Abstract

Abstract Objectives-To determine the rate of ankle injury and examine risk factors of ankle injuries in mainly recreational basketball players. Methods-Injury observers sat courtside to determine the occurrence of ankle injuries in basketball. Ankle injured players and a group of non-injured basketball players completed a questionnaire. Results-A total of 10 393 basketball participations were observed and 40 ankle injuries documented. A group of noninjured players formed the control group (n = 360). The rate of ankle injury was 3.85 per 1000 participations, with almost half (45.9%) missing one week or more of competition and the most common mechanism being landing (45%). Over half (56.8%) of the ankle injured basketball players did not seek professional treatment. Three risk factors for ankle injury were identified: (1) players with a history of ankle injury were almost five times more likely to sustain an ankle injury (odds ratio (OR) 4.94, 95% confidence interval (CI) 1.95 to 12.48); (2) players wearing shoes with air cells in the heel were 4.3 times more likely to injure an ankle than those wearing shoes without air cells (OR 4.34, 95% CI 1.51 to 12.40); (3) players who did not stretch before the game were 2.6 times more likely to injure an ankle than players who did (OR 2.62, 95% CI 1.01 to 6.34). There was also a trend toward ankle tape decreasing the risk of ankle injury in players with a history of ankle injury (p = 0.06). Conclusions-Ankle injuries occurred at a rate of 3.85 per 1000 participations. The three identified risk factors, and landing, should all be considered when preventive strategies for ankle injuries in basketball are being formulated. (Br J Sports Med 2001;35:103-108) Keywords: basketball; ankle; injury; risk; prevention In basketball, ankle injuries are among the most common injuries sustained and they are also amongst the most severe. 1-3 An Australian basketball study 2 determined that over half (53.7%) of the total time missed because of an injury in basketball was through an ankle injury. Ankle injuries may result in the player experiencing disability and residual symptoms, 4-6 the most common being pain, sense of instability, crepitus, and weakness. 5 However, arthroscopic surgery of 31 ankles 6 found that chondral lesions were evident in 95% of chronic ankle injuries and 89% of recently injured ankles. As ankle injury is a common occurrence, often with residual symptoms aVecting performance and chondral lesions, preventive strategies need to be developed, but risk factors associated with ankle injuries must first be identified and understood. Previous studies of risk factors for ankle injury have been carried out in either the laboratory, with emphasis on biomechanical assessment, or the sporting environment as a field/clinical study. Laboratory based studies examine the eVectiveness of a specific variable such as ankle tape or brace or cut of shoe on aspects of performance such as restriction of postural sway, 7 wobble board performance, 8 sporting activities such as jumping and running, 9-11 or aspects of body function such as amount of joint restriction provided, 12-15 peroneal muscle activity, 16 and peroneal reaction time. 17 18 All of these authors have inferred how these factors may aVect the incidence of ankle injuries, without assessing the actual occurrence of ankle injuries. On the other hand, field studies usually assess risk factors for ankle injury with respect to the actual incidence of ankle injuries. These field based studies may question the validity of the biomechanical studies in making inferences about the risk of ankle injury on the sports field. Therefore the aim of this study was to examine risk factors of ankle injuries, such as history of ankle injury 4 19 20 , ankle tape 15 16 and braces 12 13 , playing shoes 21 , warm up, 22 and position played 23 24 on the court, in the naturalistic environment of the basketball court. Subjects and method In Melbourne, Australia, an elite basketball competition and three recreational basketball competitions were observed to identify injuries prospectively. Injury observers were instructed to view games and note the occurrence of injuries during the game. At the end of a game, all players were asked about their injury status, and injured players completed a questionnaire. A control group was obtained by administering a questionnaire to entire teams of players who were not injured on a particular day but were from the same competition as the injured players. All games observed were played indoors on wooden floors. Whilst there exists great controversy regarding the ethics of boxing, one of the key medical issues is the risk of a boxer developing CTE either during or after his boxing career. Recent evidence suggests that exposure to boxing alone is insufficient to cause this condition. It is believed that CTE represents the cumulative long term neurological consequences of repetitive concussive and sub concussive blows to the head. 1-4 CTE ismorecommoninprofessionalratherthan amateur boxers, however, CTE has been documented in other sports such as AmericanFootball,icehockey,rugby,horse racing, and soccer. [5][6][7] CTE is clinically characterised by a combination of speech and gait disturbance, pyramidal tract dysfunction, memory impairment, extrapyramidal features, behavior or personality changes, and psychiatric disease. 1-3 8 In the early stages of this condition, the symptoms are transient and reversible, however, in the later stages they are progressive.TheneurologyofCTEincludes characteristic neuropathological features of cerebral atrophy, septal fenestration, cerebellar tonsillar scarring, cavum septum pellucidum, loss of pigmented cells, and prominent neurofibrillary tangles. 7 It is salient to review the original paper discussing the neuropathology of CTE. Although individual case reports had been published of boxers with chronic dementing illnesses, the seminal paper discussing the association of neuropathological findings in boxers was published by the English pathologist, John Corsellis. 7 He studied the brains of 15 retired boxers and retrospectively studied their fight histories. While a number of characteristic changes were noted in these brains, it is the boxers' histories that deserve specific note. Of the fighters studied, their exposure to boxing ranged between 300 and 700 bouts in the courseoftheircareers.Thiswasinaddition to sparring and other fight training that would have occurred. The issue then that needs consideration is that in this day and age we would seldom see a fighter with such a record. Even the top professionals report fight careers of 30-50 fights before retirement, an order of magnitude less than that described in Corsellis' landmark study. Recent research in boxers has also suggested that CTE in boxers may be associated with a particular genetic predisposition. The apolipoprotein E e-4 gene (ApoE), a susceptibility gene for late onset familial and sporadic Alzheimer's disease, may be associated with an increased risk of CTE in boxers. 6 9 In a non-boxing population, ApoE polymorphism was significantly associated with death and adverse outcomes following acute traumatic brain injury as seen in a neurosurgical unit. 10 In a recent prospective study, ApoE genotypes were tested for their ability to predict days of unconsciousness and functional outcome after six months. 11 There was a strongassociation demonstrated between the ApoE allele and poor clinical outcome. Furthermore, ApoE deficient (knockout) mice have been shown to have memory deficits, neurochemical changes, and diminished recovery from closed head injury when compared to controls. 12 It is suggested that ApoE plays an important role in both neuronal repair and antioxidant activity resulting in ApoE knockout mice exhibiting an impaired ability to recover from closed head injury. How then does this help the debate on the risks of boxing? Firstly we need to reconsider the original evidence on exposure as a risk factor for CTE. The simplistic assumption based on epidemiological data from previous studies that CTE is a manifestation of the length of a boxer's career and hence exposure to punches needs to be readdressed. Similarly the development in understanding of the genetic risk that a boxer may carry developing CTE means that this area may need to be re-examined in light of current day research. This issue also raises a number of ethical issues, if a boxer is found to be homozygous for the ApoE e-4 phenotype should his boxing career be curtailed? At the very least, informed consent, and genetic counseling should be undertaken. Whilst one may argue the ethics and morality of boxing, it behooves us as scientists and clinicians to at least place the medical arguments regarding risk of injury on a scientific footing. Brain injury and heading in soccer Head to ball contact is unlikely to cause injury but head to head contact might W hether repeated concussive or subconcussive blows cause permanent or cumulative brain injury is a complex and controversial question. Press coverage highlighted the case of Jeff Astle, a former England international football player, where the coroner ruled the cause of his death as an "industrial disease"-suggesting that repeated heading of balls during his professional career was the cause of his subsequent neurological decline. 1 This case was at odds with that of Billy MacPhail, a former Glasgow Celtic player, who in 1998 lost a legal battle to claim benefits for dementia that he said was due to heading the old style leather footballs. Concern has been raised over whether heading in soccer may be the basis for injury and cognitive impairment, and in the United States this has led to calls advocating the use of protective headgear for soccer players. Soccer players don't just head the ball; their heads can collide with each other, and players in positions where heading is common are also more likely to have head to head collisions more often. Although uncommon, most concussive injuries seen in soccer derive from such head to head rather than ball to head contact. 2 Heading a soccer ball results in head accelerations of less than 10 g (or less than 1000 rad/s 2 ) whereas the minimum values for the development of sport related concussion are 40-60 g (or 3500-5000 rad/s 2 ). 3 4 In contrast, head to head contact can generate enough of the forces required to cause brain injury as in any conventional head injury. Recent biomechanical research has found that commercially available soft helmets fail to reduce even this degree of head trauma to a safe level, which implies that these helmets have only a limited protective role in this setting. 5 There is no evidence that sustaining several concussions over a sporting career will necessarily result in permanent damage. 6 Research on experimental animals provides some supporting evidence against the concept that recurrent concussive injuries alone cause permanent damage. In studies of experimental concussion, animals have been subjected to repeated concussion 20-35 times in a two hour period. Despite the unusually high number of injuries no residual or cumulative effect was shown. 7 Can repeated subconcussive trauma such as might be seen in heading the ball cause a cumulative neurological injury in this setting? Although this was indicated by early retrospective studies, more recent studies have not supported this idea. [8][9][10] In a series of retrospective studies including retired Scandinavian soccer players, cognitive deficits were noted. 11 12 The results of these studies are flawed, with appreciable methodological problems. These problems include the lack of pre-injury data, selection bias, failure to control for acute head injuries, lack of blinding of observers, and inadequate controls. The authors conclude that the deficits noted in these former soccer players were explained by repetitive trauma such as heading the ball. However, the pattern of deficits seen is equally consistent with alcohol related brain impairment-a confounding variable that was not controlled for. Matser et al from the Netherlands have also implicated both concussive injury and heading as a cause of neuropsychological impairment in both amateur and professional soccer players. 2 13 Reanalysis of the data from these papers, however, indicates that purposeful heading may not be a risk factor for cognitive impairment. 14 Prospective controlled studies using clinical examination, neuroimaging, or neuropsychological testing have failed to find any evidence of cognitive impairment in soccer players. 8-10 We do not know for certain whether heading the ball in soccer may result in chronic cognitive impairment. It seems unlikely that subconcussive impacts such as seen in head to ball contact will cause chronic neurological injury. Although head to head contact may cause concussive injury, it is both uncommon and unlikely to result in cumulative brain injury. It has been speculated from other sports that particular genotypes may place athletes at heightened risk in Self reports in research with non-English speakers The challenge of language and culture is yet to be met A ssessment of the health and healthcare needs of ethnic minority populations, often relying on self reported data, is important in health and social services. 1 Major problems exist with the reliability of such information, particularly among recent and older immigrants and refugees who may have little or no competency in English and may be at high risk of health problems. Approximately 23% of immigrants to Britain born in China, Bangladesh, India, and Pakistan have no functional skill in English, and 70% cannot function fully in an English speaking social environment. 2 When a measure is probing differences within a group it must be appropriate, valid, and reliable for the group concerned. However, if the data are to be used to make comparisons between groups as in clinical trials and most epidemiological studies, then the questions must be conceptually and functionally equivalent and appropriate for all the groups compared. Non-English speakers are often excluded from clinical trials and epidemiological studies, for reasons including the lack of valid and reliable cross cultural measurements. 3 In clinical and epidemiological studies questions developed for native English speakers are usually translated into other languages. It is assumed that the modes of inquiry appropriate for native English speakers are applicable to other linguistic groups. These assumptions may reflect pragmatic issues relating to time and finance or lack of understanding of the complexities of language and culture. Translations, even by experts, may fail to achieve questions that are comparable to the original English in terms of appropriateness and meaning. 4 It is therefore important to consider conceptual matters, cultural relevance, and the subtle connotations of words and phrases. In multilingual studies, if each language is translated and compared to the English, each may resemble the English version, but the different non-English languages may differ in important ways, sometimes because it is impossible to find equivalent translations. For example the term "feeling blue," used in the original American version of the short form questionnaire 36 (SF-36), has different connotations in different languages 5 whereas the terms "check up" and "Pap smear" have no conceptual equivalent in any Chinese language. 6 Research in our department, analysing the translation of local and national health surveys, has uncovered numerous potential problems-for example, asking Muslims whether they drink more at Christmas, and the use of terms such as "weekend" and "hangover" with questionable relevance to some ethnic groups. 7 Detailed examination of translations of the Rose angina questionnaire into Punjabi and Cantonese has highlighted subtle issues potentially explaining the recently shown lesser validity of this instrument in South Asian populations. 8 In face to face interviews complications arise where different forms of the same language are used-for example, Bengali and the Sylheti variant of Bengali, the latter having no written form. For some languages the written and spoken forms are not the same-for example, Arabic or Cantonese. At interview the questions asked will not be the same as the questions written on the questionnaire or interview schedule, with unknown effects on data quality. An alternative to seeking cross cultural equivalence is to define issues as, firstly, salient and meaningful within a culture, for example, chewing paan, and, secondly, concerns of salience between cultures, for example, smoking tobacco. This strategy requires a participatory approach whereby monolingual and bilingual representatives of the target group(s) are Objective and method: To outline the direct and indirect approaches in the fight against blood doping in sports, the different strategies that have been used and are currently being used to fight efficiently against blood doping are presented and discussed. Results and conclusions: The paper outlines the different approaches and diagnostic tools that some federations have to identify and target sportspeople demonstrating abnormal blood profiles. Originally blood tests were introduced for medical reasons and for limiting misuse of recombinant human erythropoietin (rHuEPO). In this way it became possible to prevent athletes with haematocrit levels well above normal, and potentially dangerous for their health, competing in sport. Today, with nearly a decade of blood testing experience, sports authorities should be familiar with some of the limitations and specially the ability of blood tests performed prior to competitions to fight efficiently against the misuse of rHuEPO, blood transfusion, and artificial haemoglobin. E rythropoiesis is part of the large process of haematopoiesis, which involves the production of mature cells found in the blood and lymphoid organs. 1 Haematopoiesis is continuously required because of the normal turnover in the cell populations in the blood and lymphoid organs. In the normal adult human, the daily turnover of erythrocytes exceeds 10 11 cells. During periods of increased erythrocyte loss, due to haemolysis or haemorrhage, the production of erythrocytes increases rapidly and markedly. However, overproduction of erythrocytes does not occur, even after the most severe loss of erythrocytes. In haematopoiesis, a few pluripotent haematopoietic stem cells in the bone marrow proliferate and differentiate to give rise to all the cellular components of the blood and the lymphoid system. During this process, an individual haematopoietic cell undergoes an apparently random process called commitment. When a cell undergoes commitment, its potential to proliferate becomes limited and its potential to develop into multiple types of mature cell is also restricted. Thus, these haematopoietic cells are termed committed, lineage specific progenitor cells. The major stages of differentiation in mammalian erythropoiesis are as follows. The most immature stage of committed erythroid progenitors is the burst forming uniterythroid (BFU-E). The next major stage of erythroid progenitor cell development is the colony forming uniterythroid (CFU-E). A continuum of erythroid progenitor stages exists between the BFU-E and CFU-E, with decreasing proliferative potential as the progenitors approach the CFU-E stage. The descendant cells of the CFU-E are termed erythroid precursor cells. These erythroid precursors are proerythroblasts, basophilic erythroblasts, polychromatophilic erythroblasts, and orthochromatic erythroblasts. The orthochromatic erythroblasts do not divide, but they enucleate, forming the nascent erythrocyte called the reticulocyte. PRODUCTION OF ERYTHROPOIETIN Erythropoietin (EPO) is a 30 400 molecular weight glycoprotein hormone produced mainly in the kidney, and also in the liver (,10%) and, in very little quantities, in the brain. 2-5 The physiological stimulus for EPO production is tissue hypoxia, which, in the large majority of instances, is directly related to the number of circulating erythrocytes. 6 Thus, EPO and erythropoiesis are part of a negative feedback cycle that keeps tissue oxygen delivery within a narrow range by controlling the number of erythrocytes circulating in the blood. 7 ln a normal individual, any loss of erythrocytes, such as by bleeding or haemolysis, decreases delivery of oxygen to the tissues. 8 When this tissue hypoxia is sensed by cells in the kidney and liver capable of producing EPO, they produce and secrete EPO into the plasma. 9 EPO is carried to the bone marrow, where it binds to specific cell surface receptors on its target cells-the CFU-E, pro-erythroblasts, and basophilic erythroblasts. 10 11 The binding of EPO by these cells increases their ability to survive and reach the reticulocyte stage and thereby contribute to the population of circulating erythrocytes. The increased numbers of circulating erythrocytes in turn deliver more oxygen to the tissues. This increased oxygen delivery is sensed by the EPO producing cells, which then reduce EPO production so that the normal steady state number of erythrocytes is restored. The response of the kidneys to hypoxia has been shown to be exponential 12 -that is, in individuals with a normal capacity to produce EPO, a linear decline in haematocrit is accompanied by an exponential increase in plasma EPO levels. This exponential increase is not based on the release of stored, preformed EPO. Rather, the hypoxia is sensed by an intracellular molecule that interacts with an enhancer element of the Epo gene and thereby induces transcription of the gene. 9 MECHANISM OF ACTION OF ERYTHROPOIETIN ln the bone marrow, EPO binds to receptors displayed on the cell surface of CFU-E, proerythroblasts, and basophilic erythroblasts. The mature EPO receptor, with a molecular Background and objectives: Recombinant human growth hormone (rhGH) has been on the list of forbidden substances since availability of its recombinant form improved in the early 1990s. Although its effectiveness in enhancing physical performance is still unproved, the compound is likely used for its potential anabolic effect on the muscle growth, and also in combination with other products (androgens, erythropoietin, etc.). The degree of similarity between the endogenous and the recombinant forms, the pulsatile secretion and marked interindividual variability makes detection of doping difficult. Two approaches proposed to overcome this problem are: the indirect method, which measures a combination of several factors in the biological cascade affected by administration of GH; and the direct method, which measures the difference between the circulating and the recombinant (represented by the unique 22 kD molecule) forms of GH. This article gives an overview of what is presently known about hGH in relation to sport. The available methods of detection are also evaluated. Methods: Review of the literature on GH in relation to exercise, and its adverse effects and methods of detection when used for doping. Results and conclusion: The main effects of exercise on hGH production and the use and effects of rhGH in athletes are discussed. Difficulties encountered by laboratories to prove misuse of this substance by both indirect and direct analyses are emphasised. The direct method currently seems to have the best reliability, even though the time window of detection is too short. hGH doping is a major challenge in the fight against doping. The effect of exercise on hGH and its short half-life are still presenting difficulties during doping analysis. To date the most promising method appears to be the direct approach utilising immunoassays.