seminar on neonatal seizure

1. SEMINAR
on
Seizure Disorder in Newborn
Presented by
Dr. Md. Moklesur Rahman
Resident (PHO) Year - 2
Dr. Sarbari Saha
Resident (Neonatology) Year - 5

2. Case scenario 1
• S/O Santa, term (38 weeks), weighing 3200 grams,
admitted at the age of 20 hours with the H/O
convulsion at 12 hours of age. He was delivered at
home. Delivery was conducted by TBA. Resuscitation
efforts couldn’t be elicited. Liquor was clear. Baby
didn’t cry immediately after birth. O/E - Lethargic,
hypotonic, moro reflex - weak, vitals – normal, pupil-
constricted.
• What may be the cause of convulsion?

3. Case scenario 2
• S/O Halima, Term (37 weeks), LGA (5200 grams), IDM
developed convulsion at the age of 3 hour. Mother
had h/o gestational DM and treated with insulin.
HbA1c - 7.1. O/E-Baby is plumpy, plethoric, CBG-1.6
mmol/l.
• What may be the cause of convulsion?

4. Case scenario 3
• S/O Maksuda, Term (37 weeks), AGA (3400 gram)
admitted on day 3 with the complaints of less
activity, reluctant to feed, convulsion. Seizure was
difficult to manage, required multiple anti-convulsive
drugs (PHB, Fosphen and Midazolam). On query,
history revealed consanguineous marriage, H/O 1
abortion. O/E- baby is lethargic, reflex and activity-
poor, hepato-splenomegaly present. Blood gas report
shows severe metabolic acidosis.
• What may be the cause of convulsion?

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

6. Introduction
 Common manifestation of a serious CNS disease
 Most common neurological emergency in neonatal
period.
 Powerful predictor of long term cognitive and
developmental impairment
 Diagnostic and therapeutic challenge to clinicians
worldwide

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

8. Incidence
- Precise incidence is difficult to delineate and depends
on study population and criteria used for diagnosis of
seizure.
- Incidence of 10.3 per 1000 live-births.
- Incidence increase with decreasing gestation and birth
weight.
- Preterm infants vs Term infants = 20.8 vs 8.4 per 1000
live-births.
- Very low birth weight infants = 36.1 per 1000 live birth
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
 Failure of Na-K pump due to disturbance in energy
production - Hypoxemia, ischemia, and hypoglycemia
 A relative excess of excitatory neurotransmitter
- Hypoxemia, ischemia, and hypoglycemia
 A relative deficiency of inhibitory neurotransmitter
- Pyridoxine dependency
 Alteration of neuronal membrane (increase Na+
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:
GABA ion channels are relatively under expressed in
the immature brain.
In certain areas of the developing brain these
immature GABA may be depolarizing (excitatory) rather
than hyperpolarizing ( inhibitory)
Cl− gradient is reversed in the immature brain-
Under expression of the Cl− exporter KCC2
Over expression Cl− importer NKCC1
**GABA receptor is less sensitive to benzodiazepines and seizures
in the immature brain respond poorly to benzodiazepines

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
Folinic acid-responsive seizures
Urea cycle defects
Maple syrup urine disease
Propionic aciduria
Methylmalonic aciduria
Mitochondrial diseases
Glucose transporter deficiency
Perinatal asphyxia
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. • A study conducted in the Neonatology
Department of BSMMU and NICU of Central
Hospital Limited showed –
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
– Contributes 50% or more of neonatal seizures.
– most seizures due to HIE (about 50-65%) start
within the first 12 hours of life while the rest
manifest by 24-48 hours of age.
– Most severe in first 72 hours then subside
irrespective of treatment.
– Subtle, generalized tonic, myoclonic seizures most
common

25. Intracranial hemorrhage
• Seizures due to subarachnoid, intraparenchymal or
subdural hemorrhage occur more often in term
neonates while seizures secondary to intraventricular
hemorrhage (IVH) occur in preterm infants.
• Most seizures due to intracranial hemorrhage occur
between 2 and 7 days of age.
• A diagnosis of intracranial bleeding in a term baby
should lead to search for coagulation disorder
including vitamin K deficiency and testing for
hemophilia in boys.

26. Focal cerebral infarction
• Patients with arterial strokes or venous sinus
thrombosis can present with seizure.
• Perinatal stroke most commonly occur in left middle
cerebral artery distribution and present within 1st two
days.
• Accounts 10-15% of seizure in term.
• Diagnosed by neuroimaging. Venous sinus thrombosis
could be missed unless MR or CT venography studies
are requested.
• Diagnosis should trigger investigations to rule out
underlying thrombotic tendency.

27. Infection
• Bacterial and nonbacterial infections account for 5-
10% of the cases of neonatal seizures and include
bacterial meningitis, TORCH (toxoplasmosis, other
infections, rubella, cytomegalovirus, herpes simplex
virus) infections, particularly herpes simplex
encephalitis.
• Seizure usually occur after 1st week of life.

28. Metabolic cause
• Hypoglycemia-
-can cause neurologic disturbances and is very
common in IUGR and neonates whose mothers are
diabetic or prediabetic.
- The duration of hypoglycemia is very critical in
determining the incidence of neurologic symptoms.

29. Metabolic cause(cont..)
• Hypocalcemia – risk factor for LBW, asphyxiated
infant, infant with Digeorge syndrome, infant born to
mother with hyperparathyroidism
• Hypomagnesemia - is often associated with
hypocalcemia.
• Hyponatremia - is often secondary to inappropriate
antidiuretic hormone secretion.
• Hypernatremia -Inadequate breast milk, excessive
use of sodium bicarbonate

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.
 Decreased GABA and increased glutamate production
leads to intractable seizures in first days of life.
 The diagnosis is usually made by a therapeutic trial of
intravenous pyridoxine with simultaneous EEG
monitoring.
 Seizures cease after appropriate doses of pyridoxine.

31. Folinic acid-responsive seizures
May present within the first few hours as a severe
neonatal epileptic encephalopathy with myoclonic,
clonic or apneic spells
Neonatal seizures of unknown etiology that persist
after an adequate trial of anticonvulsant drugs and
pyridoxine, warrant a 24 to 48 hour trial of enteral
folinic acid
Seizures usually cease within 24 hours of treatment.
Diagnosed by CSF level of 5-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)
 Approximately 5% of seizures in term infants
 The cause for these seizures remains unknown but
may be related to a transient zinc deficiency
 Seizure onset between days 4 and 6 of life( 5th day)
 Usually clonic and apnea is common.
 Neurological state is usually normal at the onset and
no family history of seizure.
 A normal inter-ictal EEG.
 Seizures seldom persisting longer than 2 weeks.
 The long-term outcome is invariably favorable and
later epilepsy does not occur.

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. Ohtahara syndrome
 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 activities According to seizure types
• Epileptic seizures
• Non-epileptic seizures
• EEG seizures
• Subtle
• Tonic
• Clonic
• Myoclonic

38. Classification(cont..)
• Epileptic seizures: phenomena associated
with corresponding EEG seizure activity e.g.
clonic seizures.
• Non-epileptic seizures: clinical seizures
without corresponding EEG correlate e.g.
subtle and generalized tonic seizures
• EEG seizures: abnormal EEG activity with no
clinical correlation.

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. Clonic seizures(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. Myoclonic seizures
 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 stimulation Not stimulus sensitive
Stop moving if they are
grasped
Continue to move if grasped
Eye movements are normal Eye movements are abnormal
Autonomic changes- absent Autonomic changes- present
Neurological examination -
normal
Neurological examination -
normal
EEG is normal EEG abnormal

55. Benign neonatal sleep myoclonus
• Presents in the first week of life and resolves
spontaneously over weeks to months
• May be related transient dysmaturity of the
brainstem reticular-activating system
• Occurs during NREM sleep and rapidly abolished by
arousal, never occur during wakefulness
• The neurologic examination and EEG are normal
• Anticonvulsants are not indicated, benzodiazepines
may exacerbate the myoclonic jerks
• The long-term outcome is normal and later epilepsy
does not develop.

57. Refractory seizure
• Refractory means uncontrolled.
• In case of acute neonatal seizure, when seizure are not
controlled with adequate dose of 1st 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 1st 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- presence of neurocutaneous marker such as
hypopigmented macules/ash-leaf spot would be
suggestive of tuberous sclerosis

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 hepatosplenomegaly or 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,
lissencephaly and 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
Identify and characterize seizure type, manage airway, breathing,
circulation,temparature, start oxygen, start IV access, take blood sample for
baseline inv.If low Blood glucose –give 2ml/kg 10% 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 inj Fosphenytoin in 15mg/kg/dose
Consider Lorazepum, Midazolum bolus 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/hr IV on first day, reduce
by1mg/kg/hr on 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
 Maintenance therapy may not be required if loading
doses of anticonvulsant drugs control clinical seizures
 The duration of anticonvulsant drug treatment should
be as short as possible
 This will depend on diagnosis and the likelihood of
seizure recurrence.
 Babies with prolonged or difficult to treat seizures and
those with abnormality on EEG may benefit from
continuing anticonvulsant treatment.

83. Weaning of anticonvulsant therapy
 This is highly individualized and no specific guidelines
are available.
 The goal is to discontinue phenobarbitone as early as
possible.
 Discontinue all medications at discharge if clinical
examination is normal, irrespective of etiology and
EEG.
 If neurological examination is persistently abnormal
at discharge, AED is continued and the baby is
reassessed at one month.

84. If the baby is normal on examination and seizure free
at 1 month, phenobarbitone is discontinued over 2
weeks
If neurological assessment is not normal, an EEG is
obtained.
If EEG is normal , phenobarbitone is tapered and
stopped.
If EEG is abnormal, the infant is reassessed in the
same manner at 3 months and then 3 monthly till 1
year of age
Weaning of anticonvulsant therapy

86. • Although Phenobarbital and phenytoin/fosphenytoin
have traditionally been the most commonly used
medications to treat neonatal seizures, concern exists
for short-term side effects, medication interactions, the
need for frequent blood-level monitoring, and
potentially negative neurodevelopmental consequences.
• Perhaps due to these limitations, the use of other
antiepileptic medications is increasingly being reported.
• A systemic review was conducted to examine the
published evidence regarding pharmacological therapy
for neonatal seizures and recommend a treatment
algorithm.

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

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

89. PROGNOSIS
• Prognosis is variable and dependent on underlying
cause and types of seizures
• Seizures due to subarachnoid hemorrhage and late
onset hypocalcemia carry a good prognosis for long
term neurodevelopmental outcome
• Seizures related to hypoglycemia, cerebral
malformation, meningitis have a high risk for
adverse outcome
• The mortality and morbidity are greater in preterm
newborns .

90. PROGNOSIS
• Myoclonic seizures carry the worst prognosis in
terms of neurodevelopmental outcome and seizure
recurrence. Focal clonic seizures carry the best
prognosis
• Neuroimaging and EEG give a better indicator of
prognosis than neurological finding alone
• Seizures that are refractory to multiple
anticonvulsants generally have a poor prognosis.

91. Follow up
• Depend on cause of seizure and response to
treatment.
• Specialist follow-up for discharged with
anticonvulsant.
• Multidisciplinary follow up to identify physical or
cognitive deficit and to provide timely neuro-
rehabilitation is important.