An incomplete pass: inadequacies in Ohio's youth concussion legislation and the ongoing risk for players.

Author:Kane, Andrew J.
 
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  1. INTRODUCTION II. BACKGROUND OF CONCUSSION AND ITS RELATION TO YOUTH ATHLETICS A. Pathophysiology of Traumatic Brain Injury (TBI) and Concussion B. How Traumatic Brain Injury Affects Youth Differently C. Benefits of Participation in Youth Athletics D. Challenges Facing the Legislature: Unsuccessful Attempts to Make the Game Safer 1. Safety Equipment Alone Does Not Create a Meaningfully safer Environment for Contact Sports 2. Education Programs Alone Do Not Create a Meaningfully safer Environment for Contact Sports 3. Reduction of Contact Elements is Strongly Opposed; Milder Rule Changes Alone Do Not Create a Meaningfully Safer Environment for Contact Sports III. ENACTED AND PROPOSED LEGISLATIVE SOLUTIONS A. Washington's Lystedt Law: The First Attempt at Legislative Intervention B. Widespread Enactment in the Various States: 2009-2013 1. Strong legislative examples: Massachusetts, Rhode Island 2. Weak legislative example: Wyoming 3. Failed and proposed federal legislation: ConTACT, PSAC and the Care Tools Act of 2013 4. Ohio Revised Code 3313.539: Concussions and School Athletics IV. PARTICULAR DEFICIENCIES IN OHIO'S LEGISLATION AND RECOMMENDATIONS FOR IMPROVEMENT A. Failure to Require Pre-season Baseline Neurocognitive Screening B. Failure to Clarify Who May Issue Return-To-Play Decisions; Failure to Adequately Control That Decision Making C. Two Small But Significant Steps: Equipment Standards and Rule Changes 1. The Merits of a "Hit Count" System D. Immunization From Liability and Lack of Enforcement Mechanisms: Incentivizing Non-Compliance at Every Turn V. CONCLUSION I. INTRODUCTION

    Like many high school students do each spring, in 2011 Zackery Lystedt walked across the stage at the White River Amphitheatre to join his fellow Tahoma High School classmates at their senior class graduation. (1) Unlike his classmates and most others, however, Zackery rose from a wheelchair, was assisted by a cane as he made his way across the stage, and did not receive a high school diploma that day. (2)

    But there was reason to celebrate. Just to be there, Zackery had overcome numerous strokes, seven days on a ventilator, three months in a coma, three additional months of hospital rehabilitation, 13 months of immobility and 20 months on a feeding tube. (3) That afternoon, the school presented Zackery with the first-ever Lystedt Adversity Award, which observed the preceding six years he had spent overcoming a near-fatal brain injury sustained at the age of 13 while playing football for his junior high school team. (4)

    The long road to that amphitheater began on October 12, 2006. (5) Then just 13 years old, Zackery Lystedt took to the football field, bearing his school's colors and a desire to bring back victory. (6) Even an apparently significant head injury toward the end of the second quarter could not keep him out of the game. (7) Zackery was sidelined for the remainder of the half, but returned to play at the beginning of the third quarter. (8) He did not experience any loss of consciousness, and his coach was otherwise unable to detect and react to symptoms of concussion or brain injury. (9) No second thought was given to Zackery's continued play until the end of the game, when he began to complain of a severe headache. (10) During the customary end-of-game handshake, Zackary Lystedt collapsed, and was life-flighted to an area hospital in the hope that doctors could save his life. (11)

    For decades, current and former players, doctors and brain health experts have attempted to convince the National Football League and others that the short and long-term effects of concussion and other brain injuries were of serious concern and needed to be addressed. (12) In 2013, the league settled a class-action lawsuit brought by more than 4,500 retired players to compensate them for long-term neurological injuries sustained as a result of league play. (13) While the settlement agreement expressly rejected any admission of liability or weakness by the NFL that the injuries were caused by football, (14) there was much speculation that the quick out-of-court settlement and the high settlement amount ($765 million) were designed to avoid potentially damaging trial discovery. (15)

    The legal and ethical implications of adult professional athletes participating in dangerous sports in exchange for large paychecks will be left for another day. This paper focuses on the involvement of youth athletes in contact sports, and the risks of neurological injury that participation entails. (16) Many states have enacted legislation in an attempt to prevent stories like Zackery Lystedt's from recurring. (17) These statutes differ slightly, but all resemble the model legislation first enacted in 2009 by Washington State--legislation that bears Lystedt's name.

    Broadly, this paper questions whether Ohio's recently enacted youth concussion legislation adequately addresses the public health issue of sport-related brain injury, and contends that it does not. To that end, it first addresses the significance of traumatic brain injuries, including concussions, explaining that the failure to protect youth athletes from these potentially fatal conditions has largely resulted from a lack of awareness of their influence on neurological functions, and of their potential to cause serious brain injury. (18) Next, this paper examines several legislative responses enacted by other states, all of which were in place before Ohio's, and compares the recently enacted Ohio legislation to them. (19) This paper then advances several reasons why the Ohio legislation is ineffective in achieving its stated goals, and the particular ways by which it fails to protect youth athletes from the significant risks associated with traumatic brain injury and concussions. (20) Finally, it offers Ohio's legislature suggestions to bring the state's law up to a standard advocated for by brain health experts. (21)

  2. BACKGROUND OF CONCUSSION AND ITS RELATION TO YOUTH ATHLETICS

    1. Pathophysiology of Traumatic Brain Injury (TBI) and Concussion

      Traumatic brain injury (TBI) encompasses a wide range of conditions, but may be concisely defined as "an alternation in brain function, or other evidence of brain pathology, caused by an external force." (22) Within that broad category, traumatic brain injuries are graded as mild, moderate, or severe. (23) A mild form of TBI is commonly known as a concussion, which may be defined with more particularity as "a biomechanically induced neurological injury, resulting in an alteration of mental status, such as confusion or amnesia, which may or may not involve a loss of consciousness." (24) This basic definition of concussion is widely agreed upon in the field. (25) A concussion may be induced by any external biomechanical force, and may occur even if the individual is wearing protection such as a helmet. (26)

      A series of neurochemical and neurometabolic events at the cellular level is triggered by the initial trauma to the brain. (27) First, an abrupt, indiscriminate release of neurotransmitters and unchecked ionic fluxes occurs. (28) "Excitatory transmitters" such as glutamate, bind to NMDA (29) receptors. (30) This triggers a cellular event known as an "action potential", more colloquially known as a neuron firing, which is normally how neurons communicate to one another. (31) With injury, however, aberrant "action potentials" fire increasingly as a result of injury, which causes aberrant efflux of potassium and influx of calcium. (32) In an effort to correct these ionic shifts and reestablish ionic balance, the ATP-dependent (33) sodium-potassium pump works at maximum capacity. (34) In order to provide sufficient energy for the sodium-potassium pump to function, metabolism of glucose (glycolysis) is increased to supply the necessary ATP. (35) Influxes of calcium accumulate in the mitochondria, resulting in decreased ATP production and an increased need for glycolysis. (36) Under normal conditions, glycolysis is tightly coupled to cerebral blood flow, but "in a setting of increased glucose metabolism the insufficient blood supply can create a potentially damaging energy crisis." (37) These cellular changes, among others, cause a state in the neuron commonly known as "excitotoxicity," or where over-excitation of the neuron proves toxic for it. (38) This combination of cellular ionic disturbances, altered cerebral blood flow, and glucose metabolic dysfunction has been hypothesized to set the stage for more severe brain injury after a repeated concussion, described clinically as the second impact syndrome. (39)

      Another acute effect induced by concussion or other severe blunt head injury is diffuse axonal injury. (40) The traumatic impact of concussion results in traumatic axonal injury, which involves the mechanical stretching of axonal cell membranes, causing ionic flux, calcium influx and mitochondrial swelling, which is hypothesized to contribute to altered energetics, or use and production of energy, within the cell. (41) These pathophysiologic processes have been shown to interfere with axonal transport, resulting in axonal "blebbing" (42) and eventual disconnection. (43) This axonal damage was found to progress through various cortical and subcortical structures for four to six weeks, indicating signs of spatial learning and memory deficits in animal models of TBI during that time. (44) However, in the acute phase, axonal injury results in axolemmal (45) permeability, and can lead to additional influx of calcium and mitochondrial swelling. (46)

      Increases in calcium following traumatic brain injury do not necessarily lead to cell death; elevated intracellular calcium "may lead to impaired mitochondrial metabolism, but neurons may still survive." (47) Clinical signs and symptoms of impaired coordination, attention, memory, and cognition are manifestations of underlying neuronal dysfunction; (48) however, it is difficult to match clinical signs...

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