A work by Ericksen in 1866 on "Railway Injuries to the Nervous System" and Page's book in 1882 on "Injuries of the Spine" pointed the way to an extensive study of the so-called traumatic neuroses. This characterization of the functional disturbances of the nervous system following injuries was apparently the result of a monograph by Oppenheim on that subject in 1889. They had previously been considered as purely organic in origin. Traumatic hysteria was discussed very fully at various times by Charcot, whose work is so well known as to require no comment. In 1892 Friedmann described a vasomotor complex due to concussion. This is accompanied by such symptoms as headache, dizziness, loss of capacity for both physical and mental work with an increased fatigability, irritability, memory defects, and changes in personality, such as sensitiveness and eccentricity with a marked intolerance to alcohol. This condition appears some time after the symptoms of concussion and shock have subsided and may last for some months. Friedmann looked upon this as purely a vasomotor disturbance. It is probably an important factor, in some cases at least, of "shell shock". Traumatic epilepsy may result from foci of softening or other local areas of injury to the brain. Neurasthenia, hysteria and other neuroses are now generally looked upon as being essentially functional and not organic in origin, although they may follow a trauma. The simulation of these conditions has led to a great deal of discussion, notwithstanding the fact that Oppenheim found them in only about four per cent of his cases. Köppen (1897) made a very elaborate study of the postmortem lesions in the "traumatic neuroses". He found that violence to the skull often resulted in small injuries at the base of the frontal area, at the apices of the parietal lobes or in the occipital region. The pathological changes involved represented localized encephalitis with hemorrhagic infiltration. Foci of softening were often found in the cerebral cortex. He noted coma and convulsions with only minute areas of destruction of the basal cortex at autopsy. This would indicate a severe irritation, probably due to circulatory disturbances. The resulting symptoms he thought were very likely to be confused with general paresis. In cases of extreme dementia following traumatism he often found no pathological lesion other than a cicatrix in the cerebral cortex.