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Medical Research – Archive – 2017


Individuals with a history of contact sports, especially football, were studied. It revealed a threshold dose-response relationship between the exposure to trauma and risk for later life cognitive impairment. The findings also showed a rise in abnormal levels of self reported executive function problems, depression, apathy, and behavioral disregulation.


Dr. Brent Mazel, who spearheaded the idea of TBI as a chronic disease, Dr. Randal Urban and others have found that TBI victims have yet another system in their bodies chronically altered by trauma. Here it was found that TBI victims had significantly lower circulating concentrations of many amino acids. These amino acids are essential for good health in many areas of the body. This abnormal metabolic condition and abnormal relationship between amino acids, hormones and cytokines is and should be studied further.


There is currently no protocol to utilize MRI scanning at an emergency room with those suspected of having suffered TBI. The standard protocol is the quicker and cheaper CT scan. A new “brief MRI protocol” has been developed and in its initial test, in scans done within the first 48 hours after trauma, showed abnormalities in 57% of the patients. Nine of the nineteen suspected mild TBI patients with a negative CT had positive findings on the MRI. Most of the abnormalities on the MRI were noted on post contrast FLAIR.

The problem in proving objective damage in cases of mild TBI is illustrated here. The initial abnormalities are missed by the CT scan and six months or years after the event, the abnormalities can no longer be identified by radiologist. If they are seen, they are simply called “non-specific findings.” This has caused great distress in thousands of TBI victims in the last four years.


A study done in the Netherlands, a context in which litigation is non-existent and can not be a factor, showed that non hospitalized victims of mild traumatic brain injury had significant long term complaints. Six months after injury, 36% showed incomplete recovery, 25% returned to the outpatient neurology clinic within six months after injury. The findings ruled out anxiety and depression as cause of the continued difficulties.


A study involving over 6000 adolescents and young adults athletes of high school age showed that the athletes with pre-injury ADHD reported a higher rate of concussions than athletes without ADHD. Researchers were unable to determine whether the students were more susceptible to injury, have a lower threshold, or a different recovery rate than those without such a history.

Once again, this study confirms the well known observation that individuals who go into a TBI with preexisting difficulties such as ADHD, depression, anxiety, or any other brain dysfunction, have a worse outcome. This may be due to “glial activation” wherein these individual glial cells are already activated and are pathologically activated after a TBI. (See elsewhere on the site for more about glial activation).


It has been well established that TBI itself has an impact on bone density loss. Injuries to the pituitary involving sex hormones, growth hormones and others have been shown to cause osteoporosis. Cushing’s disease, the over production of cortisol, can also cause osteoporosis.

A recent study in mice showed 23 to 27% reduction in femur bone mass in animals with TBI twelve-weeks earlier. The findings indicate that TBI itself, with or without pituitary injury, can and does lead to bone loss. More research needs to be done.


The accumulation of tau molecules are a feature of many neuro-degenerative disorders following TBI such as Alzheimer’s and Parkinson’s. Tau is also associated with the development of chronic CTE in football players. Scientist have now focused in on a molecule known as “Tau Oligoners” as the culprit in starting the brain pathologies in all of these groups. This molecule apparently initiates the protein misfolding that occurs as a result of many types of brain disease. Injection of this molecule into mice started a course of severe neuro-degeneration. However, once the administration was discontinued the mice went back to normal. It is reversible in this case.

There is also a possible non-intrusive biomarker for TBI and other neuro-degenerative conditions whereby the retina in the eye is examined to see if it has been invaded by tau oligoners. A test has not yet been developed.


Another study, among many, showing observable objective changes in the brain after mild-TBI. Here brain volume in several parts of the brain, including the putamen, thalamus, amygdala and hippocampus seemed to be smaller than controls after the injury. They gradually resume most of their size after about a year, indicating recovery. (Zagorchev, L. et al. 2015).

Who is at Risk for Post Concussive Syndrome?

The study of those treated at an emergency room for mild TBI show the most commonly reported symptoms at first follow up where headache (27%), trouble falling asleep (18%), fatigue (17%), difficulty remembering (16%) and dizziness (16%). The following factors predict worse outcome:

  1. Consumption of alcohol prior to injury.
  2. The head injury resulted from a motor vehicle accident or fall.
  3. The presence of post injury headache.

Headache was more robustly associated with continued symptoms, more than loss of consciousness or alteration of consciousness or amnesia.


Methylene blue, an old well used drug, has proved to be neuroprotective to the brains of rats after a concussion. It was protective against the size of lesions and the length of functional cognitive deficits. Clinically trials are under way.


The prognostic value of DTI/MR was shown in 61 patients with mild TBI who were scanned early after trauma. The results of the abnormalities in white matter shown by DTI correlated with the patients lowered performance on neuropsychological testing and contrasted sharply with controls. DTI continues to prove itself as a biomarker for TBI in the human brain.


Microhemorrhages are one of the most common results of TBI, and with more powerful magnets and SWI/MR (Susceptibility Weighted Imaging), these micro hemorrhages can be identified. Taking it to another level, a program called SWIM (Susceptibility Weighted Imaging and Mapping) has been developed along with a Quantitative Susceptibility Mapping (QSM).

One of the problems with SWI is distinguishing between microhemorrhages and veins. These two programs substantially raise the accuracy of the identification of microhemorrhages. They can be done in a semi-automated manner with reasonable sensitivity and specificity. (Liu J. et al., 2015)


An article in the American Journal of Neuroradiology looked into the use of DTI/MR to study chronic TBI patients. It was assumed that the iron remnants of blood, which is what is seen by the SWI, would or could dissipate over years. However, they found that these microhemorrhage sites arising in the brain after a severe trauma are “time independent,” meaning that they do not fade over time. Another question answered was whether or not these tiny “tissue tears” in the brain are hemorrhagic or non hemorrhagic. Studies had determined the answer both ways. The study determined that most but not all microhemorrhages involve a hemorrhagic (blood orientated) aspect.

They also establish that traumatic microbleeds are:

  1. Located mainly in the frontal lobe and temporal lobe.
  2. The white matter of the superior frontal gyrus was most often affected.
  3. That the traumatic microbleeds were situated mainly at the gray matter-white matter border. These were further located more often next to the crowns rather than the base of the gyral stalks. Most were bilateral.
  4. Periventricular hyperintensities, (like spots close to the hollow ventricles in the center of our brain), are reported to be present in 74% of young normal persons and 89% of elderly normal persons. Therefore it is very important for your doctor and lawyer to distinguish these rather common abnormalities from those caused by trauma, particularly by location.

Unfortunately, a comment is made “diffuse axonal injury is usually related to general poor clinical status.” This statement is based on a 1991 paper written prior to even the discovery that DIA occurred in mild TBI. (Scheid R. et al. 2003)