This chapter deals with the classification, pathophysiology, prediction, prevention, and treatment of ovarian hyperstimulation syndrome (OHSS). OHSS is characterized by bilateral cystic ovarian enlargement and third-space fluid shift resulting in ascites and pleural effusion. It may be moderate or severe in severity, early or late in onset, spontaneous or iatrogenic in etiology. Prediction of OHSS is the cornerstone of prevention. It is based on identifying the characteristics of the patients who would be high responders as well as the use of ultrasonography and estradiol assessment. The pathophysiology of OHSS suggests the involvement of an inflammatory mechanism during the development of the fluid leakage associated with OHSS. Therefore, investigators hypothesized that glucocorticoids could possibly prevent OHSS in patients at high risk. Laparoscopic ovarian drilling has been used successfully for prevention of OHSS in patients with polycystic ovaries. The medical treatment of OHSS consists of correction of circulatory volume and electrolyte imbalance.

Clomiphene revolutionized the management of infertility in 1967 when it was approved for treatment of anovulation due to polycystic ovaries (PCO). The pharmacokinetics and pharmacodynamics of clomiphene explain its characteristic actions. After ovulation induction with clomiphene, serum progesterone and estradiol serum levels are increased during the luteal phase of the cycle in a direct dose-response relationship. Ultrasound of the ovaries should always be performed before initiating clomiphene treatment for the first time to rule out preexisting ovarian neoplasm, endometriomas, and persistent corpus luteum cysts to evaluate the number and size of antral follicles. Progesterone is used to confirm ovulation to determine if the dose of clomiphene is sufficient. Pregnancy rates may be increased in clomiphene cycles by increasing the number of follicles that develop, by improving endometrial conditions and cervical mucus, and by intrauterine insemination (IUI) when numbers of sperm on a postcoital test are low or absent.

The primary aim of an in vitro fertilisation (IVF) treatment cycle is the creation of two 'good quality' pre-embryos for transfer, with a secondary aim of additional embryos for cryopreservation. The use of gonadotrophin releasing hormone (GnRH) agonists with gonadotrophins has resulted in greater ease of planning the superovulation stimulation. The move towards pituitary desensitization with a GnRH agonist has become almost universal in assisted conception clinics. The GnRH agonist is commenced in either the mid-luteal or follicular phase of the cycle and continued through to the day of human chorionic gonadotrophins (HCG). Modifications of the GnRH decapeptide have enabled the development of competitive inhibitors of gonadotrophin secretion. Clinical evidence followed in therapeutic trials for IVF suggests that recombinant-follicle stimulating hormone (FSH) yields more oocytes and embryos. Particular consideration needs to be given to superovulation when polycystic ovaries are present.

This chapter discusses some of the reproductive disturbances in women with epilepsy and points out signs and symptoms that women should report to their health-care providers. Reproductive health disturbances described in women with epilepsy include menstrual abnormalities such as amenorrhea (not menstruating), oligomenorrhea (menstrual cycle length greater than 35 days), and metrorrhagia (irregular menstrual cycle with excessive menstrual flow). Menstrual cycle abnormalities, polycystic ovaries, and disruption in pituitary and ovarian hormones may cause infertility. Women with epilepsy appear to be at risk for anovulatory cycles, polycystic ovaries, and disturbance in the hypothalamic, pituitary axis, the system that regulates the menstrual cycle and ovarian production of female sex steroid hormones. Electrical epileptic discharges in the brain may alter pituitary hormones and abnormally stimulate the ovaries. Changes in ovarian hormones caused by antiepileptic drug interactions could also cause anovulatory cycles. Finally, the antiepileptic drug valproate may specifically increase the risk.