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In 2003 CDC sent a report to Congress on “mild” traumatic brain injuries. (MTBI, also sometimes called “concussion.”) The report cautioned that, contrary to past understanding, “mild” brain injuries can cause serious, permanent problems:

“In recent decades, public health and health care communities have become increasingly aware that the consequences of mild traumatic brain injury (MTBI) may not, in fact, be mild. Epidemiologic research has identified MTBI as a public health problem of large magnitude, while clinical research has provided evidence that these injuries can cause serious, lasting problems.”

Over the last 15 years , fueled in part with research funded by the US Military and the NFL, the science of MTBI has advanced. More advanced imaging, blood biomarkers, vision, hearing and balance testing, endocrine assessments, cognitive testing, and other advances have demonstrated that patients with lasting symptoms following MTBI typically show objective signs of brain damage – in other words their persistent symptoms are real and not imagined and often have an objective physiological basis. The good news is that this research has also led to interventions that can improve outcome, including such things as specially designed PT, OT, vision therapy, exercise therapy, endocrine therapy and counseling. This blog has described this research in posts over the last several years.

Despite all of this research, there has been a persistent viewpoint among a minority of medical experts that MTBI is benign and short-lived and that any persistent issues are either emotionally based or caused by unrelated physical problems. (Many of the clinicians who espouse this viewpoint are regularly retained by insurers seeking to defeat personal injury claims arising from MTBI).

The minority view that MTBI is essentially benign became further marginalized with the June 3, 2019 online publication of a significant cohert study by the AMA Journal Neurology.

The study concludes: “the term mild TBI misrepresents the immediate and long-term burden of TBI and other cooccurring factors experienced by this patient population.” The study followed 1453 patients presenting at level 1 trauma centers from February, 2014 to August 2018. Of this number, 1154 had signs of MTBI and 299 had peripheral orthopedic injury, but no signs of TBI (the later group served as the control.) One year outcomes were measured by neuropsychological measures, measures of daily functioning (the “GOSE” score) and symptoms measures. The study found that 53% of participants with MTBI were experiencing impairments at 12 months post-injury. Symptoms included headaches, fatigue, depression and forgetfulness. Patients with persistent symptoms also performed more poorly on cognitive tests than patients in the control group. Consistent with other studies, the worse outcomes were found in patients with “complicated” MBTIs, defined as patients who showed acute intercranial findings on imaging.

The importance of the study, the authors conclude, is that it highlights the need for improved treatment of MTBI, citing studies showing that early identification and treatment often improves outcomes. Perhaps it is time to adopt new terms to describe brain injury, terms less misleading than the term “mild.”

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Funded by the Brain Injury Association of New Hampshire, a group of researchers at Dartmouth assessed the effectiveness of the program by conducting semi-structured interviews of 13 participants with traumatic brain injury and 3 caregivers who had completed the 6 week, 6 session program.  The results are published in the February, 2019 issue of Disability Rehabilitation.

Kevin Pearce, a Vermont resident and world leading professional snowboarder, suffered a near fatal traumatic brain injury while training for the 2010 winter Olympics. Kevin’s remarkable resilience since his injury has inspired millions through the award-winning HBO documentary, The Crash Reel. Using the visibility generated by his success as a professional snowboarder and the international acclaim achieved by The Crash Reel, Kevin and his brother Adam created the LoveYourBrain Foundation, a non-profit organization that is working to connect, educate and empower people with Traumatic Brain Injury and to promote prevention programs. Building on Kevin’s own experience, the LoveYourBrain Yoga program has become central to the Foundation’s mission.  The program incorporates group-based breathing exercises, yoga, meditation and psychoeducation. The first six weekly sessions of the program are open only to the TBI community. Participants who complete the program can remain in the yoga community by taking gentle classes at studios throughout the country taught by yoga teachers with specialized training through the Foundation (at a discounted rate.)

As most yoga teachers recognize (including the author of this blog) one of the important benefits of the yoga program was building, through this shared experience, a sustained sense of community connection. This is particularly important to a TBI survivor isolated by her injury and impaired in the ability to make those connections. About half of the participants in the program sustained relationships built during the program and felt more capable of accessing other activities in the community. Most participants also reported physical benefits including improvements in strength, balance and flexibility and cognitive benefits, particularly the ability to control attention. Participants also reported ongoing use of tools such as breathing exercises to cope with negative emotions and stress.

Yoga practice has become increasingly popular in the general population, which is also challenged by community disconnection, stress and physical deconditioning. The LoveYourBrain yoga program customizes yoga for the TBI community and intentionally encourages connections among participants to make these recognized benefits more accessible to that community. As the Dartmouth researchers conclude, the LoveYourBrain Yoga program appears to be an effective model for community-based rehabilitation, with diverse and meaningful physical, psychological and social health benefits.

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Researchers from Berkeley, Duke, UNC Chapel Hill and University of Arizona used a new type of MRI called “diffusion kurtosis imaging” (“DKI”) to take brain scans of 16 high school football players, ages 15 to 17, before and after a single season of football. DKI is an extension of Diffusion Tensor Imaging, (DTI) discussed in prior posts. Early studies suggest that it outperforms DTI in capturing certain microstructural changes in the brain. The football players who were scanned all wore helmets and none of them were diagnosed with a concussion. The researchers also measured head impact exposure during every practice and game using the Head Impact Telemetry (HIT) system, which has been widely used in other head impact studies. The study, which is the cover story of the November issue of the journal Neurobiology of Disease, is one of the first to look at how impact sports affect the brains of children at this age.

The researchers found significant changes in the structure of the grey matter in the front and rear of the brain, where impacts are most likely to occur, as well as changes to structures deep inside the brain. These structural changes correlated with the frequency of head impacts, which, as the authors conclude “suggest(s) that DKI imaging of gray matter may yield valuable biomarkers for evaluating brain injuries associated with subconcussive head impacts in contact sports.” The most significant structural changes were found on the opposite side of the brain from impact, suggesting that “contracoup” injury may be the most prominent.

“It is becoming pretty clear that repetitive impacts to the head, even over a short period of time, can cause changes in the brain,” said study senior author Chunlei Liu, a professor of electrical engineering and computer sciences and a member of the Helen Wills Neuroscience Institute at UC Berkeley. “This is the period when the brain is still developing, when it is not mature yet, so there are many critical biological processes going on, and it is unknown how these changes that we observe can affect how the brain matures and develops.”

It should be noted that testing did not indicate any change in the athletes’ cognitive function over the course of the season, and it is yet unclear whether the changes in their brains are permanent. Nevertheless, the results raise serious concerns about the impact of football on this young population.

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There’s promising research on the use of melatonin for acute treatment of traumatic brain injury (TBI) and for treatment of sleep disturbance following TBI coming from two recent peer-reviewed papers. One, published in the Journal of Neurotrauma, reviews the literature and performs meta-analyses of the data in studies examining the use of melatonin shortly after injury.

The other, published in the journal BMC Med, reports on a randomized controlled trial examining the efficacy of melatonin in treating sleep disturbance following TBI.

Melatonin is an important hormone made by the pineal gland that helps control a person’s sleep and wake cycles.

Both studies report positive results. As explained in the first study, past studies have demonstrated that melatonin is a “potent anti-inflammatory agent” offering “therapeutic potential for many of the common post-TBI symptoms such as sleep disturbance, pain, mood disturbance and increased anxiety.” It also has few side effects. The data analyzed in the first study showed that melatonin given shortly after injury “significantly improved neurobehavioral outcome in neurological, cognitive, and motor domains, as well as in histo-pathological domains (contusion size and cerebral edema [swelling])” The authors do note that although the research is promising “there are insufficient clinical data to support routine use following TBI.” Further research is needed.

The second study examined the use of melatonin clinically to treat sleep disturbance following TBI. As we have reported in prior posts, sleep disturbance can make symptoms worse and slow recovery from TBI. The researchers in the BMC Med study found that the TBI population had reduced evening and overnight melatonin production compared to age and sex matched controls. They also had less sleep efficiency, meaning that they spent more time in non-REM sleep.

The patients who received melatonin supplements reported improved sleep quality and demonstrated increased sleep efficiency. Melatonin also reduced self-reported anxiety symptomatology and fatigue, and increased vitality and mental functioning.

Melatonin is only one of several interventions with promise in addressing sleep issues following TBI. Improving sleep “hygiene” , cognitive behavioral therapy and light therapy have also shown promise. As prior posts have emphasized, sleep disturbance often plays an influential role in prolonging symptoms following TBI and should therefore be addressed early in the clinical setting.

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A new study published in the Journal of the American Medical Association adds to a growing body of evidence pointing to traumatic brain injuries, of all levels of severity, as an important risk factor for suicide.

The significance of the study is discussed in an opinion in the same issue of JAMA.  Both the increased risk of suicide and the prevalence of depression following TBI have been discussed in prior posts in this blog.

The most recent findings further highlight the importance of continuous monitoring and treatment of depression symptoms, as urged in the literature discussed in our prior posts. The JAMA study was a retrospective population-based study that included all 7.4 million individuals aged 10 years and older living in Denmark from 1980 to 2014, representing more than 160 million person-years of follow up data. Setting it apart from other similar studies, the investigators included adjustments for relevant covariates, including preexisting psychiatric illness and preexisting nonfatal self-harm actions.

As in other studies, the investigators found that the risk of suicide was particularly elevated during the first six months following medical contact for TBI. Although the increased risk was somewhat greater for “severe” TBIs, there was increased suicide risk across all TBI severity levels, the including so-called “mild” TBIs (concussions.)

As the authors of the opinion piece point out, we do not fully understand how a TBI, a highly heterogeneous condition, increases the risk of suicide. “The answers,” they say, “ are undoubtedly multifactorial and complex.” The most important comment in the opinion appears at the end. “Suicide is preventable, but only with recognition of risk and prompt intervention.” The JAMA study should remove any doubt about the risk. Hopefully, this will lead to more attention and intervention.

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In our May, 2014 post, we reported on research showing that traumatic brain injury, including mild traumatic brain injury (mTBI), can damage and cause dysfunction in the pituitary gland resulting in deficiencies in key hormones released by the pituitary gland, such as Growth Hormone (GH). As we explained in that post, the anatomy of the pituitary gland makes it particularly susceptible to the sheering injuries seen in TBI. The pituitary gland, which is housed in a bony structure at the base of the skull, controls the function of most other endocrine glands and is therefore sometimes called the “master gland.”

Pituitary dysfunction following TBI often impacts the production of growth hormone, which regulates metabolism and body composition as well as growth. These hormone deficiencies can produce many of the persistent symptoms seen following a TBI, such as fatigue, poor memory, depression, anxiety, emotional lability, exercise intolerance, lack of concentration and attention difficulties. Left untreated they can and lead to serious physical issues, including cardiac issues. osteoporosis, neuroanatomic and neurophysiologic dysfunction. We also noted findings showing that pituitary dysfunction can worsen over the five year period following an injury – in other words, that this is an issue that deserves to be monitored on an ongoing basis.

A study published in 2015 showed that the incidence of pituitary dysfunction in mTBI cases is highest in so-called “complicated mTBI” cases, with findings of skull fracture (especially skull base fractures, where the pituitary gland is housed) and/or intracranial abnormalities on imaging.  Because of the high incidence of pituitary dysfunction in those cases, ongoing assessment was recommended, even where clinical manifestations are not clear.

In a more recent post, in 2016, we reported on a study of growth hormone deficiency following TBI published in the Journal of Neurotrauma.  That study was important for three reasons:

  • The first was the finding that the standard blood test commonly used to determine growth hormone deficiency, the IGF-1 test, is not an accurate predictor of growth hormone deficiency; a more costly and time consuming test, the “glucagon stimulation test,” proved to be a far more accurate assessment and was therefore recommended by the authors.
  • The second reason the study was important is that it highlighted the serious physical, emotional and cognitive disabilities that can develop when growth hormone deficiency is not properly monitored and treated – as the authors explain, it can lead to “morbidity and poor recovery.”
  • The third reason the study was important is that it added to the body of research showing the “high prevalence of growth hormone deficiency in patients with TBI and the necessity to monitor clinical symptoms and perform provocative testing [stimulation testing] to definitively diagnose this condition.”

The most recent study adding to this body of information was recently published (in April, 2018) in the peer-reviewed journal BMC Endocrine Disorders.  Noting that stimulation testing is “resource intensive and can be associated with adverse symptoms or risks,” the authors took another look at whether the more simple IGF-1 blood test would suffice in most cases to assess growth hormone deficiency in TBI patients. The conclusion to the study is strongly worded. “Our results demonstrate,” the author’s state, “that baseline serum IGF-1 level had no predictive value [emphasis added] in predicting GH deficiency, emphasizing the need for dynamic testing in this population.” The authors further highlight that although growth hormone deficiency (the most common hormone deficiency follow TBI) may be more common in TBI cases involving skull base fractures or intracranial abnormalities on imaging, “even individuals who sustain a single concussion from non-contact sports appear to be susceptible to developing some degree of pituitary dysfunction.”

Because of the unique features of pituitary dysfunction following TBI and the testing necessary to detect this dysfunction, it is critical that patients be followed by endocrinologists (and other providers) with specialized knowledge in this area. The consequences of not treating this dysfunction are far too serious to overlook it.

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Research scientists at the Center for Brain Health at the University of Texas at Dallas have just published a study, funded by the US Department of Defense, supporting the effectiveness of “strategy-based” cognitive training at reducing symptoms of depression commonly found in patients with chronic (greater than 6 months) traumatic brain injury (TBI) symptoms.

The training was an integrative program designed to improve cognitive control by exerting more efficient thinking strategies for selective attention and abstract reasoning. The training did not directly target psychiatric symptoms such as depression, but was nonetheless effective at reducing those symptoms.

Other studies have shown that depression alters brain structure and function. Consistent with these other studies, patients who received the cognitive training not only had reduced symptoms of depression, they also showed structural changes on imaging, including increased cortical thickness, and improved function, including increased functional connectivity.

A total of seventy‐nine individuals with chronic TBI (53 depressed and 26 non‐depressed individuals), measured using the Beck Depressive Inventory (BDI), underwent either strategy‐ or information‐based cognitive training in a small group for 8 weeks. The researchers measured psychological functioning scores, cortical thickness, and resting‐state functional connectivity (rsFC) for these individuals before training, immediately post‐training, and 3 months post‐training.

After confirming that changes in BDI scores were independent of training group affiliation, they found that the depressive‐symptoms group showed reductions in BDI scores over time relative to the non‐depressed TBI control. Within the depressive‐symptoms group, reduced BDI scores was associated with improvements in scores for post‐traumatic stress disorder, TBI symptom awareness, and functional status, increases in cortical thickness in four regions within the right prefrontal cortex, and increases in rsFC within each of these four prefrontal regions.

In addition to suggesting that cognitive training can reduce symptoms of depression associated with chronic TBI, the study suggests that cortical thickness and brain connectivity may offer promising neuroimaging markers of training‐induced improvement in mental health status in TBI patients.

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In a propensity-matched cohort study of more than 350,000 veterans with and without traumatic brain injuries (TBI), mild traumatic brain injury (mTBI) without loss of consciousness was associated with more than a twofold increase in the risk of a dementia diagnosis, even after adjusting for medical and psychiatric co-morbidities. This large epidemiological study was recently published in JAMA Neurology.  Approximately 2.8 million TBIs occur each year in the United States; approximately 80% are in the “mild” category.

Although prior studies of the association between mTBI and dementia have been mixed, this study, among the largest epidemiological studies to date, adds to the weight of evidence suggesting that even mild TBI is associated with an increased dementia diagnosis risk.

Consistent with prior studies focused on moderate and severe TBI, the study found a dose-response association between TBI severity and dementia diagnosis. In other words, with more severe TBIs, the risk of a dementia diagnosis was higher. To develop a comparison sample of veterans without TBI, the researchers selected a 2% random sample of all patients who received VHA care during the same timeframe and then used propensity matching to select one veteran without TBI for each veteran with TBI.

One of the strengths of this study is the large cohort, which provided the researchers with ample power to detect associations and to adjust for a wide range of potential confounders. Another strength was the close propensity matching of the control group.

There are some limitations in applying the study results to the population at large.

  • The database could not differentiate subjects with single TBIs from subjects with multiple TBIs – other data indicates that there is a high prevalence of multiple TBIs in the veteran population, a factor that could distinguish them from civilians.
  • The data also did not identify the mechanism of injury. The authors describe the high number of blast-related mTBI among military personnel; some researchers have suggested that this mechanism may be unique in its potential to cause long term consequences. An editorial in the same May, 2018 issue of JAMA Neurology suggests, however, that the mechanism of injury may not be as significant as the authors suggest, referring to Department of Defense data indicating that more than 75% of TBIs among their personnel occur in garrison or training; in other words, they do not involve blasts.

The authors of the study note that the young mean age of veterans in this study (50 years) raises concerns that this problem will increase as TBI-exposed veterans age. “The implications for the military health system, VA health care, and society”, they say, “are profound,” highlighting the need to further understand what physiological processes increase the risk of dementia and how this risk can be reduced.

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Although males represent a majority of emergency department visits for sports and recreation-related concussion, researchers have recently found that female athletes have a higher rate of concussion and appear to have worse outcomes than their male counterparts participating in the same sport. University of Pennsylvania researchers have recently identified anatomical differences between male and female axons that may explain this increased vulnerability.

The Penn researchers note, “while the underlying causes of concussion symptoms have yet to be fully characterized, traumatic axonal injury (TAI) has emerged as a primary neuropathological signature” which “likely reflects the unique vulnerability of axons to mechanical damage as the brain undergoes high rotational accelerations.”

Rat and human neurons were used to develop micro-patterned axon tracts in vitro (in a culture dish) that were genetically either male or female. Distinct structural differences were found. Computational modeling of TAI showed that these structural differences placed female axons at greater risk of failure during trauma under the same applied loads as the male axons. Dynamic stretch injury to the axons also induced greater pathophysiology in female axons (including more swelling and greater loss of calcium signaling.)

The researchers offer two possible evolutionary foundations for the observed sex differences. One is that although female brains are smaller in total volume, there is a functional need to maintain a similar number of axons in a given tract for both sexes, resulting in structural differences. For example, in the corpus callosum, although the average axon diameter and total tract volume is greater for males, females have a higher total number of axons. An alternative explanation offered is that since primitive times, as males have preferentially engaged in activities with a risk of head trauma, there may have been an evolutionary advantage to maintain a more mechanically resilient axonal substructure.

More research is needed to fully understand sex differences in brain structure and the implication of these differences for treatment following TBI.

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A new study published in the Journal of Neurotrauma highlights the importance of monitoring TBI patients for the presence of depression symptoms and providing clinical support to prevent minor depression from converting into major depression.

Canadian researchers assessed 236 individuals diagnosed with traumatic brain injury at 4, 8 and 12 months following injury. The results confirm prior studies showing that depression in very prevalent following TBI.

Overall, 42% of participants were diagnosed with either minor (13%) or major (29%) depression in the first year. A higher rate of major depression was found in mild TBI cases (concussion) compared to moderate/severe TBI (almost twice the percentage at 4 months, somewhat less so later on.) Not surprising, a higher rate of depression was also found in patients with a past history of depression (almost 3 times the rate in patients without a prior history.) The rate of major depression following TBI was 6 times greater than the general population.

Another important finding was that patients were just as likely to have persisting depression or get worse than recover, even with supportive services, highlighting the importance of continuous monitoring (e.g. scheduled screenings) over the months or even years following injury.

This information is important since depression, especially major depression, can interfere with recovery following TBI and in some cases can even be life threatening. As the authors point out, other studies have shown that patients with a history of TBI are 3 to 4 time more likely to commit suicide that individuals without a history of TBI.

The Bottom Line

Depression is the most common mental health issue following TBI. It cannot be ignored.

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