Newborns who experience tissue injury and pain during critical periods of development may undergo a permanent rewiring of their nervous system that increases their sensitivity to pain later in life.
Working with an animal model, scientists at the National Institute of Dental and Craniofacial Research (NIDCR) have provided the first physical evidence that pain and inflammation in newborns alters the development of pain pathway circuitry, causing a stronger response to pain in adulthood. The study, which appears in the July 28 issue of Science, calls attention to the need to assess the long-term effects of pain and tissue injury on human newborns.
"Although we have yet to directly link animal research findings to what happens in human infants, one is tempted to speculate that similar changes as those identified in the animals may occur in newborn humans exposed to pain and inflammation," said Dr. M. A. Ruda, principal investigator on the study and chief of NIDCR's Cellular Neuroscience Section.
Each year, more than 400,000 babies in the U.S. are born either prematurely or at a low birth weight. Of these, 25,000 are considered to be extremely premature--born at 27 weeks of gestation or less. While 10 or 15 years ago most of these micropreemies did not live, it is no longer unusual for them to survive, thanks to advances in medical technology. Yet these tiny babies face a host of problems. Not only are they confronted with the trauma of living in the outside world too soon, but available medical procedures used to keep them alive and monitor their progress may cause pain and tissue injury. Heel sticks to draw blood, the insertion of IV lines and nasogastric tubes, and the use of ventilators are some of the modern technologies and procedures that are both miraculous and difficult.
"A premature infant can be thought of as still in the fetal time of their life when the basic elements of brain development are occ
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Contact: Jody Dove
jody.dove@nih.gov
301-594-7558
NIH/National Institute of Dental and Craniofacial Research
26-Jul-2000