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Julian E. Bailes

Object. Transient spinal cord injury (TSCI) in athletes presents one of the most challenging clinical scenarios. Management difficulties in and subsequent return-to-play decisions are especially important in those with cervical canal stenosis.

Methods. Ten athletes (nine male and one female patients) were evaluated for TSCI. The diagnostic survey included physical and neurological examinations, plain radiographs with flexion—extension dynamic studies, computerized tomography, and magnetic resonance (MR) imaging. Clinical courses were followed and, in those who returned to contact sports activities, subsequent experience was noted.

Symptoms consisted of paralysis, weakness, or numbness in all four extremities, their duration ranging from 15 minutes to 48 hours. Radiography revealed no evidence of fracture/dislocation or ligamentous instability. Spinal stenosis of 8 to 13 mm in length at three or more levels was evident in all cases. Four patients returned to competition without recurrent TSCI (mean follow-up duration 40 months); six individuals retired.

The occurrence of TSCI is not uncommon in athletes involved in contact sports. The diagnostic workup focuses on excluding fracture/dislocation, cord contusion, ligamentous infolding or instability, herniated nucleus pulposus, syrinx, or other surgically correctable lesions. There appear to be two groups of athletes who sustain TSCI: those who experience TSCI yet in whom radiographic studies are normal, and those with cervical stenosis, the most difficult management group.

Conclusions. It does not appear that a single episode of TSCI in an athlete with spinal stenosis will substantially increase the risk of subsequent catastrophic spinal cord injury in those in whom MR imaging demonstrates preservation of cerebrospinal fluid signal.

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Vincent J. Miele, Julian E. Bailes and Neil A. Martin

✓Despite a plethora of guidelines for return to play following mild head injury, a discussion of when and if an athlete should be allowed to participate in contact or collision sports if he or she sustains a structural brain lesion or after a head injury requiring craniotomy is lacking. The structural lesions discussed include arachnoid cyst, Chiari malformation Type I, cavum septum pellucidum, and the presence of ventriculoperitoneal shunts. Issues unique to this population with respect to the possibility of increased risk of head injury are addressed. The population of athletes with epilepsy and certain genetic risk factors is also discussed. Finally, the ability of athletes to participate in contact or collision sports after undergoing craniotomies for traumatic or congenital abnormalities is evaluated. Several known instances of athletes returning to contact sports following craniotomy are also reviewed.

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Jonathan G. Hobbs, Jacob S. Young and Julian E. Bailes

Sports-related concussions (SRCs) are traumatic events that affect up to 3.8 million athletes per year. The initial diagnosis and management is often instituted on the field of play by coaches, athletic trainers, and team physicians. SRCs are usually transient episodes of neurological dysfunction following a traumatic impact, with most symptoms resolving in 7–10 days; however, a small percentage of patients will suffer protracted symptoms for years after the event and may develop chronic neurodegenerative disease. Rarely, SRCs are associated with complications, such as skull fractures, epidural or subdural hematomas, and edema requiring neurosurgical evaluation. Current standards of care are based on a paradigm of rest and gradual return to play, with decisions driven by subjective and objective information gleaned from a detailed history and physical examination. Advanced imaging techniques such as functional MRI, and detailed understanding of the complex pathophysiological process underlying SRCs and how they affect the athletes acutely and long-term, may change the way physicians treat athletes who suffer a concussion. It is hoped that these advances will allow a more accurate assessment of when an athlete is truly safe to return to play, decreasing the risk of secondary impact injuries, and provide avenues for therapeutic strategies targeting the complex biochemical cascade that results from a traumatic injury to the brain.

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James L. Stone, Vimal Patel and Julian E. Bailes

The authors trace the Oxford, England, roots of World War II (WWII)–related advances in head injury management, the biomechanics of concussion and brain injury, and postwar delineation of pathological findings in severe concussion and diffuse brain injury in man. The prominent figure in these developments was the charismatic and innovative Harvey Cushing–trained neurosurgeon Sir Hugh Cairns. Cairns, who was to closely emulate Cushing's surgical and scholarly approach, is credited with saving thousands of lives during WWII by introducing and implementing innovative programs such as helmets for motorcyclists, mobile neurosurgical units near battle zones, and the military usage of penicillin. In addition, he inspired and taught a generation of neurosurgeons, neurologists, and neurological nurses in the care of brain and spinal cord injuries at Oxford's Military Hospital for Head Injuries. During this time Cairns also trained the first full-time female neurosurgeon. Pivotal in supporting animal research demonstrating the critical role of acceleration in the causation of concussion, Cairns recruited the physicist Hylas Holbourn, whose research implicated rotary acceleration and shear strains as particularly damaging. Cairns' work in military medicine and head injury remain highly influential in efforts to mitigate and manage brain injury.

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Vincent J. Miele, John A. Norwig and Julian E. Bailes

✓Participation in contact and collision sports carries an inherent risk of injury to the athlete, with damage to the nervous system producing the most potential for significant morbidity and death. Neurological injuries suffered during athletic competition must be treated promptly and correctly to optimize outcome, and differentiation between minor and serious damage is the foundation of sideline/ringside management of the injury. In this article the authors present a guide to the sideline or ringside identification and management of head and spinal injuries.

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Ivan Sosa and Valter Stemberga

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Matthew L. Dashnaw, Anthony L. Petraglia and Julian E. Bailes

There has been a growing interest in the diagnosis and management of mild traumatic brain injury (TBI), or concussion. Repetitive concussion and subconcussion have been linked to a spectrum of neurological sequelae, including postconcussion syndrome, chronic traumatic encephalopathy, mild cognitive impairment, and dementia pugilistica. A more common risk than chronic traumatic encephalopathy is the season-ending or career-ending effects of concussion or its mismanagement. To effectively prevent and treat the sequelae of concussion, it will be important to understand the basic processes involved. Reviewed in this paper are the forces behind the primary phase of injury in mild TBI, as well as the immediate and delayed cellular events responsible for the secondary phase of injury leading to neuronal dysfunction and possible cell death. Advanced neuroimaging sequences have recently been developed that have the potential to increase the sensitivity of standard MRI to detect both structural and functional abnormalities associated with concussion, and have provided further insight into the potential underlying pathophysiology. Also discussed are the potential long-term effects of repetitive mild TBI, particularly chronic traumatic encephalopathy. Much of the data regarding this syndrome is limited to postmortem analyses, and at present there is no animal model of chronic traumatic encephalopathy described in the literature. As this arena of TBI research continues to evolve, it will be imperative to appropriately model concussive and even subconcussive injuries in an attempt to understand, prevent, and treat the associated chronic neurodegenerative sequelae.

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Julian E. Bailes, Robert F. Spetzler, Mark N. Hadley and Hillel Z. Baldwin

✓ Preliminary experience with the occasional good survival of patients in Hunt and Hess Grade IV or V with aneurysmal subarachnoid hemorrhage (SAH) led to a prospective management protocol employed during a 2½-year period. The protocol utilized computerized tomography (CT) scanning to diagnose SAH and to obtain evidence for irreversible brain destruction, consisting of massive cerebral infarction with midline shift or dominant basal ganglia or brain-stem hematoma. These patients, along with those who exhibited poor or absent intracranial filling on CT or angiography, were excluded from active treatment and given supportive care only. All other patients had immediate ventriculostomy placement and, if intracranial pressure (ICP) was controllable (≤ 30 cm H2O without an intracranial clot or ≤ 50 cm H2O in the presence of a clot), went on to have craniotomy for aneurysm clipping. Aggressive postoperative hypertensive, hypervolemic, hemodilutional therapy was subsequently employed. Of 54 patients with poor-grade aneurysms, ventriculostomy was placed in 47 (87.0%) and yielded high ICP's in the overwhelming majority, with the mean ICP being 40.2 cm H2O. Nineteen poor-grade aneurysm patients received no surgical treatment and survived a mean of 31.8 hours with 100% mortality. Thirty-five patients underwent placement of a ventriculostomy, craniotomy for aneurysm clipping and intracranial clot evacuation, and postoperative hypertensive, hypervolemic, hemodilutional therapy. The outcome at 3 months of the 35 patients who were selected for active treatment was good in 19 (54.3%), fair in four (11.4%), poor in four (11.4%), and death in eight (22.9%).

It is concluded that poor-grade aneurysm patients usually present with intracranial hypertension, even those without an intracranial clot. Based on radiographic rather than neurological criteria, a portion of these patients can be selected for active and successful treatment. Increased ICP can be present without ventriculomegaly, and immediate ventriculostomy should be performed. As long as ICP is controllable, craniotomy and postoperative intensive care can effect a favorable outcome in a significant percentage of these patients.