Within first 24 hours of life
—Hypoxic ischemic encephalopathy
—Meningitis/sepsis
—Subdural/Subarachnoid/Interventricular hemorrhage
—Intrauterine infection
—Trauma
—Pyridoxine dependency
—Drug effect/withdrawal

24-72 hours
—Meningitis/sepsis
—In premature infants: IVH
—In full-term infants: infarction, venous thrombosis
—Cerebral dysgenesis

72 hours to 1 week
—Above causes
—Inborn errors of metabolism
—Hypocalcemia
—Familial neonatal seizures

1 week to 4 weeks
—Above causes
—HSV

—Subtle seizure
—Clonic seizure
—Tonic seizure
—myoclonic

—Subtle seizure: are the most common, half of all seizure in term and preterm newborns.
Ocular phenomena: tonic eye deviation, roving nystagmus.
Oro-bucco-lingual movements: chewing, sucking, lip snacking, drooling, pedaling, boxing, cycling, swimming.
Autonomic phenomena: sudden changes in skin color, capillary size, tachycardia, bradycardia and apnea

—Clonic seizure: are stereotypic and repetitive biphasic movements with a fast contraction phase and a slower relaxation phase.
—Clonic seizures may be unifocal, multifocal or generalized.
—Unifocal seizures are not usually associated with loss of conciousness.
—Unifocal seizures: neonatal sroke, SAH or metabolic
—Multifocal : Jacksonial March
—Primarily generalized clonic seizurs are rare in newborn. Benign familial neonatal seizure.
—Tonic seizures: have a sustained period ( seconds) of muscle contraction without repetitive features. It may be focal or generalized.
—Generalized tonic seizures: in premature infants with neurologic dysfunction or major IVH. The prognosis is poor.
—Myoclonic seizures: lightning fast contraction and non rhythmic character. These seizures may occur in multifocal or generalized pattern.
—It may be elicited by tactile or auditory stimulation.
—Diffuse and serious brain dysfunction.
—Poor long term outcome.

—Seizure mimics: non- nutritive sucking, jitteriness ( abnormal but non epileptic behaviours) and true epileptic manifestation.
—Guidelines to differentiate true epileptic seizure from seizure mimic:
—First, true epileptic seizures are rarely stimulus – sensitive.
—Second, epileptic seizure cannot be abolished by passive restraint or repositioning of the infant.
—Third, epileptic seizures are associated with autonomic changes or ocular phenomena.

—EEG diagnosis of neonatal seizure:
—EEG should be recorded as soon as seizure is first suspected no later than 24 hrs.

—Etiological diagnosis:
—Hypoxic-ischemic encephalopathy
—Focal ischemic injury: neonatal arterial stroke, cerebral vein thrombosis, intracranial hemorrhage, CNS infection, metabolic disturbances.

—Pyridoxine dependency
—Nonketotic hyperglycemia
—Urea cycle defects
—Sulfite oxidase deficiency
—Glutaric aciduria type II
—Maple syrup urine disease
—Menkes disease
—Molybdenum cofactor deficiency
—Propionic aciduria
—Mitochondrial disease
—Glucose transporter deficiency.

—Phenobarbital: 20 mg/kg loading dose over 10-15 minutes. If seizures persist, bolus doses of 5 mg/kg should be given, up to a total dose 40 mg/kg or control of seizures.
—Phenytoin: second line agent 20 mg/kg in normal saline. If seizure persist 5 mg/kg may be used.
—Fosphenytoin : prodrug form that is rapidly converted into phenytoin. Safe faster rate of infusion, safe IM dosing and no tissue injury.
—The combination of phenobarbital and phenytoin will control seizure in up to 85% of infants. For neonatal seizures that remain refractory benzodiazepines may be added like lorazepam, diazepam and midazolam

—Pyridoxine:
—Rapid cessation of EEG seizures to an IV dose of 50-100 mg pyridoxine. Increases the synthesis of GABA.
—Lidocaine.