Abstract
To elucidate the mechanisms that mediate secondary amenorrhea following stroke, we studied functional alterations in hypothalamic-pituitary-ovarian axis in 7 patients having amenorrhea for at least 3 months after the onset of stroke, and 6 control patients with normal menstruation after stroke. All patients underwent evaluation of serum lutenizing hormone (LH), follicle stimulating hormone (FSH), thyroid-stimulating hormone (TSH), prolactin and estradiol. LH and FSH in response to LH-releasing hormone (LH-RH) were measured after intravenous administration of LH-RH. There was no difference in the baseline values for LH, FSH, TSH, and prolactin between the two groups. Baseline values of LH and FSH were normal in all except for one amennorhea patient in whom FSH was elevated. All amenorrhea patients demonstrated normal or good LH and FSH responses to LH-RH. In six amenorrhea patients, serum estradiol was decreased, whereas it was normal in all control patients. In 4 amenorrhea patients, menses spontaneously returned with normal estradiol. Accordingly, 6 amenorrhea patients showed normogonadotropic hypogonadism. The results suggest that, in secondary amenorrhea following stroke, the timely release of FSH and LH might be disturbed in the hypothalamus that has a positive feed-back mechanism sensitive to circulating estradiol. Another possible explanation is the influence of the primary hypogonadism due to aging. The majority of the amenorrhea patients are negative for treatment, because they regard menstruation as a burden for a disabled person.
