Seguin[22] adopts with some reservation Brown-Séquard's hypothesis that cerebral lesions produce the symptoms which point out their existence, not by destroying organs of the brain, but by setting up irritations which arrest (inhibit) the functions of other parts of the encephalon. He says that he finds no difficulty in believing that the same symptom may exist as well without as with a brain lesion. “In typical hysteria the functions of parts of the encephalon included in the right hemisphere, or in physiological relation with it, are inhibited by a peripheral irritation starting from a diseased or disordered sexual apparatus or other part; and in case of organic cerebral disease the same inhibitory action is produced. In both kinds of cases we may have loss of rational control over the emotions, loss of voluntary power over one-half of the body, and loss of sensibility in the same part.” [Footnote 22: “On Hysterical Symptoms in Organic Nervous Affections,” _Archives of Electrology and Neurology_, for May, 1875.] Simply as a matter of passing interest, the attempt of Dupuy[23] to frame a pathology of hysteria is worthy of attention. According to him, every {211} local hysterical phenomenon is dependent upon an abnormal state of either lateral half of the upper part of the pons varolii. The centres of the pons, he holds, are perhaps merely passive in the process, only becoming organically implicated when various forms of permanent contractures and paralyses ensue. [Footnote 23: _Medical Record_, New York, 1876, ii. 251.] The pathology of hysteria must be considered with reference to the explanation of the exact condition of the cerebro-spinal axis during the existence of certain special grave phenomena of hysteria, such as hemianæsthesia, hemiplegia, paraplegia, and contractures. What is the probable state of the nerve-centres and tracts during these hysterical manifestations? If, for example, in a case of hysterical hemianæsthesia it is admitted that the brain of the other side of the body is somehow implicated, although temporarily, what is the probable condition of this half of the brain? Is the cerebral change vascular or is it dynamic? If vascular, is the state one of vaso-motor spasm or one of paresis, or are there alternating conditions of spasm and paresis? Are true congestions or anaæmias present? If the condition is dynamic, what is its nature? Is it molecular? and if molecular in what does it consist? Is it possible to say absolutely what the pathological condition is in a disorder in which autopsies are obtained only by accident, and even when obtained the probabilities are that with fleeting life depart the changes that are sought to be determined?