Progress in neurological surgery
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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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There is no other sport that has come under greater scrutiny surrounding the incidence and treatment of concussion than football, and there is no other professional sports league that has experienced more intense focus of its handling of concussions than the National Football League (NFL). The NFL has received significant criticism of their management of concussion in players from both the popular press and the medical community. However, those working with active NFL players have changed their assessment and treatment of these injuries as the knowledge of concussions has evolved over time. We review the current approach to the management of concussions in the professional football player.
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A link between mild traumatic brain injury (mTBI) and neurodegenerative diseases, specifically Alzheimer's disease and chronic traumatic encephalopathy (CTE), has long been suspected. Shared clinical symptomology - most notably the prominent role of central auditory dysfunction and sleep-wake disturbances in both disease states - and similar findings on postmortem pathological examination has further reinforced suspected commonality between these seemingly disparate entities. ⋯ Recent research using diffusion tensor imaging, a novel imaging technique, and focused on patient-reported symptoms has for the first time demonstrated imaging findings in mTBI patients in vivo that are strikingly similar to Alzheimer's dementia and CTE. Moving forward, research will focus on identifying what renders certain patients with mTBI susceptible to developing full-fledged Alzheimer's disease and CTE later in life.
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The clinical presentation of concussion can vary widely as patients experience any number of symptoms including headache, dizziness, cognitive symptoms of difficulty with concentration and memory, sleep dysregulation, and mood disturbances. The variability in clinical presentation underscores the importance of thorough history-taking to clearly understand the clinical picture and to allow individualization of the treatment plan. ⋯ For those individuals whose symptoms persist or significantly impair quality of life, pharmacologic intervention may be warranted. Though few studies have investigated the use of pharmacology for treatment of postconcussion syndrome specifically, targeted treatment of medications known to improve selected symptoms can be considered.
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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.