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1.  Loss of Consciousness: Pathophysiology and Implications in Grading and Safe Return to Play 
Journal of Athletic Training  2001;36(3):249-252.
Objective:
To provide historical background and current concepts regarding the importance of loss of consciousness (LOC) in the evaluation of concussion and athletes.
Data Sources:
A MEDLINE search identified scientific and clinical articles on sport concussion management published from 1966 to present. Discussions were held with authors of selected reports. Recent research findings reported at national meetings were reviewed.
Data Synthesis:
The relative importance of LOC in the evaluation of concussion was reviewed in light of scientific and clinical evidence in the literature. Comments made by authors of concussion grading scales were considered in the development of expert consensus statements.
Conclusions/Recommendations:
The observation of LOC at the time of concussion must be viewed as reflecting a potentially worrisome traumatic brain injury. LOC is followed by more severe acute mental status abnormalities and carries a greater risk of intracranial pathology than concussion without LOC. Prolonged LOC represents a neurologic emergency, which may require neurosurgical intervention. Lingering symptoms of concussion, even without LOC, should be monitored closely and managed according to established guidelines for safe return to play.
PMCID: PMC155414  PMID: 12937492
concussion; mild traumatic brain injury; sport concussion guidelines
3.  Concussion Symptom Inventory: An Empirically Derived Scale for Monitoring Resolution of Symptoms Following Sport-Related Concussion 
Self-report post-concussion symptom scales have been a key method for monitoring recovery from sport-related concussion, to assist in medical management, and return-to-play decision-making. To date, however, item selection and scaling metrics for these instruments have been based solely upon clinical judgment, and no one scale has been identified as the “gold standard”. We analyzed a large set of data from existing scales obtained from three separate case–control studies in order to derive a sensitive and efficient scale for this application by eliminating items that were found to be insensitive to concussion. Baseline data from symptom checklists including a total of 27 symptom variables were collected from a total of 16,350 high school and college athletes. Follow-up data were obtained from 641 athletes who subsequently incurred a concussion. Symptom checklists were administered at baseline (preseason), immediately post-concussion, post-game, and at 1, 3, and 5 days post-injury. Effect-size analyses resulted in the retention of only 12 of the 27 variables. Receiver-operating characteristic analyses were used to confirm that the reduction in items did not reduce sensitivity or specificity. The newly derived Concussion Symptom Inventory is presented and recommended as a research and clinical tool for monitoring recovery from sport-related concussion.
doi:10.1093/arclin/acp025
PMCID: PMC2800775  PMID: 19549721
Brain injury; Post-concussion; Scale
4.  Stimulation by Alcohols of Cyclic AMP Metabolism in Human Leukocytes 
Journal of Clinical Investigation  1977;60(2):284-294.
In this study ethanol and certain other short-chain aryl (benzyl and phenethyl) and aliphatic (methyl, propyl, butyl, and amyl) alcohols produced up to 10-fold increases in cyclic AMP (cAMP) concentrations in purified human peripheral blood lymphocytes. Ethanol concentrations as low as 80 mg/dl produced significant elevations in lymphocyte cAMP. Significant but less marked augmentation of cAMP in response to alcohols was observed in human platelets, human granulocytes, and rabbit alveolar macrophages. The mechanism of the alcohol-induced cAMP accumulation is probably secondary to membrane perturbation and consequent activation of adenylate cyclase, because ethanol directly stimulated this enzyme in lymphocyte membrane preparations but had no effect on lymphocyte phosphodiesterase activity.
Lysosomal enzyme release, by phagocytosing human leukocytes, and aminoisobutyric acid transport in mitogen-stimulated human lymphocytes were shown to be inhibited by ethanol and other alcohols at concentrations which also elevate cAMP. In general, the magnitude of the inhibition of these inflammatory processes correlated with the ability of the alcohol to elevate cAMP concentrations. Lectin-and anti-thymocyte globulin-induced lymphocyte mitogenesis was inhibited or unaffected depending upon both the concentration and type of mitogenic stimulus and the concentration and type of alcohol utilized. Inflammatory mediator release from rat mast cells also was inhibited by ethanol and certain other alcohols, but whole cell cAMP was not increased. Ethanol may alter these inflammatory responses and other biologic processes at least in part by modulating cellular levels of cAMP.
PMCID: PMC372368  PMID: 194924

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