Progress in neurological surgery
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The following report reviews our current understanding of the neurobiological response to concussion which is often referred to as mild traumatic brain injury. The historical accomplishments to reveal the brain's response to this injury are discussed along with the neurochemical and metabolic cascade that results in an energy crisis. The massive ionic flux induced by cerebral concussion is discussed as it pertains to primarily potassium and calcium. ⋯ While experimental studies are the primary focus of this report, relevant human observations are discussed and put into context. It is now clear that cerebral concussion is not a benign event. It carries with it neuroscientific consequences that result in symptoms and an increase in risk for many other challenges to the central nervous system.
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Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative syndrome, which is caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain. CTE presents clinically as a composite syndrome of mood disorders and behavioral and cognitive impairment, with or without sensorimotor impairment. Symptoms of CTE may begin with persistent symptoms of acute traumatic brain injury (TBI) following a documented episode of brain trauma or after a latent period that may range from days to weeks to months and years, up to 40 years following a documented episode of brain trauma or cessation of repetitive TBI. ⋯ The brain of a CTE sufferer may appear grossly unremarkable, but shows microscopic evidence of primary and secondary proteinopathies. The primary proteinopathy of CTE is tauopathy, while secondary proteinopathies may include, but are not limited to, amyloidopathy and TDP proteinopathy. Reported prevalence rates of CTE in cohorts exposed to TBI ranges from 3 to 80% across age groups.
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Concussions have long been understood to be an invisible injury. Indeed, conventional imaging techniques [computed tomography and magnetic resonance imaging (MRI)] are largely ineffective in elucidating concussive injuries. More advanced techniques are being used experimentally to help delineate the underlying pathophysiology of concussive injuries on metabolic as well as ultrastructural levels. ⋯ Each technique is briefly described, followed by a summary of the findings specific to concussive injuries. Overall, there is mounting evidence to suggest that each technique has utility in describing and explaining postinjury changes in the brain. Overall, concussive injuries are evident using the various aforementioned neuroimaging modalities and suggest at a minimum the concussed brain is different in the acute and subacute postinjury phases with several other studies suggesting that changes are persistent well beyond, especially in those patients with persistent symptoms.
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Sport-related concussions affect millions of athletes every year, but they generally present no anatomic alterations when examined using conventional magnetic resonance imaging or a computed tomography scan. Because the damage occurring after a head injury seems to be more functional than structural, these techniques are unable to detect subtle alterations. ⋯ Electrophysiological methods, magnetic resonance spectroscopy, and diffusion tensor imaging are useful techniques that are sensitive to the effects of a brain trauma, which provide complementary information to allow a more complete understanding of the multiple pathophysiological processes involved in concussive events. This report summarizes recent data using neurophysiological and neuroimaging techniques to better understand the acute and chronic effects of sport-related concussions.
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The majority of traumatic brain injuries (TBI) in the USA are mild in severity. Sports, particularly American football, and military experience are especially associated with repetitive, mild TBI (mTBI). The consequences of repetitive brain injury have garnered increasing scientific and public attention following reports of altered mood and behavior, as well as progressive neurological dysfunction many years after injury. This report provides an up-to-date review of the clinical, pathological, and pathophysiological changes associated with repetitive mTBI, and their potential for cumulative effects in certain individuals.