3 – Complacency, the persisting interpretation
		Complacency seems to have been the end result of the experiments on asphyxia at birth.  The idea is still prevalent that a brief lapse in respiration is better tolerated by newborn infants than adults.  The adult victim of drowning, choking or cardiac arrest must be resuscitated within four to eight minutes at most, to avoid permanent neurological handicap [1].  Visible damage within the brains of newborn monkeys subjected to asphyxia was found only if resuscitation was delayed past six minutes; and then the damage was restricted to what Myers (1972) referred to as "a monotonous rank-order of brainstem nuclei" which he claimed was never observed in human cases [2].  Myers was wrong! Kernicterus, yellow jaundice of brainstem nuclei Ranck and Windle (1959) though puzzled that brainstem rather than cortical damage was the result of their experiments on asphyxia at birth commented, "The human neuropathologic entity most closely resembling the effects of asphyxia neonatorum in the monkey is kernicterus" [3, 4].  Kernicterus is classified as one form of cerebral palsy, and is generally thought to be the result of toxic effects of high bilirubin levels on the brain. An important thing to keep in mind when considering the supposed toxicity of bilirubin however is that bilirubin primarily affects a variable "rank order" of brainstem nuclei, not the cerebral cortex.  Bilirubin staining is not uniform throughout the brain, but only affects those areas where the blood-brain barrier has been compromised by anoxia or infection [5, 6]. Wernicke's encephalopathy Neubuerger (1954) reported a brainstem pattern of damage in a patient who survived for two weeks after being resuscitated from cardiac arrest suffered during surgery [7].  Damage of the inferior colliculi (in the midbrain auditory pathway) was a prominent part of the observed pathology, and Neubuerger noted the similarity of this brainstem pattern of damage to that of Wernicke's encephalopathy, a pattern of neuropathology most often associated with chronic alcohol intoxication [8]. Windle and Myers should perhaps have recognized the brainstem pattern of damage found in asphyxiated monkeys as a variant of Wernicke's encephalopathy.  However, Wernicke (1881) reported hemorrhagic involvement of brainstem nuclei following ingestion of sulfuric acid in one case and in two cases of chronic alcohol intoxication [9-11].  The ischemic brainstem damage observed by Windle and Myers in monkeys asphyxiated at birth was not hemorrhagic. The damage resulting from asphyxia at birth may have been caused in large part by clamping the umbilical cord, and thus preventing the transfer of respiratory blood from the placenta to the lungs and other organs of the asphyxiated monkeys.  Toxic damage on the other hand is usually associated with vasodilation and increased blood flow as a response to poisoning of metabolic enzymes; this has been shown in research like that of Grünwald et al (1993) on the metabolic effects of alcohol in the brain [12]. Reports of brainstem damage in human infants Gilles (1963) reported a case of bilateral brainstem lesions in a child that resembled the pattern of damage found by Ranck and Windle (1959) in monkeys subjected to asphyxia at birth.  Gilles went further and suggested the damage in the auditory pathway might be responsible for developmental language delay [13]. Several other reports of brainstem damage in infants were published during the 1970s and 1980s [14-22].  Natsume et al. (1995) reported brainstem damage of "type Myers" found in a newborn infant [22]. Developmental delay in childhood often precedes difficulties in school and employment problems in adulthood.  Long-term scientific studies are lacking, but medical records of patients in mental hospitals and prisons indicate, time and again, that problems existed from early childhood.  The developmentally delayed child will most often require life-long dependency on others.   Euphemisms like mild, minor, or minimal are not acceptable, especially when it's your own child designated at the lower end of "normal limits."
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