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Early reports is arthritis in dogs genetic 400 mg trental buy otc, however, suggest that many neural stem cells become glia after brain injury, and that this is a salubrious event [186]. However, indirect neuroimaging tactics are already available that should soon enable investigators to visualize human neurogenesis in vivo. First, evidence suggests that the density of neural precursor cells in rodent hippocampus is detectable as a spectroscopic metabolite peak resonating at 1. If these techniques are validated and optimized, they may soon unleash a vital new research enterprise. Investigators will finally be able to monitor the natural history of spontaneous human post-concussive neurogenesis. More clinically important, they will be able to conduct randomized controlled trials of the many agents already shown to enhance 175 176 Part I: What is a Concussion For example, stains have been found to enhance visualization of biologically interesting features. As a result of such advances, judgments about the health or sickness of brain cells, neurons, and glia, have changed, changed, and changed again. Given this iterative progress, when can we say the microscope has showed us the truth We are forced to admit that optical microscopic assessment can never be definitive, since: 1. They sacrificed the animals after three days and examined the brains with several dyes. If they had stopped with crystal violet, one would sigh with relief and infer that concussion does not kill neurons: "Staining with crystal violet showed that cortical tissue was generally intact without dramatic lesions. Hence, whatever the microscope gazer announces in 1720 or 2020 must be taken with a grain of salt. In 2050, when we will have in vivo neuroimaging technology capable of video monitoring real-time neuronal function at the sub-molecular level, gorgeous still-deaths such as those published since Micrographia [193] may be relegated to history. In fact, the authors discovered that the region in which these degenerative-but-not-fatal changes occurred was 10. In order to devise preventive treatments ­ in order to save 177 178 Part I: What is a Concussion Source: Gao and Chen, 2011 [194] by permission of Oxford University Press What Experimental Studies With Non-Human Animals Reveal Readers, rejoice! Having squeezed the last drop out of the rock of caveats, having explained why the animal data fail to answer many questions, it seems about time to impartially review that data. Hermione from slowed thinking and depression ­ we ought to know whether long-term behavioral changes are due to cell death. If you only have a dead cell stain, you may be seeing the tip of the iceberg of concussion-induced brain change. Given that different stains yield different answers about cell loss, the most earnest neuropathologist working with the wrong box of paints might be excused for failing to see and acknowledge the dire effects of "mild" concussions. In essence, the scores of peer-reviewed scientific articles reporting "intact" brains after concussion may simply be telling the same misleading story as the old reports based on conventional neuropsychological tests: "Using insensitive methods, we found nothing.

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Recall bias was virtually assured by the retrospective designs of five of six reports arthritis rheumatoid treatment natural trental 400 mg order fast delivery. The likelihood of this occurring almost without question depends on a large number of host-related and environmental factors. However, no evidence suggests that one particular clinical profile is necessary and sufficient to generate this distinctive tauopathy. But again, "trauma" was defined broadly as "any physical damage inflicted on the body. Of the 16 selected studies, only two were cohort studies of cranial injury [349, 350]. Thus, about 25% (27,406/110,993) of the head injury cohort were injured in adolescence. Based on sex, age, and year-specific disease densities, 193 cases would have been expected. Note that two factors compromise interpretation: almost all adolescents were excluded and the follow-up period was relatively short. In addition, as discussed in Chapter 7, some evidence suggests that post-concussive inflammatory change is particularly problematic among menstruating females. In late August of 2017 the Annals of Neurology accepted a paper by Montgomery et al. That concept is rapidly succumbing to the intellectual gravity of precision medicine. Genetics aside, at the very least, one expects demographically different populations to have different responses to the same health threat. By considering the possibility of an age-specific risk, a dose effect, and a late effect, Montgomery et al. That discovery, if replicated, has profound implications for medicine ­ not to mention law. Earlier chapters discussed a new model of post-concussive brain change as a neurometabolic/inflammatory/vascular melee. And a wide net has been cast seeking safe and effective treatments based on modulating inflammation [359­361]. Only time will tell which observations hold keys to either meaningful biomarkers of brain change or effective intervention. The foregoing pages in this chapter represent a very brief introduction to the nosological conundrum posed by that fact. The author tried to demonstrate that the terms of art embraced in neurological nosology tend to be loaded and biased. They make assumptions about biology that sometimes seem inconsistent with neutral scientific observation. The conventional understanding of "development," for instance, implies somatic change with the passing of time in compliance with a life history plan (and driven by a clock) that generates age-appropriate fitness-enhancing phenotypes.

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