Date:
Mar 01, 1998
Severe and prolonged loss of oxygen (severe hypoxia) to the infant during delivery can cause or contribute to brain damage and to physical and cognitive difficulties.
When there is a modest loss of oxygen (mild hypoxia) for an extended period, the consequences are less understood. If the infant with a mild degree of oxygen deprivation demonstrates no evidence of brain damage at birth and/or during the first year of life, does that mean the child will not show evidence of brain damage as it grows older (e.g.: when he/she enters school)?
A pediatric research group in Canada has studied this question in full term infants (they used full term infants to avoid the complicating issue of prematurity).1 They compared the motor skills, cognitive developed memory and child behavior of two groups of children at age 4, and then again at 6-8 years of age. One group had experienced mild oxygen deprivation during delivery but no immediate evidence of brain damage; the other group had no bio-chemical or clinical evidence of hypoxia. The two groups were otherwise similar (“matched”).
When examined at 6-8 years of age, there were no differences in performance between the two groups. Mild hypoxia did not result in performance deficits or signs of developmental brain damage in full term infants when compared to the group which did not experience mild hypoxia.
Comment:
It has been suggested that while mild oxygen deprivation during delivery does not usually result in immediate loss of brain function, there might be a modest loss of function as the child matures. This study indicates that this is probably not true. Brain injured children can certainly demonstrate difficulties in motor performance or in cognitive abilities for the first time at school age even though there was no overt evidence of such during infancy or early childhood; however, these difficulties are probably not due primarily to mild hypoxia during the birthing process. The causes for delayed evidence of difficulties probably occurred during infancy or childhood, sometimes because of a pre-existing sensitivity to brain injury due to intrauterine factors.
1 Handley-Derry, M., et al. Intrapartum Fetal Asphyxia and the Occurrence of Minor Deficits in 4 and 8 Year Old Children. Developmental Medicine and Child Neurology (1997); 39: 508-511.
© UCP Research & Educational Foundation, March 1998
Most treatments for cerebral palsy (CP) are initially directed toward children. What is not clearly established is the long- term effects of such treatments. Many appear helpful in the short term but prove to be disadvantageous in the long run. Selective dorsal rhizotomy (SDR) is a permanent, irreversible neurosurgical procedure for reducing spasticity in cerebral palsy. Parents contemplating SDR for their child would like assurance that that there will not be harmful complications from it as the child ages into adolescence and adulthood. We now have new evidence...
As I’ve discovered in the link above, Hyperbaric Oxygen Therapy hopefully can improve state of the described disorders by altering conditions of hypoxia. Hypoxic and ischemic and poorly perfused tissues and body sites with compromised blood flow are immediately and positively affected by hyperoxygenation. Hyperoxygenation is the state achieved inside Hyperbaric Chamber only when Oxygen concentrations in blood plasma elevated from 10 to 25 times its normal levels.
Comparing to normobaric conditions this equals to approximately 6 times deeper oxygen diffusion/penetration distance from the functioning blood vessels and capillaries while levels of arterial oxygen are elevating up to 1,500 mmHg!
Although this over-delivery of oxygen maintained only while the patient is inside Hyperbaric Chamber, its beneficial role is of a significance: it allows triggering a primary and secondary effects of hyperbaric treatment. Check the above link…
I know this of the subject of delivery… but what about those children who contracted pertussis as an infant and experienced oxygen deprivation over an extended period of time? Such as an infant of 6 weeks old experiencing mild O2 deprivation for periods of two to three minutes, up to 15 times a day, over a period of 30 to 35 days. What are the possibilities of cognitive functions being affected? Which areas would be most affected? Are there any outward signs of developmental brain damage or does this wait in hiding until the child matures into his teens?