Julian E. Bailes
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.
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.
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.
Vincent J. Miele, Julian E. Bailes, Robert C. Cantu and Craig H. Rabb
✓Boxing is a violent sport in which every participant accepts the risk of brain damage or death. This sport has been linked to acute neurological injury and chronic brain damage. The most common life-threatening injury encountered by its participants is subdural hematoma (SDH), and the most feared consequence of chronic insult to the nervous system is dementia pugilistica, or punch drunkenness. Although advances in imaging and neuropsychological testing have improved our ability to diagnose these injuries, the unprecedented sensitivity and wide availability of these modalities have increased the detection of mild cognitive impairment and small, asymptomatic imaging abnormalities. The question has thus been raised as to where on the spectrum of these injuries an athlete should be permanently banned from the sport.
In this report the authors describe six boxers who were evaluated for SDH sustained during participation in the sport, and who experienced remarkably different outcomes. Their presentations, clinical courses, and boxing careers are detailed. The athletes ranged in age from 24 to 55 years at the time of injury. Two were female and four were male; half of them were amateurs and half were professionals. Treatments ranged from observation only to decompressive craniectomy. Two of the athletes were allowed to participate in the sport after their injury (one following a lengthy legal battle), with no known sequelae. One boxer died within 48 hours of her injury and at least two suffered permanent neurological deficits. In a third, dementia pugilistica was diagnosed 40 years later, and the man died while institutionalized.
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.
Vin Shen Ban, Christopher J. Madden, Julian E. Bailes, H. Hunt Batjer and Russell R. Lonser
Recently, the pathobiology, causes, associated factors, incidence and prevalence, and natural history of chronic traumatic encephalopathy (CTE) have been debated. Data from retrospective case series and high-profile media reports have fueled public fear and affected the medical community's understanding of the role of sports-related traumatic brain injury (TBI) in the development of CTE. There are a number of limitations posed by the current evidence that can lead to confusion within the public and scientific community. In this paper, the authors address common questions surrounding the science of CTE and propose future research directions.
Vin Shen Ban, Julian E. Bailes, Mitchel S. Berger, Alexander R. Vaccaro and H. Hunt Batjer
Bennet Omalu, Jennifer L. Hammers, Julian Bailes, Ronald L. Hamilton, M. Ilyas Kamboh, Garrett Webster and Robert P. Fitzsimmons
Following his discovery of chronic traumatic encephalopathy (CTE) in football players in 2002, Dr. Bennet Omalu hypothesized that posttraumatic stress disorder (PTSD) in military veterans may belong to the CTE spectrum of diseases. The CTE surveillance at the Brain Injury Research Institute was therefore expanded to include deceased military veterans diagnosed with PTSD. The authors report the case of a 27-year-old United States Marine Corps (USMC) Iraqi war veteran, an amphibious assault vehicle crewman, who committed suicide by hanging after two deployments to Fallujah and Ramadi. He experienced combat and was exposed to mortar blasts and improvised explosive device blasts less than 50 m away. Following his second deployment he developed a progressive history of cognitive impairment, impaired memory, behavioral and mood disorders, and alcohol abuse. Neuropsychiatric assessment revealed a diagnosis of PTSD with hyperarousal (irritability and insomnia) and numbing. He committed suicide approximately 8 months after his honorable discharge from the USMC. His brain at autopsy appeared grossly unremarkable except for congestive brain swelling. There was no atrophy or remote focal traumatic brain injury such as contusional necrosis or hemorrhage. Histochemical and immunohistochemical brain tissue analysis revealed CTE changes comprising multifocal, neocortical, and subcortical neurofibrillary tangles and neuritic threads (ranging from none, to sparse, to frequent) with the skip phenomenon, accentuated in the depths of sulci and in the frontal cortex. The subcortical white matter showed mild rarefaction, sparse perivascular and neuropil infiltration by histiocytes, and mild fibrillary astrogliosis. Apolipoprotein E genotype was 3/4. The authors report this case as a sentinel case of CTE in an Iraqi war veteran diagnosed with PTSD to possibly stimulate new lines of thought and research in the possible pathoetiology and pathogenesis of PTSD in military veterans as part of the CTE spectrum of diseases, and as chronic sequelae and outcomes of repetitive traumatic brain injuries.