Dpmenorrhcea has been lately claimed to be an important cause of sterility, especially by the English physicians. Especially is the spasmo dic form, when severe, supposed to be efficacious. It is not clear in ex actly what way dysmenorrhcea is supposed to exercise an influence upon ovulation. We must assume that the uterine contractions which cause so much pain during menstruation, must occur during cohabitation, and either the entrance of semen be prevented by spasni of the cervical canal, or, if it has already entered it must again be expressed.
It is true that this theory would at once explain the occurrence of sterility in a large number of cases where no other abnormality is present. Dysmenorrhcea is very common, and the occurrence of this form of it in conjunction with sterility is especially noticeable. But there is no proof of its happening. It would have to be as intense as the spasm oc curring during menstruation, and would have to last much longer than the cohabitation, since, as is well known, the zoosperms retain their activity for a long time in the genital canal. Pain also should accompany it; and this is not the ease. Cohabitation often is painful in sterile women, but it is of a different nature, and can easily be referred to other causes. And if it is stated that it is the expulsion of the blood through the contracted cervix that causes the pain, and that here there is no such work t,o be done, it may be answered that violent expulsive pains often occur long before menstrual blood appears, and may even be felt when there is no question of the expulsion of blood at all. And on the other hand an exact examination will often reveal the fact that dysmenorrlicea is frequently dependent upon other pathological conditions of the genitals, so that it becomes difficult for us to accept this etiological view of this vpasm, and to reject other and more palpable disturbances as being in fluential in causing sterility.
In fact I think that dysmenorrhcea has recently been more frequently dragged into relationship with sterility than the facts warrant. I do not think the connection is by any means so intimate. There can be no doubt that bearing-down pains due to contraction of the uterine muscle may occur during menstruation, and with a fully open cervical canal, and this when it has undergone little if any change, and when the central nervous organs are affected (hysteria). But this does not surprise ns.
Uterine contractions occur when the uterus is empty and the cervix wide open, as well as when the reverse of these conditions prevails. We see it plainly during the puerperium. Why should not pathological conditions without stenosis cause it? And indeed stenosis may be present without causing dysmenorrhoio troubles, as when the effused blood is very fluid and small in amount, and slowly trickles through the stenosed os without the aid of uterine contractions. Nor must we forget that the genital canal is more succulent and distensible during menstruation than during gravidity, and we often find that we can then easily introduce a sound, to which there were in superable obstacles before. And if uterine contractions occur, dysmenor rhcea may still be absent. The diagnosis of dysmenorrlicea depends upon the subjective symptoms of the woman's expressions of pain, and we know that these do not always correspond to the actual trouble. We see great differences in the perception of pain in every-day life—how differently different women behave during childbirth, with about equal amounts of uterine contraction, and the same is the case during the puerperium; one Niroms.n will hardly feel them, while anotlivr will have most violent after pains. I have found the same thing when experimenting with secale cornutum. Is it not probable that the same differences may exist with stenosis of the cervix ? It is not out of place to note here that, of the several forms of dys menorrhcea, only the sporadic can be active in causing sterility. If the dysmenorrhcea is not marked, it will be impossible, especially in nulliparte, who have not experienced labor pains, and cannot make comparisons, to decide what form of dysmenorrhcea is present. We must not, therefore, lay too great a stress on it.
Even if we accept the proposition that the spasmodic form of dys menorrhcea is less a disease of the genitals than part of a general malady, it is not necessarily therefore a cause of sterility. Frequent uterine spasm in sterile women is not in itself alone sufficient. Dysmenorrlicea of this kind, like absence of sexual passion, points to a deficiency somewhere in the complicated mechanism of reproduction, it can only be regarded as the real cause of the infecundIty in the small proportion of cases where no other genital change can be demonstrated.