TBI Recovery in Older Persons

It used to be thought that the supply of brain cells (neurons) one was born with were meant to last a lifetime and would never increase. Now it is known that brains can use stem cells to generate new neurons which helps with preserving memories, new learning, and trauma recovery. It is also known that the outer layer of the brain, the gray matter or cortex, becomes less able to change its structure in older age. This raises the question of how do older people learn new tasks?

In  a study published in Nov. 2014 in Nature Communications a team of researchers led by  Yuko Yotsumoto of the University of Tokyo and Li-Hung Chang of Brown University scanned the brains of two groups of people before and after they learned a new visual task. The younger group (age 19-32) showed changes in their visual cortex. In the older group (age 65-80) the people who learned the new task well showed changes in their white matter beneath the visual cortex and the ones who did poorly in learning the new task showed no changes. What this indicates is that in older people the brain re-organizes itself to make new learning possible by changing the structure of its white matter, not its gray matter.

How does this relate to traumatic brain injury? In TBI a blow to the head is more likely to cause bruising to the outer layer of the brain (the gray matter or cortex) while a whiplash injury (especially with head rotation) is more likely to shear or cut the white matter. This has implications for how older people are likely to respond after TBI depending on the mechanism of brain injury.

Suicide, Self-Acceptance and Traumatic Brain Injury

The December 2007 issue of Brain Injury states that people with a traumatic brain injury are at 3-4 times the risk of suicide than the general population. Why is that? Frequently it is depression over inability to perform life tasks (including self-care, work, and/or relationships) with hopelessness that things will ever change. Attitude is key. A perfectionist approach will only lead to self-criticism, self-denigration, discouragement, and  despair. A self-compassionate and self-accepting perspective will relieve the stress and inward-directed anger caused by judgment.

Perfectionism is a major risk factor for suicide for any person not just one with a TBI. In September 2014 a group of researchers led by York University Psychology Professor Gordon Flett published an article with that finding in the APA journal Review of General Psychology.  Dr. Flett noted that people whose occupation emphasizes precision (such as physicians, lawyers and architects) or who are in leadership roles tend to be to be perfectionistic and relentlessly demanding on themselves.

Because of perfectionism, such people are unlikely to admit to suicidal feelings, ideas or plans, and unlikely to seek help, so it is up to family to spot depression and get intervention.

If you have a loved one with a TBI who exhibited perfectionism before his/her brain injury, then it would be highly appropriate to closely observe his/her mood and behavior. Is your loved one exhibiting the signs and symptoms of depression? Has he/she expressed feelings of uselessness, worthlessness, despair or hopelessness. If so, please consider getting your loved one to see a counselor, psychologist or psychiatrist.

Why are Two Concussions Close in Time so Damaging?

On 11/16/14  Zachary Weil and colleagues from Ohio State University  presented the answer to this question at the annual meeting of the Society for Neuroscience. Dr. Weil shared his research on how mice respond to two concussions. After the first concussion the mouse brain ramps us its use of glucose to power repair of damaged brain cells. This surge in glucose use is dependent upon the brain having normal signaling for the uptake of insulin. When the two concussions are 20 days apart the surge in glucose use has already occurred and the brain is protected. However, when the second concussion occurs just 3 days later brain signaling for uptake of insulin is disrupted, the brain becomes insulin resistant, and brain cells cannot utilize sugar. The result is lack of energy for brain repair, inflammation, and degeneration of brain cells with loss of attentional, memory, and learning abilities.

Dr. Weil says it appears that the surge in glucose utilization by the brain for self-repair appears about 6 days after a concussion. This not only means that soldiers and athletes with minor head injuries must be kept of out of action for more than a week. It also means that civilians must rest and not expose themselves to the risk of head injury for the same time frame. People with a brand new concussion should talk to their doctor about when it is wise to return to work and begin driving again. Being a driver or passenger in a car is definitely a risk factor for a second concussion.

New 3D Model of the Human Brain Opens Research Windows

A team of neuroscientists in Germany led by Dr. Katrin Amunts has developed a new 3D model of the human brain. As announced on 7/16/13 the team took 7,400 super thin sections of the brain of a deceased 65 year old woman in excellent health and digitized them into a 3D model on a computer. The model called Big Brain enables brain researchers to study any of these areas on a molecular level. Although the initial application of the model will be to help researchers explore causes of and cures for neuro-degenerative disorders like Alzheimer’s and Parkinson’s disease, the model can be used in other ways.

For example the model shows normal cortical thickness for older persons and this could be compared to the cortical thickness of an older person after he/she suffered a TBI (which tends to reduce cortical thickness). Over the next decade scientists in 23 countries will be helping Dr. Amunts develop the Big Brain model into a more complete and more useful model than it is right now. During this time neuroscientists may find uses for the model to help understand, diagnose or treat traumatic brain injuries.

Damage to Areas Makes TBI Worse

How come people with traumatic brain injuries have such different neuropsychological outcomes — with some people gradually returning to normal (or near-normal) and others having very significant and permanent problems? For decades neurologist have used a measure of the severity of brain injury called the Glasgow Coma Scale (GCS) to predict outcomes. Although the  GCS never explained the causes behind the different outcomes, it did offer roughly accurate predictions about neuropsychological outcome after TBI. The GCS did this based upon a statistical correlation between neuropsychological outcomes and observable factors such the length and depth of the patient’s coma along with the length of his period of post-traumatic amnesia (the amount of time before and after the brain injury he could never remember).

Now (thanks to combining a form of neuroimaging called fMRI with functional connectivity analyses, and graph theory) scientists the University of Iowa and the Washington University of St. Louis have actually found a causal explanation for why brain injury outcomes differ. Their research was just published in the September 15, 2014 Early Edition of the Proceedings of the National Academy of Sciences.

Their research shows that there are 6 “hub” areas in the brain that inter-connect with and integrate other parts of the brain to create the powerful networks responsible for the most important cognitive functions like attention, concept formation, memory, behavioral planning, decision-making, motor movement planning, and speech. When trauma causes focal damage to a brain hub the result will be much more severe than if the damage is diffused and misses all hubs. Think of it the way a major airline runs its business using a hub. If a fire, explosion or electric outage shut down the airline’s hub, the damage to the airline would be much greater than if a number of less important single airports went offline.

First PET Scan to Detect Concussional Dementia in Living Patient

In September 2014 Dr. Samuel Gandy of the Icahn School of Medicine at Mount Sinai published a cases study in the journal Translational Psychiatry detailing the use of PET scanning with a radioactive tracer called [18 F]-T807 which can diagnose dementia from significant concussive damage in a living patient’s brain. The new technique is able to visualize abnormal accumulation of tau protein in brain cells that distinguish concussion-generated dementia from the buildup of beta-amyloid protein seen in Alzheimer’s Disease (which is a non-traumatic degenerative brain disease). The people at highest risk of dementia from tau protein buildup secondary to concussion are victims of severe TBI; football and hockey players who suffer multiple concussions; and soldiers exposed to bomb blast shock waves in war.

Xenon Gas Limits Brain Damage After TBI

Traumatic brain injury (TBI) from a car crash or fall is initially a mechanical process involving bruising of brain tissue. The worst damage from TBI comes hours/days later when a bio-chemical process of inflammation and cell death occurs. Scientists have been trying for decades to understand and halt this secondary process. One way they have tried is to place patients in hyperbaric oxygen chambers. Now, a new and possibly more effective way has been discovered in mice.

In the September 2014 issue of Critical Care Medicine, Dr Robert Dickinson of Imperial College London, reported good success in limiting the bio-chemical effects of mechanical brain damage in mice by administering xenon gas to them hours after injury. Of groups of mice given a mechanical TBI the one given xenon hours after injury performed much better at tasks involving movement and balance than mice not given any xenon and mice given xenon days after injury. Dr. Dickenson hopes to get approval to try the experimental xenon treatment on human victims of TBI at  some point in the future.

Diffusion Tensor Imaging Tracks Chronic Traumatic Brain Injury

On July 21. 2014, researchers from the Center for BrainHealth at The University of Texas at Dallas published a study in the Journal of Neurotrauma, seeking to correlate the appearance of white matter damage from TBI with cognitive problems. Using the technique known as Diffusion Tensor Imaging (DTI) the researchers found that as patients’ white matter tracts healed their cognitive processing speed increased, while patients with chronic white matter damage continued to show slowed cognitive processing speed. The DTI imaging and cognitive testing were done twice, one day post TBI and again seven months post TBI.