Cerebral palsy -- the result of prolonged hypoxia
		Ranck and Windle (1959) had set out to produce and animal model of cerebral palsy, i.e. damage of the motor system of the cerebral cortex.   Instead they found that a few minutes of suffocation at birth results in visible damage only of brainstem structures., which they did liken to the lesions of kernicterus -- a recognized variant of cerebral palsy, affecting subcortical motor systems  The monkeys suffered transient delay in motor development, but appeared to recover.
			Myers (1972) obtained the cortical damage associated with cerebral palsy by inflicting prolonged hypoxia on the fetus late in gestation.  Myers stated that the brainstem pattern of damage that resulted from acute asphyxia at birth had nothing to do with any human condition.  This is wrong; many reports of brainstem damage following neonatal death have since been found; see the papers below by:
					Gilles 1963, 1969 Norman 1972 Griffiths & Laurence 1974 Grunnet et al. 1974 Schneider et al. 1975 Leech & Alvord 1977 Roland et al. 1988 Natsume et al. 1995
				And, maturation of the language areas of the cerebral cortex depends upon trophic transmitters produced in brainstem auditory nuclei.

Gilles in 1963 suggested that the lesions of brainstem auditory nuclei
reported by Ranck and Windle (1959) might be associated with
developmental language disorders.  It is almost incomprehensible why this
has not gained prominence -- learning to speak, the most important
developmental task of all human children.  And, maturation of the language
areas of the cerebral cortex m