The birth injury attorneys of Passen & Powell have often written on the various brain injuries and permanent conditions associated with fetal oxygen deprivation. Whether due to a condition during pregnancy, birth trauma, medical malpractice, or some combination of these factors, the consequences of fetal brain damage are devastating to the infant and her parents. Injuries from fetal oxygen deprivation include:
- epilepsy;
- cerebral palsy;
- mental retardation;
- autism; and
- schizophrenia.
Now, new research offers some hope for the successful treatment of these injuries in the future. Researchers from The Scripps Research Institute studying fetal oxygen deprivation in experiments on mice have found that brain injury from such deprivation is tied to the action of lysophosphatidic acid , or LPA, a particular fatty molecule which functions as a receptor transferring information into developing brain cells.
These researchers believe that their findings point to LPA as a key factor in injury developing when a fetus is deprived of oxygen. While the research is not far enough yet to even confirm the role of LPA, let alone design an effective treatment, this finding is promising indeed.
LPA normally acts as a signal to assist in the development of the human brain – both in utero and after birth. The chemical signals from LPA inflence neurogenesis, the process by which new neurons are formed in the fetal brain and the architecture of the brain is constructed.
As LPA signals the formation of new neurons, new areas of the brain form rapidly. Some of these areas are essential for survival outside the womb – for instance, the portions of the brain controlling breathing, drinking, digestion, and other basic functions. Others continue to develop after the infant enters the outside world.
To the layperson, it seems self-evident that oxygen deprivation leads to brain damage. But research leader and Scripps Research Professor Jerold Chun, MD, PhD said that his team’s research indicated that it is not the lack of oxygen itself which triggers damage in the very young, but the chemical changes which occur in the brain are actually intimately tied to the brain’s reactions to LPA.
When an fetus suffers hypoxia (oxygen deprivation), neurons in the brain become overstimulated, as they would if exposed to excessive levels of LPA. When the researchers either genetically removed LPA receptors in the subject mice, or blocked these receptors using medication, the fetal mice could suffer hypoxia without suffering brain damage.
If further research confirms and expands on this recent discovery, it is possible that infants who suffer oxygen deprivation could be successfully treated with drugs to prevent LPA from triggering the changes in the brain which turn deprivation into permanent injury and disability. This is particularly exciting as there is currently no known treatment for the brain injury caused by fetal oxygen deprivation.
While it is too soon to know whether the results achieved in mice can be replicated in humans, the brain injury lawyers of Passen & Powell are encouraged by this promising line of research. We hope that, in time, the suffering of the many infants who suffer from fetal oxygen deprivation, and that of their parents, can be mitigated or eliminated.
The research appeared in an advance, online issue of the journal Proceedings of the National Academy of Sciences (PNAS).
For a free consultation with an experienced Chicago birth injury lawyer at Passen & Powell, call us at (312) 527-4500.
