Finally, we must consider the relation of the climacteric to certain pathological conditions of the ovaries, although as yet nothing positive can be stated on this point. As introductory to this, I would refer to a fact, of which Cohnstein makes mention in his gynecological studies,' although this does not relate to the climacteric itself, but only to the early disappearance of the menstrual flow, or to an apparently premature menopause. The normally-persistent function of the ovaries in such cases of early menopause " may show itself by menstrual molimina, and may produce inflammatory and congestive processes in the ovaries and their vicinity, a point which, in Cohnstein's opinion, has hitherto been too little considered in the etiology of ovarian neoplasms, but is important pathogenetically like chlorosis (Scanzoni,. Breisky), in which in conse quence of too slight menstrual congestion and consequent persistent dehiscence of the follicles, hypersecretion of the latter occurs. The periodical congestion, which is relieved neither by uterine hemorrhage nor by rupture of the follicles, leads through increased blood-pressure to chronic hyperzemia of the ovaries with hemorrhages into the follicles, which result in cyst-formation. Blob and Blebs found blood, bloody fluid and blood-crystals within the small cysts that had developed from follicles. According to Smith, in countries where venesection is prac tised quite frequently (as in Spain at the present day), ovarian tumors are observed more rarely; this may be due to relief of the ovarian conges tion. Amenorrhcea is one of the most common menstrual disturbances observed during the development of ovarian growths (compare cases re ported by Spencer Wells, libberle, and Peaslee). Finally, the unques tionable influence of the menstrual function in the etiology of ovarian tumors is shown by the absolute increase of the affection between the twentieth and fortieth years. On the supposition that, aside from the supposed significance of the last-na,med symptom (amenorrhcea), we must also explain those cases in which this menstrual disturbance is to be re garded as a result of the already existing destruction of the normal ovarian parenchyma, I mentioned briefly Cohnheim's theory of development, since from it, as has been said, we may arrive at some definite conclusion with regard to the apparently premature menopause. If the true menopause has occurred, we must, in spite of the fact that ovarian cysts are known to develop at any age, think above all of the fact that there is now less tendency to these growths. In harmony with what has been stated, is apparently to be regarded the development of certain neoplasms with the cessation of the menstrual congestion. Olshausen lays stress upon the rare occurrence of cystomata after sixty, and regards the period of sexual activity (from twenty to fifty) as the most liable to them. A collection of cases (reported by Peaslee, Wells, Koberle and Clay), 926 in all, seems to be significant in connection with this period; of these 266 occurred between the ages of twenty and thirty, 298 between thirty and forty, 213 between forty anti fifty, and 157 after fifty. It is quite evident from this that the period of sexual activity is especially prone, but that after the menopause the tendency is decidedly less. By further statistics 01shausen shows that married women are more liable at a later period than unmar ried, the former being " more disposed between thirty and fifty, and even after fifty," but, as we asserted above, they show a certain diminished tendency after the menopause, since between thirty and thirty-nine there were 153 cases, between forty anti forty-nine 154, and above fifty 135.
Although we can, therefore, assert quite positively, that the period of the climacteric lessens the tendency to the development of ovarian cysts, it is impossible in the present state of our observations to give a satisfac tory reply to the second question concerning the influence of the meno pulse upon already-existing cystomata. I have searched in vain tho literature to which I have access for some information bearing specially on this point, and the few useful observations do not bring us to a definite conclusion in any direction. Yet, the question is certainly worth con sidering. The observations of a single individual would, of course, not be sufficient, a general interest must be awakened in it, in order to obtain any useful results from abundant clinical material. Investigations in this direction cannot be fruitless. Pregnancy and parturition often cause changes in co-existing tumors. It is known that the menopause often produces a similar result; such an effect must sometimes be observed in cystomata. A marked increase in the size of ovarian tumors is frequently observed during pregnancy (Spiegelberg, Routh, Lever, etc.), and this is certainly often noted in the case of cystomata during the climacteric.' This was explained on the supposition that each time there was an in creased supply of blood in the vessels within the adhesions, but a larger number of observations in this direction is necessary, in order to prove that this growth is sometimes really peculiar to the climacteric or post climacteric period. On the other hand, it is well-known that a retrograde
metamorphosis of certain abdominal tumors is frequently induced by the menopause. Although the " involuted, shrunken cysts " (Rokitansky) hitherto discovered in old women, were thought to have been changed by torsion of the pedicle, it is always possible that this atrophy and par tial calcification even in cystomata, is produced by the menopause alone.
Antonia of the afferent vessels (when vascular adhesions are absent) causes the same result as successive torsions of the pedicle; this latter form of torsion can alone be supposed here, since this results only in their shrink ing (shrivelling of the walls of the tumor, with absorption of the con tents '), while more rapid torsion leads to hemorrhage into the cysts and rupture, and complete strangulation of the arteries to gangrene. Besides, we know that torsion is not necessary in order to produce the effect which we are considering. Spencer Wells also observed atrophy of an ovarian tumor merely through obstruction of the circulation in the pedicle, in consequence of surrounding adhesions, a process that might occur still more readily in consequence of certain nutritive changes during, or after, the climacteric. Olshausen, also, suggests (without special reference to the menopause) the possibility of the secretion of fluid being arrested in consequence of the destruction or fatty degeneration of the epithelial lin ing of the loculi, without any torsion. By reference to a series of clinical cases of hydrops folliculi, it seems to him to be undeniable that this arrest of the secretory function may persist for years " and may in fact, be per manent." It remains to be shown whether this cessation of the secre tion and consequent diminution of cysts, even though it may be slight, does not frequently date from the period of the climacteric. Reasoning from analogy, as I have remarked, I should think that this occurrence is not improbable. There is another accident which deserves our attention, i.e., the rupture of cysts. In a paper on " The Spontaneous Rupture of Ovarian Cysts," ' I mentioned those changes in the cyst-wall which in crease their friakility to such an extent that spontaneous rupture may occur, even when there is a complete absence of external causes. I noted in this connection inflammation of the inner lining (in conseqnence of injury, strangulation of the pedicle, etc.), thrombosis of the vessel-walls (Spencer Wells, Mayne), fatty degeneration, hemorrhage into the cysts, with infiltration of blood into the wall (Spiegelberg), and finally thinning of the wall of the sac by proliferating papillomata (Rokitansky, Spiegel berg). As regards fatty degeneration in particular, I would mention here that Spencer Wells—who, in a series of 300 ovariotomies, operated in :!-1 instances after the cyst had burst, and its contents had escaped into the peritoneal cavity—describes this as the usual etiological factor in such cases.' If it is true that, as before-stated, the tendency to fatty degen eration of the cyst-wall is increased at the time of the menopause, then the disposition to spontaneous rupture of pre-existing cystomata must accordingly be regarded as greater at this period. The occurrence of a more advanced grade of fatty degeneration (according to Spencer Wells the process begins in the epithelial layer, extends to the adjacent strata, and sometimes involves the entire thickness of the wall ') would be suffi cient to explain the accident. It would be interesting to examine this point. The case of spontaneous rupture described in my paper occurred in a patient of quite advanced age. When the first rupture took place, the patient was already seventy-one years old, and had been tapped several times. The case is hardly of value in this connection, but I may by de scribing it call attention to a circumstance which I would not delay to mention.' It frequently happens, as in the case of this patient, that the point of rupture again closes, the sac refills, and laceration and refilling are again repeated. We must always bear this possibility in mind in de ciding upon individual cases. Under certain-conditions (to which I have likewise referred in the article in question), the symptoms following rup ture may be quite insignificant, and may perhaps be overlooked or mis understood in recording the history. Cases of intact (that is, unruptured) cyst can accordingly be considered in a negative sense, after somewhat prolonged and careful observation. In all positive cases we must take into account spontaneous rupture. In noting the greater percentage of such cases in younger patients, we must take into account the greater tendency to the disease during this period, the number of cases that become unavailable for observation by re,ason of operation, and, finally, the smaller number of cases observed in advanced life.