chronic traumatic encephalopathy

Symptoms of CTE, which occur in four stages, generally appear eight to ten years after an individual experiences repetitive mild traumatic brain injuries.{{cite journal |vauthors=McKee AC, Cantu RC, Nowinski CJ, Hedley-Whyte ET, Gavett BE, Budson AE, Santini VE, Lee HS, Kubilus CA, Stern RA |title=Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury |journal=J Neuropathol Exp Neurol |volume=68 |issue=7 |pages=709–35 |year=2009 |pmid=19535999 |pmc=2945234 |doi= 10.1097/NEN.0b013e3181a9d503}}

First-stage symptoms are confusion, disorientation, dizziness, and headaches. Second-stage symptoms include memory loss, social instability, impulsive behavior, and poor judgment. Third and fourth stages include progressive dementia, movement disorders, hypomimia, speech impediments, sensory processing disorder, tremors, vertigo, deafness, depression and suicidality.{{cite journal |vauthors=Fesharaki-Zadeh A |title=Chronic Traumatic Encephalopathy: A Brief Overview |journal= Frontiers in Neurology|volume=10 |page=713 |year=2019 |pmid=31333567 |pmc=6616127 |doi= 10.3389/fneur.2019.00713|doi-access=free }}

Additional symptoms include dysarthria, dysphagia, cognitive disorders such as amnesia, and ocular abnormalities, such as ptosis.{{cite journal |author=Corsellis| title=The Aftermath of Boxing |journal=Psychological Medicine |volume=3 |issue=3 |pages=270–303 |year=1973 |pmid=4729191 |doi= 10.1017/S0033291700049588 | s2cid=41879040 |display-authors=etal}} The condition manifests as dementia, or declining mental ability, problems with memory, dizzy spells or lack of balance to the point of not being able to walk under one's own power for a short time and/or Parkinsonism, or tremors and lack of coordination. It can also cause speech problems and an unsteady gait. Patients with CTE may be prone to inappropriate or explosive behavior and may display pathological jealousy or paranoia.{{cite journal |author=Mendez MF |title=The neuropsychiatric aspects of boxing |journal=International Journal of Psychiatry in Medicine |volume=25 |issue=3 |pages=249–62 |year=1995 |pmid=8567192 |doi=10.2190/CUMK-THT1-X98M-WB4C|s2cid=20238578 }}

{{See also|Chronic traumatic encephalopathy in sports}}

Most documented cases have occurred in athletes with mild repetitive head impacts (RHI) over an extended period. Evidence indicates that repetitive concussive and subconcussive blows to the head cause CTE.

• [https://www.nature.com/articles/labinvest201554 Chronic traumatic encephalopathy: A paradigm in search of evidence? Rudy J Castellani]
• [https://www.nature.com/articles/nrneurol.2017.32 New insights into the long-term effects of mild brain injury Charlotte Ridler Nature Reviews Neurology volume 13, page195 (2017)]
• [https://academic.oup.com/brain/article/141/2/422/4815697 Concussion, microvascular injury, and early tauopathy in young athletes after impact head injury and an impact concussion mouse model - Brain, Volume 141, Issue 2, February 2018]
• [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4288217/ Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome - Alzheimers Res Ther. 2014; 6(5): 68. Published online 2014 Sep 24.]
• [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4238241/ Effects of Subconcussive Head Trauma on the Default Mode Network of the Brain - J Neurotrauma. 2014 Dec 1; 31(23): 1907–1913.]
• [https://www.frontiersin.org/articles/10.3389/fnhum.2019.00294/full Understanding the Consequences of Repetitive Subconcussive Head Impacts in Sport: Brain Changes and Dampened Motor Control Are Seen After Boxing Practice - ORIGINAL RESEARCH article Front. Hum. Neurosci., 10 September 2019] In particular, it is associated with contact sports such as boxing, American football, Australian rules football, wrestling, mixed martial arts, ice hockey, rugby, and association football. In association football (soccer), whether this is just associated with prolific headers or other injuries is unclear as of 2017.{{cite journal |last1=Nitrini |first1=R |title=Soccer (Football Association) and chronic traumatic encephalopathy: A short review and recommendation. |journal=Dementia & Neuropsychologia |date=2017 |volume=11 |issue=3 |pages=218–20 |doi=10.1590/1980-57642016dn11-030002 |pmid=29213517|pmc=5674664 }} Other potential risk factors include military personnel (repeated exposure to explosive charges or large caliber ordnance), domestic violence, and repeated impact to the head. Although many military personnel are around blasts and explosions very often, it is very rare for these personnel to be diagnosed with CTE. Studies have shown that only 4.4% of deceased military veterans have been diagnosed with CTE.{{cite web |last1=Ruprecht |first1=Michał |title=Evidence of CTE Rare in Military Personnel |url=https://www.medpagetoday.com/neurology/headtrauma/99138#:~:text=Evidence%20of%20chronic%20traumatic%20encephalopathy%20(CTE)%20was,Services%20University%20in%20Bethesda%2C%20Maryland%2C%20and%20colleagues |publisher=MedPage Today |access-date=15 December 2024 |language=en |date=8 June 2022}} Exposure to blasts from explosives can produce symptoms of CTE.{{Cite web |title=Study Shows First Case Series of Chronic Traumatic Encephalopathy in Blast-Exposed Military Service Personnel and Mechanism of Injury in Blast Neurotrauma {{!}} Chobanian & Avedisian School of Medicine |url=https://www.bumc.bu.edu/camed/2012/05/17/study-shows-first-case-series-of-chronic-traumatic-encephalopathy-in-blast-exposed-military-service-personnel-and-mechanism-of-injury-in-blast-neurotrauma/#:~:text=The%20blast%20wind%20from%20an,and/or%20a%20concussive%20injury |access-date=2024-11-19 |website=www.bumc.bu.edu}} Another cause of CTE is an excessive buildup of misfolded Tau proteins, which is where the protein misfolds, setting off a reaction that slowly kills the brain cells.{{Cite web |title=What is CTE? |url=https://concussionfoundation.org/cte-resources/what-is-cte/#:~:text=According%20to%20the%20Boston%20University,her%20research%20by%20clicking%20here. |access-date=2024-11-19 |website=Concussion Legacy Foundation |language=en-usa}} The exact amount of trauma required for the condition to occur is unknown, although it is believed that it may take years to develop.

The neuropathological appearance of CTE is distinguished from other tauopathies, such as Alzheimer's disease. The four clinical stages of observable CTE disability have been correlated with tau pathology in brain tissue, ranging in severity from focal perivascular epicenters of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions.{{cite journal |vauthors=McKee AC, Stern RA, Nowinski CJ, Stein TD, Alvarez VE, Daneshvar DH, Lee HS, Wojtowicz SM, Hall G, Baugh CM, Riley DO, Kubilus CA, Cormier KA, Jacobs MA, Martin BR, Abraham CR, Ikezu T, Reichard RR, Wolozin BL, Budson AE, Goldstein LE, Kowall NW, Cantu RC |title=The spectrum of disease in chronic traumatic encephalopathy |journal= Brain |volume=136 |issue=Pt 1 |pages=43–64 |year=2013 |pmid=23208308 |pmc=3624697 |doi=10.1093/brain/aws307}}

The primary physical manifestations of CTE include a reduction in brain weight, associated with atrophy of the frontal and temporal cortices and medial temporal lobe. The lateral ventricles and the third ventricle are often enlarged, with rare instances of dilation of the fourth ventricle.{{cite journal |vauthors=Baugh CM, Stamm JM, Riley DO, Gavett BE, Shenton ME, Lin A, Nowinski CJ, Cantu RC, McKee AC, Stern RA |title=Chronic traumatic encephalopathy: neurodegeneration following repetitive concussive and subconcussive brain trauma |journal=Brain Imaging Behavior |volume=6 |issue=2 |pages= 244–54 |year=2012 |pmid=22552850 |doi=10.1007/s11682-012-9164-5 |s2cid=15955018 }} Other physical manifestations of CTE include anterior cavum septi pellucidi and posterior fenestrations, pallor of the substantia nigra and locus ceruleus, and atrophy of the olfactory bulbs, thalamus, mammillary bodies, brainstem and cerebellum.{{cite news |last=Jancin |first=Bruce |title=Chronic traumatic encephalopathy test sought |url=http://go.galegroup.com/ps/i.do?id=GALE%7CA291245393&v=2.1&it=r&p=HRCA&sw=w |access-date=15 December 2013 |newspaper=Internal Medicine News |date=1 June 2011}} As CTE progresses, there may be marked atrophy of the hippocampus, entorhinal cortex, and amygdala.

On a microscopic scale, a pathognomonic CTE lesion involves p-tau aggregates in neurons, with or without thorn-shaped astrocytes, at the depths of the cortical sulcus around a small blood vessel, deep in the parenchyma, and not restricted to the subpial and superficial region of the sulcus; the pathognomonic lesion must include p-tau in neurons to distinguish CTE from aging-related tau astrogliopathy (ARTAG).{{cite journal |last1=Bienek |first1=Kevin F. |last2=al |first2=et |title=The Second NINDS/NIBIB Consensus Meeting to Define Neuropathological Criteria for the Diagnosis of Chronic Traumatic Encephalopathy |journal=Neuropathology and Experimental Neurology |date=21 February 2021 |volume=80 |issue=3 |pages=210–219 |doi=10.1093/jnen/nlab001 |pmid=33611507 | pmc=7899277}} Supporting features of CTE are: superficial neurofibrillary tangles (NFTs); p–tau in CA2 and CA4 hippocampus; p-tau in: mammillary bodies, hypothalamic nuclei, amygdala, nucleus accumbens, thalamus, midbrain tegmentum, nucleus basalis of Meynert, raphe nuclei, substantia nigra and locus coeruleus; p-tau thorn-shaped astrocytes (TSA) in the subpial region; p-tau dot-like neurites.{{cite journal |last1=McKee |first1=Ann C.|author1-link=Ann McKee |last2=al |first2=et |title=The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy |journal=Acta Neuropathologica |date=January 2016 |volume=131 |issue=1 |pages=75–86 |doi=10.1007/s00401-015-1515-z|pmid=26667418 |pmc=4698281 }} Purely astrocytic perivascular p-tau pathology represents ARTAG and does not meet the criteria for CTE.

A small group of individuals with CTE have chronic traumatic encephalomyopathy (CTEM), which is characterized by symptoms of motor-neuron disease and which mimics amyotrophic lateral sclerosis (ALS). Progressive muscle weakness and balance and gait problems (problems with walking) seem to be early signs of CTEM.

Exosome vesicles created by the brain are potential biomarkers of TBI, including CTE.{{cite journal |vauthors=Taylor DD, Gercel-Taylor C |title=Exosome platform for diagnosis and monitoring of traumatic brain injury |journal=Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences |volume=369 |issue=1652 |page= 20130503|year=2014 |pmid=25135964 |pmc=4142024 |doi=10.1098/rstb.2013.0503}}

Loss of neurons, scarring of brain tissue, collection of proteinaceous senile plaques, hydrocephalus, attenuation of the corpus callosum, diffuse axonal injury, neurofibrillary tangles, and damage to the cerebellum are implicated in the syndrome. Neurofibrillary tangles have been found in the brains of dementia pugilistica patients, but not in the same distribution as is usually found in people with Alzheimer's.{{cite journal |vauthors=Hof PR, Bouras C, Buée L, Delacourte A, Perl DP, Morrison JH |title=Differential Distribution of Neurofibrillary Tangles in the Cerebral Cortex of Dementia Pugilistica and Alzheimer's Disease Cases |journal=Acta Neuropathologica |volume=85 |issue=1 |pages=23–30 |year=1992 |pmid=1285493 |doi=10.1007/BF00304630|s2cid=11624928 }} One group examined slices of brain from patients having had multiple mild traumatic brain injuries and found changes in the cells' cytoskeletons, which they suggested might be due to damage to cerebral blood vessels.{{cite journal | doi = 10.1007/s004010051066 | vauthors = Geddes JF, Vowles GH, Nicoll JA, Révész T | year = 1999 | title = Neuronal Cytoskeletal Changes are an Early Consequence of Repetitive Head Injury | journal = Acta Neuropathologica | volume = 98 | issue = 2| pages = 171–78 | pmid = 10442557 | s2cid = 24694052 }}

Increased exposure to concussions and subconcussive blows is regarded as the most important risk factor. In boxing, this exposure can depend on the total number of fights, number of knockout losses, duration of career, fight frequency, age of retirement, and boxing style.Jordan, B. D. (2009). "Brain injury in boxing". Clinics in Sports Medicine, 28(4), 561–78, vi.

Diagnosis of CTE cannot be made in living individuals; a clear diagnosis is only possible during an autopsy.{{Cite journal|last=Concannon|first=Leah|date=2014|title=Counseling Athletes on the Risk on Chronic Traumatic Encephalopathy|journal=Sports Health|volume=6|issue=5|pages=396–401|doi=10.1177/1941738114530958|pmid=25177414|pmc=4137675}} Though there are signs and symptoms some researchers associate with CTE, there is no definitive test to prove the existence in a living person. Signs are also very similar to those of other neurological conditions, such as Alzheimer's.Turner, Ryan C., et al. [https://pubmed.ncbi.nlm.nih.gov/27715315/ "Alzheimer's disease and chronic traumatic encephalopathy: Distinct but possibly overlapping disease entities"], Brain Injury, August 11, 2016. Accessed December 28, 2021. "Alzheimer's disease (AD) and chronic traumatic encephalopathy (CTE) have long been recognized as sharing some similar neuropathological features, mainly the presence of neurofibrillary tangles and hyperphosphorylated tau, but have generally been described as distinct entities. Evidence indicates that neurotrauma increases the risk of developing dementia and accelerates the progression of disease. Findings are emerging that CTE and AD may be present in the same patients."

The lack of distinct biomarkers is the reason CTE cannot typically be diagnosed while a person is alive. Concussions are non-structural injuries and do not result in brain bleeding, which is why most concussions cannot be seen on routine neuroimaging tests such as CT or MRI.{{cite journal |author=Poirier MP |title=Concussions: Assessment, management, and recommendations for return to activity |journal=Clinical Pediatric Emergency Medicine |volume=4|issue=3|pages=179–85|year=2003 |doi=10.1016/S1522-8401(03)00061-2}} Acute concussion symptoms (those that occur shortly after an injury) should not be confused with CTE. Differentiating between prolonged post-concussion syndrome (PCS, where symptoms begin shortly after a concussion and last for weeks, months, and sometimes even years) and CTE symptoms can be difficult. Research studies are examining whether neuroimaging can detect subtle changes in axonal integrity and structural lesions that can occur in CTE. By the early 2010s, more progress in in-vivo diagnostic techniques for CTE had been made, using DTI, fMRI, MRI, and MRS imaging; however, more research needs to be done before any such techniques can be validated.

PET tracers that bind specifically to tau protein are desired to aid the diagnosis of CTE in living individuals. One candidate is the tracer {{Not a typo|[¹⁸F]FDDNP}}, which is retained in the brain in individuals with several dementing disorders such as Alzheimer's disease, Down syndrome, progressive supranuclear palsy, corticobasal degeneration, familial frontotemporal dementia, and Creutzfeldt–Jakob disease.{{cite journal |vauthors=Villemagne VL, Fodero-Tavoletti MT, Masters CL, Rowe CC |title=Tau imaging: early progress and future directions |journal=The Lancet. Neurology |volume=14 |issue=1 |pages=114–24 |year=2015 |pmid=25496902 |doi=10.1016/S1474-4422(14)70252-2 |s2cid=10502833 }} In a small study of 5 retired NFL players with cognitive and mood symptoms, the PET scans revealed accumulation of the tracer in their brains.{{cite journal |vauthors=Small GW, Kepe V, Siddarth P, Ercoli LM, Merrill DA, Donoghue N, Bookheimer SY, Martinez J, Omalu B, Bailes J, Barrio JR |title=PET scanning of brain tau in retired national football league players: preliminary findings |journal=Am J Geriatr Psychiatry |volume=21 |issue=2 |pages=138–44 |year=2013 |pmid=23343487 |doi=10.1016/j.jagp.2012.11.019 |citeseerx=10.1.1.372.2960 }} However, {{Not a typo|[¹⁸F]FDDNP}} binds to beta-amyloid and other proteins as well. Moreover, the sites in the brain where the tracer was retained were not consistent with the known neuropathology of CTE.{{cite journal |vauthors=Montenigro PH, Corp DT, Stein TD, Cantu RC, Stern RA |title=Chronic traumatic encephalopathy: historical origins and current perspective |journal=Annual Review of Clinical Psychology |volume=11 |pages=309–30 |year=2015 |pmid=25581233 |doi=10.1146/annurev-clinpsy-032814-112814 |doi-access=free }} A more promising candidate is the tracer [¹⁸F]-T807, which binds only to tau. It is being tested in several clinical trials.{{Update inline|date=July 2024|reason=The main text says the T807 tracer is "being" tested in several clinical trials, but the cited medical reference is 9 years out of date, having been written in March 2015.}}

A putative biomarker for CTE is the presence in serum of autoantibodies against the brain. The autoantibodies were detected in football players who experienced a large number of head hits but no concussions, suggesting that even sub-concussive episodes may be damaging to the brain. The autoantibodies may enter the brain using a disrupted blood-brain barrier, and attack neuronal cells which are normally protected from an immune onslaught.John Mangels, [http://www.cleveland.com/science/index.ssf/2013/03/non-concussion_football_head_h.html Cleveland Plain Dealer], 2013/03. Given the large numbers of neurons present in the brain (86 billion), and considering the poor penetration of antibodies across a normal blood-brain barrier, there is an extended period between the initial events (head hits) and the development of any signs or symptoms. Nevertheless, autoimmune changes in blood of players may constitute the earliest measurable event predicting CTE.{{cite journal |vauthors=Marchi N, Bazarian JJ, Puvenna V, Janigro M, Ghosh C, Zhong J, Zhu T, Blackman E, Stewart D, Ellis J, Butler R, Janigro D |title=Consequences of repeated blood-brain barrier disruption in football players |journal=PLOS ONE |volume=8 |issue=3 |page=e56805 |year=2013 |pmid=23483891 |pmc=3590196 |doi=10.1371/journal.pone.0056805 |bibcode=2013PLoSO...856805M |doi-access=free }}

According to a 2017 study on the brains of deceased gridiron football players, 99% of tested brains of NFL players, 88% of CFL players, 64% of semi-professional players, 91% of college football players, and 21% of high school football players had various stages of CTE. Players still alive are not able to be tested.{{Cite web|url=https://www.bu.edu/articles/2017/cte-former-nfl-players/|title=BU Researchers Find CTE in 99% of Former NFL Players Studied|website=Boston University|date=26 July 2017 }}

Although the diagnosis of CTE cannot be determined by imaging, the effects of head trauma may be seen with the use of structural imaging.{{Cite journal|last=Concannon|first=Leah|date=October 2014|title=Counseling Athletes on the Risk of Chronic Traumatic Encephalopathy|journal=Sports Health|volume=6|issue=5|pages=396–401|doi=10.1177/1941738114530958|pmid=25177414|pmc=4137675}} Imaging techniques include the use of magnetic resonance imaging, nuclear magnetic resonance spectroscopy, CT scan, single-photon emission computed tomography, Diffusion MRI, and Positron emission tomography (PET). One specific use of imaging is the use of a PET scan is to evaluate for tau deposition, which has been conducted on retired NFL players.{{cite journal|last1=Stern|first1=Robert A.|last2=Adler|first2=Charles H.|last3=Chen|first3=Kewei|last4=Navitsky|first4=Michael|last5=Luo|first5=Ji|last6=Dodick|first6=David W.|last7=Alosco|first7=Michael L.|last8=Tripodis|first8=Yorghos|last9=Goradia|first9=Dhruman D.|last10=Martin|first10=Brett|last11=Mastroeni|first11=Diego|last12=Fritts|first12=Nathan G.|last13=Jarnagin|first13=Johnny|last14=Devous|first14=Michael D.|last15=Mintun|first15=Mark A.|last16=Pontecorvo|first16=Michael J.|last17=Shenton|first17=Martha E.|last18=Reiman|first18=Eric M.|title=Tau Positron-Emission Tomography in Former National Football League Players|journal=New England Journal of Medicine|volume=380|issue=18|year=2019|pages=1716–25|issn=0028-4793|doi=10.1056/NEJMoa1900757|pmid=30969506|pmc=6636818}}

The use of helmets and mouth guards has been put forward as a possible preventative measure; though neither has significant research to support its use,{{Cite journal|last1=Sone|first1=Je Yeong|last2=Kondziolka|first2=Douglas|last3=Huang|first3=Jason H.|last4=Samadani|first4=Uzma|date=2017-03-01|title=Helmet efficacy against concussion and traumatic brain injury: a review|url=https://thejns.org/view/journals/j-neurosurg/126/3/article-p768.xml|journal=Journal of Neurosurgery|language=en-US|volume=126|issue=3|pages=768–81|doi=10.3171/2016.2.JNS151972|pmid=27231972|issn=1933-0693|url-access=subscription}} both have been shown to reduce direct head trauma.{{Cite journal|last=Saffary|first=Roya|date=2012|title=From Concussion to Chronic Traumatic Encephalopathy: A Review|journal=Journal of Clinical Sport Psychology|pages=315–62}} Although there is no significant research to support the use of helmets to reduce the risk of concussions, there is evidence to support that helmet use reduces impact forces. The sports in which a helmet was effective in preventing TBI and concussions were skiing and snowboarding.{{Cite journal |last1=Emery |first1=Carolyn A. |last2=Black |first2=Amanda M. |last3=Kolstad |first3=Ash |last4=Martinez |first4=German |last5=Nettel-Aguirre |first5=Alberto |last6=Engebretsen |first6=Lars |last7=Johnston |first7=Karen |last8=Kissick |first8=James |last9=Maddocks |first9=David |last10=Tator |first10=Charles |last11=Aubry |first11=Mark |last12=Dvořák |first12=Jiří |last13=Nagahiro |first13=Shinji |last14=Schneider |first14=Kathryn |date=2017-06-01 |title=What strategies can be used to effectively reduce the risk of concussion in sport? A systematic review |url=https://bjsm.bmj.com/content/51/12/978 |journal=British Journal of Sports Medicine |language=en |volume=51 |issue=12 |pages=978–984 |doi=10.1136/bjsports-2016-097452 |issn=0306-3674 |pmid=28254746|s2cid=36589540 |url-access=subscription }} Mouth guards have been shown to decrease dental injuries, but again have not shown significant evidence to reduce concussions. Because repeated impacts are thought to increase the likelihood of CTE development, a growing area of practice is improved recognition and treatment for concussions and other head trauma; removal from sport participation during recovery from these traumatic injuries is essential. Proper return-to-play protocol after possible brain injuries is also important in decreasing the significance of future impacts.

Efforts are being made to change the rules of contact sports to reduce the frequency and severity of blows to the head. Examples of these rule changes are the evolution of tackling technique rules in American football, such as the banning of helmet-first tackles, and the addition of rules to protect defenseless players. Likewise, another growing area of debate is better implementation of rules already in place to protect athletes.

Because of the concern that boxing may cause CTE, there is a movement among medical professionals to ban the sport. Medical professionals have called for such a ban as early as the 1950s.

No cure exists for CTE, and it cannot be diagnosed until a post-mortem autopsy is performed.{{cite web|url=http://www.alz.org/dementia/chronic-traumatic-encephalopathy-cte-symptoms.asp|title=Alzheimer's & Dementia|website=Alzheimer's Association|publisher=alz.org|access-date=21 September 2017}} Treatment is supportive as with other forms of dementia.{{cite web |url=https://www.nhs.uk/conditions/chronic-traumatic-encephalopathy/#treating-cte |title=Treating CTE |author= |date= 1 October 2017|website=NHS Choices |publisher=GOV.UK |access-date=14 February 2018}} Those with CTE-related symptoms may receive medication and non-medication-related treatments.{{Cite journal|last1=Cantu|first1=Robert|last2=Budson|first2=Andrew|date=October 2019|title=Management of chronic traumatic encephalopathy|journal=Expert Review of Neurotherapeutics|volume=19|issue=10|pages=1015–23|doi=10.1080/14737175.2019.1633916|pmid=31215252|s2cid=195064872}} Currently, there is no way to stop or slow the development of CTE. However, medications like Aricept (donepezil) and Namenda (memantine) can mitigate memory loss and confusion, and Aricept can improve memory, motivation, and attention by increasing acetylcholine levels in the brain. Memantine is a cognitive enhancer that can help with memory loss and confusion. These medications are also treatments for Alzheimer's disease and dementia.{{Cite web |title=CTE Treatments |url=https://concussionfoundation.org/cte-resources/treatments/#:~:text=According%20to%20Dr.,mitigate%20memory%20loss%20and%20confusion. |access-date=2024-11-19 |website=Concussion Legacy Foundation |language=en-usa}} There are also antidepressants like selective serotonin reuptake inhibitors (SSRIs), which can potentially help manage some of the behavioral and emotional symptoms associated with chronic traumatic encephalopathy (CTE) and may have a small improvement in memory function, mood, and alertness. SSRIs are often the first choice of treatment for CTE due to their effectiveness.{{Cite web |last=Memory and aging center |first=Weill Institute for Neurosciences |title=A Healthcare Provider's Guide To Chronic Traumatic Encephalopathy (CTE) |url=https://memory.ucsf.edu/sites/memory.ucsf.edu/files/wysiwyg/UCSF_CTE_Providers_7-13-17.pdf}}

Rates of disease are about 30% among those with a history of multiple head injuries. Population rates, however, are unclear. Tracking the epidemiology of CTE is difficult due to the inability to diagnose this syndrome during life.{{Cite journal |last=Stein |first=Thor |date=October 16, 2024 |title=Concussion in Chronic Traumatic Encephalopathy |journal=SpringerNature Link|volume=19 |issue=10 |page=47 |doi=10.1007/S11916-015-0522-Z |pmid=26260277 |pmc=4633042 }}

Professional level athletes are the largest group with CTE, due to frequent concussions and sub-concussive impacts from play in contact sport.{{cite journal|vauthors=Saulle M, Greenwald BD|year=2012|title=Chronic traumatic encephalopathy: a review|url=http://downloads.hindawi.com/journals/rerp/2012/816069.pdf|journal=Rehabil Res Pract|volume=2012|pages=1–9|doi=10.1155/2012/816069|pmc=3337491|pmid=22567320|doi-access=free}} These contact-sports include American football, Australian rules football,{{cite web |url=https://www.theage.com.au/sport/afl/cte-discovered-in-polly-farmer-s-brain-in-landmark-afl-first-20200226-p544oq.html |title=CTE discovered in Polly Farmer's brain in AFL-first |date=26 February 2020 }} ice hockey, Rugby football (Rugby union and Rugby league),{{cite web|url=http://www.traumaticbraininjury.net/first-soccer-and-rugby-players-diagnosed-with-cte/|title=First Soccer and Rugby Players Diagnosed With CTE|author=Stone, Paul|date=18 March 2014|publisher=Neurologic Rehabilitation Institute at Brookhaven Hospital|access-date=21 March 2016}} boxing, kickboxing, mixed martial arts, association football,{{cite journal|last1=Ling|first1=Helen|last2=Morris|first2=Huw R.|last3=Neal|first3=James W.|last4=Lees|first4=Andrew J.|last5=Hardy|first5=John|last6=Holton|first6=Janice L.|last7=Revesz|first7=Tamas|last8=Williams|first8=David D.R.|date=March 2017|title=Mixed pathologies including chronic traumatic encephalopathy account for dementia in retired association football (soccer) players|journal=Acta Neuropathologica|volume=133|issue=3|pages=337–52|doi=10.1007/s00401-017-1680-3|pmc=5325836|pmid=28205009}} and wrestling.{{cite journal|vauthors=Daneshvar DH, Nowinski CJ, McKee AC, Cantu RC|year=2011|title=The epidemiology of sport-related concussion|journal=Clin Sports Med|volume=30|issue=1|pages=1–17, vii|doi=10.1016/j.csm.2010.08.006|pmc=2987636|pmid=21074078}} In association football, only prolific headers are known to have developed CTE.

Cases of CTE were also recorded in baseball.{{cite news |url=https://goodmenproject.com/featured-content/baseballs-new-three-letter-word-cte/ |title=Baseball's New Three-Letter Word: CTE |newspaper= The Good Men Project |date=2 November 2018 |last1=Cohen |first1=Neil }}

According to a 2017 study on brains of deceased gridiron football players, 99% of tested brains of NFL players, 88% of CFL players, 64% of semi-professional players, 91% of college football players, and 21% of high school football players had various stages of CTE.

As reported in a study published by Roberts, about 11% of the retired boxers he examined had a mild case of CTE, and about 6% of the boxers had major neurological problems. Through these clinical examinations, Roberts was able to establish associations between exposure to violence and the effects of CTE. He stated that among the boxers who are over the age of 50 and fought in over 150 fights, about 50% of them had CTE. This number was compared to the 7% of the boxers who had CTE and had less than 50 fights.{{Cite journal |last=Iverson |first=Grant |date=October 19, 2024 |title=Suicide and Chronic Traumatic Encephalopathy |url=https://psychiatryonline.org/doi/full/10.1176/appi.neuropsych.15070172 |journal=Neuropsychiatry |volume=28 |issue=1 |pages=9–16|doi=10.1176/appi.neuropsych.15070172 |pmid=26449269 }}

Other individuals diagnosed with CTE were those involved in military service, had a previous history of chronic seizures, were domestically abused, or were involved in activities resulting in repetitive head collisions.{{cite journal|vauthors=Daneshvar DH, Riley DO, Nowinski CJ, McKee AC, Stern RA, Cantu RC|year=2011|title=Long-term consequences: effects on normal development profile after concussion|journal=Phys Med Rehabil Clin N Am|volume=22|issue=4|pages=683–700, ix|doi=10.1016/j.pmr.2011.08.009|pmc=3208826|pmid=22050943}}{{Cite journal|last=Shetty|first=Teena|title=Imaging in Chronic Traumatic Encephalopathy and Traumatic Brain Injury|journal=Sports Health|volume=8|issue=1|pages=26–36|pmid=26733590|year=2016|doi=10.1177/1941738115588745|pmc=4702153}}

CTE was originally studied in boxers in the 1920s as "punch-drunk syndrome." The punch-drunk syndrome was first described in 1928 by a forensic pathologist, Harrison Stanford Martland, who was the chief medical examiner of Essex County in Newark, New Jersey, in a Journal of the American Medical Association article, in which he noted the tremors, slowed movement, confusion and speech problems typical of the condition.{{cite journal |author= Martland HS|title=Punch Drunk |journal=Journal of the American Medical Association |volume=91 |issue=15 |pages=1103–07|year=1928 |doi=10.1001/jama.1928.02700150029009 }} The term "punch-drunk" was replaced with "dementia pugilistica" in 1937 by J.A. Millsbaugh, as he felt the term was condescending to former boxers.{{cite journal |last1=Castellani |first1=Rudy J. |last2=Perry |first2=George |title=Dementia Pugilistica Revisited |journal=Journal of Alzheimer's Disease |date=7 November 2017 |volume=60 |issue=4 |pages=1209–21|doi=10.3233/JAD-170669 |pmid=29036831 |pmc=5676846 }} The initial diagnosis of dementia pugilistica was derived from the Latin word for boxer, pugil (akin to pugnus 'fist', pugnāre 'to fight').[http://dictionary.reference.com/browse/pugilism Pugilism (origin)], retrieved on 2 February 2013.NCERx. 2005. [http://www.about-dementia.com/dementia/brain-trauma.php Brain Trauma, Subdural Hematoma and Dementia Pugilistica] {{Webarchive|url=https://web.archive.org/web/20070527104633/http://www.about-dementia.com/dementia/brain-trauma.php |date=27 May 2007 }}. About – dementia.com. Retrieved on 19 December 2007.

Other terms for the condition have included chronic boxer's encephalopathy, traumatic boxer's encephalopathy, boxer's dementia, pugilistic dementia, chronic traumatic brain injury associated with boxing (CTBI-B), and punch-drunk syndrome.

British neurologist, Macdonald Critchley, wrote a 1949 paper titled "Punch-drunk syndromes: the chronic traumatic encephalopathy of boxers".[http://newyork.cbslocal.com/2015/12/17/concussion-bennet-omalu-nfl/ "'Concussion' Subject Bennet Omalu Exaggerated His Role, Researchers Say"]. CBS New York. 17 December 2015. CTE was first recognized as affecting individuals who took considerable blows to the head, but was believed to be confined to boxers and not other athletes. As evidence pertaining to the clinical and neuropathological consequences of repeated mild head trauma grew, it became clear that this pattern of neurodegeneration was not restricted to boxers, and the term chronic traumatic encephalopathy became most widely used.{{cite journal |author=Martland H | title=Punch Drunk|journal=The Journal of the American Medical Association |volume=91|issue=15 |pages=1103–07 |year=1928 |doi=10.1001/jama.1928.02700150029009}}{{cite journal | pmc = 2995699 |pmid=21074091 |doi=10.1016/j.csm.2010.09.007 |volume=30 |issue=1 |title=Chronic traumatic encephalopathy: a potential late effect of sport-related concussive and subconcussive head trauma |year=2011 |journal=Clin Sports Med |pages=179–88, xi |vauthors=Gavett BE, Stern RA, McKee AC}}

In 2005, Bennet Omalu{{Cite web |date=2016-11-12 |title=Physician who discovered CTE in NFL players gets AMA's highest honor |url=https://www.ama-assn.org/delivering-care/public-health/physician-who-discovered-cte-nfl-players-gets-ama-s-highest-honor |access-date=2024-11-19 |website=American Medical Association |language=en}} performed an autopsy on American football player Mike Webster. Omalu concluded that Webster was the first person to be officially diagnosed with CTE. Omalu expected the autopsy to reveal a brain affected by Alzheimer's.{{Cite web |title=tag page |url=https://www.pbs.org/wgbh/pages/frontline/oral-history/league-of-denial/cte-discovery-of-a-new-disease/#:~:text=Mike%20Webster's%20Legacy-,Dr.,chronic%20traumatic%20encephalopathy,%20or%20CTE. |access-date=2024-11-19 |website=FRONTLINE |language=en}} Instead, after fixing and dissecting the brain, Omalu observed abnormal proteins tangles that distinguish CTE from Alzheimer’s disease.

A famous case of CTE is that of former NFL player Aaron Hernandez.{{Cite web |last=Levenson |first=Eric |date=2024-10-21 |title=A timeline of Aaron Hernandez's football career, criminal cases and death |url=https://www.cnn.com/2024/10/21/us/aaron-hernandez-life-death-timeline/index.html |access-date=2024-11-19 |website=CNN |language=en}} Two years into a jail sentence for murder, Hernandez was found dead from hanging himself in his cell. An autopsy found stage 3 CTE, a severity rarely seen at his age of 27 at death.{{Cite web |last=Bracken |first=Tara |date=2020-01-20 |title=Aaron Hernandez's CTE Worst Seen in a Young Person |url=https://www.bu.edu/articles/2017/aaron-hernandez-cte-worst-seen-in-young-person/ |access-date=2024-11-19 |website=Boston University |language=en}}

In October 2022, the United States National Institutes of Health formally acknowledged there was a causal link between repeated blows to the head and CTE.{{Cite web |date=2022-10-24 |title=US health body rules collision sports cause CTE in landmark change |url=https://www.theguardian.com/sport/2022/oct/24/us-health-body-rules-collision-sports-cause-cte-in-landmark-change |access-date=2022-10-25 |website=The Guardian |language=en}}

In 2005, forensic pathologist Bennet Omalu, along with colleagues in the Department of Pathology at the University of Pittsburgh, published a paper, "Chronic Traumatic Encephalopathy in a National Football League Player", in the journal Neurosurgery, based on analysis of the brain of deceased former NFL center Mike Webster. This was then followed by a paper on a second case in 2006 describing similar pathology, based on findings in the brain of former NFL player Terry Long.{{Cite journal|title = Chronic traumatic encephalopathy in a national football league player: part II|journal = Neurosurgery|date = 2006-11-01|issn = 1524-4040|pmid = 17143242|pages = 1086–1092; discussion 1092–1093|volume = 59|issue = 5|doi = 10.1227/01.NEU.0000245601.69451.27|first1 = Bennet I.|last1 = Omalu|first2 = Steven T.|last2 = DeKosky|first3 = Ronald L.|last3 = Hamilton|first4 = Ryan L.|last4 = Minster|first5 = M. Ilyas|last5 = Kamboh|first6 = Abdulrezak M.|last6 = Shakir|first7 = Cyril H.|last7 = Wecht|s2cid = 7460284}}

In 2008, the Center for the Study of Traumatic Encephalopathy at the BU School of Medicine (now the BU CTE Center) started the VA-BU-CLF Brain Bank at the Bedford Veterans Administration Hospital to analyze the effects of CTE and other neurodegenerative diseases on the brain and spinal cord of athletes, military veterans, and civilians.{{Cite web|title=VA-BU-CLF Brain Bank {{!}} CTE Center|url=https://www.bu.edu/cte/our-research/brain-bank/|access-date=2021-08-12|website=www.bu.edu|language=en}} To date, the VA-BU-CLF Brain Bank is the largest CTE tissue repository in the world, with over 1000 brain donors.{{Cite web|title=1000 Reasons {{!}} Concussion Legacy Foundation|url=https://concussionfoundation.org/1000reasons|access-date=2021-08-12|website=concussionfoundation.org}}

On December 21, 2009, the National Football League Players Association announced that it would collaborate with the BU CTE Center to support the center's study of repetitive brain trauma in athletes.Staff. [http://www.bu.edu/cste/news/press-releases/december-21-2009/ "NFL Players Association to Support Brain Trauma Research at Boston University"], Center for the Study of Traumatic Encephalopathy press release dated 21 December 2009. Accessed 17 August 2010. Additionally, in 2010 the National Football League gave the BU CTE Center a $1 million gift with no strings attached.[http://www.bu.edu/cste/about/support-and-funding/ Support and Funding] {{webarchive |url=https://web.archive.org/web/20100715102220/http://www.bu.edu/cste/about/support-and-funding/ |date=15 July 2010 }}, Center for the Study of Traumatic Encephalopathy. Accessed 17 August 2010.Schwarz, Alan. [http://fifthdown.blogs.nytimes.com/2010/04/20/n-f-l-donates-1-million-for-brain-studies "N.F.L. Donates $1 Million for Brain Studies"], The New York Times, 20 April 2010. Accessed 17 August 2010. In 2008, twelve living athletes (active and retired), including hockey players Pat LaFontaine and Noah Welch as well as former NFL star Ted Johnson, committed to donate their brains to VA-BU-CLF Brain Bank after their deaths.{{cite news |url=http://www.canada.com/edmontonjournal/news/sports/story.html?id=4d141696-f5f9-411c-92a2-57d3aa5802b1 |title=Welch to donate brain for concussion study |access-date=18 December 2008 |newspaper=Edmonton Journal |archive-url=https://web.archive.org/web/20101006035427/http://www.canada.com/edmontonjournal/news/sports/story.html?id=4d141696-f5f9-411c-92a2-57d3aa5802b1 |archive-date=6 October 2010 }} In 2009, NFL Pro Bowlers Matt Birk, Lofa Tatupu, and Sean Morey pledged to donate their brains to the VA-BU-CLF Brain Bank.Staff. [http://www.bu.edu/cste/news/press-releases/september-14-2009/ "Three active NFL Pro Bowl players to donate brains to research"], Center for the Study of Traumatic Encephalopathy press release dated 14 September 2009. Accessed 17 August 2010.

In 2010, 20 more NFL players and former players pledged to join the VA-BU-CLF Brain Donation Registry, including Chicago Bears linebacker Hunter Hillenmeyer, Hall of Famer Mike Haynes, Pro Bowlers Zach Thomas, Kyle Turley, and Conrad Dobler, Super Bowl Champion Don Hasselbeck and former pro players Lew Carpenter, and Todd Hendricks. In 2010, professional wrestlers Mick Foley, Booker T and Matt Morgan also agreed to donate their brains upon their deaths. Also in 2010, MLS player Taylor Twellman, who had to retire from the New England Revolution because of post-concussion symptoms, agreed to donate his brain upon his death. As of 2010, the VA-BU-CLF Brain Donation Registry consists of over 250 current and former athletes.Staff. [http://www.bu.edu/cste/news/press-releases/february-1-2010/ "20 more NFL stars to donate brains to research"], Center for the Study of Traumatic Encephalopathy press release dated 1 February 2010. Accessed 17 August 2010.

In 2011, former North Queensland Cowboys player Shaun Valentine became the first Australian National Rugby League player to agree to donate his brain upon his death, in response to recent concerns about the effects of concussions on Rugby League players, who do not use helmets. Also in 2011, boxer Micky Ward, whose career inspired the film The Fighter, agreed to donate his brain upon his death. In 2018, NASCAR driver Dale Earnhardt Jr., who retired in 2017 citing multiple concussions, became the first auto racing competitor to agree to donate his brain upon his death.Boren, Cindy. [https://www.washingtonpost.com/news/early-lead/wp/2016/03/28/dale-earnhardt-jr-plans-to-donate-his-brain-for-concussion-research/ "Dale Earnhardt Jr. plans to donate his brain for concussion research"], The Washington Post, March 28, 2016. Accessed December 28, 2021. "He announced the most Dale Earnhardt Jr. way possible, with a nonchalant tweet on a Saturday night. That's how NASCAR's most popular driver disclosed that he would donate his brain posthumously to science. His announcement came in response to a Sports Illustrated tweet and responses about three members of the Oakland Raiders decided to donate their brains to the Concussion Legacy Foundation after learning that Hall of Famer Ken Stabler's brain showed evidence of chronic traumatic encephalopathy at autopsy."

In related research, the Center for the Study of Retired Athletes, which is part of the Department of Exercise and Sport Science at the University of North Carolina at Chapel Hill, is conducting research funded by National Football League Charities to "study former football players, a population with a high prevalence of exposure to prior Mild Traumatic Brain Injury (MTBI) and sub-concussive impacts, in order to investigate the association between increased football exposure and recurrent MTBI and neurodegenerative disorders such as cognitive impairment and Alzheimer's disease (AD)".{{cite web |url=http://exss.unc.edu/research-and-laboratories/center-for-the-study-of-retired-athletes/current-research/ |title=A Study on the Association Between Football Exposure and Dementia in Retired Football Players |publisher=UNC College of Arts and Sciences |access-date=1 August 2012 |archive-url=https://web.archive.org/web/20120811082425/http://exss.unc.edu/research-and-laboratories/center-for-the-study-of-retired-athletes/current-research/ |archive-date=11 August 2012 }}

In February 2011, former NFL player Dave Duerson committed suicide via a gunshot to his chest, thus leaving his brain intact.Smith, Michael David, [http://profootballtalk.nbcsports.com/2012/05/03/boston-researchers-request-junior-seaus-brain/ "Boston researchers request Junior Seau's brain"]. NBC Sports Pro Football Talk, 3 May 2012. Retrieved 3 May 2012. Duerson left text messages to loved ones asking that his brain be donated to research for CTE.{{cite web |url=http://www.nbcchicago.com/blogs/grizzly-detail/Dave-Duerson-Committed-Suicide-Medical-Examiner-116539023.html |title=Dave Duerson Committed Suicide: Medical Examiner |access-date=20 February 2011 |last=Kusinski |first=Peggy |date=1 February 2011|work=NBC Chicago}} The family got in touch with representatives of the Boston University center studying the condition, said Robert Stern, the co-director of the research group. Stern said Duerson's gift was the first time of which he was aware that such a request had been made by someone who had committed suicide that was potentially linked to CTE.{{cite news |url=https://www.nytimes.com/2011/02/20/sports/football/20duerson.html |title=Before Suicide, Duerson Asked for Brain Study |work=The New York Times |first=Alan |last=Schwarz |author-link=Alan Schwarz |date=20 February 2011}} Stern and his colleagues found high levels of the protein tau in Duerson's brain. These elevated levels, which were abnormally clumped and pooled along the brain sulci, are indicative of CTE.{{cite news |url=http://www.latimes.com/health/cbsports-study-duerson-had-brain-damage-at-time-of-suicide-20110502,0,1748318.story |title=Study: Duerson had brain damage at time of suicide |author= Deardorff, Julie |newspaper=Los Angeles Times |date=2 May 2011 |access-date=2 May 2011}}{{dead link|date=June 2021|bot=medic}}{{cbignore|bot=medic}}

In July 2010, NHL enforcer Bob Probert died of heart failure. Before his death, he asked his wife to donate his brain to CTE research because it was noticed that Probert experienced a mental decline in his 40s. In March 2011, researchers at Boston University concluded that Probert had CTE upon analysis of the brain tissue he donated. He was the second NHL player from the program at the BU CTE Center to be diagnosed with CTE postmortem.{{cite news |url=https://www.nytimes.com/2011/03/03/sports/hockey/03fighter.html |author= Schwarz, Alan |title=Hockey Brawler Paid Price, With Brain Trauma |newspaper=The New York Times |date=2 March 2011 |access-date=14 March 2011}}

The BU CTE Center has also found indications of links between amyotrophic lateral sclerosis (ALS) and CTE in athletes who have participated in contact sports. Tissue for the study was donated by twelve athletes and their families to the VA-BU-CLF Brain Bank at the Bedford, Massachusetts VA Medical Center.[http://www.bumc.bu.edu/busm-news/2010/08/17/researchers-discover-brain-trauma-in-sports-may-cause-a-new-disease-that-mimics-als/ "Researchers Discover Brain Trauma in Sports May Cause a New Disease That Mimics ALS"], BUSM press release, 17 August 2010 3:41 pm. Retrieved 11 September 2011.

In 2013, President Barack Obama announced the creation of the Chronic Effects of Neurotrauma Consortium or CENC, a federally funded research project devised to address the long-term effects of mild traumatic brain injury in military service personnel (SMs) and veterans.{{cite web |title=Obama Introduces New PTSD and Education Programs | website=military.com |last=Jordan |first=Bryant |date=12 August 2013 |url=http://www.military.com/daily-news/2013/08/12/obama-introduces-new-ptsd-and-education-programs.html |access-date=2 May 2014}}{{cite web|title=Obama administration to research TBI, PTSD in new efforts Read more: Chronic Effects of Neurotrauma Consortium |website=fiercegovernment.com |url=http://www.fiercegovernment.com/story/obama-administration-research-tbi-ptsd-new-efforts/2013-08-14 |access-date=2 May 2014 |archive-url=https://web.archive.org/web/20140502230312/http://www.fiercegovernment.com/story/obama-administration-research-tbi-ptsd-new-efforts/2013-08-14 |archive-date=2 May 2014 }}{{cite web |title=DoD, VA Establish Two Multi-Institutional Consortia to Research PTSD and TBI |website=va.gov |url=http://www.va.gov/opa/pressrel/pressrelease.cfm?id=2473 |access-date=2 May 2014}} The CENC is a multi-center collaboration linking premiere basic science, translational, and clinical neuroscience researchers from the DoD, VA, academic universities, and private research institutes to effectively address the scientific, diagnostic, and therapeutic ramifications of mild TBI and its long-term effects.{{cite web |title=RTI to research mild traumatic brain injury effects in US soldiers |website=army-technology.com |url=http://www.army-technology.com/news/newsrti-brain-injury-effects-soldiers |access-date=2 May 2014|date=2 August 2013}}

Nearly 20% of the more than 2.5 million U.S. service members (SMs) deployed since 2003 to Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) have sustained at least one traumatic brain injury (TBI), predominantly mild TBI (mTBI),Warden D. Military TBI during the Iraq and Afghanistan wars. J Head Trauma Rehabil. 2006; 21 (5): 398–402.{{cite web |title=DoD Worldwide Numbers for TBI |website=dvbic.dcoe.mil |url=http://dvbic.dcoe.mil/dod-worldwide-numbers-tbi |access-date=4 February 2013 |archive-date=17 January 2014 |archive-url=https://web.archive.org/web/20140117020937/http://dvbic.dcoe.mil/dod-worldwide-numbers-tbi }} and almost 8% of all OEF/OIF Veterans demonstrate persistent post-TBI symptoms more than six months post-injury.{{cite journal |vauthors=Scholten JD, Sayer NA, Vanderploeg RD, Bidelspach DE, Cifu DX |title=Analysis of US Veterans Health Administration comprehensive evaluations for traumatic brain injury in Operation Enduring Freedom and Operation Iraqi Freedom Veterans |journal=Brain Inj |volume=26 |issue=10 |pages=1177–84 |year=2012 |pmid=22646489 |doi=10.3109/02699052.2012.661914 |s2cid=37365962 }}{{cite journal |vauthors=Taylor BC, Hagel EM, Carlson KF, Cifu DX, Cutting A, Bidelspach DE, Sayer NA |title=Prevalence and costs of co-occurring traumatic brain injury with and without psychiatric disturbance and pain among Afghanistan and Iraq War Veteran V.A. users | journal = Med Care |volume=50 |issue=4 |pages= 342–46 |year=2012 |pmid=22228249 |doi=10.1097/MLR.0b013e318245a558 |s2cid=29920171 |url=https://zenodo.org/record/894896}} Unlike those head injuries incurred in most sporting events, recent military head injuries are most often the result of blast wave exposure.{{cite journal | vauthors = Weppner J, Linsenmeyer M, Ide W | title = Military Blast-Related Traumatic Brain Injury | journal = Current Physical Medicine and Rehabilitation Reports | publisher = Brain Injury Medicine and Rehabilitation | date = 1 August 2019 | url = https://link.springer.com/article/10.1007/s40141-019-00241-8 | volume = 7 | issue = 4 | pages = 323–32 | doi=10.1007/s40141-019-00241-8 | s2cid = 199407324 | access-date = 10 May 2020 | url-access = subscription }}

After a competitive application process, a consortium led by Virginia Commonwealth University was awarded funding to study brain injuries in military veterans.{{cite web |title=Fact Sheet: Largest federal grant in VCU's history |website=spectrum.vcu.edu| url=http://www.spectrum.vcu.edu/inside-research/vcu-will-lead-62-million-study-of-traumatic-brain-injuries-in-military-personnel/ |access-date=2 May 2014}}{{cite web |title=VCU to lead major study of concussions |website=grpva.com |url=http://www.grpva.com/news-and-media/details/vcu-to-lead-major-study-of-concussions |access-date=2 May 2014 |archive-url=https://web.archive.org/web/20140503003008/http://www.grpva.com/news-and-media/details/vcu-to-lead-major-study-of-concussions |archive-date=3 May 2014 }}{{cite web |title=Brain trust – the US consortia tacking military PTSD and brain injury | website=army-technology.com |url=http://www.army-technology.com/features/featurebrain-trust-us-consortia-tacking-military-ptsd-brain-injury/ |access-date=2 May 2014| date=9 March 2014 }}{{Unreliable source? |reason=domain on WP:BLACKLIST|date=June 2016}}{{cite web |title=DOD partners to combat brain injury |website=army.mil|date=19 August 2013 | url=https://www.army.mil/article/109492/DOD_partners_to_combat_brain_injury/|access-date=2 May 2014}}{{cite web |title=Fact Sheet: The Obama Administration's Work to Honor Our Military Families and Veterans | url=https://obamawhitehouse.archives.gov/the-press-office/2013/08/10/fact-sheet-obama-administration-s-work-honor-our-military-families-and-v |access-date=2 May 2014|via=National Archives |work=whitehouse.gov |date=1 August 2013}}{{cite web |title=Fact Sheet: VCU will lead $62 million study of traumatic brain injuries in military personnel |website=news.vcu.edu| url=http://www.news.vcu.edu/article/VCU_Will_Lead_62_Million_Study_of_Traumatic_Brain_Injuries_in |access-date=2 May 2014}} The project principal investigator for the CENC is David Cifu, chairman and Herman J. Flax professor[http://www.pmr.vcu.edu/Department/Default.aspx About Us] {{webarchive |url=https://web.archive.org/web/20151222213718/http://www.pmr.vcu.edu/Department/Default.aspx |date=22 December 2015 }}, Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University. Retrieved 21 December 2015. of the Department of Physical Medicine and Rehabilitation (PM&R) at Virginia Commonwealth University (VCU) in Richmond, Virginia, with co-principal investigators Ramon Diaz-Arrastia, Professor of Neurology, Uniformed Services University of the Health Sciences, and Rick L. Williams, statistician at RTI International.

In 2017, Aaron Hernandez, a former professional football player and convicted murderer, committed suicide at the age of 27 while in prison. His family donated his brain to the BU CTE Center. Ann McKee, the head of Center, concluded that "Hernandez had Stage 3 CTE, which researchers had never seen in a brain younger than 46 years old."{{cite news |last=Kilgore |first=Adam |title=Aaron Hernandez suffered from most severe CTE ever found in a person his age |url=https://www.washingtonpost.com/sports/aaron-hernandez-suffered-from-most-severe-cte-ever-found-in-a-person-his-age/2017/11/09/fa7cd204-c57b-11e7-afe9-4f60b5a6c4a0_story.html|access-date=12 July 2020 |newspaper=Washington Post |date=9 November 2017}}

In 2022, former NRL player and coach Paul Green died by suicide at the age of 49. Green's brain was donated to the Australian Sports Brain Bank, with his family posting on the website "In memory of our beloved Paul, we ask that you support the pioneering work of the Australian Sports Brain Bank" to raise money for further understanding of CTE.{{cite news |last1=Proszenko |first1=Adrian |title=Paul Green's brain donated to Australian Sports Brain Bank |url=https://www.brisbanetimes.com.au/sport/nrl/paul-green-s-brain-donated-to-australian-sports-brain-bank-20220818-p5bavo.html |access-date=18 August 2022 |work=Brisbane Times |publisher=Nine Media}} A post-mortem examination revealed that Green was suffering from one of the most "severe forms" of CTE. Professor Michael Buckland said Green had "an organic brain disease which robbed him of his decision-making and impulse control." He added Green would likely have been "symptomatic for some time."{{cite web |last1=Waterworth |first1=Ben |title='Daddy's brain was sick': Paul Green's wife Amanda reveals truth behind death that rocked NRL |url=https://www.foxsports.com.au/nrl/nrl-news-2022-paul-green-cause-of-death-was-cte-brain-disease-wife-amanda-green-interview/news-story/509fec274b55b3d1879875b276f6b5f9 |website=foxsports.com.au |publisher=News Corporation Australia |access-date=26 October 2022 |date=22 October 2022}}

Research into the genetic component of CTE is evolving and well summarized in a recent review.{{Cite journal |last1=Abdolmohammadi |first1=Bobak |last2=Dupre |first2=Alicia |last3=Evers |first3=Laney |last4=Mez |first4=Jesse |date=August 2020 |title=Genetics of Chronic Traumatic Encephalopathy |journal=Seminars in Neurology |volume=40 |issue=4 |pages=420–429 |doi=10.1055/s-0040-1713631 |issn=1098-9021 |pmid=32712945|s2cid=220798883 }} The minor allele of TMEM106B is associated with a protective phenotype.

In 2023, Australian rules football player Heather Anderson became the first female athlete diagnosed with CTE after her death by suicide on 13 November 2022, at the age of 28. Her brain, which was donated to the Australian Sports Brain Bank, was found to contain multiple CTE lesions, and abnormalities were found "nearly everywhere" in the cortex.{{cite web |title=Heather Anderson diagnosed with CTE in 1st case for female athlete |url=https://www.espn.com/afl/story/_/id/37956773/aflw-player-heather-anderson-first-woman-diagnosed-cte |website=ESPN |date=4 July 2023 }} Also in 2023, a study was published on August 28 in JAMA Neurology regarding brain autopsies of athletes, one of whom was the first American female athlete diagnosed with CTE; her name is unknown, but she died at age 28 and was a collegiate soccer player.{{Cite web|url=https://simhcottumwa.org/autopsy-study-of-athletes-who-died-young-shows-many-had-signs-of-cte/|title=Autopsy Study of Athletes Who Died Young Shows Many Had Signs of CTE|first=Alan|last=Mozes|date=29 August 2023}}

In March 2024, former rugby union player Billy Guyton became the first New Zealand-based athlete diagnosed with CTE following his forced retirement in 2018, due to the complications of multiple concussions, and his death by suspected suicide in 2023.{{Cite web |last=RNZ |author-link=Radio New Zealand |date=14 March 2024 |title=Brain injury from head knocks discovered in late Blues halfback |url=https://www.nzherald.co.nz/sport/rugby/brain-injury-from-head-knocks-discovered-in-late-blues-halfback-billy-guyton/5W7WY5CREFHK3HPZMDJTDMFNHY/ |access-date=16 March 2024 |website= |publisher=The New Zealand Herald |language=en-NZ}}{{Cite news |last=Aylwin |first=Michael |date=14 March 2024 |title=First professional rugby union player confirmed to have died with CTE |url=https://www.theguardian.com/sport/2024/mar/14/first-professional-rugby-union-player-cte-billy-guyton |access-date=16 March 2024 |work=The Guardian |language=en-GB |issn=0261-3077}} His brain had been donated by his family to the Neurological Foundation Human Brain Bank at the University of Auckland, with post-mortem analyses conducted in New Zealand and Australia eventually finding "background changes consistent with global hypoxic ischaemic encephalopathy", as well as trauma-induced cavum septum pellucidum and age-related tau deposits.

{{sister project|project=Wikiversity|text= Wikiversity is calling for essays on Concussions in Sports}}

• Acquired brain injury
• Brain damage
• Chronic traumatic encephalopathy in sports
• Concussions in American football
• Concussions in rugby union
• Health issues in American football
• List of NFL players with chronic traumatic encephalopathy
• Chuck Bednarik
• The Hit (Chuck Bednarik)
• Traumatic brain injury

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• {{commons category-inline}}

{{Medical condition classification and resources

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| ICD10 = {{ICD10|G93.8}}

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| eMedicineSubj = sports

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{{Neurotrauma}}

{{Trauma|state=autocollapse}}

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