Neonatal Neurology
What to know
Hypoxic-ischemic encephalopathy is staged by Sarnat criteria (I mild, II moderate, III severe) using tone, reflexes, level of consciousness, and seizures. Supportive evidence: cord pH below 7.0, base deficit ≥12–16 mEq/L, Apgar ≤5 at 5 minutes, and need for resuscitation. Therapeutic hypothermia is offered for infants ≥36 weeks and ≥1800–2000 g with moderate-to-severe encephalopathy, begun within 6 hours and continued 72 hours; it is not indicated for mild encephalopathy. MRI at days 3–5 shows basal ganglia/thalamic injury after acute profound asphyxia and watershed injury after prolonged partial asphyxia.
Neonatal seizures are usually subtle - apnea, eye deviation, cycling, autonomic change - and frequently electrographic without clinical correlate, so EEG is required. HIE is the most common cause; others include hypoglycemia, hypocalcemia, meningitis, and inherited epilepsies. Phenobarbital 20 mg/kg is first line, with levetiracetam or fosphenytoin next; refractory seizures should prompt a pyridoxine trial and consideration of KCNQ2 or SCN1A testing.
Preterm brain injury: germinal matrix intraventricular hemorrhage (Papile grades I–IV, grade IV being periventricular hemorrhagic infarction) and periventricular leukomalacia, which produces spastic diplegia. Neonatal hypotonia requires separating central (normal reflexes, other CNS signs) from peripheral (areflexia, weakness, preserved cognition) causes; check CK and consider SMA, congenital myopathy, and myotonic dystrophy.
Brachial plexus injury: Erb (C5–C6) gives a "waiter's tip" posture; Klumpke (C8–T1) includes Horner syndrome.
Traps
Cooling eligibility windows are strict, and mild HIE is excluded. A neonate with apnea has a seizure until EEG says otherwise.
Rule of thumb
In a floppy newborn, preserved facial expression and cognition with absent reflexes point to anterior horn cell or neuromuscular disease, not a central cause.