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This accumulation gives rise to the two classic neuropathological phenotypes of axonal swelling: singular axonal bulbs (previously called retraction balls) and axonal varicosities, which occur as a series of protrusions along individual axons.13, 19 At a critical threshold of axonal swelling, the axons disconnect at the location of the injury (secondary axotomy).16, 17, 20, 21 Neuronal damage consisting of axonal bulbs and swellings is most commonly located in the deep gyri at the interface between the grey and white matter.13, 22 Studies using advanced MRI techniques, such as diffusion tensor imaging, show that the extent of white matter abnormalities after mild TBI correlates with the severity of postconcussion http://www.fakeoakleysaler.com cognitive problems.23, 24, 25Many practicing clinicians have assumed that the axonopathy and metabolic stress in patients with mild TBI is reversed within 1 weeks, because this is when clinical symptoms have most often disappeared.26 However, magnetic resonance spectroscopy findings, electrophysiological data and neuropsychological assessments suggest that patients‘ physiological parameters return to baseline after 30 days.27, 28 Moreover, neuropathological analyses indicate that axonopathy might continue for years after TBI.13 Another important consideration affecting the patient’s recovery fake ray ban sunglasses after mild TBI is their age, since the developing brain seems to be more vulnerable to repeated concussions than is the adult brain,29 owing to differences in the degree of myelination, volume ratio of brain to water, elastic properties, and blood barrier (BBB) integrity.30, 31 This knowledge, in conjunction with available biomechanical, radiological and clinical data,32, 33 should be communicated to parents with the aim of discouraging the participation of children in contact sports that target the head.A form of TBI induced early dementia was first reported in 1928 among professional boxers, Fake ray bans years after their careers had ended.34 Initially termed dementia pugilistica or punch drunk syndrome, the prevalence of this neuropsychiatric manifestation is now estimated at around 20% in former professional boxers.35, 36 These observations aroused great interest in the long term outcomes of patients who developed chronic or progressive symptoms after a single episode or repeated episodes of mild TBI.37 Such symptoms can include changes in cognition (memory and executive functioning), mood (depression, Cheap Oakleys apathy and suicidal thoughts), personality and behaviour (poor impulse control and behavioural disinhibition), and movement (including parkinsonism and symptoms of motor neuron dysfunction), which are similar to those described in ex boxers.38 Some investigators have started to describe this constellation of symptoms as chronic traumatic encephalopathy (CTE);39, 40, 41 however, vigorous debate is ongoing among researchers regarding the definition of CTE from both neuropsychiatric and neuropathological perspectives.The brains of former boxers with CTE also display the hallmark pathologies of Alzheimer disease (AD), including neurofibrillary tangles composed of hyperphosphorylated tau and amyloid (A plaques.42, 43 Progressive axonopathy in these patients might underlie the rapid formation of A plaques after TBI.44 The risk factors for CTE in ex boxers are a long career, many bouts, high sparring exposure, many knockouts, poor performance, and being able to tolerate many blows without being knocked out, all of which are associated with cumulative exposure to repetitive brain trauma.40 According to one study, a positive apolipoprotein E status, commonly associated with AD, is a risk factor for CTE in these individuals.36 Similarly, tau and A pathology, as well as TAR DNA binding protein 43 (TDP Authentic Jerseys Sale 43) deposition, have been found in the brains of patients with CTE approximately 10 years after professional participation in nfl jerseys cheap contact sports such as American football.45 Notably, neuritic A plaques and neurofibrillary tangles have also been found in patients a few years to four decades after a single episode of moderate or severe TBI.46 However, TDP 43 deposition was not found in these patients, suggesting that this pathological feature might be used to distinguish patients with CTE due to a single episode of TBI from those with CTE due to repetitive TBI.47Top of pageCurrently available fluid biomarkersCSF biomarkers of acute brain injuryThe cerebrospinal fluid (CSF) is in direct contact with the extracellular matrix in the brain, and its composition reflects Fake Oakley Outle biochemical changes that occur in this organ.48 For these reasons, the CSF might be considered an optimal source of biomarkers of brain injury.