ABSTRACT
Abstract Background Professional soccer athletes are exposed to repetitive head impacts and are at risk of developing chronic traumatic encephalopathy. Objective To evaluate regional brain glucose metabolism (rBGM) and gray matter (GM) volume in retired soccer players (RSPs). Methods Male RSPs and age and sex-matched controls prospectively enrolled between 2017 and 2019 underwent neurological and neuropsychological evaluations, brain MRI and [18F]FDG-PET in a 3.0-Tesla PET/MRI scanner. Visual analysis was performed by a blinded neuroradiologist and a blinded nuclear physician. Regional brain glucose metabolism and GM volume were assessed using SPM8 software. Groups were compared using appropriate statistical tests available at SPM8 and R. Results Nineteen RSPs (median [IQR]: 62 [50-64.5] years old) and 20 controls (60 [48-73] years old) were included. Retired soccer players performed worse on mini-mental state examination, digit span, clock drawing, phonemic and semantic verbal fluency tests, and had reduced rBGM in the left temporal pole (pFDR = 0.008) and the anterior left middle temporal gyrus (pFDR = 0.043). Semantic verbal fluency correlated with rBGM in the right hippocampus, left temporal pole, and posterior left middle temporal gyrus (p ≤ 0.042). Cray matter volume reduction was observed in similar anatomic regions but was less extensive and did not survive correction for multiple comparisons (pFDR ≥ 0.085). Individual [18F]FDG-PET visual analysis revealed seven RSPs with overt hypometabolism in the medial and lateral temporal lobes, frontal lobes, and temporoparietal regions. Retired soccer players had a higher prevalence of septum pellucidum abnormalities on MRI. Conclusion Retired soccer players had reduced rBCM and CM volume in the temporal lobes and septum pellucidum abnormalities, findings possibly related to repetitive head impacts.
Resumo Antecedentes Jogadores profissionais de futebol estão expostos a impactos cranianos repetitivos e ao risco de desenvolver encefalopatia traumática crônica. Objetivo Avaliar o metabolismo glicolítico cerebral regional (MCCr) e o volume de substância cinzenta (vSC) em jogadores de futebol aposentados (JFAs). Métodos Jogadores de futebol aposentados masculinos e controles pareados por idade e sexo foram incluídos prospectivamente entre 2017 e 2019. Foram realizadas avaliações neurológica e neuropsicológica, ressonância magnética (RM) e [18F]FDG-PET cerebrais (3.0-Tesla PET/RM). As imagens foram analisadas visualmente por um neurorradiologista e um médico nuclear cegos ao grupo de cada participante. O metabolismo glicolítico cerebral regional e o vSC foram avaliados através do programa SPM8. Os grupos foram comparados através de testes estatísticos apropriados disponíveis em SPM8 e R, de acordo com a distribuição e o tipo dos dados. Resultados Dezenove JFAs (mediana [IIQ]: 62 [50-64.5] anos) e 20 controles (60 [48-73] anos) foram incluídos. Os JFAs tiveram pior desempenho no mini-exame do estado mental e nos testes de dígitos, desenho do relógio, fluência verbal e fluência semântica e apresentaram MCCr significativamente reduzido no polo temporal e no giro temporal médio anterior esquerdos. Fluência semântica (animais) apresentou correlação positiva com MCCr no hipocampo direito, no polo temporal esquerdo e no aspecto posterior do giro temporal médio esquerdo. Menor vSC foi observado nas mesmas regiões, porém este achado não sobreviveu à correção para comparações múltiplas. Análise individual do [18F]FDG-PET cerebral revelou sete JFAs com claro hipometabolismo nas faces medial e lateral dos lobos temporais, nos lobos frontais e nas regiões temporoparietais. Os JFAs apresentaram ainda maior prevalência de anormalidades do septo pelúcido. Conclusão Os JFAs apresentam MCCr e vSC reduzidos nos lobos temporais, além de anormalidades do septo pelúcido, achados possivelmente relacionados a impactos cranianos repetitivos.
ABSTRACT
Traumatic brain injury (TBI) has been recognized as a risk factor for developing dementia. Currently, around 69 million people worldwide suffer from TBI each year, while the overall incidence of TBI among Chinese residents is on a rapid rise. Such a large population of TBI patients may lead to a future surge in the number of dementia patients, bringing heavy burdens on families and societies. However, it seems to be suggested by numerous studies that not all TBI patients are associated with an increased risk of dementia. Dementia can result in disability as well as interfere with caregivers ′ normal lives. Therefore, it will be significant to clarify the relationship between TBI and dementia as well as explain the process of onset and development of post-TBI dementia. In this study, the authors summarize post-TBI dementia from aspects of influencing factors and pathogenic mechanisms, so as to provide relevant references for related studies, therapy, and prophylaxis of post-TBI dementia.
ABSTRACT
The competitive sports are beneficial to cardiovascular system and brain health. However, physical exercise is accompanied with risks. Severe trauma is possible in competitive sports that may impact on the head and body. In recent years, more interests are aroused in sports-related traumatic brain injury(TBI), especially the mild TBI(mTBI). Repetitive mTBI can cause persistent cognitive, behavioral and mental problems, leading to chronic traumatic encephalopathy(CTE) and eventually resulting in neurodegeneration. In this study, the authors summarize the pathological characteristics and mechanism of CTE induced by mTBI due to competitive exercise so as to reveal the pathogenesis of CTE and provide valuable information for early diagnosis, development of disease biomarkers and explore effective therapeutic targets.
ABSTRACT
Soccer is the most popular sport worldwide, with over 265 million participants. Soccer is unique in that the ball can be directed deliberately and purposefully with the head, an act referred to as ‘heading’. In recent years, there has been concern about the association between repetitive subconcussive head impacts associated with heading and chronic traumatic encephalopathy. Heading causes immediate changes in biochemical and electrophysiological markers of traumatic brain injury, and some studies have reported brain structural changes and dysfunction in former soccer players. In 2019, it was reported that the mortality associated with neurodegenerative diseases was about 3.5 times higher among former professional soccer players. Following that, in early 2020, the guidance have been published to limit heading by age in some regions including England and Scotland. In this review, we will expound the immediate and long-term effects of heading associated with chronic traumatic encephalopathy and the measures that should be taken into consideration in the practice of soccer instruction, based on the latest findings.
ABSTRACT
Chronic traumatic encephalopathy (CTE) is a distinct neurodegenerative disease that associated with repetitive head trauma. CTE is neuropathologically defined by the perivascular accumulation of abnormally phosphorylated tau protein in the depths of the sulci in the cerebral cortices. In advanced CTE, hyperphosphorylated tau protein deposits are found in widespread regions of brain, however the mechanisms of the progressive neurodegeneration in CTE are not fully understood. In order to identify which proteomic signatures are associated with CTE, we prepared RIPA-soluble fractions and performed quantitative proteomic analysis of postmortem brain tissue from individuals neuropathologically diagnosed with CTE. We found that axonal guidance signaling pathwayrelated proteins were most significantly decreased in CTE. Immunohistochemistry and Western blot analysis showed that axonal signaling pathway-related proteins were down regulated in neurons and oligodendrocytes and neuron-specific cytoskeletal proteins such as TUBB3 and CFL1 were reduced in the neuropils and cell body in CTE. Moreover, oligodendrocyte-specific proteins such as MAG and TUBB4 were decreased in the neuropils in both gray matter and white matter in CTE, which correlated with the degree of axonal injury and degeneration. Our findings indicate that deregulation of axonal guidance proteins in neurons and oligodendrocytes is associated with the neuropathology in CTE. Together, altered axonal guidance proteins may be potential pathological markers for CTE.
Subject(s)
Humans , Axons , Blotting, Western , Brain Injury, Chronic , Brain , Cell Body , Cerebral Cortex , Craniocerebral Trauma , Cytoskeletal Proteins , Gray Matter , Immunohistochemistry , Neurodegenerative Diseases , Neurons , Neuropathology , Neuropil , Oligodendroglia , tau Proteins , White MatterABSTRACT
ABSTRACT Sports activities associated with repetitive cranial trauma have become a fad and are popular in gyms and even among children. It is important to consistently characterize the consequences of such sports activities in order to better advise society on the real risks to the central nervous system. We present the case of a former boxer reporting cognitive and behavioral symptoms that began six years after his retirement as a boxer, evolving progressively with parkinsonian and cerebellar features suggestive of probable chronic traumatic encephalopathy (CTE). Using our case as a paradigm, we extended the range of differential diagnosis of CTE, including corticobasal degeneration, multiple system atrophy, vitamin B12 deficiency, neurosyphilis, frontotemporal dementia and Alzheimer's disease.
RESUMO As atividades esportivas associadas ao trauma craniano repetitivo tornaram-se uma moda e são populares nas academias e entre as crianças. É importante fazer uma caracterização consistente das consequências de tais atividades esportivas, a fim de aconselhar melhor uma sociedade sobre os riscos reais para o sistema nervoso central. Apresentamos um antigo boxeador relatando sintomas cognitivos e comportamentais que começaram seis anos após sua aposentadoria como boxeador e evoluiu progressivamente com características parkinsonianas e cerebelares sugestivas de provável encefalopatia traumática crônica (ETC). Usando nosso caso como paradigma, ampliamos a gama de diagnóstico diferencial de ETC, incluindo degeneração corticobasal, atrofia de múltiplos sistemas, deficiência de vitamina B12, neurossífilis, demência frontotemporal e doença de Alzheimer.
Subject(s)
Humans , Brain Diseases , Spinocerebellar Degenerations , Multiple System Atrophy , Dementia , Diagnosis, Differential , Chronic Traumatic Encephalopathy , Frontal LobeABSTRACT
Objective To detect the long term effect of pure and multiple concussions on spatial cognitive of rats.Methods One hundred and eighty 7-week-old Spragne-Dawley male rats with weight of 280 ± 30g were chosen and randomly divided into a control group and a concussion group.The cerebral concussion was induced in the rats using a metallic pendulum striker concussive device.After the first strike,the brain injury group was randomly divided into a pure cerebral concussion(PCC)group and a multiple cerebral concussion(MCC) group.After the second strike,the MCC group was randomly divided into two-fold cerebral concussion(2MCC) group and three-fold cerebral concussion(3MCC) group.The striking interval was 24h.One,3 and 6 months after trauma,their cognitive function was tested using Morris water maze.Results One month later after injury,there was no significant difference in the escape latency between the control group and PCC group.Significant differences in the measurement were observed between the control/PCC group and 2MCC group on the 7th day after the injury,also between the control/PCC and 3MCC groups on the 6th and 7th day.And there were significant differences between the 2MCC and 3MCC groups on the 6th and 7th days.The non-platform test did not observe any significant differences among the four groups.Three months after injury,there was still no significant difference between the control group and PCC group,PCC and 2MCC groups,as well as 2MCC and 3MCC groups in the escape latency.However,there was significant difference between the control group and 2MCC group on the 5th,6th and 7th days,between the control group and 3MCC group on the 4th,5th,6th and 7th days,as well as between PCC group and 3MCC group on the 6th and 7th days.In the non-platform test,there was no significant difference between the control group and PCC group,between PCC group and 2MCC group,as well as between 2MCC group and 3MCC group.However,2MCC and 3MCC groups spent significantly less time in the former platform quadrant,when compared with the control group and 3MCC group spent significantly less time than PCC group.Six months after injury,significant differences in the escape latency were observed between the control group and PCC group on the 6th and 7th days,and 2MCC group on the 5th,6th and 7th days,also and 3MCC groups on the 2nd,3rd,4th,5th,6th and 7th days,still between PCC group and 2MCC group on the 6th and 7th days,as well as between PCC group and 3MCC group on the 4th,5th,6th and 7th days.Moreover,there was significant difference between 2MCC and 3MCC groups only on the 7th day.In the non-platform test,PCC group,2MCC group and 3MCC group spent significantly less time in the former platform quadrant compared with the control group.Moreover,in this test significant differences were found between PCC group and 2MCC/3MCC group,but not between 2MCC group and 3MCC group.Conclusion With the increase of cerebral concussion times,earlier and more serious damage of spatial cognition will appear,with a significant cumulative effect in rats.Such rat model can be used to study the pathological changes of cognitive impairment in chronic traumatic encephalopathy.
ABSTRACT
Resumen La exposición repetitiva a traumas craneales es una de las características de la encefalopatía traumática crónica. Neuropatológicamente en esta patología encontramos depósitos de proteína hiperfosforilada tau (p-tau). Inicialmente fue descrita como demencia pugilística, pero se ha asociado a otros tipos de deportes, traumas por explosión entre otros. Los síntomas de esta enfermedad incluyen pérdida de memoria, alteración cognitiva, cambios de ánimo y demencia. Presentamos una revisión de la literatura sobre esta interesante enfermedad.
Abstract Repetitive exposure to cranial trauma is one of the hallmarks of chronic traumatic encephalopathy. Neuropathologically, hyperphosphorylated protein tau (p-tau) deposits are found. Initially it was described as pugilistic dementia, but it has been associated with other types of sports, explosive traumas among others. Symptoms of this disease include memory loss, cognitive impairment, mood swings and dementia. We present a review of the literature on this interesting disease.
ABSTRACT
ABSTRACT Chronic traumatic encephalopathy (CTE) was initially described in boxers, but in recent years it has been reported in other settings, particularly in contact sports and military personnel. Soccer (football association) had previously been (and still is) considered relatively safe when compared to other sports, such as American football. However, a few cases of professional soccer players with CTE have been reported in the last few years. It is still unknown how frequent this condition is in soccer players, and the role played by heading the ball remains elusive. Other traumas to the head, face and neck caused by contact with another player's head, arm or other body parts are among the most frequent in soccer. In spite of the lack of more in-depth knowledge, there is reasonable evidence for recommending severe punishment (red card and suspension for several matches) for players causing avoidable trauma to another player's head.
RESUMO Encefalopatia traumática crônica (ETC) foi inicialmente descrita em boxeadores, mas nos últimos anos tem sido relatada em outras situações, particularmente nos esportes de contato e no pessoal militar. O futebol ou futebol de associação foi (e ainda é) considerado relativamente mais seguro quando comparado a outros esportes, como o futebol americano. No entanto, alguns casos de jogadores de futebol profissional com CTE foram relatados nos últimos anos. Ainda não se sabe a frequência dessa condição nos jogadores de futebol bem como qual o papel desempenhado por cabecear a bola. Outros traumas de crânio e pescoço causados pelo contato com o crânio, braço ou outras partes do corpo de outros jogadores estão entre os mais frequentes no futebol. Apesar da falta de um conhecimento mais aprofundado, há razoável evidência para recomendar punição severa (cartão vermelho e suspensão por várias partidas) para jogadores que causarem trauma evitável na cabeça de outro jogador.
Subject(s)
Humans , Soccer , Chronic Traumatic Encephalopathy , Craniocerebral TraumaABSTRACT
La encefalopatía traumática crónica (ETC) es una enfermedad neurodegenerativa que se produce como consecuencia traumatismos cerebrales repetitivos; concusiones, que son un síndrome clínico que se caracteriza por una alteración de la función cerebral. Una concusión, bajo su estricta definición, no debiese causar cambios estructurales en el cerebro por lo que no sería visible a través de imágenes, sí existen cambios a nivel microscópicos, bioquímicos y biomecánicos. La mayoría de los pacientes tienen completa resolución de sus síntomas dentro de 10 días (90 por ciento), pero existe un pequeño porcentaje que persiste con estos, pudiendo presentarse como un síndrome postconcusional, síndrome de segundo impacto o una encefalopatía traumática crónica. La ETC se caracteriza por la acumulación de prot-tau hiperfosforilada en neuronas y astrocitos. Estas se van a presentar en forma de ovillos o hilos neurofibrilares. En etapas iniciales las encontraremos de forma focalizada en la corteza frontal y en las formas más severas su distribución será más generalizada, distribuyéndose en la mayoría de las regiones del cerebro. Su diagnóstico se realiza a través de histopatología, por lo que hasta el momento sólo se ha logrado post-mortem. Se está trabajando en nuevas tecnologías asociadas a biomarcadores y PET para lograr una diagnostico premortem. El mayor énfasis en el manejo de esta taupatía es la prevención y adecuado manejo de las concusiones.
Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease which is produced as a consequence of repeated brain trauma: concussions, which are a clinical syndrome characterized by an alteration in brain functions. A concussion, understrict definition, should not cause structural changes to the brain. Therefore, it would not be possible to see through images if there were changes at a microscopic, biochemical level. Most patients see their symptoms completely resolved within 10 days (90 percent), but there is a small percentage which persists, and these might cause a post-concussional syndrome, second impact syndrome of chronic traumatic encephalopathy. CTE is characterized by the accumulation of hyper-phosphorylated Tau protein in neurons and astrocytes. These appear in the form of neurofibrillary tangles. During the initial stages they are focalized in the frontal cortex and, in more severe cases, their distribution is more generalized, spreading through the majority of the regions in the brain. It is diagnosis is done through histopathology. Thus, it has only been possible to do post mortem. New technologies associated with bio-markers and PET are being worked on to achieve a pre-mortem diagnosis. The greatest emphasis in the handling of this tauopathy lies in the prevention and the adequate handling of concussions.
Subject(s)
Humans , Brain Concussion/complications , Chronic Traumatic Encephalopathy/diagnosis , Chronic Traumatic Encephalopathy/etiology , Chronic Traumatic Encephalopathy/prevention & control , tau Proteins , Tauopathies , Brain Damage, Chronic , Cadaver , Brain Damage, Chronic/complications , Neurodegenerative DiseasesABSTRACT
ABSTRACT Traumatic brain injury (TBI) represents a significant public health problem in modern societies. It is primarily a consequence of traffic-related accidents and falls. Other recently recognized causes include sports injuries and indirect forces such as shock waves from battlefield explosions. TBI is an important cause of death and lifelong disability and represents the most well-established environmental risk factor for dementia. With the growing recognition that even mild head injury can lead to neurocognitive deficits, imaging of brain injury has assumed greater importance. However, there is no single imaging modality capable of characterizing TBI. Current advances, particularly in MR imaging, enable visualization and quantification of structural and functional brain changes not hitherto possible. In this review, we summarize data linking TBI with dementia, emphasizing the imaging techniques currently available in clinical practice along with some advances in medical knowledge.
RESUMO O traumatismo cranioencefálico (TCE) representa um importante problema de saúde pública nas sociedades modernas. As suas principais causas são: os acidentes de trânsito e as quedas. O traumatismo leve e repetido relacionado com os esportes de contato ou o traumatismo relacionado com as ondas de choque provenientes de explosões em cenário de guerra são hoje reconhecidas como importantes causas de TCE. A mortalidade e morbilidade associada ao TCE é considerável. TCE representa o fator de risco ambiental melhor reconhecido para o desenvolvimento de demência. Com o reconhecimento recente de que até o TCE leve pode determinar déficts cognitivos, os estudos de imagem adquiriram grande importância neste contexto. Contudo, não está definido qual o melhor estudo de imagem para caracterizar o TCE. Avanços tecnológicos, como a ressonância magnética, permitem atualmente identificar e quantificar alterações intra-parenquimatosas estruturais e funcionais, não detectáveis nos estudos convencionais. Neste artigo os autores resumem os estudos que relacionam TCE e demência, dando particular ênfase às técnicas de imagem atualmente disponíveis na prática clínica, bem como alguns avanços nos métodos de imagem ainda limitados ao plano da investigação.
Subject(s)
Humans , Magnetic Resonance Spectroscopy , Dementia , Post-Concussion Syndrome , Brain Injuries, Traumatic , Chronic Traumatic EncephalopathyABSTRACT
Dementia pugilistica (DP) or chronic traumatic encephalopathy (CTE) is a neurodegenerative disease or dementia that may affect amateur or professional boxers as well as athletes in other sports who suffer concussions. The condition is thought to affect around 15% to 20% of professional boxers and caused by repeated concussive or subconcussive blows. CTE was in the past referred to as dementia pugilistica, which reflected the prevailing notion that this condition was restricted to boxers. Recent research, however, has demonstrated neuropathological evidence of CTE in retired American football players, a professional wrestler, a professional hockey player and a soccer player, as well as in nonathletes. It is probable that many individuals are susceptible to CTE, including those who experience falls, motor vehicle accidents, assaults, epileptic seizures, or military combat, and that repeated mild closed head trauma of diverse origin is capable of instigating the neurodegenerative cascade leading to CTE. We report a 62-year old man suspicious of dementia pugilistica with clinical features of frontotemporal dementia and parkinsonism.
Subject(s)
Humans , Athletes , Brain Injury, Chronic , Dementia , Epilepsy , Football , Frontotemporal Dementia , Head Injuries, Closed , Hockey , Military Personnel , Motor Vehicles , Neurodegenerative Diseases , Parkinsonian Disorders , Soccer , SportsABSTRACT
A 61-year-old ex-boxer presented with a three-year history of progressive memory decline. During a seven-year follow-up period, there was a continuous cognitive decline, very similar to that usually observed in Alzheimer's disease. Parkinsonian, pyramidal or cerebellar signs were conspicuously absent. Neuropathological examination revealed the typical features of dementia pugilistica: cavum septi pellucidi with multiple fenestrations, numerous neurofibrillary tangles in the cerebral isocortex and hippocampus (and rare senile plaques). Immunohistochemistry disclosed a high number of tau protein deposits and scarce beta-amyloid staining. This case shows that dementia pugilistica may present with clinical features practically undistinguishable from Alzheimer's disease.
Um ex-boxeador de 61 anos apresentou-se com história de três anos de perda progressiva de memória e evoluiu com declínio cognitivo lentamente progressivo, sugestivo de doença de Alzheimer, durante seguimento de sete anos. Sinais parkinsonianos, piramidais ou cerebelares estiveram ausentes durante toda a evolução. Exame neuropatológico evidenciou características típicas de dementia pugilistica: cavum do septo pelúcido com múltiplas fenestrações, numerosos emaranhados neurofibrilares no isocórtex cerebral e hipocampo (e raras placas senis). Imuno-histoquímica confirmou número elevado de depósitos de proteína tau e raros de beta-amilóide. Este caso demonstra que dementia pugilistica pode apresentar quadro clínico indistinguível daquele da doença de Alzheimer.