Why Rest Following Concussion is Critical

Doctors who order several days of rest after a person suffers a concussion are giving sound advice, say researchers, and new data from animal models explains why.

Georgetown University Medical Center neuroscientists say rest — for more than a day — is critical for allowing the brain to reset neural networks and repair any short-term injury. The new study in mice also shows that repeated mild concussions with only a day to recover between injuries leads to mounting damage and brain inflammation that remains evident a year after injury.

“It is good news that the brain can recover from a hit if given enough time to rest and recover. But on the flip side, we find that the brain does not undertake this rebalancing when impacts come too close together,” says the study’s lead researcher, Mark P. Burns, PhD, assistant professor of neuroscience at GUMC and director of the Laboratory for Brain Injury and Dementia.

This first-of-its-kind study, published in the March 2016 issue of American Journal of Pathology, modeled repeated mild head trauma as a means to investigate brain damage that occurs after a sports, military or domestic abuse injury.

Investigators developed a mouse model of repetitive, extremely mild concussive impacts conducted while the mouse is anesthetized. They compared the brain’s response to a single concussion with an injury received daily for 30 days and one received weekly over 30 weeks.

Mice with a single insult temporarily lose 10-15 percent of the neuronal connections in their brains, but no inflammation or cell death resulted, Burns says. With three days rest, all neuronal connections were restored. This neuronal response is not seen in mice with daily concussions, but the pattern is restored when a week of rest is given between each insult, Burns says.

When a mild concussion occurred each day for a month, inflammation and damage to the brain’s white matter resulted. “This damage became progressively worse for two months and remained apparent one year after the last impact,” Burns says.

Image shows MRI scans from a concussion patient.
When a mild concussion occurred each day for a month, inflammation and damage to the brain’s white matter resulted. MRI brain scans of a concussion patient image is for illustrative purposes only. Credit: M J Richardson.

“The findings mirror what has been observed about such damage in humans years after a brain injury, especially among athletes,” Burns says. “Studies have shown that almost all people with single concussions spontaneously recover, but athletes who play contact sports are much more susceptible to lasting brain damage. These findings help fill in the picture of how and when concussions and mild head trauma can lead to sustained brain damage.”

About this concussion research

Georgetown co-authors are first author Charisse N. Winston, PhD, Maia Parsadanian, David N. Zapple, Sonia Villapol, PhD, and undergraduate students David Barton, Tiffany E. Wilkins, Aidan Neustadtl, Deepa Chellappa, and Andrew D. Alikhani. Contributors also include Emmanuel Planel, PhD, and Anastasia Noel, PhD, from the Centre Hospitalier de l’Université Laval, Neurosciences, Québec, Canada.

Funding: The study was supported by Georgetown University’s Neural Injury and Plasticity Training Program, the National Institute for Neurological Disorders and Stroke (R01 NS067417), a supplement to Promote Diversity in Health-Related Research, a donation from KPB Corporation, the Canadian Institute of Health Research, Fonds de Recherche en Santé du Québec and the Natural Sciences and Engineering Research Council of Canada.

Source: Karen Teber – Georgetown University Medical Center
Image Source: The image is credited to M J Richardson and is licensed CC BY SA 2.0
Original Research: Abstract for “Dendritic Spine Loss and Chronic White Matter Inflammation in a Mouse Model of Highly Repetitive Head Trauma” by Charisse N. Winston, Anastasia Noël, Aidan Neustadtl, Maia Parsadanian, David J. Barton, Deepa Chellappa, Tiffany E. Wilkins, Andrew D. Alikhani, David N. Zapple, Sonia Villapol, Emmanuel Planel, and Mark P. Burns in American Journal of Pathology. Published online February 4 2016 doi:10.1016/j.ajpath.2015.11.006


Abstract

Dendritic Spine Loss and Chronic White Matter Inflammation in a Mouse Model of Highly Repetitive Head Trauma

Mild traumatic brain injury (mTBI) is an emerging risk for chronic behavioral, cognitive, and neurodegenerative conditions. Athletes absorb several hundred mTBIs each year; however, rodent models of repeat mTBI (rmTBI) are often limited to impacts in the single digits. Herein, we describe the effects of 30 rmTBIs, examining structural and pathological changes in mice up to 365 days after injury. We found that single mTBI causes a brief loss of consciousness and a transient reduction in dendritic spines, reflecting a loss of excitatory synapses. Single mTBI does not cause axonal injury, neuroinflammation, or cell death in the gray or white matter. Thirty rmTBIs with a 1-day interval between each mTBI do not cause dendritic spine loss; however, when the interinjury interval is increased to 7 days, dendritic spine loss is reinstated. Thirty rmTBIs cause white matter pathology characterized by positive silver and Fluoro-Jade B staining, and microglial proliferation and activation. This pathology continues to develop through 60 days, and is still apparent at 365 days, after injury. However, rmTBIs did not increase β-amyloid levels or tau phosphorylation in the 3xTg-AD mouse model of Alzheimer disease. Our data reveal that single mTBI causes a transient loss of synapses, but that rmTBIs habituate to repetitive injury within a short time period. rmTBI causes the development of progressive white matter pathology that continues for months after the final impact.

“Dendritic Spine Loss and Chronic White Matter Inflammation in a Mouse Model of Highly Repetitive Head Trauma” by Charisse N. Winston, Anastasia Noël, Aidan Neustadtl, Maia Parsadanian, David J. Barton, Deepa Chellappa, Tiffany E. Wilkins, Andrew D. Alikhani, David N. Zapple, Sonia Villapol, Emmanuel Planel, and Mark P. Burns in American Journal of Pathology. Published online February 4 2016 doi:10.1016/j.ajpath.2015.11.006

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