Explosives used in World War I caused many blast injuries; the large number of TBIs that resulted allowed researchers to learn about localization of brain functions. Blast-related injuries are now common problems in returning veterans from Iraq & Afghanistan; research shows that the symptoms of such TBIs are largely the same as those of TBIs involving a physical blow to the head. In the 1970s, awareness of TBI as a public health problem grew, and a great deal of progress has been made since then in brain trauma research, such as the discovery of primary and secondary brain injury. The 1990s saw the development and dissemination of standardized guidelines for treatment of TBI, with protocols for a range of issues such as drugs and management of intracranial pressure. Research since the early 1990s has improved TBI survival; that decade was known as the "Decade of the Brain" for advances made in brain research. Research directions Diagnosis Quantitative EEG and EEG, which has no specific patterns in TBI is used in research settings to differentiate between mild TBI and no TBI. Medications No medication is approved to halt the progression of the initial injury to secondary injury. The variety of pathological events presents opportunities to find treatments that interfere with the damage processes. Neuroprotection methods to decrease secondary injury, have been the subject of interest follows TBI. However, trials to test agents that could halt these cellular mechanisms have met largely with failure. For example, interest existed in cooling the injured brain; however, a 2020 Cochrane review did not find enough evidence to see if it was useful or not. Maintaining a normal temperature in the immediate period after a TBI appeared useful. One review found a lower than normal temperature was useful in adults but not children. While two other reviews found it did not appear to be useful. Further research is necessary to determine if the vasoconstrictor indomethacin (indometacin) can be used to treat increased pressure in the skull following a TBI. In addition, drugs such as NMDA receptor antagonists to halt neurochemical cascades such as excitotoxicity showed promise in animal trials but failed in clinical trials. These failures could be due to factors including faults in the trials' design or in the insufficiency of a single agent to prevent the array of injury processes involved in secondary injury. Other topics of research have included investigations into mannitol, dexamethasone,