THE pREMENSTRUAL SyNDRoME G09

Andersch et al (1979) looked ar gonadotrophin levels. He showed no difference in follicle-stimulating hormone (FSH) or luteinising hormone (LH) in the two groups ar an)'stage of the cycle. Biicksrrbm er al (1976), however, shou'ed slightly elevated levels of FSH in the follicular phase of the cycle which probably parallels his oestrogen findings, O'Brien (1979) showed no difference between FSH or LH measurements between the two groups, nor *'as there anv statistical correlation between the premenstrual mood score and gonadotrophin levels.

Anti-diuretic hormone
Although anri-diureric hormone (ADH) has been measured in PMS, there are no conclusive srudies- A preliminaryreport has shor*-n c1'clical ADH r-ariadon but rhese finding_= have not been confirmed (Chan'at & Holececk, i966)Testosterone
Testosterone has been measured dail1'. Epstein et al
r

Prolactin

give rise to PMS. First, prolactin causes retention of sodium, u'ater and potassium. Secondly, it has a direct effecr on the breasts and may be responsible foi at least the breast sl,mptoms. Thirdly, it is well-established that prolacdn is secreted in response to stress, and lastly it has err i.nrer-relationship with dopamine metabolism. Horrobin (197-l) suggested that the hormone may play a crucial aetiological role, though he did not measure the hormone in either the menstrual cycle or in women complaining of Pl{S. Many other workers have assessed the significance of prolacdn levels during the menstrual cycle. Halbreich and co-workers showed higher levels of prolactin throughout the course of the menstrual cycle in the symp_ tomaric group; there was also a rise in the prolactin levels during the premenstrual phase, but this was found in s!-mptomatic and control subiects. The absolute rise was approximately the same in both groups (Halbreich et al, 1976). Two other studies have shown elevated prolactin Ievels in the premenstrual phase (Friesen et al, 197); Veke_ mans er al, 1977). The remaining studies have nor shown such a clearcut picture. In symptomatic subjects, Andersch and colleagues showed lower levels of prolactin in the follicular phase, compared with controls. The luteal phase no difference between control and symptomatic patients (McNeilly & Chard, 1974; Harrison & Letchworrt, i976; Andersen et at, L977; O'Brien & Symonds, 19g2). Because prolactin is released in a pulsatile manner, there are often dramatic fluctuations even throughout the course of a day. The most convincing studies are those in which at leasr daily samples are taken. In a study by Epstein et al (1975) daily samples were taken and although he confirmed the considerable day-to-day fluctuations, there were no consistent alterations during the course of the menstrual cycle itself. No mention was made in this study of the occurrence of PMS symproms, but a study by Backstrom & Aakvaag (1981) reported daily values and showed no difference between the symptomatic and asymptomatic
sublects. levels, however, were no different from those of the control group (Andersch et al, 1979). The majority of studies show

There are several reasons why prolactin may be thought to

showed raised levels of aesrosrerone around ihe tine oi ovulation, but no alteradon premtrstruallv. Backstrora & Aakvaag (1981) shorved no difference ar anv suge of *. menstrual cycle, nor rras there anv difference benr-een lhe symptomatic and control groups.

19ij

Adrenal hormones

In addition to the piruitarl'and

ovarian hormones- o-.ae: endocrine changes have been considered i:: rhe aeioirSl-

of the syndrome. Adrenal hormoqes.

carechol:'-i:.-:_*-

pancreatic hormones and prosreglaadins hat'e all bee ::e subject of hypotheses if nor acruali1- s;uciied. Th=e evirtually no good investigative srudies ol adrenal fuaciions in this syndrome with the exception cri aldosrerole a=i

testosterone which hate previousil- been discu:sc.jAdrenal sex steroids could theorericailr. accounr ioi ine persistence of the svndrome after oophorectoml' aad after the menopause a suggestion put fors-ard bv Dalton (1964). The amount of adrenal sex -sreroid produced i.s much less than that producoJ b1' rhe or-an- ciuring reprG. ductive life and a cyclical panera has not,rei be--n shcrqa. There is as yet no research to con-fir= tiese as_su-tir.dons. Cortisol is another 'stress' ho:moce a:i ir also ha_s 5s3. mineralo-corticoid activir-v. Cyclical rarieiion doe ccur: however this is onll'slight and is characreriseci b1,a siighr increase in the premensuual phase iSri-irergel<i er al. 19;i . Differences betu-een s1'mptomatic a::d non-sr.mprorlarj. women have not been demonstrated. i Catecholamines from adrenal or oiher svmpathetic ganglia, mav weii cause or contribuie to the svndrome. Catecholamines exerr their effecr rhroughour the bodr. particularly on the cardiovascular system and on the iuxraglomerular appararus, rherefore indirectlv affecting sodium handling. However, the role of the sl,mpathetic nervous
s-vstem remains unknos-n

P-\IS.

Pancreatic hormones There appear ro be aherations in glucose tolerance in the mensrrual c1,cle and thus the roles of glucagon, insulin and carbohydrate hare been considered. Flattening of the glucose tolerance test occurs premensrruaily (Billig & Spaulding, 1974; Morton er al, 1950). This phase of the cycle is somerimes associated with hunger, sweating, ner-