Biochemical hypotheses of premenstrual tension syndrome

As information has evolved concerning the incidence of cyclical emotional changes preceding theonset of menses, th e premenstrual tension syndrome (PMT) has gained increased attention in boththe lay and professional literature. Although there has been some disagreement as to the exact nature,the time of occurrence, or even the existence of PMT (Koeske, 1981), ther ies considerable consensusthat the PMT syndrome indeed exists (Janowsky al. et 1966, 1967, 1969, 1973). Steine al.r et (1980)and Halbreich & Endicott (1982) have now operationalized psychodiagnostic criteria for PMT whichcan allow separate studies to attain diagnostic consensus more accurately.Several methodological problems in PMT research have limited exploration ho owf premenstrualphysiology might influence mood. A major problem has been the strong reliance on the use ofcorrelative techniques. Man hormones,y electrolytes, , neurotransmitters and somatic parameterschange within the menstrual cycle, and a tradition has existed for assuming the aetiologicalimportance of a favourite correlate which changes premenstrually. Although such correlations area reasonable place to start, it may be naive to believe that temporal correlations necessarily implyaetiology.Another problem in PMT research is the general assumption that circulating ovarian-linkedhormones as such are of fundamental significance in triggering and sustaining premenstrualemotional symptoms. It is equally possible that central neurotransmitters, neuromodulators, andneuroendocrine mechanisms control the onset and intensity of PMT, and that peripheral ovarianand other hormonal changes are merely simultaneous epiphenomena, and/or are driven by the abovecentral influences, but do not actually exert behavioural effects.The use of retrospective reports in PMT research has caused additional problems, withexaggerated incidences being reported, probably due to societal expectations (Koeske 1981, Parlee; ,1973; Sommer, 1978). In contrast, the incidence of PMT symptoms reported usually is relativelylow in prospective PMT studies. Thus, many subjects who report PMT do not show symptoms inactual experiments. Also, since the intensity of PMT may vary from month to month (Green, 1982),such variation may introduce serious inconsistencies and variance problems into research studies.One recent step forward in this area has been the administration of repeated mood and behaviouralratings to prospective subjects over several cycles to screen for and document cyclic emotionalchanges before a given subject is used in a specific PMT study.Also, there is some evidence that the stress of the experimental method itself may influence andconfound studies exploring menstrual cycle-behavioural relationships (Koeske 1981, ; Parlee , 1982). Conversely, a major impediment to understanding and treating PMT has been its remarkablesensitivity to treatment by placebo. Many promising aetiological hypotheses have been based onobserved ameliorative effects in uncontrolled studies of compounds which have specific centralbiochemical effects. Subsequent controlled studies have shown these treatments to be no moreeffective than placebo.There have been several hormonal hypotheses proposed to explain the aetiology of premenstrualtension. The most obvious o thesf e involves an aetiological role for fluctuations in ovarian steroids.The oestrogen withdrawal hypothesis suggests that PMT is due to premenstrual oestrogenwithdrawal. The observation that high levels of oestrogen have antidepressant effects (Klaiber etal. 1979) lends support to this possibility. However, the premenstrual fall in oestrogen is not the