forms of insanity to occur at the puberal epoch. Only superficial observation sufficed to maintain this contention, and hence, the causative relation between puberty and hebephrenia became a mooted question. Notwithstanding this, the appearance of certain stuporous and confused states at the time of puberty was so constant that Kahlbaum refused to discard the early evolutional stage as an etiological element, and contented himself with recognizing two forms of the disease, namely: "The classic form terminating in dementia, known as hebephrenia vera; and another less severe and curable form to be called heboidophrenia." From our conception of hebephrenia, or the simple form of dementia precox, in its present clinical status, we would not be justified in maintaining the views of Kahlbaum; especially in so far as they relate to the cause and the time of the occurrence of the disease. It must be conceded, however, that the involutional period of life is accompanied by remarkable mental and physical changes. These are especially pronounced in the female. The emotions begin to develop; new sensations are ushered into our natures; the reproductive sense becomes magnified, and with it we pass into a stage of imaginary, sentimental, emotional and physiological activity. This development period in life, gentlemen, is nature's great test of the survival of the fittest; those natures, either through a weakened inheritance or acquired instability, that can not withstand this terrible evolutional storm must fall. Is it so remarkable, then, that with dementia precox there is almost invariably linked an hereditary predisposition? The reasoning is as obvious as the sparkling water that flows from an undefiled fount; it is simply the picture of cause and effect. I maintain therefore, that puberty, per se, does not possess an etiological equivalent in the disease before us, but on the contrary is the prin

cipal factor in bringing into activity, with its symptom complex, a latent neuropathic element which is either acquired or congenital. In further corroboration of a primary degenerative factor in the development of dementia precox, I wish to cite the marked frequency of tuberculosis in this class of patients as highly significant of this fact. It is not generally conceded that tuberculosis, as a disease, is transmitted from one generation to another, but there is a unanimous acceptance of an inherited predisposing weakness that favors its development. Taking the history of tuberculosis in these cases, dating back from generation to generation, taking the history of insanity, moral depravity, and other manifestations of inherited stigmata, both direct and remote, we can come to a reasonable conclusion that precocious dementia is a primary degenerative psychosis, with its most potent causative factor resting latent in a quiescent inherited instability. We now wish to consider acquired predispositions. Cases are on record in which children born under the most favorable circumstances, with clear family histories and bright minds, may become victims of serious illness and accident; upon these are visited weakened physical states, with cerebral inferiority, terminating sometimes in dementia precox. Furthermore, certain infectious diseases, such as typhoid fever (2), rubeola, and scarlatina occurring during adolescence may be followed by what appears to be a primary dementia. Among the occasional causes. might be mentioned mental strain. This is especially frequent in children coming into the active life of cities from the country, where the tax upon the nervous system is more than they can bear. Onanism is also considered to be an occasional cause. This practice is supposed to bring about a kind of neuropsychic exhaustion, but it is too common to merit much consideration as a causative factor.

PATHOGENESIS.

There is very little information to be obtained upon the morbid anatomy of dementia precox, and, especially the organic changes in the brain. The specific pathogenesis as suggested by Dr. J. Christian (2) of the National Asylum, Charenton, to me is only plausible in so far as it recognizes an underlying defective state.

His claims of a constant and identical alteration in the brain cells is intangible unless he accepts as an anatomical basis for such changes a pre-existing neuropathic tendency. We could just as reasonably contend that in the first stages of acute mania or melancholia there is a specific cytolotic change in the brain. I am willing to admit that we do get cellular changes in the brain secondary to any of the psychoses, but the fact has not yet been established that with each and every alienation we get primarily a characteristic change in the brain structure. The investigation that is now being made by Dr. Wm. Rush Dunton, of Shepard and Enoch Pratt Hospital, is highly valuable and quite suggestive, but the pathologic findings noted by him come from those causes that have progressed slowly into dementia, and have died well advanced in years. This links with his observations a secondary consideration which of necessity must undervalue his findings. I have been unable to find any report of a case dying early in the disease that went to autopsy with microscopic findings noted. Dr. Dunton (3) observed certain organic changes in the cells from different regions of the cortex, such as chromatolysis, swelling and displacement of the nuclei with degeneration and atrophy, but as stated above, these were in cases that had been existing for years. His investigation as yet has been quite limited, and these changes are in no sense to be considered conclu

sive. It is highly probable that these changes in the cortex are not peculiar to dementia precox, but are only such pathological states that might arise in the course of any of the chronic progressive psychoses. The gross pathological findings in Dr. Dunton's cases are very interesting, but in no respect peculiar. As mentioned before, tuberculosis, and especially pulmonary, is quite frequent, and is probably due to the susceptible condition of these patients in their natural weakened state.

CLINICAL COURSE-SYMPTOMATOLOGY.

We now come to look at dementia precox in its hospital aspect. The disease, if considered in a collective sense, possesses a clinical course and chain of symptoms that is quite distinctive and uniform. If we observe the affection in an abstract sense many and varied are the symptoms that come before us. The initial symptoms of the disease, in its several distinctive types, are always confusing and complex. Much embarrassment was produced among the earliest observers, and even among alienists of to-day, by this varied symptomatology. Hence, it is highly probable that so many of the early writers describe this same affection under many different classifications. Dementia primary, adolescent insanity, pubescent insanity, juvenile insanity, katatonia and hebephrenia all representing a nomenclature that may be summed up in one meaning, namely, dementia precox. We are thankful to say that out of this chaos of unscientific terminology is rising a new hope and definite course for the great science of psychiatry. To Emil Kreplein we should bow our heads for his ingenuity in bringing into one category this class of mental alienation. To him should be given the credit for that inspiration that is transforming and revolutionizing psychiatry throughout the world. The time

has come when the study of mental diseases has come to be a science. The honest thinkers in this field of great abstruseness are no longer content to regard every horseface apprehensive woman as acute or chronic melancholia; they are no longer content to look upon every case of psychomotor excitement, with alternate stupor and delirium extending over a period of from several months to many years, as acute or chronic mania; no longer content to look upon the lucid intervals of maniac-depressive insanity and dementia precox as cures, and diagnose these cases from year to year as they return to the asylums as recurrent mania. Kreplein's classification is still open to criticism, but through it we are offered a satisfactory working basis. His (4) observations led him to conclude that a large majority of mental diseases fall under one of two groups—the maniac-depressive group, ending in a certain per cent. of recoveries; and those cases terminating in some form of dementia, representing one of the types of dementia precox. It is quite probable that a large per cent. of the secondary and terminal dements in our hospitals to-day are but cases of dementia precox in its more advanced stage. In taking up the symptoms of dementia precox it is best to be more general than specific. Hairsplitting diagnoses made upon special symptoms, without

nsidering the history of the disease as a whole, is ilable to produce as much confusion as an abstract passage from the Bice. The physical characteristics of the disease present a more striking and interesting picture than does the mental symptoms.

The motor phenomena exhibited through certain grimaces, stereotypy, impulsive movements, eccentricities of manner and verbigerations can not be forgotten. The systematic distortion of the face; the peculiar puckering of the lips-snout-lip--and the pacing of the floor, and