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SummaryPostmenopausal hyperandrogenism can be tumour-or non-tumour-related, with pathology residing either in the ovary or adrenal gland(s). The tempo of investigation is determined by the clinical severity of hyperandrogenism (presence/absence of actual virilisation) and degree of serum testosterone elevation. When clinical or biochemical hyperandrogenism is severe, rapidly developing, or associated with hypercortisolism, screening for adrenocortical or ovarian carcinoma with crosssectional imaging should be prioritised over detailed biochemical evaluation. Adrenal hyperandrogenism is readily characterised, both biochemically and radiologically. By contrast, even a combination of high-resolution imaging with laboratory evaluation, including dynamic endocrine testing, often cannot distinguish between ovarian hyperthecosis (OH) and virilising ovarian tumour (VOT); a definitive diagnosis usually emerging only after histological examination of excised ovaries. VOTs are typically below the resolution-limit of current imaging modalities and exhibit suppression of gonadotropin-dependent androgen secretion with GnRH-analogue therapy. Thus, for well-characterised ovarian hyperandrogenism, laparoscopic bilateral salpingo-oophorectomy may serve both as a diagnostic and therapeutic procedure. Nevertheless, women unable or unwilling to undergo ovarian surgery can be reassured that malignant VOTs are exceedingly rare and that long-term medical therapy with oral antiandrogens or GnRH-analogues is safe and well-tolerated. OH is strongly associated with insulin-resistance, with hyperinsulinaemia acting synergistically with raised gonadotropin levels to stimulate thecal cell hyperplasia and androgen secretion by the postmenopausal ovary, which lacks granulosa cell aromatase activity and thus cannot convert testosterone to 17 beta estradiol. Thus, features of metabolic syndrome may indicate OH, and significant reductions in androgens can thereby potentially be achieved with lifestyle measures and/or insulin-sensitising drugs. K E Y W O R D Shirsutes, management of ovarian hyper thecosis, post-menopausal androgen excess, virilisation testosterone

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Forty-six adult male subjects have been exposed to strong vestibular stimulation produced by controlled cyclic nodding of the head while being rotated in the horizontal plane on a turntable at constant angular velocity. Forearm blood flow was measured with a mercury-in-rubber strain gauge plethysmograph standardized against a conventional plethysmographic technique. There was wide variability among the subjects in the amount of vestibular stimulation needed to cause nausea just short of emesis. Motion sickness, when unequivocal, was accompanied by increased blood flow in the forearm and nearly always by an increase in the circumference of the forearm when venous flow was not occluded. Resistant subjects, in whom motion sickness was either minimal or not apparent, showed either no increase in forearm blood flow or increases that were equivocal. It is concluded that increased muscle blood flow may now be added to antidiuresis, nausea, pallor, and sweating, as a physiological response common to the vasovagal syndrome and to motion sickness caused by vestibular stimulation. A possible explanation of the results and their relation to aviation are discussed.