Head Injury Death Research Articles

A cost-effectiveness and value of information analysis to inform future research of tranexamic acid for older adults experiencing mild traumatic brain injury

BackgroundTranexamic acid reduces head injury deaths in patients with CT scan evidence of intracranial bleeding after mild traumatic brain injury (TBI). However, the cost-effectiveness of tranexamic acid for people with mild TBI in the pre-hospital setting, prior to CT scanning, is uncertain. A large randomised controlled trial (CRASH-4) is planned to address this issue, but the economic justification for it has not been established. The aim of the analysis was to estimate the likelihood of tranexamic acid being cost-effective given current evidence, the treatment effects required for cost-effectiveness, and the expected value of performing further research.MethodsAn early economic decision model compared usual care for mild TBI with and without tranexamic acid, for adults aged 70 and above. The evaluation was performed from a UK healthcare perspective over a lifetime time horizon, with costs reported in 2020 pounds (GBP) and outcomes reported as quality-adjusted life years (QALYs). All analyses used a £20,000 per QALY cost-effectiveness threshold.ResultsIn the base case analysis, tranexamic acid was associated with an incremental cost-effectiveness ratio of £4885 per QALY gained, but the likelihood of it being cost-effective was highly dependent on the all-cause mortality treatment effect. The value of perfect information was £22.4 million, and the value of perfect information for parameters that could be collected in a trial was £21.9 million. The all-cause mortality risk ratio for tranexamic acid and the functional outcomes following TBI had the most impact on cost-effectiveness.ConclusionsThere is a high degree of uncertainty in the cost-effectiveness of tranexamic acid for older adults experiencing mild TBI, meaning there is a high value of performing future research in the UK. The value in a global context is likely to be far higher.

Tranexamic acid to reduce head injury death in people with traumatic brain injury: the CRASH-3 international RCT.

Tranexamic acid safely reduces mortality in traumatic extracranial bleeding. Intracranial bleeding is common after traumatic brain injury and can cause brain herniation and death. We assessed the effects of tranexamic acid in traumatic brain injury patients. To assess the effects of tranexamic acid on death, disability and vascular occlusive events in traumatic brain injury patients. We also assessed cost-effectiveness. Randomised trial and economic evaluation. Patients were assigned by selecting a numbered treatment pack from a box containing eight packs that were identical apart from the pack number. Patients, caregivers and those assessing outcomes were masked to allocation. All analyses were by intention to treat. We assessed the cost-effectiveness of tranexamic acid versus no treatment from a UK NHS perspective using the trial results and a Markov model. 175 hospitals in 29 countries. Adults with traumatic brain injury within 3 hours of injury with a Glasgow Coma Scale score of ≤ 12 or any intracranial bleeding on computerised tomography scan, and no major extracranial bleeding, were eligible. Tranexamic acid (loading dose 1 g over 10 minutes then infusion of 1 g over 8 hours) or matching placebo. Head injury death in hospital within 28 days of injury in patients treated within 3 hours of injury. Secondary outcomes were early head injury deaths, all-cause and cause-specific mortality, disability, vascular occlusive events, seizures, complications and adverse events. Among patients treated within 3 hours of injury (n = 9127), the risk of head injury death was 18.5% in the tranexamic acid group versus 19.8% in the placebo group (855/4613 vs. 892/4514; risk ratio 0.94, 95% confidence interval 0.86 to 1.02). In a prespecified analysis excluding patients with a Glasgow Coma Scale score of 3 or bilateral unreactive pupils at baseline, the results were 12.5% in the tranexamic acid group versus 14.0% in the placebo group (485/3880 vs. 525/3757; risk ratio 0.89, 95% confidence interval 0.80 to 1.00). There was a reduction in the risk of head injury death with tranexamic acid in those with mild to moderate head injury (166/2846 vs. 207/2769; risk ratio 0.78, 95% confidence interval 0.64 to 0.95), but in those with severe head injury (689/1739 vs. 685/1710; risk ratio 0.99, 95% confidence interval 0.91 to 1.07) there was no apparent reduction (p-value for heterogeneity = 0.030). Early treatment was more effective in mild and moderate head injury (p = 0.005), but there was no obvious impact of time to treatment in cases of severe head injury (p = 0.73). The risk of disability, vascular occlusive events and seizures was similar in both groups. Tranexamic acid is highly cost-effective for mild and moderate traumatic brain injury (base case of £4288 per quality-adjusted life-year gained). Early tranexamic acid treatment reduces head injury deaths. Treatment is cost-effective for patients with mild or moderate traumatic brain injury, or those with both pupils reactive. Further trials should examine early tranexamic acid treatment in mild head injury. Research on alternative routes of administration is needed. Time to treatment may have been underestimated. Current Controlled Trials ISRCTN15088122, ClinicalTrials.gov NCT01402882, EudraCT 2011-003669-14, Pan African Clinical Trial Registry PACTR20121000441277. The project was funded by the National Institute for Health Research (NIHR) Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 25, No. 26. See the NIHR Journals Library website for further project information. In addition, funding was provided by JP Moulton Charitable Trust, Joint Global Health Trials (Medical Research Council, Department for International Development and the Wellcome Trust). This project was funded by the NIHR Global Health Trials programme.

Effect of tranexamic acid on intracranial haemorrhage and infarction in patients with traumatic brain injury: a pre-planned substudy in a sample of CRASH-3 trial patients

BackgroundEarly tranexamic acid (TXA) treatment reduces head injury deaths after traumatic brain injury (TBI). We used brain scans that were acquired as part of the routine clinical practice during the...

Cost-effectiveness analysis of tranexamic acid for the treatment of traumatic brain injury, based on the results of the CRASH-3 randomised trial: a decision modelling approach

IntroductionAn estimated 69 million traumatic brain injuries (TBI) occur each year worldwide, with most in low-income and middle-income countries. The CRASH-3 randomised trial found that intravenous administration of tranexamic acid...

Accuracy of time to treatment estimates in the CRASH-3 clinical trial: impact on the trial results

BackgroundEarly treatment with tranexamic acid may reduce deaths after traumatic brain injury (TBI). In mild and moderate TBI, there is a time to treatment interaction, with early treatment being most beneficial. Time to treatment was recorded by clinicians and is subject to error. Using monitoring data from the CRASH-3 trial, we examine the impact of errors in time to treatment on estimated treatment effects.MethodsThe CRASH-3 trial was a randomised trial of the effect of tranexamic acid on death and vascular occlusive events in 12,737 TBI patients. This analysis includes the 8107 patients with a Glasgow coma scale score of 9 to 15 since previous analyses showed that these patients benefit most from early treatment. Clinician-recorded time to treatment was checked against ambulance and hospital records for 1368/12,737 (11%) patients. Patients who died were preferentially selected for monitoring and we monitored 36% of head injury deaths. We describe measurement errors using Bland-Altman graphs. We model the effect of tranexamic acid on head injury death using logistic regression with a time-treatment interaction term. We use regression calibration, multiple imputation and Bayesian analysis to estimate the impact of time to treatment errors.ResultsClinicians rounded times to the nearest half or full hour in 66% of cases. Monitored times were also rounded and were identical to clinician times in 63% of patients. Times were underestimated by an average of 9 min (95% CI − 85, 66). There was more variability between clinician-recorded and monitored times in low- and middle-income countries than in high-income countries. The treatment effect estimate at 1 h was greater for monitored times OR = 0.61 (95% CI 0.47, 0.81) than for clinician-recorded times OR = 0.63 (95% CI 0.48, 0.83). All three adjustment methods gave similar time to treatment interactions. For Bayesian methods, the treatment effect at 1 h was OR = 0.58 (95% CI 0.43, 0.78). Using monitored times increased the time-treatment interaction term from 1.15 (95% CI 1.03, 1.27) to 1.16 (95% CI 1.05, 1.28).ConclusionsAccurate estimation of time from injury to treatment is challenging, particularly in low resource settings. Adjustment for known errors in time to treatment had minimal impact on the trial results.Trial registrationClinicalTrials.gov NCT01402882. Registered on 25 July 2011

Tranexamic acid in traumatic brain injury: an explanatory study nested within the CRASH-3 trial

PurposeThe CRASH-3 trial is a randomised trial of tranexamic acid (TXA) on death and disability in patients with traumatic brain injury (TBI). It is based on the hypothesis that early TXA treatment can prevent deaths from post-traumatic intracranial bleeding. The results showed that timely TXA treatment reduces head injury deaths in patients with reactive pupils and those with a mild to moderate GCS at baseline. We examined routinely collected CT scans in a sample of 1767 CRASH-3 trial patients to explore if, why, and how patients are affected by TXA.MethodsThe CRASH-3 IBMS is an explanatory study nested within the CRASH-3 trial. We measured the volume of intracranial bleeding on CT scans using established methods (e.g. ABC/2).ResultsPatients with any un-reactive pupil had a median intracranial bleeding volume of 60 ml (IQR 18–101 ml) and patients with reactive pupils had a median volume of 26 ml (IQR 1–55 ml). Patients with severe GCS had median intracranial bleeding volume of 37 ml (IQR 3–75 ml) and patients with moderate to mild GCS had a median volume of 26 ml (IQR 0.4–50 ml). For every hour increase from injury to the baseline scan, the risk of new bleeding on a further scan decreased by 12% (adjusted RR = 0.88 [95% CI 0.80–0.96], p = 0.0047).ConclusionPatients with reactive pupils and/or mild to moderate GCS may have benefited from TXA in the CRASH-3 trial because they had less intracranial bleeding at baseline. However, because bleeding occurs soon after injury, treatment delay reduces the benefit of TXA.

Tranexamic acid for significant traumatic brain injury (The CRASH-3 trial): Statistical analysis plan for an international, randomised, double-blind, placebo-controlled trial.

Background: Worldwide, traumatic brain injury (TBI) kills or hospitalises over 10 million people each year. Early intracranial bleeding is common after TBI, increasing the risk of death and disability. Tranexamic acid reduces blood loss in surgery and death due to bleeding in trauma patients with extra-cranial injury. Early administration of tranexamic acid in TBI patients might limit intracranial bleeding, reducing death and disability. The CRASH-3 trial aims to provide evidence on the effect of tranexamic acid on death and disability in TBI patients. We will randomly allocate about 13,000 TBI patients (approximately 10,000 within 3 hours of injury) to an intravenous infusion of tranexamic acid or matching placebo in addition to usual care. This paper presents a protocol update (version 2.1) and statistical analysis plan for the CRASH-3 trial. Results: The primary outcome is head injury death in hospital within 28 days of injury for patients treated within 3 hours of injury (deaths in patients treated after 3 hours will also be reported). Because there are reasons to expect that tranexamic acid will be most effective in patients treated immediately after injury and less effective with increasing delay, the effect in patients treated within one hour of injury is of particular interest. Secondary outcomes are all-cause and cause-specific mortality, vascular occlusive events, disability based on the Disability Rating Scale and measures suggested by patient representatives, seizures, neurosurgical intervention, neurosurgical blood loss, days in intensive care and adverse events. Sub-group analyses will examine the effect of tranexamic acid on head injury death stratified by time to treatment, severity of TBI and baseline risk. Conclusion: The CRASH-3 trial will provide reliable evidence of the effectiveness and safety of tranexamic acid in patients with acute TBI. Registration: International Standard Randomised Controlled Trials registry ( ISRCTN15088122) 19/07/2011, and ClinicalTrials.gov ( NCT01402882) 25/07/2011.

Tranexamic acid for significant traumatic brain injury (The CRASH-3 trial): Statistical analysis plan for an international, randomised, double-blind, placebo-controlled trial.

Background: Worldwide, traumatic brain injury (TBI) kills or hospitalises over 10 million people each year. Early intracranial bleeding is common after TBI, increasing the risk of death and disability. Tranexamic acid reduces blood loss in surgery and death due to bleeding in trauma patients with extra-cranial injury. Early administration of tranexamic acid in TBI patients might limit intracranial bleeding, reducing death and disability. The CRASH-3 trial aims to provide reliable evidence on the effect of tranexamic acid on death and disability in TBI patients. We will randomly allocate about 13,000 TBI patients to an intravenous infusion of tranexamic acid or matching placebo in addition to usual care. This paper presents a protocol update (version 2.1) and statistical analysis plan for the CRASH-3 trial. Results: The primary outcome is head injury death in hospital within 28 days of injury for patients treated within 3 hours of injury (deaths in patients treated after 3 hours will also be reported). Because there are strong scientific reasons to expect that tranexamic acid will be most effective in patients treated immediately after injury and less effective with increasing delay, the effect in patients treated within one hour of injury is of particular interest. Secondary outcomes are all-cause and cause-specific mortality, vascular occlusive events (myocardial infarction, pulmonary embolism, deep vein thrombosis, stroke), disability based on the Disability Rating Scale and measures suggested by patient representatives, seizures, neurosurgical intervention, neurosurgical blood loss, days in intensive care and adverse events. Sub-group analyses will examine the effect of tranexamic acid on head injury death stratified by time to treatment, severity of TBI and baseline risk. Conclusion: The CRASH-3 trial will provide reliable evidence of the effectiveness and safety of tranexamic acid in patients with acute TBI. Registration: International Standard Randomised Controlled Trials registry ( ISRCTN15088122) 19/07/2011, and ClinicalTrials.gov ( NCT01402882) 25/07/2011.

An audit of head trauma care and mortality.

To analyze the factors contributing to deaths from head trauma by using standardized assessment parameters and to provide a peer-review of head injury deaths with focus on identifying deficiencies and analyzing contributory factors. Descriptive study. The study was carried out at the Emergency, Aga Khan University Hospital during January 1998 to December 1999. One hundred and three patients above the age of 15 years presenting alive to the Aga Khan University Hospital (AKUH) emergency with head injury were included in this study. Identified deaths data was reviewed by the Hospital Trauma Peer Review Committee and consensus arrived at for categorization of deaths. The potential deficiencies in care were identified and final recommendations made. The data was computed on CDC Trauma Registry (V 3.0) and SPSS (V 8.0). Mean age was 31.9 years (n=103) with predominant male population (4:1). Severe head injury (GCS<8) accounted for 21.3 % (n=22) of all cases with a total number of deaths being 12.6 % (n=13). Deaths were categorized preventable in 3 cases with non-preventable and potentially preventable in 4 and 6 cases respectively. Road traffic accidents were the predominant mechanism (n=8) in all deaths (n=13). The time interval in relation to mortality was biphasic, most deaths occurring either within 24 hours or between 3-7 days of injury. Inappropriate pre-hospital treatment, pre-hospital delays and inappropriate mode of transportation without inter-hospital communication were the process-related defects in pre-hospital care with major determinant of deaths outside AKUH (n=5). Prolonged emergency stay, delayed intensive care availability were the process-related deficiencies whereas inappropriate initial resuscitation, inappropriate initial head injury management were provider-related deficiencies in in-hospital care. Transfer of inappropriately managed patients, lapses in inter-hospital communications, delayed transfers were identified as the major pre-hospital factors whereas lack of ICU beds, portable ventilators in emergency room, delays in CT scan facilities were the deficiencies in the hospital services. Opportunities for improvement in head trauma care are needed to focus on initial resuscitation and appropriate surgical management.

Did Emperor Moctezuma II's head injury and subsequent death hasten the fall of the Aztec nation?

This article analyzes the head injury of Emperor Moctezuma as one of those injuries that affected the course of history. The Emperor's death arguably changed the fate of an entire nation and led to the destruction of the Aztec civilization. Moctezuma died in the evening hours of June 30, 1520, in his palace in the Aztec capital, Tenochtitlan, while a prisoner of the Spanish conquistadors. The Emperor had been speaking to his people in an effort to persuade them to cease hostilities against Hernán Cortés, his Spanish soldiers, and Indian allies. Both Spanish and Indian contemporary sources document that he sustained a severe head injury when one of his own warriors hit him with a rock thrown from a sling. However, after the Conquest of Mexico some of the information collected by Spanish friars from Indian stories, songs, and pictorial representations raised the possibility that Moctezuma died of strangulation or stabbing at the hands of the Spaniards. There is even a suggestion of suicide. This issue remains unresolved and emotionally charged. The historical and clinical analysis of the events surrounding Moctezuma's death indicates that the Emperor most likely died as a consequence of head injury. The author has attempted to present a neutral analysis but agrees with Benjamin Keen that neutrality may be unattainable, no matter how remote the subject of historical inquiry is from the present.

Mortality from Head Injury over Four Decades in Scotland.

Although the causes of head injury, the population at risk, and approaches to prevention and treatment are continually evolving, there is little information about how these are reflected in patterns of mortality over time. We used population-based comprehensive data uniquely available in Scotland to investigate changes in the total numbers of deaths from 1974 to 2012, as well as the rates of head injury death, from different causes, overall and in relation to age and gender. Total mortality fell from an annual average of 503 to 339 with a corresponding annual decrease in rate from 9.6 to 6.4 per 100,000 population, the decline substantially occurring between 1974 and 1990. Deaths in children fell strikingly, but rose in older people. Deaths in males fell to a greater extent than females, but remained at a higher rate overall. Initially, a transport accident accounted for most deaths, but these fell by 80%, from 325 per year to 65 per year over the 39-year period. Deaths from falling and all other causes did not decline, coming to outnumber transport accident deaths by 1998, which accounts for the overall absence of change in total mortality in recent years. In order to reduce mortality in the future, more-effective measures to prevent falls are needed and these strategies will vary in younger adults (where alcohol is often a factor), as well as in older adults where infirmity can be a cause. In addition, measures to sustain reductions in transport accidents need to be maintained and further developed.

G13 Trends in admission and death rates due to Paediatric Head injury in England and Wales 2000–2012

Over the last ten years there has been a steady rise in short paediatric admissions. This is likely to be multi-factorial but is in part attributed to the introduction of...

Report of a Case of a Head Injury in a Mule (Eqqus ferus caballus) A Pathological Study

The aim of this study was to report of a case of a head injury in a mule (Eqqus ferus caballus) by pathological study. Were studied a mule of 3 months old, with history of a head injury, collapse, shock and sudden death. Was to examined by necropsy and samples of tissue were recollected. Necropsy revealed a traumatic in head with brain injury obliquely with an open fracture of the frontal bone, about 15 cm long, 1.5 cm wide, exposure of brain tissue and significant bleeding. Severe hydrocephalus acquired approximately 15 cubic centimeters.Submeningeal hematoma on the ventral side of the frontal bone, as well as a hematoma in the left hemisphere. The histopathology of brain evidence severed edema and hemorrhage submeningeal and marked coagulation necrosis acute encephalomalacia and leukoencephalomalacia. Increased Virchow-Robbins space. Evidence is not suppurative meningitis with presence of lymphocytic diffuse. In conclusion were reported a case of trauma of head injury in a mule underlying a viral meningitis by pathological study on a mule.

Helmet use by cyclists and head injury

Although the use of helmets by cyclists reduces head injury deaths and hospitalizations, their compulsory use is hotly debated. Neal Cook discusses both the positive and negative impact of cycling helmet legislation.

Regional neuropathology referral practice before and after new organ retention legislation

Previous organ retention controversies in the United Kingdom have resulted in public concern in relation to the retention of organs following post mortem examination. Therefore, protocols were devised and implemented to facilitate adequate sampling for diagnostic purposes for neuropathology autopsy referrals, without the need for organ retention. We have examined various aspects of referral practice before and after the introduction of these new sampling protocols. All neuropathology autopsy referral cases were reviewed between 1993 and 1995, and 2003 and 2005 and data such as: referral source, nature of samples (whether whole organ or limited sampling) and final diagnosis were recorded. Overall, the number of autopsy cases referred for neuropathology opinion reduced, particularly those originating from hospital consented autopsies. Forensic referrals also reduced, with a shift in practice from referrals of whole fixed brains, to both whole brains and sampled brain slices. Within the referrals from forensic practice, whilst cases of 'natural deaths' and head injury cases secondary to road traffic accidents or falls reduced, cases involving inflicted, traumatic head injury and sudden unexpected death in epilepsy and infancy remained static. The introduction of protocols to facilitate sampling of brains at autopsy, so minimising organ retention, proved successful and, whilst there has been a reduction in neuropathology referrals, cases in which neuropathology input is deemed best practice remained static.

The effect of a celebrity death on children's injury-related emergency department visits

BackgroundFollowing a skiing-related head injury death of the actor Natasha Richardson, we noted a marked increase in injury-related visits to the Emergency Department (ED) of the Montreal Children's Hospital (MCH)....

Histopathological changes of the hippocampus neurons in brain injury.

The glial fibrillary acidic protein (GFAP) is known as a peculiar marker of mature astrocytes of the central nervous system (CNS). However, we found distinct immunopositivity to a monoclonal anti-GFAP reagent in the hippocampus neurons in head injury fatalities. The present study investigated the neuronal and neuroglial GFAP-immunopositivity in the hippocampus in a series of head injury cases, which included acute and subacute/delayed deaths (n=17 and n=73, respectively), and acute cardiac death (n=13), delayed death due to multiple organ failure from non-head injury (n=6), and pneumonia (n=9) cases were examined as controls. GFAP-immunopositivity in the neurons was frequently observed in CA4, CA3 and CA2 regions in cases of subacute/delayed head injury death that showed marked brain swelling accompanied by secondary brain stem hemorrhages, showing an inverse relationship to that in astrocytes. These findings suggest possible induction of GFAP or a related protein in hippocampus neurons depending on the severity of brain swelling following head injury.

Evaluation of postmortem S100B levels in the cerebrospinal fluid with regard to the cause of death in medicolegal autopsy

Previous studies have suggested the usefulness of the postmortem serum S100B level as a marker of the severity of brain damage. In this study, we investigated the S100B level in the cerebrospinal fluid (CSF) in serial autopsy cases ( n = 216, within 3 days postmortem), including those of blunt injury ( n = 34: fatal head injury, n = 20; others, n = 14), sharp instrument injury ( n = 9), mechanical asphyxiation ( n = 19), drowning ( n = 11), fire fatality ( n = 26), intoxication ( n = 20), hypothermia (cold exposure, n = 16), hyperthermia (heat stroke, n = 9), acute cardiac death ( n = 52) and pneumonia ( n = 20). The CSF S100B level showed a moderate postmortem time-dependent increase for acute cardiac death ( r = 0.58, p < 0.0001) and asphyxia ( r = 0.741, p < 0.001). In cases of survival time within 48 h, drowning and hypothermia usually showed a lower CSF S100B level (around 500 ng/ml), and the level was higher for delayed head injury death, asphyxia, intoxication, and hyperthermia (around 1500 ng/ml) ( p < 0.05). In fatal head injury cases, however, CSF S100B did not correlate with the survival time or postmortem interval. A CSF S100B level of >2000 ng/ml in the early postmortem period might be considered a biochemical sign of fatally severe brain damage.

Fatal Head Injury in Children Younger Than 2 Years in New York City and an Overview of the Shaken Baby Syndrome

Shaken baby syndrome is a controversial topic in forensic pathology. Some forensic pathologists state that shaking alone is insufficient to explain death and that an impact must have occurred even if there is no impact site on the head. To examine a large cohort of fatal, pediatric head injuries for patterns of specific autopsy findings and circumstances that would support or dispute pure shaking as the cause of death. We retrospectively reviewed 59 deaths due to head injuries in children younger than 2 years certified in our office during a 9 year period (1998-2006). The review included autopsy, toxicology, microscopy, neuropathology, and police and investigators' reports. There were 46 homicides, 8 accidents, and 1 undetermined death from blunt-impact injury of the head. In 10 (22%) of the homicides, there was no impact injury to the head, and the cause of death was certified as whiplash shaking. In 4 (40%) of these 10 deaths, there was a history of shaking. In 5 (83%) of the other 6, there was no history of any purported accidental or homicidal injury. All 8 accidental deaths had impact sites. Of the 59 deaths, 4 (6.7%) had only remote injuries (chronic subdural hematomas, remote long bone fractures) that were certified as undetermined cause and manner. These 4 deaths were excluded from the study. We describe a subset of fatal, nonaccidental head-injury deaths in infants without an impact to the head. The autopsy findings and circumstances are diagnostic of a nonimpact, shaking mechanism as the cause of death. Fatal, accidental head injuries in children younger than 2 years are rare.

Changes in Motorcycle-Related Head Injury Deaths, Hospitalizations, and Hospital Charges Following Repeal of Pennsylvania’s Mandatory Motorcycle Helmet Law

To evaluate the 2003 repeal of Pennsylvania's motorcycle helmet law, we assessed changes in helmet use and compared motorcycle-related head injuries with non-head injuries from 2001-2002 to 2004-2005. Helmet use among riders in crashes decreased from 82% to 58%. Head injury deaths increased 66%; nonhead injury deaths increased 25%. Motorcycle-related head injury hospitalizations increased 78% compared with 28% for nonhead injury hospitalizations. Helmet law repeals jeopardize motorcycle riders. Until repeals are reversed, states need voluntary strategies to increase helmet use.