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Over half of all reported traumatic brain injuries are the result of a motor vehicle accident. Other then the direct head impact itself, the sheer forces of the accident can cause the brain also to collide against the internal bone of the skull. In fact, when a moving head comes to a quick stop, the brain continues in its movement, striking the interior of the skull. This can cause bruising of the brain and/or bleeding form vessels tearing. The consequences are immediate, with a scarcely predictable spectrum of lesions: from simple scalp lacerations (SLs), up to the most severe types of diffuse axonal injury (DAI). SLs can bleed profusely, causing dangerous acute hypotension and may act as a conduit for infection when associated with depressed skull fractures (SFs). SFs generally correlate with severity of injury, and patients with a SFs have a much higher likelihood of having an intracranial hematoma, such as extradural hematomas. Contusions are found to have a characteristic distribution, with the frontal poles, orbital gyri, the cortex above and below the Sylvian fissure, the temporal poles, and the lateral and inferior aspects of the temporal lobes. Lacerations of the frontal and temporal lobes are frequently associated with acute subdural bleeding and/or intraparenchymal hemorrhage. DAI causes by itself 35% of all deaths after head injury, and may or may not be accompanied by intracranial mass lesion. Approximately half of severe cases of DAI exhibit focal lesions of the corpus callosum, the rostral brainstem, and microscopic evidence of widespread damage of the white matter. Urgent surgical candidates are those patients in whom a mass lesion is causing a significant mass effect. Radiographically, lesions are considerable when they are more than 25 cc of volume, and/or cause effacement of the basal cisterns or midline shift > 5mm. More important, clinically significant lesions are those causing progressive neurologic symptoms. The decision to operate is based on a combination of the history of the trauma, significance of the patient’s neurologic deficits, and the significance of findings on cerebral imaging. Prognosis for victims of severe brain injury has improved in the past two decades, with a decreasing mortality. Still, however, one out of two will face permanent neurological deficits. Undoubtedly, after the urgent surgical treatment that represents the crucial action to stop the “run against the clock”, a better understanding of the pathophysiology and the development of new pharmacological strategies is mandatory. Continual improvements in the training of pre-hospital medical personnel, rapid transport of head injury victims to definitive care, and the increase of the Trauma Centers and Neuroscience Intensive Care Units will play a role in the next future.

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Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) which causes demyelination of the nerve fibers. The etiology of this disease is not well understood but it is believed that T helpers play a central role in MS. Numerous findings support the view that Th17 cells play an essential role in pathogenesis of MS and IL-17 secreting T (Th17) cells have a role in inflammation and demyelination of the CNS.In some studies suggest that “There was no significant relationship between the serum levels of these cytokines and Expanded Standard Disability Stated Scale (EDSS) and disease Progression Index (PI)”. New drugs targeting specific points of the Th17 pathways are already being tested in clinical trials and provide basis for the development of biomarkers to monitor disease activity. Some examples of the results of other studies are given below: 1. TGF-β negatively regulates the differentiation of encephalitogenic Th17 cells. 2. miR-27a may probably inhibit negative regulators of Th17 cell differentiation, thus promoting its differentiation while miR-214 has an adverse effect. Also both miR-141 and miR-200a show up-regulation in relapsing phase of MS patients compared to remitting and control groups. 3. IFN-β inhibits the expansion of Th17 cells in active multiple sclerosis. 4. JAK2 as a critical factor that stabilizes IFN-γR2 surface expression in Th17 cells from AMS patients, making them sensitive to IFN-γ. 5. Vitamin A modulate the imbalance of Th17 and Treg cells through multiple molecular pathways. 6. IL-11 as a new Th17-promoting cytokine. 7. CXCR3 signaling in glial cells in negatively regulating Th17 cell expansion during EAE. According to these results focusing on the role of Th17 cells and use of its pathways and their biomarkers of diagnosis and disease activity are new windows to effective therapies.