Ischemic brainstem damage
			Ranck and Windle (1959) described brain damage in monkeys subjected to suffocation at birth -- the infant head was delivered into a saline sac and the umbilical cord cut.  They reported a pattern of ischemic damage of brainstem nuclei that resembled the lesions usually observed in kernicterus.  Damage of the motor areas of the cortex had been expected, but was not found.  Asphyxia at birth had been intended to provide an animal model for cerebral palsy.
		Kernicterus is a form of cerebral palsy, most often associated with bilirubin staining of the basal ganglia.  Because only the brainstem was affected, asphyxia of this kind at birth was considered a possible cause of "minimal cerebral dysfunction" (MCD).  But, examination of the brains of monkeys allowed to survive for several months or years showed that development of the brain had not followed the normal course (Faro & Windle 1969).
			An infant that does not breathe right away at birth, but is nevertheless per protocol subjected to immediate clamping of the umbilical cord, is likely to suffer some degree of suffocation and impairment of the same brainstem centers affected in monkeys subjected to neonatal asphyxia.
				Auditory nuclei in the midbrain were most prominently and severely affected in monkeys subjected to asphyxia at birth.  Monkeys are not expected to learn to speak, but human children learn to speak "by ear" before maturation of the language areas of the cortex is complete.  Maturation of the cortical language areas is dependent upon trophic transmitters produced in brainstem auditory nuclei.  Impairment of brainstem auditory nuclei cannot be considered "minimal."