TBI

Complex link between head trauma and Alzheimer’s

Studies linking head trauma with increased risk and earlier age of onset for Alzheimer's disease have yielded contradictory results. Now a population-based study involving 448 healthy older adults (70+) and 141 seniors with mild cognitive impairment

Bright light therapy may help those with mild TBI

Bright light therapy lamp

A small study involving 18 individuals with at least one mild traumatic brain injury with related sleep disturbance has shown that six weeks of morning bright light therapy resulted in a marked decrease in subjective daytime sleepiness, and improved nighttime sleep.

Sleep, because of its role in brain plasticity, is likely to be important for brain recovery, but unfortunately sleep problems are common in those with TBI.

The research was presented on June 3, in Baltimore, Md., at SLEEP 2013, the 27th annual meeting of the Associated Professional Sleep Societies LLC.

Repeated hits to the head without concussion still dangerous

football game

A study involving 67 college football players has found that a protein biomarker for traumatic brain injury (S100B) was present in varying degrees in the blood samples of all the players after every game, even though none of them suffered a concussion. This demonstrates that even the most routine hits have some impact on the blood-brain barrier and possibly the brain itself.

Concussions in high school athletes may need longer recovery & better testing

Two small studies suggest that standard testing of concussed high school athletes might be insufficiently sensitive.

I’ve talked before about how even mild head injuries can have serious consequences, and in recent years we’ve seen growing awareness of the long-term dangers of sports’ concussions (especially for young people). This has been followed by a number of initiatives to help protect athletes. However, while encouraging, they may still be under-estimating the problem. Two recent studies, involving high school athletes who had experienced concussions, point to quite subtle impairment lasting for longer than expected.

In one study, 20 concussed adolescents were tested on their attention and executive function within 72 hours post injury, and then again at one week, two weeks, one month, and two months post injury. Compared with matched controls, they had a significantly greater switch cost on the Task-Switching Test and a significantly greater reaction time for the Attentional Network Test conflict effect component, with this lasting up to two months after injury.

The results suggest that longer recovery periods than the standard 7-10 days may be warranted, given that the slower reaction times (although only a matter of milliseconds) might make further injury more likely.

In another study, 54 adolescent athletes who had been concussed but who reported being symptom-free and had returned to baseline neurocognitive-test levels, were given, further testing. This revealed that over a quarter of them (27.7%) showed cognitive impairment following moderate physical exertion (15 to 25 minutes on a treadmill, elliptical, or stationary bicycle). These athletes scored significantly lower on verbal and visual memory, although processing speed and reaction was not affected (suggesting that tests focusing mainly on these latter abilities are insufficient).

The group affected did not differ from the rest in terms of symptoms or concussion history.

The findings suggest that computerized neurocognitive testing following moderate exertion should be part of the standard procedure when making return-to-play decisions.

Correlation between emotional intelligence and IQ

A study shows that IQ and conscientiousness significantly predict emotional intelligence, and identifies shared brain areas that underlie this interdependence.

By using brain scans from 152 Vietnam veterans with a variety of combat-related brain injuries, researchers claim to have mapped the neural basis of general intelligence and emotional intelligence.

There was significant overlap between general intelligence and emotional intelligence, both in behavioral measures and brain activity. Higher scores on general intelligence tests and personality reliably predicted higher performance on measures of emotional intelligence, and many of the same brain regions (in the frontal and parietal cortices) were found to be important to both.

More specifically, impairments in emotional intelligence were associated with selective damage to a network containing the extrastriate body area (involved in perceiving the form of other human bodies), the left posterior superior temporal sulcus (helps interpret body movement in terms of intentions), left temporo-parietal junction (helps work out other person’s mental state), and left orbitofrontal cortex (supports emotional empathy). A number of associated major white matter tracts were also part of the network.

Two of the components of general intelligence were strong contributors to emotional intelligence: verbal comprehension/crystallized intelligence, and processing speed. Verbal impairment was unsurprisingly associated with selective damage to the language network, which showed some overlap with the network underlying emotional intelligence. Similarly, damage to the fronto-parietal network linked to deficits in processing speed also overlapped in places with the emotional intelligence network.

Only one of the ‘big five’ personality traits contributed to the prediction of emotional intelligence — conscientiousness. Impairments in conscientiousness were associated with damage to brain regions widely implicated in social information processing, of which two areas (left orbitofrontal cortex and left temporo-parietal junction) were also involved in impaired emotional intelligence, suggesting where these two attributes might be connected (ability to predict and understand another’s emotions).

It’s interesting (and consistent with the growing emphasis on connectivity rather than the more simplistic focus on specific regions) that emotional intelligence was so affected by damage to white matter tracts. The central role of the orbitofrontal cortex is also intriguing – there’s been growing evidence in recent years of the importance of this region in emotional and social processing, and it’s worth noting that it’s in the right place to integrate sensory and bodily sensation information and pass that onto decision-making systems.

All of this is to say that emotional intelligence depends on social information processing and general intelligence. Traditionally, general intelligence has been thought to be distinct from social and emotional intelligence. But humans are fundamentally social animals, and – contra the message of the Enlightenment, that we have taken so much to heart – it has become increasingly clear that emotions and reason are inextricably entwined. It is not, therefore, all that surprising that general and emotional intelligence might be interdependent. It is more surprising that conscientiousness might be rooted in your degree of social empathy.

It’s also worth noting that ‘emotional intelligence’ is not simply a trendy concept – a pop quiz question regarding whether you ‘have a high EQ’ (or not), but that it can, if impaired, produce very real problems in everyday life.

Emotional intelligence was measured by the Mayer, Salovey, Caruso Emotional Intelligence Test (MSCEIT), general IQ by the Wechsler Adult Intelligence Scale, and personality by the Neuroticism-Extroversion-Openness Inventory.

One of the researchers talks about this study on this YouTube video and on this podcast.

Reference: 

Self-imagination helps memory in both healthy and memory-impaired

A small study involving patients with TBI has found that the best learning strategies are ones that call on the self-schema rather than episodic memory, and the best involves self-imagination.

Sometime ago, I reported on a study showing that older adults could improve their memory for a future task (remembering to regularly test their blood sugar) by picturing themselves going through the process. Imagination has been shown to be a useful strategy in improving memory (and also motor skills). A new study extends and confirms previous findings, by testing free recall and comparing self-imagination to more traditional strategies.

The study involved 15 patients with acquired brain injury who had impaired memory and 15 healthy controls. Participants memorized five lists of 24 adjectives that described personality traits, using a different strategy for each list. The five strategies were:

  • think of a word that rhymes with the trait (baseline),
  • think of a definition for the trait (semantic elaboration),
  • think about how the trait describes you (semantic self-referential processing),
  • think of a time when you acted out the trait (episodic self-referential processing), or
  • imagine acting out the trait (self-imagining).

For both groups, self-imagination produced the highest rates of free recall of the list (an average of 9.3 for the memory-impaired, compared to 3.2 using the baseline strategy; 8.1 vs 3.2 for the controls — note that the controls were given all 24 items in one list, while the memory-impaired were given 4 lists of 6 items).

Additionally, those with impaired memory did better using semantic self-referential processing than episodic self-referential processing (7.3 vs 5.7). In contrast, the controls did much the same in both conditions. This adds to the evidence that patients with brain injury often have a particular problem with episodic memory (knowledge about specific events). Episodic memory is also particularly affected in Alzheimer’s, as well as in normal aging and depression.

It’s also worth noting that all the strategies that involved the self were more effective than the two strategies that didn’t, for both groups (also, semantic elaboration was better than the baseline strategy).

The researchers suggest self-imagination (and semantic self-referential processing) might be of particular benefit for memory-impaired patients, by encouraging them to use information they can more easily access (information about their own personality traits, identity roles, and lifetime periods — what is termed the self-schema), and that future research should explore ways in which self-imagination could be used to support everyday memory tasks, such as learning new skills and remembering recent events.

Genes, brain size, brain atrophy, and Alzheimer’s risk

A round-up of genetic news. Several genes are linked to smaller brain size and faster brain atrophy in middle- & old age. The main Alzheimer's gene is implicated in leaky blood vessels, and shown to interact with brain size, white matter lesions, and dementia risk. Some evidence suggests early-onset Alzheimer's is not so dissimilar to late-onset Alzheimer's.

Genetic analysis of 9,232 older adults (average age 67; range 56-84) has implicated four genes in how fast your hippocampus shrinks with age (rs7294919 at 12q24, rs17178006 at 12q14, rs6741949 at 2q24, rs7852872 at 9p33). The first of these (implicated in cell death) showed a particularly strong link to a reduced hippocampus volume — with average consequence being a hippocampus of the same size as that of a person 4-5 years older.

Faster atrophy in this crucial brain region would increase people’s risk of Alzheimer’s and cognitive decline, by reducing their cognitive reserve. Reduced hippocampal volume is also associated with schizophrenia, major depression, and some forms of epilepsy.

In addition to cell death, the genes linked to this faster atrophy are involved in oxidative stress, ubiquitination, diabetes, embryonic development and neuronal migration.

A younger cohort, of 7,794 normal and cognitively compromised people with an average age of 40, showed that these suspect gene variants were also linked to smaller hippocampus volume in this age group. A third cohort, comprised of 1,563 primarily older people, showed a significant association between the ASTN2 variant (linked to neuronal migration) and faster memory loss.

In another analysis, researchers looked at intracranial volume and brain volume in 8,175 elderly. While they found no genetic associations for brain volume (although there was one suggestive association), they did discover that intracranial volume (the space occupied by the fully developed brain within the skull — this remains unchanged with age, reflecting brain size at full maturity) was significantly associated with two gene variants (at loci rs4273712, on chromosome 6q22, and rs9915547, on 17q21). These associations were replicated in a different sample of 1,752 older adults. One of these genes is already known to play a unique evolutionary role in human development.

A meta-analysis of seven genome-wide association studies, involving 10,768 infants (average age 14.5 months), found two loci robustly associated with head circumference in infancy (rs7980687 on chromosome 12q24 and rs1042725 on chromosome 12q15). These loci have previously been associated with adult height, but these effects on infant head circumference were largely independent of height. A third variant (rs11655470 on chromosome 17q21 — note that this is the same chromosome implicated in the study of older adults) showed suggestive evidence of association with head circumference; this chromosome has also been implicated in Parkinson's disease and other neurodegenerative diseases.

Previous research has found an association between head size in infancy and later development of Alzheimer’s. It has been thought that this may have to do with cognitive reserve.

Interestingly, the analyses also revealed that a variant in a gene called HMGA2 (rs10784502 on 12q14.3) affected intelligence as well as brain size.

Why ‘Alzheimer’s gene’ increases Alzheimer’s risk

Investigation into the so-called ‘Alzheimer’s gene’ ApoE4 (those who carry two copies of this variant have roughly eight to 10 times the risk of getting Alzheimer’s disease) has found that ApoE4 causes an increase in cyclophilin A, which in turn causes a breakdown of the cells lining the blood vessels. Blood vessels become leaky, making it more likely that toxic substances will leak into the brain.

The study found that mice carrying the ApoE4 gene had five times as much cyclophilin A as normal, in cells crucial to maintaining the integrity of the blood-brain barrier. Blocking the action of cyclophilin A brought blood flow back to normal and reduced the leakage of toxic substances by 80%.

The finding is in keeping with the idea that vascular problems are at the heart of Alzheimer’s disease — although it should not be assumed from that, that other problems (such as amyloid-beta plaques and tau tangles) are not also important. However, one thing that does seem clear now is that there is not one single pathway to Alzheimer’s. This research suggests a possible treatment approach for those carrying this risky gene variant.

Note also that this gene variant is not only associated with Alzheimer’s risk, but also Down’s syndrome dementia, poor outcome following TBI, and age-related cognitive decline.

On which note, I’d like to point out recent findings from the long-running Nurses' Health Study, involving 16,514 older women (70-81), that suggest that effects of postmenopausal hormone therapy for cognition may depend on apolipoprotein E (APOE) status, with the fastest rate of decline being observed among HT users who carried the APOe4 variant (in general HT was associated with poorer cognitive performance).

It’s also interesting to note another recent finding: that intracranial volume modifies the effect of apoE4 and white matter lesions on dementia risk. The study, involving 104 demented and 135 nondemented 85-year-olds, found that smaller intracranial volume increased the risk of dementia, Alzheimer's disease, and vascular dementia in participants with white matter lesions. However, white matter lesions were not associated with increased dementia risk in those with the largest intracranial volume. But intracranial volume did not modify dementia risk in those with the apoE4 gene.

More genes involved in Alzheimer’s

More genome-wide association studies of Alzheimer's disease have now identified variants in BIN1, CLU, CR1 and PICALM genes that increase Alzheimer’s risk, although it is not yet known how these gene variants affect risk (the present study ruled out effects on the two biomarkers, amyloid-beta 42 and phosphorylated tau).

Same genes linked to early- and late-onset Alzheimer's

Traditionally, we’ve made a distinction between early-onset Alzheimer's disease, which is thought to be inherited, and the more common late-onset Alzheimer’s. New findings, however, suggest we should re-think that distinction. While the genetic case for early-onset might seem to be stronger, sporadic (non-familial) cases do occur, and familial cases occur with late-onset.

New DNA sequencing techniques applied to the APP (amyloid precursor protein) gene, and the PSEN1 and PSEN2 (presenilin) genes (the three genes linked to early-onset Alzheimer's) has found that rare variants in these genes are more common in families where four or more members were affected with late-onset Alzheimer’s, compared to normal individuals. Additionally, mutations in the MAPT (microtubule associated protein tau) gene and GRN (progranulin) gene (both linked to frontotemporal dementia) were also found in some Alzheimer's patients, suggesting they had been incorrectly diagnosed as having Alzheimer's disease when they instead had frontotemporal dementia.

Of the 439 patients in which at least four individuals per family had been diagnosed with Alzheimer's disease, rare variants in the 3 Alzheimer's-related genes were found in 60 (13.7%) of them. While not all of these variants are known to be pathogenic, the frequency of mutations in these genes is significantly higher than it is in the general population.

The researchers estimate that about 5% of those with late-onset Alzheimer's disease have changes in these genes. They suggest that, at least in some cases, the same causes may underlie both early- and late-onset disease. The difference being that those that develop it later have more protective factors.

Another gene identified in early-onset Alzheimer's

A study of the genes from 130 families suffering from early-onset Alzheimer's disease has found that 116 had mutations on genes already known to be involved (APP, PSEN1, PSEN2 — see below for some older reports on these genes), while five of the other 14 families all showed mutations on a new gene: SORL1.

I say ‘new gene’ because it hasn’t been implicated in early-onset Alzheimer’s before. However, it has been implicated in the more common late-onset Alzheimer’s, and last year a study reported that the gene was associated with differences in hippocampal volume in young, healthy adults.

The finding, then, provides more support for the idea that some cases of early-onset and late-onset Alzheimer’s have the same causes.

The SORL1 gene codes for a protein involved in the production of the beta-amyloid peptide, and the mutations seen in this study appear to cause an under-expression of SORL1, resulting in an increase in the production of the beta-amyloid peptide. Such mutations were not found in the 1500 ethnicity-matched controls.

 

Older news reports on these other early-onset genes (brought over from the old website):

New genetic cause of Alzheimer's disease

Amyloid protein originates when it is cut by enzymes from a larger precursor protein. In very rare cases, mutations appear in the amyloid precursor protein (APP), causing it to change shape and be cut differently. The amyloid protein that is formed now has different characteristics, causing it to begin to stick together and precipitate as amyloid plaques. A genetic study of Alzheimer's patients younger than 70 has found genetic variations in the promoter that increases the gene expression and thus the formation of the amyloid precursor protein. The higher the expression (up to 150% as in Down syndrome), the younger the patient (starting between 50 and 60 years of age). Thus, the amount of amyloid precursor protein is a genetic risk factor for Alzheimer's disease.

Theuns, J. et al. 2006. Promoter Mutations That Increase Amyloid Precursor-Protein Expression Are Associated with Alzheimer Disease. American Journal of Human Genetics, 78, 936-946.

http://www.eurekalert.org/pub_releases/2006-04/vfii-rda041906.php

Evidence that Alzheimer's protein switches on genes

Amyloid b-protein precursor (APP) is snipped apart by enzymes to produce three protein fragments. Two fragments remain outside the cell and one stays inside. When APP is produced in excessive quantities, one of the cleaved segments that remains outside the cell, called the amyloid b-peptides, clumps together to form amyloid plaques that kill brain cells and may lead to the development of Alzheimer’s disease. New research indicates that the short "tail" segment of APP that is trapped inside the cell might also contribute to Alzheimer’s disease, through a process called transcriptional activation - switching on genes within the cell. Researchers speculate that creation of amyloid plaque is a byproduct of a misregulation in normal APP processing.

[2866] Cao, X., & Südhof T. C. (2001).  A Transcriptively Active Complex of APP with Fe65 and Histone Acetyltransferase Tip60. Science. 293(5527), 115 - 120.

http://www.eurekalert.org/pub_releases/2001-07/aaft-eta070201.php

Inactivation of Alzheimer's genes in mice causes dementia and brain degeneration

Mutations in two related genes known as presenilins are the major cause of early onset, inherited forms of Alzheimer's disease, but how these mutations cause the disease has not been clear. Since presenilins are involved in the production of amyloid peptides (the major components of amyloid plaques), it was thought that such mutations might cause Alzheimer’s by increasing brain levels of amyloid peptides. Accordingly, much effort has gone into identifying compounds that could block presenilin function. Now, however, genetic engineering in mice has revealed that deletion of these genes causes memory loss and gradual death of nerve cells in the mouse brain, demonstrating that the protein products of these genes are essential for normal learning, memory and nerve cell survival.

Saura, C.A., Choi, S-Y., Beglopoulos, V., Malkani, S., Zhang, D., Shankaranarayana Rao, B.S., Chattarji, S., Kelleher, R.J.III, Kandel, E.R., Duff, K., Kirkwood, A. & Shen, J. 2004. Loss of Presenilin Function Causes Impairments of Memory and Synaptic Plasticity Followed by Age-Dependent Neurodegeneration. Neuron, 42 (1), 23-36.

http://www.eurekalert.org/pub_releases/2004-04/cp-ioa032904.php

Reference: 

[2858] Consortium, E. N. I. G. M. - A.(E. N. I. G. M. A.), & Cohorts Heart Aging Research Genomic Epidemiology(charge) (2012).  Common variants at 12q14 and 12q24 are associated with hippocampal volume. Nature Genetics. 44(5), 545 - 551.

[2909] Taal, R. H., Pourcain B. S., Thiering E., Das S., Mook-Kanamori D. O., Warrington N. M., et al. (2012).  Common variants at 12q15 and 12q24 are associated with infant head circumference. Nature Genetics. 44(5), 532 - 538.

[2859] Cohorts Heart Aging Research Genomic Epidemiology,(charge), & Consortium E. G. G.(E. G. G.) (2012).  Common variants at 6q22 and 17q21 are associated with intracranial volume. Nature Genetics. 44(5), 539 - 544.

[2907] Stein, J. L., Medland S. E., Vasquez A. A., Hibar D. P., Senstad R. E., Winkler A. M., et al. (2012).  Identification of common variants associated with human hippocampal and intracranial volumes. Nature Genetics. 44(5), 552 - 561.

[2925] Bell, R. D., Winkler E. A., Singh I., Sagare A. P., Deane R., Wu Z., et al. (2012).  Apolipoprotein E controls cerebrovascular integrity via cyclophilin A. Nature.

Kang, J. H., & Grodstein F. (2012).  Postmenopausal hormone therapy, timing of initiation, APOE and cognitive decline. Neurobiology of Aging. 33(7), 1129 - 1137.

Skoog, I., Olesen P. J., Blennow K., Palmertz B., Johnson S. C., & Bigler E. D. (2012).  Head size may modify the impact of white matter lesions on dementia. Neurobiology of Aging. 33(7), 1186 - 1193.

[2728] Cruchaga, C., Chakraverty S., Mayo K., Vallania F. L. M., Mitra R. D., Faber K., et al. (2012).  Rare Variants in APP, PSEN1 and PSEN2 Increase Risk for AD in Late-Onset Alzheimer's Disease Families. PLoS ONE. 7(2), e31039 - e31039.

Full text available at http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0031039

[2897] Pottier, C., Hannequin D., Coutant S., Rovelet-Lecrux A., Wallon D., Rousseau S., et al. (2012).  High frequency of potentially pathogenic SORL1 mutations in autosomal dominant early-onset Alzheimer disease. Molecular Psychiatry.

McCarthy, J. J., Saith S., Linnertz C., Burke J. R., Hulette C. M., Welsh-Bohmer K. A., et al. (2012).  The Alzheimer's associated 5′ region of the SORL1 gene cis regulates SORL1 transcripts expression. Neurobiology of Aging. 33(7), 1485.e1-1485.e8 - 1485.e1-1485.e8

Long-lasting effects of early-childhood brain injuries

A 10 year follow-up of children hospitalized for brain injuries in early childhood suggests that young brains are not as resilient as we thought.

I recently discussed some of the implications of head injuries and how even mild concussions can have serious and long-term consequences. A follow-up study looking at the effects of childhood traumatic brain injury ten years after the event has found that even those with mild TBI showed some measurable effects, while those with severe TBI had markedly poorer performance on a number of cognitive measures.

The study involved 40 children who were admitted to hospital with TBI in early childhood (between 2 to 7 years; average just under 5), and 16 healthy controls. The children’s cognitive functions were assessed at the time of accident, and again at 12 and 30 months and 10 years later. Of the 40 with TBIs, 7 had mild injuries, 20 had moderate, and 13 severe.

Unsurprisingly, children with severe TBI had the poorest outcomes. This group was significantly poorer (compared to controls) on full scale IQ; performance IQ; verbal IQ; verbal comprehension; perceptual organization, processing speed. Those who had moderate TBI were significantly poorer on full scale IQ and verbal comprehension only, and those with mild TBI performed more poorly than the controls on verbal comprehension only. Note the size of these effects: the average scores of the group with severe TBI were 18-26 points lower than the control group. In comparison, those with moderate TBI were around 10 points lower on the two significant measures.

These findings are in contrast to research involving adults and older children, where IQ tends to remain intact.

They also contradict the belief that young brains have greater ability to ‘bounce back’ from injury.

Interestingly, the recovery trajectory wasn’t significantly affected by severity of injury — all the groups followed a similar pattern and they all tended to plateau from 5 to 10 years after injury. In general, the findings paint a picture of a long period of disrupted development immediately after the injury, lasting perhaps as long as 30 months, before the brain has recovered sufficiently to progress relatively normally. In other words, intervention may be helpful even years after the injury.

One weakness in the study is the small number of mild TBI cases. It should also be noted that the IQ of the control group was surprisingly high (113). However, given that they had similar IQ levels to the TBI groups prior to injury, it is possible that this reflects a practice effect (but remember that all groups got the same amount of practice).

One thing I wonder about, given recent research pointing to the value of schooling in raising IQ, is the extent to which some of this is due to loss of education that may have resulted from severe injury.

Frequent 'heading' in soccer can lead to brain injury and cognitive impairment

A small study extends the evidence that even mild concussions can cause brain damage, with the finding that frequent heading of the ball in soccer can cause similar damage.

American football has been in the news a lot in recent years, as evidence has accumulated as to the brain damage incurred by professional footballers. But American football is a high-impact sport. Soccer is quite different. And yet the latest research reveals that even something as apparently unexceptional as bouncing a ball off your forehead can cause damage to your brain, if done often enough.

Brain scans on 32 amateur soccer players (average age 31) have revealed that those who estimated heading the ball more than 1,000-1,500 times in the past year had damage to white matter similar to that seen in patients with concussion.

Six brain regions were seen to be affected: one in the frontal lobe and five in the temporo-occipital cortex. These regions are involved in attention, memory, executive functioning and higher-order visual functions. The number of headings (obviously very rough estimates, based presumably on individuals’ estimates of how often they play and how often they head the ball on average during a game) needed to produce measurable decreases in the white matter integrity varied per region. In four of temporo-occipital regions, the threshold number was around 1500; in the fifth it was only 1000; in the frontal lobe, it was 1300.

Those with the highest annual heading frequency also performed worse on tests of verbal memory and psychomotor speed (activities that require mind-body coordination, like throwing a ball).

This is only a small study and clearly more research is required, but the findings indicate that we should lower our ideas of what constitutes ‘harm’ to the brain — if repetition is frequent enough, even mild knocks can cause damage. This adds to the evidence I discussed in a recent blog post, that even mild concussions can produce long-lasting trauma to the brain, and it is important to give your brain time to repair itself.

At the moment we can only speculate on the effect such repetition might have to the vulnerable brains of children.

The researchers suggest that heading should be monitored to prevent players exceeding unsafe exposure thresholds.

Reference: 

Kim, N., Zimmerman, M., Lipton, R., Stewart, W., Gulko, E., Lipton, M. & Branch, C. 2011. PhD Making Soccer Safer for the Brain: DTI-defined Exposure Thresholds for White Matter Injury Due to Soccer Heading. Presented November 30 at the annual meeting of the Radiological Society of North America (RSNA) in Chicago.

Even mild head injuries can seriously affect the brain

Traumatic brain injury is the biggest killer of young adults and children in the U.S., and in a year more Americans suffer a TBI than are diagnosed with breast, lung, prostate, brain and colon cancer combined. There are many causes of TBI, but one of the more preventable is that of sports concussion.

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