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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, Vimal Patel, Hamad Farhat, Brian Sindelar and James Stone

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Patrick W. McCormick, Robert F. Spetzler, Julian E. Bailes, Joseph M. Zabramski and James L. Frey

✓ A retrospective review of 42 patients (mean age 61.4 years) with surgically managed symptomatic internal carotid artery occlusion is reported. A standardized surgical protocol aimed at restoration of flow in the vessel was used. Presenting symptoms included hemispheric transient ischemic attacks in 68% of patients, new fixed neurological deficits in 28%, amaurosis fugax in 28%, and stroke-in-evolution in 9%. Twenty-four arteries were successfully reopened. A proximal remnant angioplasty (stumpectomy) was performed alone in nine patients or in combination with an external carotid endarterectomy in nine. In four patients with persisting symptoms who failed to achieve primary restoration of flow, a superficial temporal-to-middle cerebral artery bypass procedure was performed.

The permanent surgical morbidity rate was 2% and the surgical mortality rate was 0%. Transient postoperative deficits were present in three patients (7%). Follow-up review at a mean of 40 months was obtained in 39 patients (93%). Following surgical intervention, five patients died of unrelated causes, two had neurological events consistent with a transient cerebral ischemic attack, and two had vertebrobasilar insufficiency. No patient suffered from stroke.

Of the 24 successfully reopened vessels, follow-up ultrasound evaluations were obtained in 17 (73%) at a mean of 28 months after surgery. In 15 patients (88%) the vessels were widely patent, one (5.8%) had stenosis greater than 70%, and one (5.8%) showed asymptomatic reocclusion.

Reopening occluded internal carotid arteries in selected patients is associated with low surgical morbidity and mortality rates. Further studies are necessary to determine the impact of this surgical therapy on the natural history of this condition.

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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.

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Vin Shen Ban, Julian E. Bailes, Mitchel S. Berger, Alexander R. Vaccaro and H. Hunt Batjer

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Julian E. Bailes, Marc L. Leavitt, Edward Teeple Jr., Joseph C. Maroon, Shou-Ren Shih, Merlin Marquardt, Amr El Rifai and Leo Manack

✓ The potential for hypothermia to prevent or ameliorate ischemic injury to the central nervous system is well known. To determine if a more prolonged period of metabolic suppression with blood substitution is possible, a method was developed to lower body temperature to near the freezing point. Eight adult mongrel dogs underwent closed-chest extracorporeal circulation with both external and internal body cooling. As they were cooled, progressive hemodilution was employed until complete exsanguination and blood substitution with an aqueous solution was accomplished. Continuous circulation and a core temperature at a mean of 1.7°C were maintained from 2½ to 3 hours. After rewarming to 20°C, the animals were autotransfused and allowed to recover. Of the eight animals, two died due to technical factors related to cardiac defibrillation. Of the six surviving animals, five survived over a long period and one died on the 10th postoperative day with hepatorenal failure resulting from a presumed blood transfusion incompatability reaction. All six showed normal neurological function and kennel behavior, except one dog with mild weakness of a hindlimb. When the dogs were sacrificed 1 to 2 months postoperatively, all organs were histologically normal. Specifically, there was no gross or microscopic evidence of ischemic or hypoxic injury to any central nervous system structures.

This pilot study demonstrates that it is possible to successfully achieve complete exsanguination, blood substitution, and ultraprofound body temperature, while continuous circulation of the blood substitute is maintained. With the capability of controlling and repeatedly performing washout of the extracellular environment and by reaching lower temperatures, it may be possible to attain greater cellular metabolic suppression. This perhaps will extend the allowable times for circulatory arrest procedures. In addition, “bloodless ischemia” may be beneficial in removing both blood substances and formed elements which may mediate organ ischemia. With replacement of blood at warm temperatures, coagulopathy is avoided. This preliminary evidence demonstrates potential in the combination of ultraprofound hypothermia and complete blood component substitution. However, further study is required to confirm the potential of achieving circulatory arrest of longer duration.

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Ryan C. Turner, Zachary J. Naser, Julian E. Bailes, David W. Smith, Joseph A. Fisher and Charles L. Rosen

Object

Helmets successfully prevent most cranial fractures and skull traumas, but traumatic brain injury (TBI) and concussions continue to occur with frightening frequency despite the widespread use of helmets on the athletic field and battlefield. Protection against such injury is needed. The object of this study was to determine if slosh mitigation reduces neural degeneration, gliosis, and neuroinflammation.

Methods

Two groups of 10 adult male Sprague-Dawley rats were subjected to impact-acceleration TBI. One group of animals was fitted with a collar inducing internal jugular vein (IJV) compression prior to injury, whereas the second group received no such collar prior to injury. All rats were killed 7 days postinjury, and the brains were fixed and embedded in paraffin. Tissue sections were processed and stained for markers of neural degeneration (Fluoro-Jade B), gliosis (glial fibrillary acidic protein), and neuroinflammation (ionized calcium binding adapter molecule 1).

Results

Compared with the controls, animals that had undergone IJV compression had a 48.7%–59.1% reduction in degenerative neurons, a 36.8%–45.7% decrease in reactive astrocytes, and a 44.1%–65.3% reduction in microglial activation.

Conclusions

The authors concluded that IJV compression, a form of slosh mitigation, markedly reduces markers of neurological injury in a common model of TBI. Based on findings in this and other studies, slosh mitigation may have potential for preventing TBI in the clinical population.

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James D. Mills, Julian E. Bailes, Cara L. Sedney, Heather Hutchins and Barry Sears

Object

Traumatic brain injury remains the most common cause of death in persons under 45 years of age in the Western world. Recent evidence from animal studies suggests that supplementation with omega-3 fatty acid (O3FA) (particularly eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) improves functional outcomes following focal neural injury. The purpose of this study is to determine the benefits of O3FA supplementation following diffuse axonal injury in rats.

Methods

Forty adult male Sprague-Dawley rats were used. Three groups of 10 rats were subjected to an impact acceleration injury and the remaining group underwent a sham-injury procedure (surgery, but no impact injury). Two of the groups subjected to the injury were supplemented with 10 or 40 mg/kg/day of O3FA; the third injured group served as an unsupplemented control group. The sham-injured rats likewise received no O3FA supplementation. Serum fatty acid levels were determined from the isolated plasma phospholipids prior to the injury and at the end of the 30 days of supplementation. After the animals had been killed, immunohistochemical analysis of brainstem white matter tracts was performed to assess the presence of β-amyloid precursor protein (APP), a marker of axonal injury. Immunohistochemical analyses of axonal injury mechanisms—including analysis for caspase-3, a marker of apoptosis; RMO-14, a marker of neurofilament compaction; and cytochrome c, a marker of mitochondrial injury—were performed.

Results

Dietary supplementation with a fish oil concentrate rich in EPA and DHA for 30 days resulted in significant increases in O3FA serum levels: 11.6% ± 4.9% over initial levels in the 10 mg/kg/day group and 30.7% ± 3.6% in the 40 mg/kg/day group. Immunohistochemical analysis revealed significantly (p < 0.05) decreased numbers of APP-positive axons in animals receiving O3FA supplementation: 7.7 ± 14.4 axons per mm2 in the 10 mg/kg/day group and 6.2 ± 11.4 axons per mm2 in the 40 mg/kg/day group, versus 182.2 ± 44.6 axons per mm2 in unsupplemented animals. Sham-injured animals had 4.1 ± 1.3 APP-positive axons per mm2. Similarly, immunohistochemical analysis of caspase-3 expression demonstrated significant (p < 0.05) reduction in animals receiving O3FA supplementation, 18.5 ± 28.3 axons per mm2 in the 10 mg/kg/day group and 13.8 ± 18.9 axons per mm2 in the 40 mg/kg/day group, versus 129.3 ± 49.1 axons per mm2 in unsupplemented animals.

Conclusions

Dietary supplementation with a fish oil concentrate rich in the O3FAs EPA and DHA increases serum levels of these same fatty acids in a dose-response effect. Omega-3 fatty acid supplementation significantly reduces the number of APP-positive axons at 30 days postinjury to levels similar to those in uninjured animals. Omega-3 fatty acids are safe, affordable, and readily available worldwide to potentially reduce the burden of traumatic brain injury.

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Julian E. Bailes, Anthony L. Petraglia, Bennet I. Omalu, Eric Nauman and Thomas Talavage

Research now suggests that head impacts commonly occur during contact sports in which visible signs or symptoms of neurological dysfunction may not develop despite those impacts having the potential for neurological injury. Recent biophysics studies utilizing helmet accelerometers have indicated that athletes at the collegiate and high school levels sustain a surprisingly high number of head impacts ranging from several hundred to well over 1000 during the course of a season. The associated cumulative impact burdens over the course of a career are equally important. Clinical studies have also identified athletes with no readily observable symptoms but who exhibit functional impairment as measured by neuropsychological testing and functional MRI. Such findings have been corroborated by diffusion tensor imaging studies demonstrating axonal injury in asymptomatic athletes at the end of a season. Recent autopsy data have shown that there are subsets of athletes in contact sports who do not have a history of known or identified concussions but nonetheless have neurodegenerative pathology consistent with chronic traumatic encephalopathy. Finally, emerging laboratory data have demonstrated significant axonal injury, blood-brain barrier permeability, and evidence of neuroinflammation, all in the absence of behavioral changes. Such data suggest that subconcussive level impacts can lead to significant neurological alterations, especially if the blows are repetitive. The authors propose “subconcussion” as a significant emerging concept requiring thorough consideration of the potential role it plays in accruing sufficient anatomical and/or physiological damage in athletes and military personnel, such that the effects of these injuries are clinically expressed either contemporaneously or later in life.

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Julian E. Bailes, Jeffrey W. Cozzens, Alan R. Hudson, David G. Kline, Ivan Ciric, Peter Gianaris, Lawrence P. Bernstein and Daniel Hunter

✓ Studies on the peripheral nerves in rats and other species have helped in the development of laser-assisted nerve anastomosis (LANA), but offer little in evaluating the efficacy of this technique in primates. The authors present a study of LANA in the peripheral nerves of rhesus monkeys. Twelve adult rhesus monkeys underwent bilateral resection of a portion of the peroneal nerve followed by placement of autogenous sural nerve interposition fascicular grafts. The grafts were completed with conventional microsurgical suture technique on one side and with LANA on the other. At 5, 8, 10, and 12 months, the grafted nerves were evaluated for continuity, nerve conduction, and histology (both light and electron microscopy). No significant difference in continuity, conduction velocity, nerve degeneration, nerve regeneration, axon fiber number, or axon fiber density was found in any animal between grafts performed by conventional microsuture and LANA grafts. There was no difference in distal or proximal myelinated fiber density between the LANA grafts and the conventional microsuture grafts. It was concluded that LANA is as effective as microsurgical suture nerve anastomosis in a primate model of nerve repair and grafting.