The clinical appearances of a severely hypotonic neonate with cranial nerve involvement and a comatose neonate are very similar. The only neonatal disease that produces this degree of hypotonia is botulism. Botulism is characterized by a history of constipation preceding the absence of limb movements and a history of normal mental status as weakness develops. Peripheral nerve stimulation in neonates with botulism does not produce muscle twitching due to myoneural junction block. Patients with botulism usually have normal EEGs unless there is superimposed hypoxia due to respiratory failure or hyponatremia due to inappropriate secretion of antidiuretic hormone. Neonates with botulism and hypoxia or hyponatremia may present with EEG background abnormalities and electroencephalographic seizures.

There are many causes of coma. Most causes of coma are readily identified from the initial clinical evaluation and laboratory findings while others require a high index of suspicion and special laboratory investigations.

Coma due to asphyxia is associated with profound metabolic or mixed acidemia (pH < 7.00) at the time of the event or shortly after. Evidence of multi-organ system failure is often present. Lactic acid is elevated but ketosis is not present. The absence of ketosis distinguishes lactic acidosis due to asphyxia from lactic acidosis due to an inborn error of metabolism. The mechanisms of asphyxia during labor, delivery, and immediate postpartum are: (1) an interruption of the umbilical circulation; (2) altered placental gas exchange; (3) inadequate perfusion of the maternal side of the placenta, (4) impaired maternal oxygenation; or (5) failure of the neonate to accomplish lung inflation.