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Penn Researchers Explain The Mechanics Behind The Delayed Effects Of Brain Trauma; Findings May Chart Paths To Therapeutic Relief

Date:
April 4, 2001
Source:
University Of Pennsylvania Medical Center
Summary:
The initial twist and snap of physical injury to nerve cells and fibers in the brain during head trauma is only the beginning of the damage. Researchers at the University of Pennsylvania Medical Center have determined that one of the initial events triggering these long-term problems includes a massive flood of calcium ions, electrically charged calcium atoms, that enter axons following brain trauma.
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(Philadelphia, PA) – The initial twist and snap of physical injury to nerve cells and fibers in the brain during head trauma is only the beginning of the damage. In particular, the stretching of nerve fibers, or "axons", can induce progressive damage leading to long-term problems such as memory dysfunction and difficulties with concentration.

Researchers at the University of Pennsylvania Medical Center have determined that one of the initial events triggering these long-term problems includes a massive flood of calcium ions, electrically charged calcium atoms, that enter axons following brain trauma. In addition, their study suggests a possible course of treatment for this pathologic process. The results of the study are published in The Journal of Neuroscience’s March issue.

Previously, researchers had only postulated that calcium entry into damaged axons was an important indicator for the start of progressive damage. Now this has not only been demonstrated, but a mechanism of this calcium entry has been discovered. "It appears that that the physical motions of trauma literally tears open proteins that act as gates on the axon membrane," explains Douglas Smith, MD, an associate professor in the Penn Department of Neurosurgery.

Surprisingly, the gates that were forced open were not for calcium ions, but for sodium ions. "We have now found that it is the rapid flow of sodium ions through the damaged gates that triggers a subsequent inflow of calcium ions," said Smith. "With this knowledge, we can evaluate therapies that block the sodium channels."

Early therapy targeting sodium channels may be critical to preventing the progressive damage to axons, which has been previously found by this research team. "It can be hours, even months, after a head injury before the damage to the axons becomes so severe that the neurons can no longer function," says Smith. "There is currently no cure to stop the delayed effect of head trauma, but we are convinced that the damage can be slowed down and, eventually, even stopped."


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The above story is based on materials provided by University Of Pennsylvania Medical Center. Note: Materials may be edited for content and length.


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University Of Pennsylvania Medical Center. "Penn Researchers Explain The Mechanics Behind The Delayed Effects Of Brain Trauma; Findings May Chart Paths To Therapeutic Relief." ScienceDaily. ScienceDaily, 4 April 2001. <www.sciencedaily.com/releases/2001/04/010402072253.htm>.
University Of Pennsylvania Medical Center. (2001, April 4). Penn Researchers Explain The Mechanics Behind The Delayed Effects Of Brain Trauma; Findings May Chart Paths To Therapeutic Relief. ScienceDaily. Retrieved May 25, 2015 from www.sciencedaily.com/releases/2001/04/010402072253.htm
University Of Pennsylvania Medical Center. "Penn Researchers Explain The Mechanics Behind The Delayed Effects Of Brain Trauma; Findings May Chart Paths To Therapeutic Relief." ScienceDaily. www.sciencedaily.com/releases/2001/04/010402072253.htm (accessed May 25, 2015).

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