INHIBITION OF OVULATION IN THE HUMAN 



John Rock 



Free Hospital for Women, Massachusetts 

 I. AUTOGENOUS INHIBITION OF OVULATION 



Before discussing methods of suppressing ovulation in the human, it might 

 be well to review briefly various aspects of autogenous failure of ovulation. 

 We find this process inhibited not only in many different clinical conditions, 

 but also in several physiological states (1,2). 



A. In Physiological States 



There is physiological anovulation before puberty, as also after the cUmac- 

 terium. Moreover, oligo-ovulation is a comparatively frequent gynecological 

 diagnosis among adults (1,3). It denotes habitual failure of ovum release each 

 year, for more than four weeks, or even for a few months, yet without 

 discernible pathology. Of course in such cases we infer dysfunction of the 

 "feed-back" or "push-pull" process, either as a weak "push" from gonadal 

 hormones, or resistance to "push" in the hypothalaraic-pituitary partnership. 

 Furthermore, even in normally cyclic women, anovulatory cycles are occa- 

 sionally interspersed among the usual ovulatory ones (1). 



During the normal cycle, we have, of course, the postovulatory relative 

 progestinism, the latter prevailing also in pregnancy with a hyperestrogeno- 

 progestinism; and in lactation, we relate the usual anovulation to a similar 

 prolactinism. 



Anovulation may also occur as an accompaniment of a stress reaction 

 disturbing hypothalamic function. The follicular inactivity of anorexia 

 nervosa may be similarly indicted with probable assistance from dietary 

 deficiency (4). 



B. In Pathological Conditions 



Leaving aside intrinsic ovarian insufficiency (hypoplasia ovarii) as an 

 obvious cause of anovulation, other clinical conditions accompanied by 

 failure of ovulation may be considered under two headings : those involving 

 (1) extrapituitary pathology and (2) intrapituitary pathology. 



1. Extrapituitary pathology. Extrapituitary pathology may cause sex 

 hormone imbalance toward what one might rather vaguely term androgenicity 

 — as with an arrhenoblastoma, or a hylar-cell tumor, or with hyperadrenalism 

 — and thus hinder ovulation. In like manner, the ovulatory mechanism may 



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