Hypoparathyroidism ( Hypocalcemia)
•Vascular events (Venous thrombosis, hemorrhage)
•Kernicterus ( Venous encephalopathy)
•Acidurias (Methylmalonic or propionic acidemia)
•Urea cycle disorders
•Tuberous sclerosis

52. Non-epileptic behavior in newborn
•Jitteriness
•Benign neonatal sleep myoclonus

53. Jitteriness vs Seizure
Jitteriness Seizure
Movements are of a fine
nature
Movements are of a coarser
nature
Provoked by stimulationNot stimulus sensitive
Stop moving if they are
grasped
Continue to move if grasped
Eye movements are normalEye movements are abnormal
Autonomicchanges-absentAutonomicchanges-present
Neurological examination -
normal
Neurological examination -
normal
EEG is normal EEG abnormal

55. Benign neonatal sleep myoclonus
•Presentsinthefirstweekoflifeandresolves
spontaneouslyoverweekstomonths
•Mayberelatedtransientdysmaturityofthe
brainstemreticular-activatingsystem
•OccursduringNREMsleepandrapidlyabolishedby
arousal,neveroccurduringwakefulness
•TheneurologicexaminationandEEGarenormal
•Anticonvulsantsarenotindicated,benzodiazepines
mayexacerbatethemyoclonicjerks
•Thelong-termoutcomeisnormalandlaterepilepsy
doesnotdevelop.

57. Refractory seizure
•Refractory means uncontrolled.
•In case of acute neonatal seizure, when seizure are not
controlled with adequate dose of 1
st
line two
anticonvulsant drug (Inj. Phenobarbitone/ Inj.
Fosphenytoin) is called refractory seizure.

58. Approach to a newborn
with seizure

59. Detail of seizure event
•Onset
•Duration
•Associated eye movements
•Seizure type
•conscious/ sleeping at the time of seizure
History

60. History
Postnatal age at the time of seizure
Seizures occuring on 1
st
3 days of life
•perinatal asphyxia
•intracranial hemorrhage
•metabolic disorder.
Seizures occuring on day 4-7
Meningitis
metabolic causes
developmental defects
Between 1-4 week-
•Late onset hypocalcemia
•IEM, Cerebral dysgenesis

61. Antenatal history
•Maternal H/O Diabetes
•PET
•Maternal TORCH infection
•History of drug intake
•Maternal H/O fever
•Prolonged rupture of membrane
•H/O chorioamnionitis
History

62. Natal history
•H/O fetal distress
•decreased fetal movement
•information regarding maternal analgesia
•place of delivery
•mode of delivery
•duration of labour
•H/O obstructed or prolonged labour
•H/O instrumental delivery
History

63. Postnatal history:
–H/O delayed cry
–resuscitative measures in the labor room
–Apgar score
–abnormal cord pH
History

64. Feeding history:
–reluctant to feed
–vomiting after initiation of breast milk may be
suggestive of Inborn error of metabolism
–Late onset hypocalcemia should be considered in
the presence of feeding with cow’s milk.
History

65. Family history:
History of consanguinity, family history of seizures or
mental retardation and early fetal/neonatal deaths -
suggestive of IEM
History of seizures in either parent or sibs in the
neonatal period may suggest benign familial neonatal
convulsions
History

66. Physical findings
–Vital signs should be recorded in all infant with
seizure.
–Thorough general physical examination
–Neurologic examination
–Direct observation of the seizure pattern

67. General physical examination
•Gestation, birth weight, weight for age
•Dysmorphic face
•Color-pale in Intracranial hemorrhage.
•Activities–lethargic, less active in sepsis.
•Fontanels-full or bulged in meningitis
•Head-evidence of the birth injuries
•Skin-presenceofneurocutaneousmarkersuchas
hypopigmentedmacules/ash-leafspotwouldbe
suggestiveoftuberoussclerosis
•

68. Neurologic evaluation
–level of alertness
–Pupillary size and reaction to light
–Changes in muscle tone
–Status of primitive reflexes
–Cranial nerves examination
–Motor function
–Sensory function
–Fundus examination –for features of
chorioretinitis

69. Systemic examination
Presence of hepatosplenomegalyor an abnormal
urine odor may be suggestive of IEM

70. Investigations
First line
Sepsis work up
CBC, PBF with IT ratio, ANC
CRP, Blood culture
CSF study
Blood glucose
Serum electrolyte
Calcium & magnesium
Cranial sonography-recommended for all babies with
seizures to exclude ICH
EEG

71. EEG
Has both diagnostic and prognostic role
It should be done in all neonates who need
anticonvulsant therapy
Assess the severity of brain dysfunction and to decide
the duration of anticonvulsant drugs
It should be done as soon as the neonate is stable,
preferably within first week.

72. Lumbar puncture
LP is done in neonatal seizures to rule out bacterial
and viral infections
It may also help in the diagnosis of nonketotic
hyperglycinemia (NKH)
CSF study may be withheld temporarily if severe
cardio-respiratory compromise is present or in
cases with severe birth asphyxia

73. Additional investigations
May be considered in neonates-
Do not respond to a combination of phenobarbitone
and phenytoin
Earlier in neonates with specific features
These include
Neuroimaging (CT, MRI),
Screen for -Congenital infections (TORCH)
-Inborn errors of metabolism

74. Neuroimaging
CT scan
should be done if an etiology is not available after the
first line of investigations
It can be diagnostic in sub-arachnoid hemorrhage and
developmental malformations
MRI
Indicated only if investigations do not reveal any
etiology and seizures are resistant to usual anti-epileptic
therapy.
It can be diagnostic in cerebral dysgenesis,
lissencephalyand other neuronal migration disorders.

75. Metabolic screen
Helps early identification & management of
inborn metabolic errors causing seizures
Include
Blood and urine pH
Urinary reducing substances
Blood ammonia, Lactate
Urine and serum aminoacidogram
serum and CSF lactate/pyruvate ratio

76. Management

77. TREATMENT OUTLINE
•Stepwise acute management of neonatal seizures
•Identification and treatment of underlying disorders
•Choice of antiepileptic drugs(AED)
•Maintenance of antiepileptic drugs(AED)
•Weaning of antiepileptic drugs

78. Neonate with seizure
Identifyandcharacterizeseizuretype,manageairway,breathing,
circulation,temparature,startoxygen,startIVaccess,takebloodsamplefor
baselineinv.IflowBloodglucose–give2ml/kg10%DA
If Hypocalcaemia-give 2ml/kg Inj 10% Cal gluconate IV slowly
Administer Inj phenobarbitone 20 mg/kg IV stat over 20 min
Repeat phenobarbitone 10 mg/kg/dose until 40 mg/kg dose reached
Repeat injFosphenytoinin 15mg/kg/dose
Consider Lorazepum, Midazolumbolus and Infusion, other AED, Pyridoxine
If seizure persists
If seizure persists
If seizure persistsf
If seizure persists
If seizure persists
Fosphenytoin-loading: 30 mg/kg IV stat over 30 mins under cardiac monitoring

79. Other anti-epileptic drug-
i)Lidocaine-Start with 4mg/kg/hrIV on first day, reduce
by1mg/kg/hron each subsequent day
ii)Paraldehyde-0.1-0.2 ml/kg/dose may be given IM or 0.3
ml/kg/dose mixed with coconut oil in 3:1 may be used by per
rectal route
iii)Levetiracetam-20-30mg/kg iv, then 10mg/kg/day, upto
30mg/kg/day
iv)Valproic acid-10-20mg/kg, then 20mg/kg/day
v)Topiramate
Management cont..

80. ANTI-EPILEPTIC DRUG THERAPY
•Anticonvulsant drugs should be considered to
treat seizures after cause specific treatment
when-
Prolonged–greater than 3 minutes
Frequent –greater than 2-3 per hour
In specialized care facilities where EEG is available,all
electric seizure even in absence of clinically
apparent seizure should be treated

81. The expected response to anticonvulsants-
40% to the initial 20-mg/kg loading dose of
phenobarbitone
70% to a total of 40 mg/kg of Pb
85% to a 20-mg/kg loading dose of PHT
95% to 100% to 0.05 to 0.10 mg/kg lorazepam

82. Maintenance and duration of
Antiepileptic drugs
Maintenancetherapymaynotberequiredifloading
dosesofanticonvulsantdrugscontrolclinicalseizures
Thedurationofanticonvulsantdrugtreatmentshould
beasshortaspossible
Thiswilldependondiagnosisandthelikelihoodof
seizurerecurrence.
Babieswithprolongedordifficulttotreatseizuresand
thosewithabnormalityonEEGmaybenefitfrom
continuinganticonvulsanttreatment.

83. Weaning of anticonvulsant therapy
Thisishighlyindividualizedandnospecificguidelines
areavailable.
Thegoalistodiscontinuephenobarbitoneasearlyas
possible.
Discontinueallmedicationsatdischargeifclinical
examinationisnormal,irrespectiveofetiologyand
EEG.
Ifneurologicalexaminationispersistentlyabnormal
atdischarge,AEDiscontinuedandthebabyis
reassessedatonemonth.

84. Ifthebabyisnormalonexaminationandseizurefree
at1month,phenobarbitoneisdiscontinuedover2
weeks
Ifneurologicalassessmentisnotnormal,anEEGis
obtained.
IfEEGisnormal,phenobarbitoneistaperedand
stopped.
IfEEGisabnormal,theinfantisreassessedinthe
samemannerat3monthsandthen3monthlytill1
yearofage
Weaning of anticonvulsant therapy

86. •AlthoughPhenobarbitalandphenytoin/fosphenytoin
havetraditionallybeenthemostcommonlyused
medicationstotreatneonatalseizures,concernexists
forshort-termsideeffects,medicationinteractions,the
needforfrequentblood-levelmonitoring,and
potentiallynegativeneurodevelopmentalconsequences.
•Perhapsduetotheselimitations,theuseofother
antiepilepticmedicationsisincreasinglybeingreported.
•Asystemicreviewwasconductedtoexaminethe
publishedevidenceregardingpharmacologicaltherapy
forneonatalseizuresandrecommendatreatment
algorithm.

87. Fig: Suggested treatment algorithm for neonatal seizure
Seizure suspected
Confirm by EEG
Phenobarbitone
20 mg/kg IV
If seizure continueAdditionalPhenobarbitone
20 mg/kg IV
If seizure continue
Levetiracetam50MG/KG IV
then 40 mg/kg
maintenance
Phenytoin/
Fosphenytoin20mg/kg Iv and
start 2
nd
maintenance with
Phenytoin/Levetiracetam
Lidocaine 2mg/kg bolus,then
6mg/kg/hr in drip
Also start 2
nd
maintenance i.e.
Levetiracetam

88. Fig: Suggested treatment algorithm for neonatal seizure(cont..)
If seizure continue
Midazolam0.15mg/kgIVbolus then 1 ug/kg/min
Begin weaning after 24 hrs of EEG seizure freedom
If seizure continue,considerPENTOBARBITAL
Drip/Lidocainedrip if not yet tried

89. PROGNOSIS
•Prognosisisvariableanddependentonunderlying
causeandtypesofseizures
•Seizuresduetosubarachnoidhemorrhageandlate
onsethypocalcemiacarryagoodprognosisforlong
termneurodevelopmentaloutcome
•Seizuresrelatedtohypoglycemia,cerebral
malformation,meningitishaveahighriskfor
adverseoutcome
•Themortalityandmorbidityaregreaterinpreterm
newborns.

90. PROGNOSIS
•Myoclonicseizurescarrytheworstprognosisin
termsofneurodevelopmentaloutcomeandseizure
recurrence.Focalclonicseizurescarrythebest
prognosis
•NeuroimagingandEEGgiveabetterindicatorof
prognosisthanneurologicalfindingalone
•Seizuresthat arerefractorytomultiple
anticonvulsantsgenerallyhaveapoorprognosis.

91. Follow up
•Dependoncauseofseizureandresponseto
treatment.
•Specialistfollow-upfordischargedwith
anticonvulsant.
•Multidisciplinaryfollowuptoidentifyphysicalor
cognitivedeficitandtoprovidetimelyneuro-
rehabilitationisimportant.