Previous studies suggest the etiology of pain after an MVC is not solely due to tissue damage at the time of trauma, but rather may also be strongly influenced by physiologic systems involved in the body's response to the collision. These physiologic systems influence the function of nerve cells that process pain in the brain, spinal cord and body tissues.

Researchers from the University of North Carolina collected data from 948 patients who came to one of eight emergency departments in four states for care after an MVC. Participants provided a blood sample at the time of their emergency department evaluation. The extent and severity of patient pain symptoms were assessed at the time of the emergency department visit and also six weeks after the emergency department visit (via a telephone or web-based interview). The researchers used the data for two separate studies.

The first study analyzed the role of dopamine, an important neurotransmitter in the brain. Out of the five different dopamine receptors, dopamine receptor 2 has been shown to play an important role in neurologic function. The first study assessed whether genetic variations influencing the function of the dopamine receptor 2 are associated with acute pain severity after an MVC. One specific single nucleotide polymorphism in the dopamine receptor 2, rs6276, was significantly associated with pain severity in the acute aftermath of a collision.

"The findings suggest dopamine pathways involving the dopamine receptor 2 contribute to the intensity of pain experienced immediately after an MVC," said study author Andrey V. Bortsov, M.D., Ph.D., Assistant Professor of Anesthesiology, University of North Carolina, Chapel Hill.

The second study assessed the role of the hypothalamic-pituitary adrenal (HPA) axis, a physiologic system of central importance to the body's response to stressful events. The study evaluated whether the HPA axis influences pain severity six weeks after MVC. Findings revealed the FKBP5 gene variant was associated with a 20 percent higher risk of moderate to severe neck pain six weeks after an MVC, as well as a greater extent of body pain.

"Unfortunately, patients who experience persistent pain after an MVC are often viewed with suspicion, as if they are making up their symptoms for financial gain or some other reason," said senior study author Samuel A. McLean, M.D., Assistant Professor of Anesthesiology, University of North Carolina, Chapel Hill. "Our study is the first to identify a genetic risk factor for persistent pain after an MVC, and contributes further evidence that persistent pain after a collision has a neurobiological basis. These findings also will help us begin to identify physiologic systems involved in chronic pain development after an MVC. Understanding these systems will help us to develop new interventions to prevent the transition from acute to chronic pain after a collision."

Note: If no author is given, the source is cited instead.

• Pain Control
• Fibromyalgia
• Neuropathy

• Brain Injury
• Caregiving
• PTSD

• Dopamine hypothesis of schizophrenia
• Sensory neuron
• Phantom limb
• Neurotransmitter
• Pain
• Nociceptor