Traumatic brain injuries (TBIs) contribute to 50,000 deaths annually and many cases of permanent disability in the United States. Each year, approximately 1.7 million people in the U.S. sustain a TBI, according to the Centers for Disease Control and Prevention. TBI is a contributing factor to approximately one-third of all injury-related deaths in this country.

TBI often results when an object hits a person’s head violently, when an object pierces the brain, or when a bomb explodes nearby. Athletes, soldiers and car accident victims are at high risk for TBI. Since mild head injuries may not produce obvious disruption of normal brain function, symptoms of TBI range from mild (headache, dizziness, or blurred vision) to severe (convulsions, seizures, or death). What’s more, TBI patients surviving an initial trauma are frequently left with debilitating neurological impairment.

A group of mechanical engineers at the University of Utah is studying the biomechanics of traumatic brain injuries. Although damage to neurons and neuronal connections are the essence of TBI, a patient commonly also sustains injury to blood vessels of the brain. The U researchers focus specifically on this trauma to the blood vessels.

“Nearly all significant traumatic brain injuries include some element of injury to the blood vessels,” says Ken Monson, assistant professor of mechanical engineering at the University of Utah. “However, mechanisms and thresholds for vascular damage are not well understood.”

Monson and his associates are studying both mechanical loading on blood vessels and also the response of blood vessels to these forces.  In a healthy human brain, the complex structure of blood vessels provides a tightly regulated supply of blood to meet the brain’s metabolic demands and to remove waste products from brain cells. The blood–brain barrier formed by the vessels also keeps whole blood isolated from brain tissue.

When a TBI occurs, the brain’s blood vessels respond in several ways, says Monson. The blood vessels may tear and release blood inside the skull—a structure that cannot easily expand—thereby creating pressure on the brain. Damaged vessels may also release proteins toxic to brain tissue through the dysfunctional blood-brain barrier. Either way, excess pressure may cause brain damage or death, and leaking proteins may kill neurons.

“Cerebral blood vessels sometimes stop functioning properly after a head injury,” says Monson. “It’s not clear whether loss of cerebral blood flow control occurs because vessels become unresponsive due to mechanical deformation, or whether these vessels are uninjured but are receiving ‘bad’ signals from their injured environment. We are investigating both mechanisms.”

Because Monson cannot study blood vessels in a live human being, he studies isolated vessels in the lab under conditions similar to those of a head injury. “We run tests to address mechanical questions,” he says. “What are the material properties?  How far can the blood vessel stretch before it fails or becomes unresponsive?”  But testing in the confines of a lab goes only so far in explaining trauma to the brain’s blood vessels, says Monson.  Monson’s group is also developing computational models focused on mechanical interactions between the brain and vessels. One goal is to construct a model at the microscopic level of the brain’s cortex. “With a working model, we can show how individual blood vessels are deformed during TBI,” says Monson. “The results can then be used to predict injury and its subsequent progression, and could aid in the development of more effective treatments for TBI.”

Monson expects these findings to help inform the design of automotive interiors and protective equipment for athletes and soldiers.

Reprinted from the University of Utah College of Engineering 2012 Research Report

To learn more about this and other related research projects visit the Head Injury and Vessel Biomechanics Laboratory