2. SEIZURES
• A seizure is an abnormal paroxysmal electrical activity in the brain
resulting in motor, sensory, behavioural or autonomic manifestations.
• Occurs due to electrical disturbances in the brain, i.e. due to excessive
surge of electrical activity in the brain that cause a variety of
symptoms, depending on which parts of brain are involved.
EPILEPSY
• Is the occurrence of 2 unprovoked seizures over a day apart beyond
the neonatal period i.e a neurological disorders.
3. CONVULSION
• The involuntary action of jerking and contraction.
• A sudden, violent, irregular movement of body, caused by involuntary
contraction of muscles & associated especially with brain disorder.
NEONATAL SEIZURES
• Are the paroxysmal alterations in the neurological functions.
• Defined as a sudden, repetitive, evolving and stereotyped episode of
abnormal electrographic activity with a minimum duration of 10 sec.
• And are more common in newborn period than in any other time of
life.
4. EPIDEMIOLOGY
• 10.3/1000 in term babies.
• 20.8/1000 in preterm .
• 36.1/1000 in VLBW .*
• 6 to 12% in babies < 1.5 kg.
*NNPD,2002-3
5. •PATHOPHYSIOLOGY
• Immature brain has many differences from the mature brain that
render it more excitable and more likely to develop seizures.
• The balance of excitatory and inhibitory processes in the immature
brain are weighted toward excitation with an excess of glutamatergic
synapses over inhibitory (usually gamma-aminobutyric acid [GABA]-
ergic) synapses.
• These developmental features may underlie the neonate's tendency
to frequently developmemt of recurrent seizures.
• Thus,
• GABA in the immature brain has an excitatory function.
• Delay in the development of inhibitory GABAergic transmission
9. PERINATAL COMPLICATIONS
• Birth asphyxia and intra-cranial injuries together account for about half of
the neonatal seizures.
• In perinatal asphyxia, the seizures occur in the context of a newborn who
has a history of difficulty during labor and delivery with alterations of the
fetal heart rate, decreased umbilical artery pH, and Apgar score <5 at 5
minutes.
• Convulsions occur on 1 st DOL.
• Cephalhematoma or fracture of skull and bulging anterior fontanel due to
raised intracranial tension may be associated.
• Although the insult is global, the seizures are usually focal and may be
multifo- cal. They are typically of short duration (<1 minute) but may be
very frequent and refractory.
10.
11. Therapeutic hypothermia
• In recent years, therapeutic hypothermia has become the standard of
care in neonates with suspected hypoxic injury. Therapeutic hypo-
thermia may decrease the rate of both death and disability in
neonates with hypoxic injury. It may also decrease the overall seizure
burden in patients with moderate hypoxic injury. A rebound increase
in seizure frequency has been documented during rewarming.
Although rare.
• It raises the threshold for seizures, by reducing release of excitatory
neurotransmitters. Thus neuroprotective effect.
• ( core temperature < 34•c ).
12. Infarction & hemorrhage
• ICH are responsible for 10% to 15% of neonatal seizures.
• The convulsive manifestations of intracranial bleed appear between 2 and
7 days of age.
• Normal delivery or de- liveries with instrumentation and/or trauma may be
associated with more substantial subarachnoid hemorrhages, which may
present with seizures, usually on the second day of life. These infants
appear clinically well between seizures and have a very good outcome.
• Subdural hemorrhages are related to large infant size, breech delivery, and
instrumentation. They are often associated with underlying cerebral
contusions, which may be responsible for the seizures in some cases.
• Presenting seizures are usually focal and occur in the first few days of life.
13. Infections
• Congenital intrauterine infections such as with cytomegalovirus (CMV),
toxoplasma, rubella, and herpes viruses may present early (first 2 days)
with seizures in severe cases.
• About one- third of patients with neonatal meningitis, present with
convulsions.
• Clinical scenario may include microcephaly; poor intrauterine growth:
prematurity; and other skin, ophthalmic, and systemic findings.
Meningoencephalitis, cerebral calcification, and dysgenesis (in cases of
early intrauterine infection) contribute to the pathogenesis of seizures in
these cases.
• Postnatal sepsis, for example, with group B Streptococcus or Escherichia
coli, is often complicated by meningitis and may be associated with
seizures.
14. Malformations
• Five percent of neonatal seizures are caused by cerebral dysgenesis.
• Cerebral dysgenesis can cause seizures from the first day of life.
• This is most likely with the more severe disorders such as
hemimegalencephaly, lissencephaly, and poly- microgyria,
hydrocephalus, agenesis of corpus callosum.
• Seizures are often refractory to medications.
• Some disorders may be amenable to surgical treatments, such as
hemimegalencephaly and focal polymicrogyria.
• Neuroimaging is primary in making these diagnosis.
15.
16. Metabolic disorders
• Hypocalcemia (serum calcium <7 mg/dL) is the commonest biochemical
abnormality causing neonatal seizures.
• Symptoms of hypocalcemia include jitteriness, stimulus-induced muscle
jerks, seizures, and rarely, laryngospasm.
• Early onset hypocalcaemia occurs in the first 3 DOL & associated with
prematurity, IDM, IUGR & perinatal asphyxia. Most are asymptomatic.
• Late onset >10 DOL hypocalcaemia occur due to hypoparathyroidism,
feeding high phosphate formulas, Digeorge syndrome( chromosome
22q11.2 deletion) & hypomagnesemia.
• In the absence of perinatal complications, the prognosis in this group is
excellent.
17. • Hypoglycemia In neonates, hypoglycemia is diagno- sed when blood
glucose level is <40 mg/dL, irrespec- tive of period of gestation.
• The diagnosis is suspected, if any of the situations known to
predispose to hypogly- cemia such as immaturity, severe IUGR, large-
for-dates, Rhesus isoimmunization, and infants of diabetic mothers
coexist.
• Symptoms are jitteriness /tremor, hypotonia, alteration of
consciousness, poor feeding, apnea and seizures.
• In hypoglycemia, the main excitatory amino acid glutamate is poorly
reabsorbed due to its extreme secretion in the synaptic area and
thus leads to increased amounts of secondary extracellular glutamate
which in turn induces convulsions.
18. Causes of neonatal hypoglycaemia
• Decreased glucose supply, as in the premature and small for
gestational age infant.
• Increased utilization, such as hyperinsulinemic states, most
commonly seen in the infant of the diabetic mother.
• Disorders in which pathways of gluconeogenesis are deficient or
suppressed (e.g.. glycogen storage disorders, aminoacidopathies such
as maple syrup urine disease, fatty acid oxidation defects).
19. • Hypomagnesemia
• The m/c cause is transient neonatal hypomagnesemia.
• It causes parathyroid hormone resistance & so leads to
hypocalcaemia.
• Thus, hypomagnesemia must be corrected before hypocalcemia can
be corrected.
• Levels < 1.4 mg/ dl are considered low.
20. Hyponatremia
• Though uncommon, severe & rapidly evolving hyponatremia cause ld
seizures.
• Are generalised clonic.
• Occurs with sodium levels of < 115meq/L.
• Its seen in condition such as in inappropriate ADH, renal anomalies,
congenital adrenal hyperplasia.
• May be Associated with Perinatal hypoxia.
21. Drug withdrawal
• Seizures can rarely be caused by the neonate's passive addiction and then drug
withdrawal after birth.
• Such drugs include narcotic analgesics, sedative-hypnotics, Theophylline,
propylene glycol[diluent in IV nutritional formulation] & alcohol.
• The use of large doses of phenothiazines
for eclampsia management may lead to
toxicity in neonate evident via excessive
jitteriness, rigidity & ophisthotonus.
• The associated seizures appear after 48
hours of life.
• The withdrawal symptoms are mediated
through release of epinephrine when baby is
no longer exposed to maternal opiods after
birth.
22. Local anaesthesia intoxication seizures
• Results from neonatal intoxication with local anesthetics during
paracervical block, that are inadvertently administered into the
infant's scalp, leads to intractable convulsions.
• Pupils are usually dilated & non reactive to light, doll’s eye
phenomenon is lost due to complete external ophthalmoplegia.
• Careful examination may show the needle mark.
23. Oculocephalic reflex
Normal – eyes moving in direction
opposite to head movement.
Abnormal – Asymmetrical
uncomfortable eye deviation &
movements – indicates damage to
brainstem.
Absent – occurs in severe neuro
dysfunction, brainstem damage, brain
death & deep coma.
Doll’s eye reflex – examines 3,6 cranial
nerves.
Occulomotor = innervates eye muscles.
Abducent = innervates ext. rectus
muscle.
24. IEM
• Typically caused by an enzyme defect in the metabolic pathways of
carbohydrates, proteins, or fat, many cause disease due to
accumulation of toxic products unable to proceed along the appropri-
ate metabolic pathways.
• In these disorders, infants initially appear well, due to the benefits of
placental clearance of toxins until birth, and only become
encephalopathic and have seizures after 2 to 3 days.
• Biochemical markers for these disorders include hypoglyce- mia,
metabolic acidosis, hyperammonemia, as well as specific patterns of
alteration in amino acid or organic acid profiles.
• Symptoms appear after introduction of milk feeding.
25. Pyridoxine dependancy
• It is a rare autosomal recessive disorder of an enzyme involved in production of inhibitory
neurotransmitter GABA and presents with First-day early-onset intractable seizures.
• Prolonged maternal administration of vitamin B6, during pregnancy for Hyperemesis
gravidarum may predispose to this condition.
• Seizures may be focal or generalized having onset during first 12 hours and are resistant to
conventional therapy.
• Condition should be suspected in any infant having intractable cryptogenic focal seizures
with developmental retardation having onset during first 18 months of life. Irritability,
restlessness, crying and vomiting may precede the seizures.
• There may be a history of severe or fatal cryptogenic convulsive disorder in a sibling. There
may be consanguinity among the parents.
• EEG may show generalized bursts of bilaterally synchronous high voltage 1–4 Hz activity with
interspersed spikes
• Seizures are controlled with intravenous administration of 50-100 mg pyridoxine and they
reappear within 3 weeks of withdrawal of Pyridoxine.
26. • Patients with pyridoxine-dependency may have generalized 1-4Hz
sharp and slow wave activity.
•
27.
28.
29. Age of onset of seizures
• First day
• Hypoxic-ischemic encephalopathy, cerebral contusion, 'first day' hypocalcemia,
pyridoxine dependency, accidental injection of local anesthetic into fetal scalp.
• Between 1 and 3 day
• Intracranial hemorrhage, hypoglycemia, narcotic withdrawal and inborn error of
metabolism.
• 4th to 7th day
• Tetany, meningitis, TORCH infections, developmental malformations, acute
bilirubin encephalopathy, and benign neonatal seizures.
• 1-4 weeks
• Late-onset hypocalcemia, sepsis, progressive hydro- cephalus, herpes
encephalitis, inborn error of metabolism, cerebral dysgenesis and epileptic
syndromes.
30. Types of Seizures
• Due to incomplete development of axons, dendritic processes,
arborization and poor myelination, the manifestations are more
subtle and pleomorphic.
• The severity of convulsive movements is related to the size of the
baby.
• Larger the baby, more powerful are the twitchings.
• The clinical morphology of the seizures generally offers little clue to
the etiology or prognosis.
• Many newborns may have more than one seizure type.
31. • Subtle seizures or motor automatisms
• They account for over 50% of all seizures and are more common in
preterm babies. They can be easily missed.
• Jerking of eyes (with or without conjugate deviation), blinking or
fluttering of eyelids, staring look, sucking, chewing, or smacking
orobuccal movements and apneic attacks are included among subtle
seizures.
• Oral, facial and lingual phenomena are common due to advanced
maturation of the limbic system. There is tachycardia at the onset
followed by bradycardia after the apnea and hypoxemia.
• EEG may be normal.
32.
33. • Clonic seizures
• Multifocal –
• These are the rhythmic movements of body parts – consists of rapid
flexion phase f/b slower extensor movement.
• The Clonic convulsive movements migrate haphazardly from one limb
to another.
• They may occur due to hypoxic-ischemic encephalopathy and birth
trauma.
• Migrate in non jacksonian pattern ( random ) may also involve face.
34. • Focal –
• They are well localized and often associated with loss of
consciousness.
• They are common due to metabolic disorder, birth trauma and
cerebral infarc- tion.
• It has good prognosis.
35.
36. • Tonic seizures
• There is generalized stiffening, akin to decerebrate (tonic extension of
all limbs) or decorticate (flexion of upper limbs and extension of
lower limbs) posturing and may be associated with stertorous
breathing and eye signs.
• They may be associated with intraventricular hemorrhage and acute
bilirubin encephalopathy.
• In general, the prognosis of tonic seizures is poor.
37.
38.
39. • Myoclonic seizures
• Sudden jerky movements which are non rhythmic, rapid of <50msec
& repetitive pro- duced by episodic contractions of a group of
muscles.
• These may occur in babies with developmental defects including
anencephaly.
• Common symptoms: quick jerking often after awakening, rhythmic
movements, electric shock sensation, unusual clumsiness.
• Worst prognosis in terms of neurodevelopmental
Outcome & seizure recurrence.
40. Myoclonic seizures types
• Focal –
Mostly flexors of UL.
• Multifocal –
Asynchronous twitching of several parts of the body.
• Generalised –
B/L jerks of Upper & sometimes LL.
41.
42. Spasm – Infantile spasm
• Occurs – 4-18 months of age in early infancy.
• Traid – Hypsarrhythmia (random, high voltage, slow waves with multifocal
spikes)
- Developmental retardation
- infantile spasms
• Traid is called West syndrome.
• Seizure types –
1. Flexor 14% - flexion of neck, arms, legs ; B/L symmetrical seizures. Bows
head & flexes UL for greeting – SALAAM SEIZURES.
2. Extension 23% - extension of neck, arms, legs .
43. • Spasms-
• are seen in clusters .
• Persisting for minutes with brief intervals.
• Develops while drowsy/ immediate unon awakening , not during sleep.
• Etiology –
• HIE with PVL.
• Neurocutaneous – tuberous, neurofibromatosis.
• Infection – IUI – CMV or postnatal infection – meningoencephalitis.
• Head injury
• Brain malformations- lissencephaly
• IEM – PKU, nonketotic hyperglycinaemia.
44. • Rx –
• ACTH – 20U SC daily for 2 wks then inc. to 30U then inc. to 40 U if
seizures persists.
• Monitor BP, salt restriction only breast feed, potassium rich diet.
• Prednisolone – in patients not affording ACTH –
• 2mg/kg/day BD for 2 wks , if no improvement
continue another 2 wks.
• Antiepileptics – if steriod failure
• Valproate, lamotrigine, vigabatrin, clobazam,etc.
45.
46. D/D
Paroxysmal Nonepileptic
Event
Hx C/F Differentiating features
Benign neonatal sleep
myoclonus .
Most common entity
misdiag- nosed as seizure
in the neonate.
Neonate is term, healthy,
and thriving.
May be present from
birth to 3 months, after
spontaneously
disappears.
Multifocal jerks seen in
transition to and during
sleep.
Only present during sleep.
Upon wakening,. the
jerking ceases.
Jitteriness (tremors) May have expo- sure to
maternal substance abuse
or use of medica- tions,
meta- bolic disorder.
Hypoglycemia, perinatal
insult.
Stimulus sensitive, high
frequency, low amplitude.
and oscillatory (not
jerking movement)
Activated/exacerbated by
arousal.
Extinguishes or decreases
with flexion of the
extremity and gentle
restraint.
No associated abnormal
eye movements or
autonomic change.
Apnea of prematurity Neonate is preterm. Apnea & bradycardia. Apnea associated with
tachycardia suggests
seizure. Assess for other
associated features (i.e.,
automatisms, oculomotor
events, motor
movements, etc.).
47.
48. Why do seizures have different manifestations
in Neonatal age ?
• Poor cortical organisation.
• Poor myelination.
• Less efficient synapses.
• Predominance of excitatory neurotransmitter receptors ( e.g
Glutamate).
• Decreased GABA channels/receptors.
• Advanced development of limbic system.
49. Diagnosis
• Seizure hx – regarding type of seizure, its onset & asso. Movements.
• Antenatal hx –IUI, PROM, foul smelling liquor, maternal DM, narcotic
addiction & fetal distress.
• Perinatal hx- resuscitation in labour room i.e. fetal distress, Apgar
score, instrumental delivery & LA injection.
• Feeding hx – appearance, lethargy, poor activity, vomiting after
initiation of breast feed[IEM].
• Family hx – consanguinity, F/H of seizures or MR, early fetal or
neonatal deaths{IEM}.
• H/O seizures in either parent or siblings in neonatal period suggestive
of Benign familial neonatal convulsions.
50. •EXAMINATION
• Vitals - HR, RR, CRT, Temp, BP.
• General examination –
• Gestation.
• Birth wt.
• LBW & hepatosplenomegaly seen in IUI.
• Seizures in term well baby may be due to SAH.
• Seizures in large for date babies may be due to hypoglycemia.
• Apparently well child seen in Metabolic seizures.
51. • CNS examination - presence of bulging AF may be suggestive of
meningitis or ICH.
• Consciousness (alert /drowsy/comatose).
• Tone (hypo/hyper).
• Needle mark – suggestive of LA instillation.
• Fundus examination for chorioretinitis – suggestive of congenital
toxoplasmosis.
• Systemic examination - presence of hepatosplenomegaly or
abnormal urine odour may be suggestive of IEM.
• Skin should be examined for neurocutaneous markers.
52. • First-line investigations –
• Check CBC, haematocrit, blood glucose, calcium, phosphorus,
magnesium, sodium, venous pH and base excess.
• Hypocalcemia can be suspected by looking for prolonged QTc interval
(>0.2 sec) on EKG.
• CSF examination and blood culture should be taken in all cases to
exclude meningitis or other infections.
• Cranial ultrasound and EEG should be done once metabolic disorders
are excluded.
53. • Second-line investigations –
• When convulsions persist and first-line investigations are unable to
identify the cause, non-contrast CT scan and MRI of brain is advised
to exclude structural or developmental defects like cerebral
dysgenesis, lissencephaly and neuronal migration disorders.
• Appropriate tests including serology for TORCH-infections should be
undertaken to exclude intrauterine infections.
• Screening tests for exclusion of inborn error of metabolism include
ABG anion gap, blood ammonia, lactate/pyruvate level, plasma and
urinary amino acid profile (high performance liquid chromatography
or tandem mass spectrometry).
• If facilities exist, mother's urine and baby's meconium should be
screened for maternal drug abuse.
• Therapeutic trial with pyridoxine is usually reserved as a last resort.
54. EEG
• • Continuous electroencephalogram (cEEG): >3 hours of monitoring is gold
standard for the diagnosis of neonatal seizures. Including video analysis can
be very helpful to correctly characterize events & avoid misinterpretation
of artifacts.
• • Routine neonatal EEG recording, typically of 1 hour duration, allows
assessment of background activity, developmental maturity, and
sometimes, epileptic potential. A typical clinical event unlikely be captured
in such short time, thus where possible 24 hr continous monitoring is
preferred.
• • Amplitude-integrated electroencephalogram (aiEEG): a bedside
technique increasingly being used by neonatologists for neuromonitoring.
60. Management
• Airway patency [suction, positioning, O2].
• IV line set up [drugs, fluid-electrolytes, anticonvulsants & bld sampling].
• Nurse in thermoregulatory environment.
• Monitor perfusion & ventilation.
• If hypoglycaemia-
• Glucose 5-10 mL/kg of 10% solution as a bolus followed by 10% dextrose at
a rate of 8 mg/kg/minute.
• The blood glucose should be maintained between 70 and 120 mg/dl.
61. • If Hypocalcemia –
• Calcium gluconate 200 mg/kg of 10% solution (2 mL/kg) diluted with equal
volume of DW is injected slowly in 5-10 minutes under cardiac monitoring
for bradycardia.
• If hypomagnesemia-
• Magnesium sulphate 50-100 mg/ kg IV given.
• When seizures persist even after correction of hypo- calcemia, and
hypoglycemia, anticonvulsants should be given.
• Hyponatremia –
• Rapid IV bolus of 4-6 ml/kg of 3% saline.
• Anticonvulsant Therapy –
• Phenobarbital has been the gold standard for manage- ment of neonatal
seizures for over 90 years.
62. • Parenteral loading dose of Phenobarbitone 20mg/kg is administered slowly
intravenously over 20 minutes. If there is no response in 15 minutes, additional
doses of Phenobarbitone 10 mg/kg every 15 minutes are administered
intravenously till the seizures are controlled or a total dose of 40 mg/kg has been
given
• If convulsions are still uncontrolled despite maximal dose of Phenobarbitone,
Phenytoin is administered intravenously in a loading dose of 20 mg/kg.
• Fosphenytoin, a pro-drug of phenytoin, is preferred because of its solubility in
standard intravenous solutions, neutral pH, feasibility to administer at a faster
rate and lack of necrosis of subcutaneous tissues on extravasation & a safe IM. It
is given in a loading dose of 15-20 mg/kg IV over 20 min dil. In DW.
• The maintenance therapy in with phenobarbitone and phenytoin is started after
12 hours of loading dose and given in a dose of 5 mg/ kg/day in two divided
doses for 6-8 wks.
• And if , abnormal neurostatus or EEG persist , then continued maintenance for 6-
12 months .
63. • BENZODIAZEPINES -
• If convulsions are intractable and baby is in a status convulsions, give
lorazepam 50 µg/kg IV slowly over 2-5 min.
• Diazepam should be avoided as it has a short duration of action, carries the
risk of inducing apneic attacks and may predispose the baby to develop
kernicterus by displacement of bilirubin from the binding sites in the protein
because it contains sodium benzoate as a preservative.
• Alternatively, clonazepam, 100-200 µg/kg can be given IV over 30 sec.
• Midazolam 0.05–0.15 mg/kg/dose is effective when given through
intramuscular route because it is highly soluble in water or continuous IV
infusion at 0.2-1.0 microgram/kg/min may repeat 0.05mg/kg in 2-3 min
interval upto max dose of 0.2 mg/kg.
• S/E – Sedation, thus not used for longer duration.
64. • Paraldehyde can also be given in a dose of 200-400 mg/kg deep IM as
5% solution in 5% dextrose or diluted with double volume of olive oil
or coconut oil and given per rectum.
• Belongs to aldehydes group, works by damping down nervous system,
has sedative effect.
• Lidocaine 2 mg/kg IV bolus over 10 minutes followed by 6 mg/kg/hr
for 6 hrs as a constant infusion has been used with success to abort
intractable seizures. However, it should never be co-administered
with phenytoin due to potential risk of myocardial damage and
arrhythmia.
65. • Levetiracetam is given in a loading dose of 50 mg/kg IV followed by
maintenance dose of 5 mg/kg every 8-12 hours..
• Sodium valproate 20 mg/kg oral or IV as a loading dose followed by
10 mg/kg every 12 hr has been used in newborn babies. It is
associated with a serious risk of hepatotoxicity.
• Vigabatrin a dose of 50 mg/kg/day has been used in neonates with
refractory infantile spasms & also in Tuberous sclerosis.
• Inborn errors of metabolism: Prompt cessation of milk feeding, while
trying to identify the underlying metabolic defect, may be life saving.
71. • Pyridoxine-dependent Seizures
• Give pyridoxine 100 mg IV under EEG control and close clinical
observation.
• Repeat 100 mg IV every 10 min till seizures are controlled or a cumu- lative
dose of 500 mg is given.
• In the absence of suitable intravenous formulation of pyridoxine in India, it
is given intramuscularly (1.0 mL neurobion provides 50 mg pyridoxine) and
1.0 mL each may be administered intramuscularly in the anterolateral
aspect of each thigh.
• The maintenance dose of pyridoxine is 5 mg/kg (or 50 mg/d) single oral
dose daily.
• If Pyridoxine is stopped, seizures would reappear within 3 weeks.
• There is no need to administer any other anticonvulsant agent in infants
with pyridoxine- dependent seizures.
72. • Exchange blood transfusion is indicated in the following situations:
• Life-threatening metabolic disorder.
• Accidental injection of local anesthetic to the fetus.
• Acute bilirubin encephalopathy
• Diuretic therapy and gastric lavage are effective to enhance excretion
of inadvertently injected local anesthetic into infant's scalp during
pudendal block.
• Infections - Appropriate and early antibiotic therapy for bacterial
meningitis.
73. • PROGNOSIS –
• Focal clonic seizures carry the best prognosis.
• Myoclonic seizures carry the worst prognosis in terms of
neurodevelopmental outcome and seizure recurrence.
• Seizures related to hypoglycemia, cerebral malformations and
meningitis have adverse outcome.
• Uncomplicated hypocalcemia, narcotic withdrawal & subarachnoid
haemorrhage carry good prognosis.
• Long term sequelae in infants including CP & intellectual disabilities,
still occur at high rate of 30%~35% with postneonatal seizures
occurring in 20%.
• Metabolic seizures also carry best prognosis.
74. • With the outcome-
• Long term Neurodeficit risk is seen in :
• Onset of seizures on DOL 1.
• Persistent seizures for >48 hrs despite anticonvulsants.
• And Myoclonic seizures.
• The overall risk of epilepsy & brain damage among survivors is 30-
40%
