In a new research paper published in the latest issue of Neurotherapeutics by the researchers at the University Of Maryland School Of Medicine (UM SOM), it has been argued that our understanding about the true nature of traumatic brain injury and how it causes chronic degenerative problems is misunderstood.
The two authors of the paper – Alan Faden, MD, a neurologist and professor of anesthesiology, and David Loane, PhD, an assistant professor of anesthesiology are of the opinion that the cause of chronic brain damage and neuropsychiatric problems after trauma are more due to long-term inflammation in the brain. According to them, this inflammation is a key culprit behind the various symptoms that a person experiences after suffering traumatic brain injury and mild traumatic brain injury like brain atrophy, depression and cognitive decline.
Dr. Faden and Dr. Loane stated that in general more emphasis is given to a specific diagnosis like chronic traumatic encephalopathy (CTE). Some former football players have been diagnosed with it. They seriously think that this takes away the focus from other mechanisms, which are more common and hence more important and may be more treatable. There is no doubt that chronic traumatic encephalopathy is a very serious problem. However, relatively few people have been diagnosed with this condition. So, it definitely make sense for researchers and journalists to focus more things like repeated concussive impacts or mild traumatic brain injury which can also trigger chronic brain inflammation that can last for years and cause lasting irreversible damage.
Dr. Faden emphasized that brain inflammation is a very key issue and one that has been not taken very seriously. He added that in some recent brain imaging studies, which also includes those of former professional football players, it is indicated that persistent brain inflammation after a single moderate head injury or repeated milder traumatic brain injury may be very common, and that it may eventually contribute to cognitive problems. Some larger studies also reveal that brain inflammation actually stays for several months or years in many people with traumatic brain injury.
In their paper Dr. Faden and Dr. Loane also state that chronic brain inflammation related to traumatic brain injury may be treatable. There are recent researches that show that some experimental drugs, along with controlled exercise programs, can control brain inflammation caused by traumatic brain injury. That is why these avenues should be pursued on priority.
Prior to this there have been two groundbreaking publications were done by Dr. Faden. In these works, he studied and observed animal models of traumatic brain injury, examined the mechanisms by which even mild brain injuries can cause sustained cognitive and psychiatric problems. In his work he elucidated how this process occurs. One of the study was published in Cerebral Blood Flow and Metabolism and the other one in Journal of Neuropathology and Experimental Neurology. Dr. Faden opined that in these studies it was found how repeated mild injuries can lead to the injuries that are similar to those which occur after a single moderate or severe traumatic brain injury. The loss of brain cells and the brain inflammation look quite similar. He remarked that since the mechanism behind the damage is understood now, strategies to prevent or minimize the problems should be developed.
During the study for the paper published in the Journal of Cerebral Blood Flow and Metabolism, Dr. Faden and team studied the brains of animals with mild traumatic brain injury. It was seen that there was a substantial loss of neurons, and an increase a kind of inflammatory immune cell active in the brain called microalgia. These changes were long-lasting and resulted in decreased function in the hippocampus.
In the other paper, it was found that traumatic brain injury triggers certain long-term molecular changes which results in increased inflammation lasting up to a year. Such inflammation causes death of brain neurons and result in cognitive loss.