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Epidemiology of ischaemic stroke and traumatic brain injury
Best Practice & Research Clinical Anaesthesiology 24 (2010) 485–494
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Epidemiology of ischaemic stroke and traumatic brain injury Valery L. Feigin, Professor a, *, Suzanne Barker-Collo, MD b, Rita Krishnamurthi, MD a, Alice Theadom a, Nicola Starkey, MD c a
National Institute for Stroke and Applied Neurosciences, School of Rehabilitation and Occupation Studies, School of Public Health and Psychosocial Studies, Faculty of Health and Environmental Studies, AUT University, AUT North Shore Campus, AA254, 90 Akoranga Dr, Northcote 0627, Private Bag 92006, Auckland 1142, New Zealand b Faculty of Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand c Department of Psychology, Faculty of Arts and Social Sciences, University of Waikato, Private Bag 3105, Hamilton, New Zealand
Keywords: ischaemic stroke brain injury epidemiology risk factors
Acquired brain injury, including both Ischaemic stroke (IS) and Traumatic Brain injury (TBI), is one of the most common causes of disability and death in adults. Yet there are vast differences in our knowledge of their epidemiology. While the incidence, casefatality and risk factors for stroke are well established, work needs to continue particularly in low-income countries, where these data remain sparse; and in relation to specific stroke subtypes such as IS. Similar data regarding the epidemiology of TBI are generally lacking. The majority of TBI incidence studies have focussed on hospital-based samples and there are no established criteria from which to design high quality epidemiological studies. The need to establish such criteria separate from those already available for stroke is suggested given the differing demographic profile of TBI as well as differences in seeking of medical attention for TBI. The immense burden of stroke can be reduced by prevention of modifiable risk factors particularly in developing countries where both changing lifestyle and lack of healthcare resources are contributing to rising stroke incidence and mortality. Similarly, studies to date indicate that TBI incidence can be reduced by addressing modifiable risk factors such as alcohol abuse, risktaking behaviour and socioeconomic disparities. Ó 2010 Elsevier Ltd. All rights reserved.
* Corresponding author. Tel.: þ64 9 921 9166; Fax: þ64 9 921 9620. E-mail address: [email protected] (V.L. Feigin). 1521-6896/$ – see front matter Ó 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.bpa.2010.10.006
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Introduction Acquired brain injury (an injury to the brain occurring after birth) is one of the most common causes of disability and death in adults.1,2 Stroke and Traumatic brain Injury (TBI) are the two most common causes of acquired brain injury, yet there are vast differences in our knowledge of their epidemiology. In this review we identify important issues regarding current epidemiological data on ischaemic stroke (IS) and TBI, including incidence, case-fatality and known risk factors with the emphasis on populationbased studies; identifying differences between these conditions and implications for epidemiological studies and future management. Epidemiology of ischaemic stroke The World Health Organisation (WHO) defines stroke as “rapidly developing signs of focal (or global) disturbance of cerebral function, lasting longer than 24 h (unless interrupted by death) with no apparent non-vascular cause”.3 Strokes can be either ischaemic (occlusion of a blood vessel) or haemorrhagic (rupture of a blood vessel). Distinguishing between stroke subtypes is critical to appropriate management, and diagnosis is predominantly made using Computerised tomography (CT) or Magnetic resonance imaging (MRI) .4 Prognosis and treatment post-stroke differ according to the specific nature of stroke and therefore stroke subtype needs to be identified.5 IS constitutes 80–85% of all strokes3,6 and is therefore the focus of this review. IS carries an enormous emotional and socio-economical impact with lifetime costs per patient estimated at US$59,800 to US$230,000.7 The risk of recurrent IS is 2% 7-days post-stroke and 29% 5-years post-stroke.8 Moreover, stroke is a common cause of disability adjusted life-years (DALYs; the sum of life-years lost as a result of premature death and years lived with disability adjusted for severity) with estimates that it will be the fourth most common cause of disability in western countries by 2030.4 Wide variability in incidence may reflect true differences or methodological differences used to study stroke epidemiology in different countries9 and differences within countries (e.g. higher incidence in rural areas).10 A recent systematic review of worldwide stroke incidence9 revealed distinct trends in stroke incidence according to income levels, with >100% increase in low- to middle-income countries and a 42% decrease in high-income countries since 1970; but similar age-adjusted incidence of IS between high-income and low- to middle-income countries in the last decade. However, the pooled proportional frequencies of IS in high-income countries were higher (83%) in 2000–08 compared to low- to middle-income countries (67%), who had higher haemorrhagic stroke incidence. Case-fatality rates (21–30 days) following IS have declined in high-income countries from 10–32% (1990–99) to 13–23% (2000–08).9 Case-fatality rates for low- to middle-income countries for IS have only recently been published and suggest higher case-fatality in these countries (range 17.8–23.2%) possibly reflecting differences in acute care.5 Years of life lost due to premature mortality (YLLs) attributed to stroke (80–85% IS) vary widely but global estimates are 9.5% and 9.9% of total deaths for low-income countries and high-income countries respectively, making it the second leading cause of death after ischaemic heart disease.11 IS can be further differentiated into 5 subtypes, using the Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria: larger artery atherosclerosis, cardioembolism, small vessel occlusion (lacune) stroke of other undetermined etiology, and stroke of undetermined etiology.12 In a population-based study,13 incidence of subtypes was: cardioembolism is 30.2 (25.6–35.7), small artery occlusion 25.8 (21.5–30.9), and larger artery atherosclerosis 15.3 (12–19.3) per 100,000 person-years (adjusted to WHO standard European population) with the incidence of large artery disease twice as high in men as women. In this study IS subtype was a significant predictor for long-term survival but not long-term recurrence up to 2 years. Longer-term IS mortality rates also vary by subtype.14 This heterogeneity of IS suggests its epidemiology should be evaluated, where possible, by subtype. Major risk factors for ischaemic stroke Age Advancing age is associated with increased IS prevalence and is its principal non-modifiable risk factor.15–18 For each decade after age 55, the risk of stroke more than doubles,19 presumably due to
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increased exposure to environmental risk factors and higher prevalence of risk factors including atrial fibrillation (AF), hypertension, diabetes, and coronary heart disease. Hypertension Hypertension is responsible for 60–70% of strokes worldwide and is considered it’s most important modifiable factor.20 In IS, damage to the arteries caused by hypertension impairs blood flow by causing plaque to build up thus creating a clot which leads to stroke. The American Heart Association Stroke Council identified elevated systolic blood pressure (with or without elevated diastolic blood pressure) as increasing stroke risk,21 as is also evidenced in other studies.22 Unfortunately, a significant proportion of people remain undiagnosed or inadequately treated for hypertension23 despite readily available pharmacological treatment. Gender A range of findings for gender differences in the epidemiology, outcomes and treatment of stroke are reported. Men have higher age-specific stroke rates than women and men are more likely to have their first-ever stroke at a younger age.24 However, due to increased stroke incidence for women >84 years, women overall, experience more strokes.25 Women are also typically identified as experiencing poorer outcomes post-stroke.26 The causes of this disparity may be partly explained by women: being older at stroke onset; having poorer pre-stroke functioning; having more co-morbidities; being less likely to have social support, and more likely to be widowed/divorced.26 Ethnicity Numerous studies report ethnic disparities in prevalence and incidence of IS as well as related disability and mortality. The NOMASS study reported a higher annual incidence of age-adjusted firstever stroke incidence per 100,000 in blacks than whites and Hispanics.27 In New Zealand, Maori/Pacific populations had higher rates of IS (age-adjusted risk ratio (RR) 1.7) than Europeans and were likely to experience stroke at a younger age.28 The subtype of IS also differs between ethnic populations.29 Atherosclerosis Atherosclerosis, the thickening of artery walls due to the build up of plaques made from fatty materials (e.g., cholesterol, calcium) found in the blood can obstruct blood flow by narrowing or blocking blood vessels. The narrowing of brain arteries (i.e., intracranial atherosclerosis) causes or contributes to >70% of strokes worldwide.30 Atrial fibrillation AF is the most powerful and treatable embolic stroke precursor. The slow, abnormal rhythm in AF causes clot formation in the heart, which can then travel to the brain and cause a stroke. AF rises markedly with age31 and is well identified as an independent stroke risk factor.32 Incidence of stroke associated with AF has been estimated to increase from five33 to seven34 times. IS that occurs with AF is almost twice as likely to be fatal than stroke without AF.35 Tobacco Tobacco use is an established significant independent risk factor for IS.36 Chemicals in tobacco smoke increase plaque build up in arteries and promote development of blood clots that can cause strokes. Smoking doubles the risk of IS versus non-smokers.37 Moreover there is an unambiguous relationship between number of cigarettes smoked and stroke risk with smoking 15 cigarettes/day increasing stroke risk up to four times.38 A positive correlation between the length of time smoking and increased stroke risk is also reported.39 As well as increasing the risk of IS, tobacco use has also been demonstrated to increase the risk of haemorrhagic stroke, especially subarachnoid haemorrhage.40,38 Second-hand smoke is also established as contributing to stroke incidence.41,42 Alcohol Heavy drinking is associated with hypertension and AF and thus is related to increased stroke risk.43 However, any direct relationship between alcohol and stroke is unclear.43 A 2003 meta-analysis of 35
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studies indicated that >60 g of alcohol daily increased risk of stroke, although light or moderate consumption (<24 g/day) decreased stroke risk compared to abstainers.44 Physical inactivity Several studies have demonstrated an inverse relationship between increased physical activity and an increase in the risk of stroke45 as well as stroke risk factors including hypertension, high cholesterol, obesity, diabetes and atherosclerosis.46 Two meta-analyses concluded that there was a lower risk of both ischaemic and haemorrhagic stroke in moderately and highly active individuals.47,48 Obesity/diet The relationship between obesity and stroke remains controversial due to methodological inconsistencies across studies. Nevertheless, obesity (particularly abdominal adiposity and waist circumference) is positively related to IS.49,50 This is thought to occur through hypertension and diabetes37 though a positive correlation has been found between BMI and stroke independent of hypertension, diabetes and high cholesterol.38 Due to the association of diet and obesity and its complex interactions with other risk factors (e.g., hypertension) determining the exact extent to which diet affects stroke risk is difficult. Good nutrition can mitigate other stroke risk factors including hypertension, high cholesterol, diabetes and cardiac disease.51 Diets high in fat, sugar and salt increase stroke risk52 by raising low-density cholesterol, triglycerides and increasing blood pressure. Conversely, diets low in saturated fats and sodium and high in fruit and vegetables significantly reduce stroke risk.53–55 Research into diet and stroke subtype is scarce although there is some evidence that consumption of fish is associated with a decreased IS risk.56 Summary There are difficulties in making direct comparisons between studies that limit case ascertainment to hospitals and those that are population-based. Different clinical definitions, use of subtypes, hospital admission patterns and access to diagnostic tools (e.g. CT scans) may account for some variations in incidence rates. Population-based studies provide a most robust evidence of the burden of IS in the world. Evidence strongly suggests IS incidence can be reduced by targeting modifiable risk factors such as hypertension, smoking and poor diet/lifestyle. Projections estimate that by 2030 stroke will be one of the main causes of lost healthy life-years, thus further work is needed to complete the picture and to broaden our understanding of its risk factors, prevention and management. Epidemiology of traumatic brain injury TBI is defined by the WHO as ‘an acute brain injury resulting from mechanical energy to the head from external physical forces’. Operational criteria for clinical identification of TBI include 1 of: (1) confusion or disorientation; (2) loss of consciousness; (3) post-traumatic amnesia; (4) other neurological abnormalities (e.g., focal neurological signs, seizure, intracranial lesion).57 TBI severity is classified as mild, moderate or severe, based on Glasgow Coma Scale (GCS) scores.57 According to the literature, irrespective of age, 70–90% of TBIs are mild with 5–20% being moderate & severe.58 Incidence of TBI in developed countries (e.g., United Kingdom, Australia) is z200–300 people per 100,000 population annually.59 A recent WHO systematic review60 suggests the annual incidence of mild TBI is probably >600/100,000. Incidence rates for low and middle-income countries are scarce, varying from 160 per 100,000 in India,61 360 per 100,000 in Brazil,62 and 219 per 100,000 in Yemen.63 Those in low-middle-income countries often lack access to basic medical care, particularly in rural areas.64 Even in high-income countries the cost of care is high and the registration of new TBI cases is poor, leading to underestimated incidence with many cases unrecorded. TBI incidence in African countries is unknown, but in Nigeria, 31% of all trauma related deaths are due to TBI.65 In contrast to stroke, in Europe and North America, only z25% of persons who experience TBI are admitted to hospital.66 In New Zealand, it is estimated that for every 100 people seen at hospital regarding TBI, 60 are managed by their general practitioner.67 Studying TBI in a population-wide context is therefore particularly important. Moreover, changes in patterns of referral can distort
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longitudinal trends derived from hospital data.68 Official statistics are of limited use as they are incomplete (due to selection bias) and do not collect all data relevant to interpreting variations in outcome. Further, inconsistent and inaccurate diagnosis of TBI is evident in coding of hospital discharges for TBI,67 emphasizing the importance of appropriate TBI case ascertainment. Unlike IS, 28-day case-fatality is rarely reported for TBI. Estimates indicate that 30–35% of patients admitted to hospital with moderate or severe TBI die within the first 30-days.69 In the USA, >3% of all deaths during 2001 were due to brain injury.70 However, reported annual case-fatality ranges widely (3.2%71 to 19.7%72) and there are too few good quality studies to draw any conclusions. The difference in rates may reflect the lack of specificity of cause of death on the death certificates (e.g. massive multiple trauma not specifying body regions involved).73 Furthermore, mortality is significantly higher (19.5%) in low compared to high-income countries,74 with violent assaults accounting for a larger proportion of TBIs.61,65 In rapidly developing countries such as India, car use has increased dramatically over the last 20 years (from 5.3 million to 59 million between 1981 and 2002), with few safety regulations or road rules. As a consequence, 44% of road deaths worldwide occur in Asia.61 Combined with poor access to medical care TBI is a rapidly increasing public health problem in these countries.65 Due to the high incidence of TBI at an early age and long-term impact on employment and disability,75 the DALY lost due to TBI is significant.76 The economic cost of TBI varies significantly, due to both individual characteristics and the nature of the injury.77 TBI in children and young adults has a significant economic cost; in the USA in 2006, children admitted to hospital with a TBI following a motor vehicle accident (MVA) or falls incurred hospital charges of zUS$2.6 billion78 whilst in the UK young adults (18–25 years) with TBI cost z47.2 million GBP per year.79 WHO estimate TBI will be the 3rd leading cause of premature death across all ages by 2020.80 Moderate and severe TBI results in the greatest disability and consumes the most resources per individual, yet mild TBI’s (mTBI) magnitude and societal ramifications are often underestimated.60 Despite the label ‘mild’, many of these injuries result in long-term difficulties81–83 (e.g., post-concussion symptoms,84 epilepsy,85 depression,86 cognitive deficits,87 sleep disturbances,88 and persistent headache89). These are often unrecognized in the acute phase, as patients do not seek medical attention, are not systematically assessed or are lost to medical follow-up.81 It has been estimated that 40–80% of mTBI survivors experience post-concussive syndrome, a constellation of physical, cognitive, and behavioural difficulties90 that may persist up to 2 years post-TBI.91 A hospital-based cohort study found that 47% of mTBI cases had moderate to severe physical disability 1-year post-injury.92 Along with the significant number of mTBIs, these outcomes underline the value of accurate identification and adequate management.57,67
Risk factors for traumatic brain injury Age TBI incidence peaks between 15 and 24 years of age, with smaller peaks in infancy (<5 years) and older age93,94 Self-reports suggest 31% of children experience a head injury before age 18,95 whilst 44% of 14–15 year olds reported a head injury in previous 3 years.96,97 The mechanism of TBI differs with age. Falls are most common in young and old age groups, with MVA and assaults most common in middle age.70 Cycling and sports related accidents also account for a significant proportion of TBI in 8–14 year olds.93 Overall, the most common cause of TBI worldwide is transport related, whether it be in a car, or as a cyclist or pedestrian.93 Categorisation of TBI severity in children is based on criteria for adults and is frequently difficult to apply, particularly in pre-verbal children.97,98 However, existing criteria suggest 80–90% of childhood TBI’s are mild.70,97 Consequences of TBI in children can be more severe than in adults, potentially impacting previously acquired skills, inhibiting learning of new skills, and adversely impacting attainment of developmental milestones, which may not be apparent for years post-injury.97,99–101 Studies are inconsistent, but evidence suggests that outcomes for children and adolescents after uncomplicated (i.e., no evidence of intracranial abnormality) mTBI are good.98 However, there are few studies beyond 5 years, leaving the full impact of TBI on normal developmental processes (e.g., executive functions) unclear.97,102
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Alcohol Alcohol use increases risk of TBI as a result of falls, MVA and assault.61 In an American emergency department, 56% of people with TBI had positive blood alcohol, with half of these over the legal limit.103 Alcohol abuse is associated with recurrent TBI104 and parental alcohol misuse is a risk factor for childhood TBI (relative risk ratio 1.99).105 Gender Males are at approximately twice the risk of TBI compared to females 1.6–2.8.94,106 However, the gender ratio varies with age; in those <5 years of age, incidence rates are similar, but after this, incidence increases faster in males resulting in an incidence over double that in females, particularly apparent during adolescence.97,107 This is largely due to the increased risk-taking behaviour, reflecting the higher incidence of MVA in young males drivers.108 Ethnicity, socioeconomic status and education There are ethnic inequalities in TBI incidence and outcomes109; with ethnic minority groups having greater TBI risk and higher post-TBI mortality.110,111 While at 1-year post-injury, Caucasian and minority group TBI survivors reported similar impairments and activity, minorities report significantly less social integration.112 Furthermore, parents of ethnic minority children with a TBI rate injury outcomes less favourably than Caucasians, even when socioeconomic status (SES) is controlled for.113 Proportionally, fewer TBI from minorities are employed at 1-year, even if employed prior to injury.114 Compared to Caucasians, minority groups receive less medical care post-TBI (e.g., longer wait for doctor)115 and receive fewer inpatient rehabilitation therapies.116 Separating the effects of ethnicity and SES is challenging. Even so, studies indicate that lower SES is associated with increased risk of TBI. For example, even though 16% of the South Carolina residents are uninsured, they make up 26% of TBIs seen in emergency departments.117 Similarly, in the UK, children with severe TBI requiring intensive care reside in significantly poorer parts of the country.118 Lower SES is also linked to poorer TBI outcomes.113 In contrast, higher levels of pre-injury education are associated with better outcomes in all areas of functioning.119 Clearly, it is important to understand how ethnic/ socioeconomic factors impact TBI incidence and outcomes, and the reasons for these inequalities, in order to improve these outcomes for vulnerable groups.120
Summary To date TBI epidemiological studies are limited to small and hospitalised samples, underestimating its true incidence and outcomes. Case ascertainment has focused on hospital admission or discharge records; capturing moderate to severe TBI cases where death hasn’t occurred at the time of injury. However, as most mTBI cases are not hospitalised (few seek immediate medical attention) and those who die before reaching hospital are not recorded in the hospital admission records, these are overlooked. Significant differences in study methods and TBI classification (particularly in children) make comparisons difficult; therefore consistent comprehensive approaches to case ascertainment are needed. Overarching summary and practice points Accurate and representative population-based data are crucial for: determining the true incidence, causes and outcome of TBI and IS; evidence-based healthcare planning across the care spectrum; evaluating the impact of preventative/management strategies; addressing persistent uncertainty about socioeconomic and health service factors influencing recovery; examining the natural course of recovery; providing information about access and satisfaction with services and identifying service gaps and ensuring evidence-informed policy, resource and service allocation, planning of relevant prevention, and evaluation of sector and service performance. This review indicates a wide level of epidemiological knowledge about stroke generally, yet a dearth of similar information in regards to IS and its subtypes; and an even greater gap in knowledge in
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relation to TBI where few population-based studies are available and issues related to age and capture of cases with mTBI are particularly important. Criteria proposed to inform the design of high quality epidemiological studies and enabling the comparison of stroke incidence worldwide could be applied to IS more specifically.121 The need to establish such criteria separate from those already available for stroke is suggested for TBI to encompass the differing demographic profile of TBI as well as differences in seeking of medical attention.122 Conflict of interest statement None.
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Vegetable and fruit intake and stroke mortality in the Hiroshima/Nagasaki life span study. Stroke 2003; 34(10): 2355–2360 [Research Support, Non-U.S. Gov’t Research Support, U.S. Gov’t, Non-P. H.S.]. 54. Dauchet L, Amouyel P, Dallongeville J et al. Fruit and vegetable consumption and risk of stroke: a meta-analysis of cohort studies [Meta-Analysis Research Support, Non-U.S. Gov’t]. Neurology 2005; 65(8): 1193–1197 [Summary for patients in Neurology. 2005 Oct 25;65(8):E17–8; PMID: 16247035]. 55. Fung TT, Rexrode KM, Mantzoros CS et al. Mediterranean diet and incidence of and mortality from coronary heart disease and stroke in women [Erratum appears in Circulation. 2009 Mar 31;119(12):e379]. Circulation 2009; 119(8): 1093–1100 [Comparative Study Research Support, N.I.H., Extramural]. 56. He K, Song Y, Daviglus ML, et al. Fish consumption and incidence of stroke: a meta-analysis of cohort studies. 2004;35 (7):1538–42.
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Neurological Research 2002; 24(1): 24–28. 62. de Andrade AF, Marino R, Ciquini O et al. Guidelines for neurosurgical trauma in Brazil. World Journal of Surgery 2001; 25(9): 1186–1201. 63. Shukri AA, Bersnev VP & Riabukha NP. The epidemiology of brain injury and the organization of health care to victims in Aden (Yemen). In Hyder AA, Wunderlich CA, Puvanachandra P et al (eds.). The impact of traumatic brain injuries: a global perspective. NeuroRehabilitation 2007: 341–353. 64. Gabella B, Hoffman RE, Marine WW & Stallones L. Urban and rural traumatic brain injuries in Colorado. Annals of Epidemiology 1997; 7(3): 207–212. 65. Hyder AA, Wunderlich CA, Puvanachandra P et al. The impact of traumatic brain injuries: a global perspective. NeuroRehabilitation 2007; 22(5): 341–353. 66. Vink R, Nimmo AJ. Novel therapies in development for the treatment of traumatic brain injury. 2002;11(10):1375–86. 67. Group NZG. Traumatic brain injury: diagnosis, acute management and rehabilitation. Wellington: New Zealand Guidelines Group, 2006. 68. Stephenson S, Langley J & Cryer C. Effects of service delivery versus changes in incidence on trends in injury: a demonstration using hospitalised traumatic brain injury. Accident, Analysis and Prevention 2005; 37(5): 825–832. 69. Baguley IJ, Nott MT, Slewa-Younan S. Long-term mortality trends in functionally-dependent adults following severe traumatic-brain injury. 2008;22(12):919–25. 70. Bazarian JJ, McClung J, Shah MN et al. Mild traumatic brain injury in the United States, 1998–2000. Brain Injury 2005; 19(2): 85–91. 71. Rutland-Brown W, Langlois JA, Thomas KE & Xi YL. Incidence of traumatic brain injury in the United States, 2003. Journal of Head Trauma Rehabilitation 2006; 21(6): 544–548. 72. Vázquez-Barquero A, Vázquez-Barquero JL, Austin O et al. The epidemiology of head injury in Cantabria. European Journal of Epidemiology 1992; 8(6): 832–837. 73. Sosin DM, Sniezek JE & Waxweiler RJ. Trends in death associated with traumatic brain injury, 1979 through 1992. Success and failure. JAMA 1995; 14(273): 1778–1780. 74. Mauritz W, Wilbacher I, Majdan M et al. Epidemiology, treatment and outcome of patients after severe traumatic brain injury in European regions with different economic status. European Journal of Public Health 2008; 18(6): 575–580. 75. Donders J & Warschausky S. Neurobehavioral outcomes after early versus late childhood traumatic brain injury. Journal of Head Trauma Rehabilitation 2007; 22(5): 296–302. *76. WHO. Injuries in the WHO European region: burden, challenges and policy response. Background paper for the 55th session of the WHO Regional Committee (RC55). World Health Organization, 2005. 77. McGarry LJ, Thompson D, Millham FH et al. Outcomes and costs of acute treatment of traumatic brain injury. Journal of Trauma 2002; 53(6): 1152–1159. 78. Shi J, Xiang H, Wheeler K et al. Costs, mortality likelihood and outcomes of hospitalized US children with traumatic brain injuries. Brain Injury 2009; 23(7): 602–611. 79. Beecham J, Perkins M, Snell T & Knapp M. Treatment paths and costs for young adults with acquired brain injury in the United Kingdom. Brain Injury 2009; 23(1): 30–38. 80. Murray CJ & Lopez AD. Global health statistics: a compendium of incidence, prevalence and mortality estimates for over 200 conditions. Cambridge: Harvard University Press, 1996. 81. Dischinger P, Read K, Kerns T et al. Causes and outcomes of mild traumatic brain injury: an analysis of CIREN data. Annual Proceedings – Association for the Advancement of Automotive Medicine 2003; 47: 577–589. 82. Hoge CW, McGurk D, Thomas DJ et al. Mild traumatic brain injury in U.S. soldiers returning from Iraq. New England Journal of Medicine 2008; 358(5): 453–463. 83. Kashluba S, Hanks RA, Casey JE & Millis SR. Neuropsychologic and functional outcome after complicated mild traumatic brain injury. Archives of Physical Medicine and Rehabilitation 2008; 89(5): 904–911. 84. Yang C-C, Tu Y-K, Hua M-S & Huang S-J. The association between the postconcussion symptoms and clinical outcomes for patients with mild traumatic brain injury. Journal of Trauma 2007; 62(3): 657–663. 85. Bruns Jr. J & Hauser WA. The epidemiology of traumatic brain injury: a review. Epilepsia 2003; 44(Suppl. 10): 2–10. 86. Ganesalingam K, Yeates KO, Ginn MS et al. Family burden and parental distress following mild traumatic brain injury in children and its relationship to post-concussive symptoms. Journal of Pediatric Psychology 2008; 33(6): 621–629. 87. Malojcic B, Mubrin Z, Coric B et al. Consequences of mild traumatic brain injury on information processing assessed with attention and short-term memory tasks. Journal of Neurotrauma 2008; 25(1): 30–37. 88. Milroy G, Dorris L & McMillan TM. Sleep disturbances following mild traumatic brain injury in childhood. Journal of Pediatric Psychology 2008; 33(3): 242–247. 89. Packard RC. Chronic post-traumatic headache: associations with mild traumatic brain injury, concussion, and postconcussive disorder. Current Pain and Headache Reports 2008; 12(1): 67–73. 90. Corrigan JD, Wolfe M, Mysiw WJ et al. Early identification of mild traumatic brain injury in female victims of domestic violence. Clinical Journal of Women’s Health 2001; 1: 184–190. 91. O’Shaughnessy E, Fowler R & Reid V. Sequelae of mild closed head injuries. Journal of Family Practice 1984; 18: 391–394.
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92. Thornhill S, Teasdale GM, Murray GD et al. Disability in young people and adults one year after head injury: prospective cohort study. British Medical Journal 2000; 320(7250): 1631–1635 [see comment]. 93. Kraus JF & Chu LD. Epidemiology. In Silver JM, McAllister TW & Yudofsky SC (eds.). Textbook of traumatic brain injury. Washington DC: American Psychiatric Publishing Inc., 2005, pp. 3–26. 94. Barker-Collo SL, Wilde NJ & Feigin VL. Trends in head injury incidence in New Zealand: a hospital-based study from 1997/1998 to 2003/2004. Neuroepidemiology 2009; 32(1): 32–39. 95. Segalowitz SJ & Brown D. Mild head injury as a source of developmental disabilities. Journal of Learning Disabilities 1991; 24(9): 551–559. 96. Body C & Leathem J. Incidence and aetiology of head injury in a New Zealand adolescent sample. Brain Injury 1996; 10 (8): 567–573. *97. McKinlay A, Grace RC, Horwood LJ et al. Prevalence of traumatic brain injury among children, adolescents and young adults: prospective evidence from a birth cohort. Brain Injury 2008; 22(2): 175–181. 98. Kirkwood MW, Yeates KO, Taylor HG et al. Management of pediatric mild traumatic brain injury: a neuropsychological review from injury through recovery. The Clinical Neuropsychologist 2008; 22(5): 769–800. 99. Fay TB, Yeates KO, Wade SL et al. Predicting longitudinal patterns of functional deficits in children with traumatic brain injury. Neuropsychology 2009; 23(3): 271–282. 100. Babikian T & Asarnow R. Neurocognitive outcomes and recovery after pediatric TBI: meta-analytic review of the literature. Neuropsychology 2009; 23(3): 283–296. 101. Muscara F, Catroppa C, Eren S & Anderson V. The impact of injury severity on long-term social outcome following paediatric traumatic brain injury. Neuropsychological Rehabilitation 2009; 19(4): 541–561. 102. Catroppa C & Anderson V. Planning, problem-solving and organizational abilities in children following traumatic brain injury: intervention techniques. Pediatric Rehabilitation 2006; 9(2): 89–97. 103. Kraus JF, Morgenstern H & Fife D. Blood alcohol tests, prevalence of involvement, and outcomes following brain injury. American Journal of Public Health 1989; 79: 294–299. 104. Ruff R, Marshall L, Klauber M et al. Alcohol abuse and neurological outcome of the severely head injured. Journal of Head Trauma Rehabilitation 1990; 5(3): 21–31. 105. Winqvist S, Jokelainen J, Luukinen H & Hillbom M. Parental alcohol misuse is a powerful predictor for the risk of traumatic brain injury in childhood. Brain Injury 2007; 21(10): 1079–1085. 106. Bener A, Omar AO, Ahmad AE et al. The pattern of traumatic brain injuries: a country undergoing rapid development. Brain Injury 2010; 24(2): 74–80. 107. Kraus JF, Rock A, Hemyari P. Brain injuries among infants, children, adolescents, and young adults. 1990;144(6):684–91. 108. Lewis-Evans B, Lukkien C. Crash profile of New Zealand novice drivers strategy and sustainability. Wellington, New Zealand; 2007 [Contract No.: Document Number]. 109. Rutland-Brown W, Wallace LJD, Faul MD & Langlois JA. Traumatic brain injury hospitalizations among American Indians/Alaska Natives. Journal of Head Trauma Rehabilitation 2005; 20(3): 205–214. 110. Frankowski R, Annegers J & Whitman S. The descriptive epidemiology of head trauma in the United States. In Becker DP (ed.). Central nervous system research status report. Bethesda: NINCDS, 1985, pp. 33–43. *111. Thurman D, Alverson C, Dunn K et al. Traumatic brain injury in the United States: a public health perspective. Journal of Head Trauma Rehabilitation 1999: 14. 112. Rosenthal MD, Harrison-Felix C et al. Impact of minority status on functional outcome and community integration following traumatic brain injury. Journal of Head Trauma Rehabilitation 1996; 11: 40–57. 113. Yeates KO, Taylor HG, Woodrome SE et al. Race as a moderator of parent and family outcomes following pediatric traumatic brain injury. Journal of Pediatric Psychology 2002; 27(4): 393–403. 114. Livingston DH, Lavery RF, Mosenthal AC et al. Recovery at one year following isolated traumatic brain injury: a Western Trauma Association prospective multicenter trial. Journal of Trauma 2005; 59(6): 1298–1304. discussion 304. 115. Bazarian J, Pope C, McClung J et al. Ethnic and racial disparities in emergency department case. Academic Emergency Medicine 2003; 10: 1209–1217. 116. Rappaport M, Hall K, Hopkins K & Belleza T. Disability rating scale for severe head trauma: Coma to community. Archives of Physical Medicine and Rehabilitation 1982; 63: 118–123. 117. Selassie AW, Pickelsimer EE, Frazier LJ & Ferguson PL. The effect of insurance status, race, and gender on ED disposition of persons with traumatic brain injury. American Journal of Emergency Medicine 2004; 22(6): 465–473. 118. Parslow RC, Morris KP, Tasker RC et al. Epidemiology of traumatic brain injury in children receiving intensive care in the UK. Archives of Disease in Childhood 2005; 90(11): 1182–1187. 119. Ponsford J, Draper K & Schönberger M. Functional outcome 10 years after traumatic brain injury: its relationship with demographic, injury severity, and cognitive and emotional status. Journal of the International Neuropsychological Society 2008; 14(2): 233–242. 120. Feigin VL & Barker-Collo S. Applied brain injury research in New Zealand: can we do better? New Zealand Medical Journal 2008; 121(1268). *121. Sudlow CL & Warlow CP. Comparing stroke incidence worldwide: what makes studies comparable? Stroke 1996; 27(3): 550–558. *122. Barker-Collo SL & Feigin VL. Capturing the spectrum: suggested standards for conducting population-based traumatic brain injury incidence studies. Neuroepidemiology 2009; 32(1): 1–3.
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1
Epidemiology of ischaemic stroke and traumatic brain injury Valery L. Feigin, Professor a, *, Suzanne Barker-Collo, MD b, Rita Krishnamurthi, MD a, Alice Theadom a, Nicola Starkey, MD c a
National Institute for Stroke and Applied Neurosciences, School of Rehabilitation and Occupation Studies, School of Public Health and Psychosocial Studies, Faculty of Health and Environmental Studies, AUT University, AUT North Shore Campus, AA254, 90 Akoranga Dr, Northcote 0627, Private Bag 92006, Auckland 1142, New Zealand b Faculty of Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand c Department of Psychology, Faculty of Arts and Social Sciences, University of Waikato, Private Bag 3105, Hamilton, New Zealand
Keywords: ischaemic stroke brain injury epidemiology risk factors
Acquired brain injury, including both Ischaemic stroke (IS) and Traumatic Brain injury (TBI), is one of the most common causes of disability and death in adults. Yet there are vast differences in our knowledge of their epidemiology. While the incidence, casefatality and risk factors for stroke are well established, work needs to continue particularly in low-income countries, where these data remain sparse; and in relation to specific stroke subtypes such as IS. Similar data regarding the epidemiology of TBI are generally lacking. The majority of TBI incidence studies have focussed on hospital-based samples and there are no established criteria from which to design high quality epidemiological studies. The need to establish such criteria separate from those already available for stroke is suggested given the differing demographic profile of TBI as well as differences in seeking of medical attention for TBI. The immense burden of stroke can be reduced by prevention of modifiable risk factors particularly in developing countries where both changing lifestyle and lack of healthcare resources are contributing to rising stroke incidence and mortality. Similarly, studies to date indicate that TBI incidence can be reduced by addressing modifiable risk factors such as alcohol abuse, risktaking behaviour and socioeconomic disparities. Ó 2010 Elsevier Ltd. All rights reserved.
* Corresponding author. Tel.: þ64 9 921 9166; Fax: þ64 9 921 9620. E-mail address: [email protected] (V.L. Feigin). 1521-6896/$ – see front matter Ó 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.bpa.2010.10.006
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Introduction Acquired brain injury (an injury to the brain occurring after birth) is one of the most common causes of disability and death in adults.1,2 Stroke and Traumatic brain Injury (TBI) are the two most common causes of acquired brain injury, yet there are vast differences in our knowledge of their epidemiology. In this review we identify important issues regarding current epidemiological data on ischaemic stroke (IS) and TBI, including incidence, case-fatality and known risk factors with the emphasis on populationbased studies; identifying differences between these conditions and implications for epidemiological studies and future management. Epidemiology of ischaemic stroke The World Health Organisation (WHO) defines stroke as “rapidly developing signs of focal (or global) disturbance of cerebral function, lasting longer than 24 h (unless interrupted by death) with no apparent non-vascular cause”.3 Strokes can be either ischaemic (occlusion of a blood vessel) or haemorrhagic (rupture of a blood vessel). Distinguishing between stroke subtypes is critical to appropriate management, and diagnosis is predominantly made using Computerised tomography (CT) or Magnetic resonance imaging (MRI) .4 Prognosis and treatment post-stroke differ according to the specific nature of stroke and therefore stroke subtype needs to be identified.5 IS constitutes 80–85% of all strokes3,6 and is therefore the focus of this review. IS carries an enormous emotional and socio-economical impact with lifetime costs per patient estimated at US$59,800 to US$230,000.7 The risk of recurrent IS is 2% 7-days post-stroke and 29% 5-years post-stroke.8 Moreover, stroke is a common cause of disability adjusted life-years (DALYs; the sum of life-years lost as a result of premature death and years lived with disability adjusted for severity) with estimates that it will be the fourth most common cause of disability in western countries by 2030.4 Wide variability in incidence may reflect true differences or methodological differences used to study stroke epidemiology in different countries9 and differences within countries (e.g. higher incidence in rural areas).10 A recent systematic review of worldwide stroke incidence9 revealed distinct trends in stroke incidence according to income levels, with >100% increase in low- to middle-income countries and a 42% decrease in high-income countries since 1970; but similar age-adjusted incidence of IS between high-income and low- to middle-income countries in the last decade. However, the pooled proportional frequencies of IS in high-income countries were higher (83%) in 2000–08 compared to low- to middle-income countries (67%), who had higher haemorrhagic stroke incidence. Case-fatality rates (21–30 days) following IS have declined in high-income countries from 10–32% (1990–99) to 13–23% (2000–08).9 Case-fatality rates for low- to middle-income countries for IS have only recently been published and suggest higher case-fatality in these countries (range 17.8–23.2%) possibly reflecting differences in acute care.5 Years of life lost due to premature mortality (YLLs) attributed to stroke (80–85% IS) vary widely but global estimates are 9.5% and 9.9% of total deaths for low-income countries and high-income countries respectively, making it the second leading cause of death after ischaemic heart disease.11 IS can be further differentiated into 5 subtypes, using the Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria: larger artery atherosclerosis, cardioembolism, small vessel occlusion (lacune) stroke of other undetermined etiology, and stroke of undetermined etiology.12 In a population-based study,13 incidence of subtypes was: cardioembolism is 30.2 (25.6–35.7), small artery occlusion 25.8 (21.5–30.9), and larger artery atherosclerosis 15.3 (12–19.3) per 100,000 person-years (adjusted to WHO standard European population) with the incidence of large artery disease twice as high in men as women. In this study IS subtype was a significant predictor for long-term survival but not long-term recurrence up to 2 years. Longer-term IS mortality rates also vary by subtype.14 This heterogeneity of IS suggests its epidemiology should be evaluated, where possible, by subtype. Major risk factors for ischaemic stroke Age Advancing age is associated with increased IS prevalence and is its principal non-modifiable risk factor.15–18 For each decade after age 55, the risk of stroke more than doubles,19 presumably due to
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increased exposure to environmental risk factors and higher prevalence of risk factors including atrial fibrillation (AF), hypertension, diabetes, and coronary heart disease. Hypertension Hypertension is responsible for 60–70% of strokes worldwide and is considered it’s most important modifiable factor.20 In IS, damage to the arteries caused by hypertension impairs blood flow by causing plaque to build up thus creating a clot which leads to stroke. The American Heart Association Stroke Council identified elevated systolic blood pressure (with or without elevated diastolic blood pressure) as increasing stroke risk,21 as is also evidenced in other studies.22 Unfortunately, a significant proportion of people remain undiagnosed or inadequately treated for hypertension23 despite readily available pharmacological treatment. Gender A range of findings for gender differences in the epidemiology, outcomes and treatment of stroke are reported. Men have higher age-specific stroke rates than women and men are more likely to have their first-ever stroke at a younger age.24 However, due to increased stroke incidence for women >84 years, women overall, experience more strokes.25 Women are also typically identified as experiencing poorer outcomes post-stroke.26 The causes of this disparity may be partly explained by women: being older at stroke onset; having poorer pre-stroke functioning; having more co-morbidities; being less likely to have social support, and more likely to be widowed/divorced.26 Ethnicity Numerous studies report ethnic disparities in prevalence and incidence of IS as well as related disability and mortality. The NOMASS study reported a higher annual incidence of age-adjusted firstever stroke incidence per 100,000 in blacks than whites and Hispanics.27 In New Zealand, Maori/Pacific populations had higher rates of IS (age-adjusted risk ratio (RR) 1.7) than Europeans and were likely to experience stroke at a younger age.28 The subtype of IS also differs between ethnic populations.29 Atherosclerosis Atherosclerosis, the thickening of artery walls due to the build up of plaques made from fatty materials (e.g., cholesterol, calcium) found in the blood can obstruct blood flow by narrowing or blocking blood vessels. The narrowing of brain arteries (i.e., intracranial atherosclerosis) causes or contributes to >70% of strokes worldwide.30 Atrial fibrillation AF is the most powerful and treatable embolic stroke precursor. The slow, abnormal rhythm in AF causes clot formation in the heart, which can then travel to the brain and cause a stroke. AF rises markedly with age31 and is well identified as an independent stroke risk factor.32 Incidence of stroke associated with AF has been estimated to increase from five33 to seven34 times. IS that occurs with AF is almost twice as likely to be fatal than stroke without AF.35 Tobacco Tobacco use is an established significant independent risk factor for IS.36 Chemicals in tobacco smoke increase plaque build up in arteries and promote development of blood clots that can cause strokes. Smoking doubles the risk of IS versus non-smokers.37 Moreover there is an unambiguous relationship between number of cigarettes smoked and stroke risk with smoking 15 cigarettes/day increasing stroke risk up to four times.38 A positive correlation between the length of time smoking and increased stroke risk is also reported.39 As well as increasing the risk of IS, tobacco use has also been demonstrated to increase the risk of haemorrhagic stroke, especially subarachnoid haemorrhage.40,38 Second-hand smoke is also established as contributing to stroke incidence.41,42 Alcohol Heavy drinking is associated with hypertension and AF and thus is related to increased stroke risk.43 However, any direct relationship between alcohol and stroke is unclear.43 A 2003 meta-analysis of 35
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studies indicated that >60 g of alcohol daily increased risk of stroke, although light or moderate consumption (<24 g/day) decreased stroke risk compared to abstainers.44 Physical inactivity Several studies have demonstrated an inverse relationship between increased physical activity and an increase in the risk of stroke45 as well as stroke risk factors including hypertension, high cholesterol, obesity, diabetes and atherosclerosis.46 Two meta-analyses concluded that there was a lower risk of both ischaemic and haemorrhagic stroke in moderately and highly active individuals.47,48 Obesity/diet The relationship between obesity and stroke remains controversial due to methodological inconsistencies across studies. Nevertheless, obesity (particularly abdominal adiposity and waist circumference) is positively related to IS.49,50 This is thought to occur through hypertension and diabetes37 though a positive correlation has been found between BMI and stroke independent of hypertension, diabetes and high cholesterol.38 Due to the association of diet and obesity and its complex interactions with other risk factors (e.g., hypertension) determining the exact extent to which diet affects stroke risk is difficult. Good nutrition can mitigate other stroke risk factors including hypertension, high cholesterol, diabetes and cardiac disease.51 Diets high in fat, sugar and salt increase stroke risk52 by raising low-density cholesterol, triglycerides and increasing blood pressure. Conversely, diets low in saturated fats and sodium and high in fruit and vegetables significantly reduce stroke risk.53–55 Research into diet and stroke subtype is scarce although there is some evidence that consumption of fish is associated with a decreased IS risk.56 Summary There are difficulties in making direct comparisons between studies that limit case ascertainment to hospitals and those that are population-based. Different clinical definitions, use of subtypes, hospital admission patterns and access to diagnostic tools (e.g. CT scans) may account for some variations in incidence rates. Population-based studies provide a most robust evidence of the burden of IS in the world. Evidence strongly suggests IS incidence can be reduced by targeting modifiable risk factors such as hypertension, smoking and poor diet/lifestyle. Projections estimate that by 2030 stroke will be one of the main causes of lost healthy life-years, thus further work is needed to complete the picture and to broaden our understanding of its risk factors, prevention and management. Epidemiology of traumatic brain injury TBI is defined by the WHO as ‘an acute brain injury resulting from mechanical energy to the head from external physical forces’. Operational criteria for clinical identification of TBI include 1 of: (1) confusion or disorientation; (2) loss of consciousness; (3) post-traumatic amnesia; (4) other neurological abnormalities (e.g., focal neurological signs, seizure, intracranial lesion).57 TBI severity is classified as mild, moderate or severe, based on Glasgow Coma Scale (GCS) scores.57 According to the literature, irrespective of age, 70–90% of TBIs are mild with 5–20% being moderate & severe.58 Incidence of TBI in developed countries (e.g., United Kingdom, Australia) is z200–300 people per 100,000 population annually.59 A recent WHO systematic review60 suggests the annual incidence of mild TBI is probably >600/100,000. Incidence rates for low and middle-income countries are scarce, varying from 160 per 100,000 in India,61 360 per 100,000 in Brazil,62 and 219 per 100,000 in Yemen.63 Those in low-middle-income countries often lack access to basic medical care, particularly in rural areas.64 Even in high-income countries the cost of care is high and the registration of new TBI cases is poor, leading to underestimated incidence with many cases unrecorded. TBI incidence in African countries is unknown, but in Nigeria, 31% of all trauma related deaths are due to TBI.65 In contrast to stroke, in Europe and North America, only z25% of persons who experience TBI are admitted to hospital.66 In New Zealand, it is estimated that for every 100 people seen at hospital regarding TBI, 60 are managed by their general practitioner.67 Studying TBI in a population-wide context is therefore particularly important. Moreover, changes in patterns of referral can distort
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longitudinal trends derived from hospital data.68 Official statistics are of limited use as they are incomplete (due to selection bias) and do not collect all data relevant to interpreting variations in outcome. Further, inconsistent and inaccurate diagnosis of TBI is evident in coding of hospital discharges for TBI,67 emphasizing the importance of appropriate TBI case ascertainment. Unlike IS, 28-day case-fatality is rarely reported for TBI. Estimates indicate that 30–35% of patients admitted to hospital with moderate or severe TBI die within the first 30-days.69 In the USA, >3% of all deaths during 2001 were due to brain injury.70 However, reported annual case-fatality ranges widely (3.2%71 to 19.7%72) and there are too few good quality studies to draw any conclusions. The difference in rates may reflect the lack of specificity of cause of death on the death certificates (e.g. massive multiple trauma not specifying body regions involved).73 Furthermore, mortality is significantly higher (19.5%) in low compared to high-income countries,74 with violent assaults accounting for a larger proportion of TBIs.61,65 In rapidly developing countries such as India, car use has increased dramatically over the last 20 years (from 5.3 million to 59 million between 1981 and 2002), with few safety regulations or road rules. As a consequence, 44% of road deaths worldwide occur in Asia.61 Combined with poor access to medical care TBI is a rapidly increasing public health problem in these countries.65 Due to the high incidence of TBI at an early age and long-term impact on employment and disability,75 the DALY lost due to TBI is significant.76 The economic cost of TBI varies significantly, due to both individual characteristics and the nature of the injury.77 TBI in children and young adults has a significant economic cost; in the USA in 2006, children admitted to hospital with a TBI following a motor vehicle accident (MVA) or falls incurred hospital charges of zUS$2.6 billion78 whilst in the UK young adults (18–25 years) with TBI cost z47.2 million GBP per year.79 WHO estimate TBI will be the 3rd leading cause of premature death across all ages by 2020.80 Moderate and severe TBI results in the greatest disability and consumes the most resources per individual, yet mild TBI’s (mTBI) magnitude and societal ramifications are often underestimated.60 Despite the label ‘mild’, many of these injuries result in long-term difficulties81–83 (e.g., post-concussion symptoms,84 epilepsy,85 depression,86 cognitive deficits,87 sleep disturbances,88 and persistent headache89). These are often unrecognized in the acute phase, as patients do not seek medical attention, are not systematically assessed or are lost to medical follow-up.81 It has been estimated that 40–80% of mTBI survivors experience post-concussive syndrome, a constellation of physical, cognitive, and behavioural difficulties90 that may persist up to 2 years post-TBI.91 A hospital-based cohort study found that 47% of mTBI cases had moderate to severe physical disability 1-year post-injury.92 Along with the significant number of mTBIs, these outcomes underline the value of accurate identification and adequate management.57,67
Risk factors for traumatic brain injury Age TBI incidence peaks between 15 and 24 years of age, with smaller peaks in infancy (<5 years) and older age93,94 Self-reports suggest 31% of children experience a head injury before age 18,95 whilst 44% of 14–15 year olds reported a head injury in previous 3 years.96,97 The mechanism of TBI differs with age. Falls are most common in young and old age groups, with MVA and assaults most common in middle age.70 Cycling and sports related accidents also account for a significant proportion of TBI in 8–14 year olds.93 Overall, the most common cause of TBI worldwide is transport related, whether it be in a car, or as a cyclist or pedestrian.93 Categorisation of TBI severity in children is based on criteria for adults and is frequently difficult to apply, particularly in pre-verbal children.97,98 However, existing criteria suggest 80–90% of childhood TBI’s are mild.70,97 Consequences of TBI in children can be more severe than in adults, potentially impacting previously acquired skills, inhibiting learning of new skills, and adversely impacting attainment of developmental milestones, which may not be apparent for years post-injury.97,99–101 Studies are inconsistent, but evidence suggests that outcomes for children and adolescents after uncomplicated (i.e., no evidence of intracranial abnormality) mTBI are good.98 However, there are few studies beyond 5 years, leaving the full impact of TBI on normal developmental processes (e.g., executive functions) unclear.97,102
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Alcohol Alcohol use increases risk of TBI as a result of falls, MVA and assault.61 In an American emergency department, 56% of people with TBI had positive blood alcohol, with half of these over the legal limit.103 Alcohol abuse is associated with recurrent TBI104 and parental alcohol misuse is a risk factor for childhood TBI (relative risk ratio 1.99).105 Gender Males are at approximately twice the risk of TBI compared to females 1.6–2.8.94,106 However, the gender ratio varies with age; in those <5 years of age, incidence rates are similar, but after this, incidence increases faster in males resulting in an incidence over double that in females, particularly apparent during adolescence.97,107 This is largely due to the increased risk-taking behaviour, reflecting the higher incidence of MVA in young males drivers.108 Ethnicity, socioeconomic status and education There are ethnic inequalities in TBI incidence and outcomes109; with ethnic minority groups having greater TBI risk and higher post-TBI mortality.110,111 While at 1-year post-injury, Caucasian and minority group TBI survivors reported similar impairments and activity, minorities report significantly less social integration.112 Furthermore, parents of ethnic minority children with a TBI rate injury outcomes less favourably than Caucasians, even when socioeconomic status (SES) is controlled for.113 Proportionally, fewer TBI from minorities are employed at 1-year, even if employed prior to injury.114 Compared to Caucasians, minority groups receive less medical care post-TBI (e.g., longer wait for doctor)115 and receive fewer inpatient rehabilitation therapies.116 Separating the effects of ethnicity and SES is challenging. Even so, studies indicate that lower SES is associated with increased risk of TBI. For example, even though 16% of the South Carolina residents are uninsured, they make up 26% of TBIs seen in emergency departments.117 Similarly, in the UK, children with severe TBI requiring intensive care reside in significantly poorer parts of the country.118 Lower SES is also linked to poorer TBI outcomes.113 In contrast, higher levels of pre-injury education are associated with better outcomes in all areas of functioning.119 Clearly, it is important to understand how ethnic/ socioeconomic factors impact TBI incidence and outcomes, and the reasons for these inequalities, in order to improve these outcomes for vulnerable groups.120
Summary To date TBI epidemiological studies are limited to small and hospitalised samples, underestimating its true incidence and outcomes. Case ascertainment has focused on hospital admission or discharge records; capturing moderate to severe TBI cases where death hasn’t occurred at the time of injury. However, as most mTBI cases are not hospitalised (few seek immediate medical attention) and those who die before reaching hospital are not recorded in the hospital admission records, these are overlooked. Significant differences in study methods and TBI classification (particularly in children) make comparisons difficult; therefore consistent comprehensive approaches to case ascertainment are needed. Overarching summary and practice points Accurate and representative population-based data are crucial for: determining the true incidence, causes and outcome of TBI and IS; evidence-based healthcare planning across the care spectrum; evaluating the impact of preventative/management strategies; addressing persistent uncertainty about socioeconomic and health service factors influencing recovery; examining the natural course of recovery; providing information about access and satisfaction with services and identifying service gaps and ensuring evidence-informed policy, resource and service allocation, planning of relevant prevention, and evaluation of sector and service performance. This review indicates a wide level of epidemiological knowledge about stroke generally, yet a dearth of similar information in regards to IS and its subtypes; and an even greater gap in knowledge in
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relation to TBI where few population-based studies are available and issues related to age and capture of cases with mTBI are particularly important. Criteria proposed to inform the design of high quality epidemiological studies and enabling the comparison of stroke incidence worldwide could be applied to IS more specifically.121 The need to establish such criteria separate from those already available for stroke is suggested for TBI to encompass the differing demographic profile of TBI as well as differences in seeking of medical attention.122 Conflict of interest statement None.
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