A Collection of Medical & Legal Information About Brain Injury


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Latest Medical Research about Brain Injury

Updated: 21 February 2020


Since 2014 Neuropsychologist in the United States have been engaged in a bitter battle over the proper way to address the part of their test batteries which try to determine if the patientis giving full effort or is faking it. ("malingering") Effort testing is often used by the defense in particularly mild TBI cases. However while more and more "effort tests" are piled into the test, the chances of being mistakenly identified as a malingerer, who fails one or more of these tests,is much higher. However, the false-positive rate of most of these tests (percentage of people whoare mistakenly diagnosed as being malingerers) if the false-positive rate was 30%, would mean that three out of ten people. We are working to clean this up.


Reviewing over 20 years of TBI research, the study found a significant association ofprior TBI with subsequent neurologic and psychiatric diagnosis. They found higher rates of Alzheimer's, Parkinson's, mild impairment, depression and bipolar disorder in individuals with a previous TBI compared to those without TBI. Analysis of mild TBI found no evidence that multiple TBI's were associated with higher odds of disease than a single TBI.


In a study of martial art and boxing athletes, who sustained repeated sub-concussive blows, it was found that the brain blood barrier, a protective highly regulated gateway into the central nervous system (the spine in the brain) was found to be damaged by trauma. The brain does not like large molecules. You may have heard that certain compounds can make their way to the brain. With a tear or leak in the protective system during trauma or MS, the brain becomes inflamed when large molecules enter the system that should not be in the system. New technology regarding MRI will enable patients to determine if the BBB is torn or not, in the near future.


Sleep disturbance after TBI is extremely common, yet it has been relatively ignored by researchers. In a 2008 study it showed that insomnia, largely goes undiagnosed. Sleep problems and deprivation can severely compromise the recovery process and lead to worse outcomes. Those suffering from sleep problems after TBI should go to the local hospital and sign up for a sleep study, which can identify the particular problem. Sleep apnea, if caused by TBI, can lead to cognitive problems and a shortened life.


Studies from Australia, as well as British medical journals have shown what most of us have long suspected. That is, that ER personnel are not keen on wading into a diagnosis of mild TBI. This is a major concern for those headed into TBI litigation because the EMT and ER records form the foundation for the presence or absence of TBI, according to the insurance companies. A recent article in the Journal of Neurotrauma from 2019 shows that the diagnosis of mild TBI is difficult because the symptoms are vague and not specific. After looking at the records of 1600 patients, they found that less than half of those with a confirmed TBI were actually diagnosed with a mild TBI.


This study found that presence of at least one or two pituitary hormone dysfunction was 32%. While most pituitary dysfunction's resolve within 12 to 24 monoths, a third of those with TBI might have ongoing problems, especially with the hormone known as human growth hormone. The diagnosis of this condition is not a blood test as commonly believed. It is a four hour, rather difficult test, which involves drinking glucose and taking blood samples over that period of time. Only a few centers in the country are currently doing this type of testing. In our experience, 10 out of 20 of our clients, so tested, have been found to be HGH deficient. All ofthem have shown a great deal of recovery in energy, motivation and initiative after receiving their daily shots of growth hormone. Insurance companies are terrible to work with regarding human growth hormone shots, so if coverage is cut off on someone properly diagnosed an attorney must be called.

Updated: 25 April 2019


In April 2019, a heartbreaking New York Times article outlined the tragic suicide of Olympic cyclist Kelly Katlynn. She came from an enormously competitive and successful family and was going to be a probable medalist in the 2020 Tokyo Olympics. However, after an accident while cycling, she received a mild TBI which adversely affected her cognition. The accident did not involve an injury to her head but afterwards she felt dizzy, had headaches, sensitivity to light and trouble sleeping. Personality changes occurred as well as social isolation and loss of focus and drive. Because her life had been derailed, she decided on suicide. That is the power of a mild traumatic brain injury.


In the 2019 Journal of Neurotrauma patients with cognitive symptoms after a single blunt trauma TBI, with normal CT and normal MRI, were given PET scans of the brain. PET scans measure the rate at which the brain's fuel, glucose, is consumed - injured areas consuming less. They found that compared to normals the glucose uptake was significantly decreased in the bilateral pre-frontal area and significantly increased around the limbic system. This increased activity is likely a compensatory strategy by the brain to work around injured areas.


The corpus callosum is a thick band of white matter which literally connects both sides of the brain and allows for communication between the two hemispheres (right brain/left brain). The corpus callosum is the most sensitive area of the brain to high velocity changes as in a car accident . Adults with severe chronic TBI underwent MRI/DTI testing of the corpus callosum and performed on the awareness of social inference test (TASIT)which showed a strong correlation between injury to that area and test scores on social awareness testing. Again, confirming that TBI caused severe social disabilities.


We owe the returning veterans a great deal of thanks for forcing the medical establishment to finally do peer reviewed research on mild TBI. Since the veterans started returning, the last decade has truly been the decade of mild TBI, with hundreds of new studies being done.

This particular study looked at insomnia symptoms one year after TBI. Interestingly those with mild TBI were significantly more likely to have insomnia than those with moderate to severe TBI. They also found that depressive symptoms and general anxiety were significantly associated with insomnia symptoms after TBI, as well as headache and binge drinking.


Sleep disorders are reported with 30 to 70% of TBI cases and they have negative impacts on quality-of-life and rehabilitation. They aggravate psychiatric problems, and sleep apnea has been shown to be highly detrimental in many ways. In the study a total of 72% experienced sleep disturbances compared to 24% in the control group, a significant difference. Another study, found in the Journal of Head Trauma Rehabilitation in 2016, looked at the risks of sleep apnea. A significant predictor of apnea was age. Given the progressive nature of sleep apnea and the serious problems associated with it, earlier identification of apnea is needed.


As if we didn't have enough to worry about with injuries to our traditional brain, recent studies have shown that our gut microbiome is sending more signals to the brain than the brain sends to the gut. It has been shown that the gut biome is adversely affected by TBI. These changes in the gut can lead to a pro-inflammatory state within the central nervous system. New interventions are being developed.


Researchers in Galveston Texas, including Dr. Randall Urban and Dr Brent Masel, both of whom developed the breakthrough idea of TBI as a chronic disease, were involved in the study. By studying the blood work of chronic TBI patients, it was found that even many years after injury these patients exhibited abnormal metabolic responses and altered relationships between circulating amino acids and hormones. This is a chronic disease state whose effects are just being discovered. The condition, known as hypoaminoacidemia, causes a large reduction in the amount of circulating amino acids in the body.


The study looked at life expectancy after traumatic brain injury in those completing inpatient rehabilitation in the US between 2001 and 2010. They found that individuals with TBI were 2.23 times more likely to die than individuals of comparable age, giving them a reduced life expectancy of nine (9) years. Individuals with TBI had a greater risk of death from seizures, accidental poisoning, mental or behavioral problems, external injuries. Those with TBI requiring rehabilitation following acute hospital care were 49 times more likely to die of pneumonia, 22 times more likely to die of seizures, three times more likely to commit suicide, and 2.5 times more likely to die of digestive conditions versus matched populations.

Updated: 23 July 2018


MRS is a new diagnostic tool to detect brain injury by looking at the levels of common brain chemicals after injury. If these metabolites are at certain levels as to each other, an injury is likely. MRS can be done as part of a standard MRI and is available in most cities in the U.S. A recent review of almost 1000 studies on MRS shows that it is effective on all TBIs, except for mild TBI and acute injuries.


The intrusive and sometimes severe symptom commonly following TBI - tinnitus, a loud constant ringing in the ears, has long evaded a cure. Now, however, tinnitus retaining therapy (TRT) seems to work in up to 80% of patients. The treatment now can show improvements in one month instead of one year. Hopefully TRT will soon be covered by heath insurance, if not already.


Depression seems to be associated with disruptions in the body caused by neuro-inflammation such as TBI, stroke, chronic pain, diabetes and other illnesses. Inflammatory reactions in the brains microglia (immune cells) as well as brain blood barrier (BBB) disruption seem to be the cause. Depression occurs in the presence of a high brain inflammatory load. Researchers are racing to learn more about these causes and cures. (Benattin, C et al. 2016).


The microglia of the brain, which were ignored by scientists for 70 years until recently, appear to have a great deal to do with our health. Microglia are activated after TBI and often do not shut down after their immune response should be over. This causes chronic neuro-inflammation, which can lead to dementia, depression, anxiety, Parkinson's and more. Stress has been found to create microglia activation - yet another strike against stress in our stressful lives.

In fact, stress caused by "repeated social defeat" failure at dating or work, for example, actually activates microglial and harms the immune system, leading to widespread susceptibility to a variety of illnesses. (Ramirez, K. et al. 2016)


Insulin-like growth factor (IGF-1) is involved in both growth hormones and diabetes and is produced by the pituitary gland. Commonly in TBI we see damage to the pituitary/hypothalamic axis which results in lowered IGF-1/growth hormone levels (although do not rely on IGF-1 testing alone after a TBI, the levels can be normal; do only a Glucagon tolerance test). IGF-1 is now thought to be involved in regulation of the human body's "homeostasis" - or normal metabolic levels. Disruption can lead to Alzheimers and diabetes. IGF-1 itself shows promise as a possible therapy. (Zheng P. 2017).


Fatigue, after a headache, is the most common symptom of TBI. An injured brain consumes far more fuel (glucose) than a normal brain, leading to such fatigue. When an injured brain goes around injured areas, thus consuming more fuel.

With this new therapy of using short blue wavelength light (blue), after four weeks most patients showed lessened fatigue and increased attention. Yellow lights and no lights showed no improvement. Better yet, no pills needed! (Sinclair, KL et al 2014)


Injured brain cells, neurons, can have damage to the energy producing component to the cell - the mitochondria. These essential parts of any cell are needed for a cells very survival. Now researchers have discovered that one of the brain's immune cells called an astrocyte, actually donates its own mitochondria to the wounded cell. The cell signals "help me" and the signal is picked up by an enzyme called CD38. Efforts are underway to see if CD38 itself can aid recovery in TBI and mouse data seems to say "yes," as mice with CD38 faired twice as well post TBI. (Lo E. 2016)


Studies have shown that 80% of TBI patients show mild to moderate Vitamin D deficiency. Further, these patients showed lower cognitive ability and depression. It is thought that Vitamin D aids in neuro-protection of the brain. Eat you salmon, milk, sardines and get some sunlight.


Beta blockers, especially propranolol (Inderal), administered early after moderate to severe TBI, showed shorter time for ventilation, hospital stay and higher rates of survival. (Ko A. 2016)


While most doctors treating MTBI continue to opine that it cannot be the cause of chronic impairments, with three months being the cut off, they are being shown to be wrong. A total of 45 studies, many on returning Veterans, were reviewed. Half of the patients in these studies showed symptoms for far longer than three months from a single MTBI (McInnes K et al. 2017).


A new type of MRI scan, know as fast mean kurtosis tensor (MKT or diffusion kurtosis imaging - DKI) is showing promise in viewing structural damage in MTBI, as well as in cancer detection. They found micro-structural changes in the thalamus and corpus callosum 14 days to three months after MTBI. MKI promises to be more sensitive than even DTI in the future. (Naess-Schmidt ES et al. 2017).

Updated: 1 March 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)


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