Neurology

Neonatal Seizures

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Etiologies of Neonatal Seizures

Underlying Defect

Points to Remember

Hypoxic–ischemic encephalopathy

  • Leading cause of neonatal seizures in full-term infants.
  • This diagnosis should never be one of exclusion.
  • Data supporting this diagnosis (history of prolonged labor, perinatal depression, prolonged resuscitation) should be obtained and documented.

Focal ischemia/infarction

  • Second most common cause of neonatal seizures in full-term infants.
  • Most common presentation is right-sided clonic seizures due to infarction in the left middle cerebral artery territory.
  • Cerebral vein thromboses can lead to venous infarcts.

Intracranial hemorrhage

  • In term infants, subarachnoid hemorrhage is more associated with subsequent seizure than subdural hemorrhage.
  • Infratentorial subdural hemorrhages require urgent evaluation due to risk of brainstem compression.
  • In preterm infants, intraventricular hemorrhage is the most common type of ICH (see below).

Infections of the CNS

  • Can occur in utero (CMV, toxoplasmosis) or perinatally (herpes simplex, bacterial meningitis with GBS or Escherichia coli being most common).
  • Prognosis can be very grim.

Metabolic derangement

  • Transient causes (hypoglycemia, hypocalcemia, hyponatremia); see Chapter 34 for further information.
  • Inborn errors of metabolism (pyridoxine dependency, nonketotic hyperglycinemia, urea cycle defects, glutaric aciduria (type II), maple syrup urine disease, organic acidurias, cofactor deficiencies, mitochondrial defects , Zellweger Syndrome).

Structural defects

  • Defects of neuronal migration (heterotopias).
  • Defects of neuronal organization (polymicrogyria).
  • Cerebral malformation (holoprosencephaly).
  • Usually will display associated dysmorphic features on physical examination.

Common Causes of Neonatal Seizures by Age at Presentation

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Day of Life

Possible Causes

1

Hypoxic ischemic encephalopathy

Infection

Hypocalcemia

Maternal drug use

Hypoglycemia

2–3

All of the above

Inborn errors of metabolism

Drug withdrawal

CNS malformation

Hypernatremia

Hyponatremia

Classification of Neonatal Seizures

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Seizure Type

Clinical Manifestation

Subtle

Oral–buccal–lingual or ocular movements

Autonomic dysfunction (Δ in HR, BP, Spo2)

Stereotypical stepping/swimming

Clonic

Rhythmic, slow jerking

Facial, extremity, or axial involvement

Focal or generalized

Tonic

Sustained limb posturing

Asymmetric position of trunk/neck

Focal or generalized

Myoclonic

Rapid isolated jerks

Limb/trunk involvement

Generalized, multifocal, or focal

Neonatal Seizure Mimics

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Seizure Mimic

Clinical Manifestation

Jitteriness

Spontaneous or provoked by stimulus

Flexion/extension are equivalent

Diminished by repositioning

Abolished with containment

Benign neonatal sleep myoclonus

Bilateral or unilateral

Synchronous or asynchronous

Occurs during sleep

Not due to a stimulus

Stimulus-evoked myoclonus

Focal or generalized

Severe CNS dysfunction

EEG may show cortical spike-wave discharge

Hyperekplexia (stiff-man syndrome)

Generalized stiffness

Autosomal dominant and recessive forms

Excessive startle responses to unexpected stimuli

Excessive stiffness following startle response

Benzodiazepines reduce symptoms

Management

  • Support respiratory and cardiovascular function (may require endotracheal intubation and mechanical ventilation).
  • Place on continuous cardiorespiratory monitoring.
  • Correct any known causes of seizures (see above).
  • If seizures continue after correction of transient metabolic derangements, load with phenobarbital (20 mg/kg IV); can be followed by repeat doses of 5–10 mg/kg IV to a total dose of 40 mg/kg IV, if needed.
  • If seizures continue, load with a benzodiazepine such as midazolam (0.1 mg/kg IV; repeat doses can be given to a total dose of 0.3 mg/kg IV).
  • If seizures continue, load with fosphenytoin 20 mg/kg.
  • If seizures continue, can consider loading with pyridoxine (100 mg/kg IV), preferably with EEG monitoring. Maintenance dosing can be 50-100 mg/dose once daily (orally)
  • Newer agents that are used in older children, adolescents, and adults may sometimes be given (in consultation with the neurology service), but no data exist on the safety and efficacy of these medications in neonates.

Intraventricular Hemorrhage

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  • Definition: an intracranial hemorrhage that originates in the paraventricular subependymal germinal matrix and may extend into the lateral ventricular system.
    • 50% of IVH occurs in the first 24 h after birth, and 90% by 7-10 days of life..
    • Incidence and severity are inversely proportional to gestational age.
    • Antenatal steroid administration is associated with a lower incidence.
    • Major risk factors:
      • Extreme prematurity
      • Need for assisted ventilation
      • Pneumothorax
    • Clinical presentation can be very diverse:
      • May be asymptomatic
      • May have nonspecific symptoms (bulging fontanelle, sudden drop in hematocrit, apnea/bradycardia, metabolic acidosis, seizures, change in level of consciousness)
      • May present with a catastrophic constellation of symptoms (profound hypotension, severe neurogenic pulmonary edema, rapid deterioration in neurologic exam, decerebrate posturing)
    • All infants with birth weight <1500 g and any infant who the attending physician feels is at risk for IVH should receive a screening head US between 7 and 10 DOL.
      • If abnormalities are noted on the initial screening US, follow-up is recommended at weekly intervals to monitor for the development of posthemorrhagic hydrocephalus.
      • If no abnormalities are noted on the initial screening US, follow-up cranial imaging can be done at 36–40 wk postmenstrual age to evaluate for evidence of periventricular leukomalacia.

Papile’s Grading of Ivh

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Grade I

Germinal matrix hemorrhage

Grade II

Germinal matrix hemorrhage with intraventricular hemorrhage but without ventricular dilation

Grade III

Germinal matrix hemorrhage with intraventricular hemorrhage and dilation

Grade IV

Germinal matrix hemorrhage with parenchymal involvement

  • Prognosis:
    • Mortality in severe IVH (grades III/IV) is approximately 20%–50%.
    • Incidence of posthemorrhagic hydrocephalus in severe IVH (grades III/IV) is approximately 55%–80%.
    • Long-term major neurologic sequelae are related to the extent of parenchymal injury:
      • 15%–20% of infants with minor degrees of hemorrhage will have a major neurodevelopmental impairment (slightly higher than those without IVH).
      • 50%–80% of infants with severe hemorrhage will have major developmental impairment.

Neonatal Encephalopathy

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  • A diagnosis of neonatal encephalopathy can be considered when an infant has both a change in mental status and an abnormal neurologic examination.
  • The Sarnat classification is most frequently used to describe the severity of encephalopathy and is most appropriate for infants with HIE.

Sarnat Stages of HIE

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Stage 1 (Mild)

Stage 2 (Moderate)

Stage 3 (Severe)

Level of consciousness

Hyperalert

Lethargic

Stuporous, comatose

Tone

Normal

Hypotonic

Flaccid

Posture

Normal

Flexed

Decerebrate

Reflexes

Hyperactive

Hypoactive

Absent

Pupils

Mydriasis

Miosis

Unequal, poor light reflex, midline

Oculovestibular

Normal

Overactive

Weak or absent

Seizures

None

Common

Decerebrate

EEG

Normal

Low voltage with seizures

Burst suppression to isoelectric

Duration of symptoms

<24 h

2–14 d

Hours to weeks

Outcome

Nearly 100% normal

80% normal

∼50% die; survivors have severe sequelae

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Jan 9, 2019 | Posted by in PEDIATRICS | Comments Off on Neurology

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