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10.1192/apt.7.6.469Access the most recent version at DOI:2001, 7:469-477.APT

Moira ConnollymanagementPremenstrual syndrome: an update on definitions, diagnosis and

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APT (2001), vol . 7, p. 469Managing premenstrual syndromeAdvances in Psychiatric Treatment (2001), vol. 7, pp. 469477

Premenstrual syndrome:an update on definitions, diagnosis

and managementMoira Connolly

the cyclic occurrence of symptoms that are ofsufficient severity to interfere with some aspects oflife and which appear with consistent and predictable

relationships to menses (Endicott et al, 1981)

show at least a 30% increase from the intensity ofsymptoms measured in the follicular phase, that is,in days 510 of the menstrual cycle, compared withthose measured in the premenstrual phase (on the6 days before menstruation). In addition, pre-menstrual changes must be prospectively docu-mented for at least two consecutive menstrual cycles.Some research authorities stipulate a 50% worseningof symptoms by the premenstrual phase (Steiner &Wilkins, 1996). The 30% change in ratings ofsymptoms has been shown to be too liberal and apoor discriminator when comparing women withself-reported severe PMS, women using contracep-tives whose natural cyclicity has been suppressedand women with normal cyclicity who report nopremenstrual symptoms (Gallant et al, 1992). Gallantet alemphasise that what may be more clinicallyrelevant is womens perceptions of variations insocial and occupational functioning and the wayin which having PMS is meaningful in a womanslife. The authors concern is that ever more stringentcriteria might result in the exclusion from studies ortreatment of significantly troubled individuals.

The diagnosis of PMS was operationalised withthe introduction of the term late luteal phase dys-

phoric disorder (LLPDD) into DSMIIIR (APA,1987) under the section headed Proposed diagnos-tic categories needing further study. Subsequently,a work group on LLPDD reported to the DSMIVTask Force, culminating in its inclusion in DSMIV

Most articles on the management of the premenstrualsyndrome (PMS) begin by noting that the term pre-menstrual tension was first coined by R. T. Frank

in 1931 and pre-menstrual syndrome by Greene& Dalton in 1953. However, in 1847, Dr Ernst F. vonFeuchtersleben wrote:

The menses in sensitive women is almost alwaysattended by mental uneasiness, irritability andsadness. (quoted by Rubinow & Schmidt, 1995)

Difficulties remain in defining the condition,identifying its aetiology and in understanding whysome women are sensitive to developing thiscyclical condition, which is linked to the menstrualcycle and characterised by mainly affective symp-toms such as irritability and dysphoria.

In this paper, we aim to summarise what we cur-

rently understand about PMS and the more narrowand operationally defined premenstrual dysphoricdisorder (PMDD; American Psychiatric Association(APA), 1994), which probably equates with the mostsevere end of the PMS spectrum. In addition, theassessment and management of patients will bedescribed with reference to both the physical andpsychological components of severe PMS.

Definition and diagnosisof premenstrual syndrome

Premenstrual syndrome(s) has (have) been various-ly defined. The National Institute of Mental Healthdefinition states that premenstrual changes or:

Moira Connolly is a consultant general psychiatrist at Gartnavel Royal Hospital (Glasgow G12 0XH) with interests in psychiatricrehabilitation and cognitivebehavioural therapy (CBT). She is a supervisor on the South of Scotland CBT course and honorarysenior lecturer in the Department of Psychological Medicine, University of Glasgow.

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APT (2001), vol . 7, p. 470 Connolly

(APA, 1994) as premenstrual dysphoric disorder in the section Mood disorders not otherwisespecified, with its clinical criteria laid out inAppendix B For further study(see Box 1).

It is widely agreed that the dysphoric symptomsof PMS are among the most troublesome. This isreflected in the DSMIV diagnostic criteria, with 10

of 11 symptoms being emotional or behavioural innature, while the 11th covers multiple physicalsymptoms. In ICD10 (World Health Organisation(WHO), 1992), it is listed as a physical disorder N943, premenstrual tension syndrome, underPain and other conditions associated with femalegenital organs and the menstrual cycle. There is norequirement for a minimum number of symptoms orfor functional impairment to make the ICD10diagnosis of PMS. For the purposes of this article,the abbreviation PMS will be used, as few studies

have exclusively dealt with patient populationswhose diagnosis conforms to the narrower DSMIV definition.

DSMIV allows the diagnosis of premenstrualdysphoric disorder to be made alongside otherdisorders, but offers no guidance on differentiatingbetween the two. Two disorders may coexist or

indeed be intricately related to one another. Forexample, persistent symptoms across the earlyfollicular phase may represent a reaction to severePMS. Alternatively, PMS may prove the final stressorleading to an inability to cope for someone with anunderlying affective disorder. This may explain theincrease in psychiatric hospital admission rates forwomen in weeks 1 and 4 of their menstrual cycle,reported by ODwyer et al(1997).

The association between dysphoric PMS andother physical and psychiatric disorders in womens

Box 1 Research criteria for premenstrual dysphoric disorder (from DSMIV, with kind permissionfrom the American Psychiatric Association)

A. In most menstrual cycles during the past year, five (or more) of the following symptoms werepresent for most of the time during the last week of the luteal phase, began to remit within a fewdays after the onset of the follicular phase, and were absent in the week post-menses, with at leastone of the symptoms being either (1), (2), (3), or (4):

1. markedly depressed mood, feelings of hopelessness, or self-depreciating thoughts2. marked anxiety, tension, feeling of being keyed up or on edge3. marked affective lability (e.g. feeling suddenly sad or tearful or increased sensitivity to

rejection)4. persistent and marked anger or irritability or increased interpersonal conflicts5. subjective sense of difficulty in concentrating

6. lethargy, easy fatigability, or marked lack of energy7. marked change in appetite, overeating, or specific food cravings8. hypersomnia or insomnia9. a subjective sense of being overwhelmed or out of control10. other physical symptoms, such as breast tenderness or swelling, headaches, joint or muscle

pain, a sensation of bloating, weight gain.

Note: In menstruating females, the luteal phase corresponds to the period between ovulation and theonset of menses, and the follicular phase begins with menses. In non-menstruating females (e.g.those who have had a hysterectomy), the timing of luteal and follicular phase may requiremeasurement of circulating reproductive hormones.

B. The disturbance markedly interferes with work or school or with usual social activities andrelationships with others (e.g. avoidance of social activities, decreased productivity and efficiency

at work or school).

C. The disturbance is not merely an exacerbation of the symptoms of another disorder, such as majordepressive disorder, panic disorder, dysthymic disorder, or a personality disorder (although it maybe superimposed on any of these disorders).

D.Criteria A, B and C must be confirmed by prospective daily ratings during at least two consecutivesymptomatic cycles. (The diagnosis may be made provisionally prior to this confirmation.)

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APT (2001), vol . 7, p. 471Managing premenstrual syndrome

when assessing treatment efficacy in a researchsetting. Shortened versions of these are in existence,for example, the Premenstrual Tension Scale (PMTS)derived from the MDQ, and although less fullyevaluated are probably more acceptable to womenprepared to keep prospective diaries. Other comm-only used rating scales include the Daily Record of

Severity of Problems (incorporating DSMIV PMDDsymptoms) and the Prospective Record of the Impactand Severity of Menstruation (PRISM).

Single sheets in calendar, visual analogue or diaryforms, such as the Calendar of PremenstrualExperiences (COPE), are probably most acceptablein clinical practice. Other diagnostic instrumentssuch as commonly used anxiety and depressionquestionnaires may also play a valid role in helpingclinicians to assess symptom severity and identifycomorbid disorders. For full details and referencesto specific scales, see Budeiri et al (1994) andPearlstein & Stone (1998).

Ideally, prospective daily ratings should demon-

strate a premenstrual increase in symptom severitymeasurable as a percentage change, or in relation toan absolute severity requirement. This is achievedby dividing the cycle into phases and comparingthe symptom scores for each phase. Despite limitedagreement in the research literature as to phaseidentification, comparing average scores in thetroublesome days premenstrually with thoseobtained in the days after menstruation would havemost relevance clinically. Confirming subjectivelyreported functional impairment can be problematic,but the use of social adjustment scales and qualityof life measures holds promise (see Box 2 for a

summary of the assessment process).Steiner & Wilkins (1996) propose using both ICD10 and DSMIV when assessing individual patients.Doing so helps to delineate the severity of symptoms,takes into account other possible comorbid con-ditions and helps guide appropriate treatment. They

life cycles has been comprehensively reviewed byHalbreight (1996). These include other hormonallyrelated disorders such as post-partum depression,dysphoric adverse effects with some contraceptivemedication and dysphoric mood during sequentialhormonal replacement therapy, in addition to majordepressive disorders and seasonal affective disorder.

Widening the net, a high lifetime comorbidity ofdysphoric PMS has also been reported withdysthymic disorder, panic disorder, various anxietydisorders, alcohol and drug misuse, acute or chronicdepression, various personality disorders andphysical disorders such as hypertension, systemiclupus erythematosis and endometriosis.

The differential diagnosis of women presentingwith premenstrual symptoms includes a broad rangeof psychiatric and physical disorders that can mimic,exacerbate, or coincide with PMS. It is imperativethat history-taking and examination are detailed(Pearlstein & Stone, 1998).

Steps in assessmentand diagnosis

The literature on PMS is fraught with variations indiagnostic procedures, assessment schedules andoutcome measures, making it difficult to makemeaningful assessments of the efficacy of specifictreatments. For example, Budeiri et al(1994) havereviewed the entry criteria and scales used formeasuring treatment outcomes in 350 clinical trials

of 115 drug treatments for PMS and recorded 65different assessment scales. Useful recent reviewsof clinically relevant diagnostic procedures andprospective rating scales are those of Steiner &Wilkins (1996) and Pearlstein & Stone (1998).

Symptoms must be rated prospectively in order toavoid the inaccuracies inherent in retrospectiverating. These include incorrect symptom timing andamplification of symptom severity. Symptomsrecorded over several cycles will illustrate anyintercycle variability in the nature and severity ofsymptoms. Psychological stressors in the lives ofindividuals will vary irrespective of the cycle graphically illustrated in one study when anunpredicted symptom peak occurred with severalwomen and the actual calendar date (as opposed tomenstrual date) was noted to be 24 December(Sampson, 1988)!

Budeiri et al(1994) advocate using existing scalessuch as the Menstrual Distress Questionnaire (MDQ47 items), the Premenstrual Experience Assess-ment (PEA 88 items) and the PremenstrualAssessment Form (PAF 95 items), particularly

Box 2 Summary of steps in the assessmentprocess

Full history, relevant physical examinationand investigation

Exclude the presence of any other physicalor psychiatric illness

Prospective rating of symptoms using agreedquestionnaires or calendar sheets for atleast two cycles

Check for symptom patterns and particularlythe presence of an increase in symptomsin the premenstrual phase

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recommend the use of the term premenstrualmagnification, PMM, where other conditions suchas depression are exacerbated in the premenstrualphase. Box 3 outlines the diagnostic categories thatthey propose for use in clinical practice.

Demographics and aetiology

Most women can detect the physiological changesassociated with the pre-menstruum, but onlybetween 3% and 8% experience severe symptoms inkeeping with a diagnosis of PMDD (Steiner &Wilkins, 1996), with the vulnerable years being thelate 20s and early 30s (Freeman, 1995). Retrospectivereporting and postal surveys account for some ofthe variations in prevalence studies.

Gonadal st eroi ds

The link to the menstrual cycle strongly implicatesgonadal sex steroids in the genesis of symptoms,however, endocrinological studies have not revealedconvincing abnormalities to date. Basal anddynamic gonadal hormone studies have failed toshow any luteal phase-specific biological ab-normalities in PMS (Roca et al, 1996). A frequentlycited study by Schmidt et al (1991) used a pro-gesterone antagonist to manipulate PMS patients

hormones such that some were fooled as to wherethey were in their cycle by artificially inducingmenstruation early. They then experienced PMSsymptoms in what was hormonally changed to theearly follicular phase, that is, immediately post-menstruation. This study suggests that hormonalevents before the late luteal phase could set in motion

interactions resulting in symptoms premenstruallyand, from the psychological perspective, it alsosuggests that premenstrual symptoms cannot beexplained solely by expectation bias.

The rol e of serot oni n

Rapkin (1992) has summarised the role of serotoninin human and animal behaviour and the relevanceof this research for the premenstrual syndrome. Shecites studies on vervet monkeys, which demon-strated that the higher serotonin level seen indominant males is not a fixed trait marker but is

influenced by the social interactions the animalexperiences. Subsequent alterations in whole bloodserotonin levels become evident 710 days afterchanges to the animals social experience. Rapkinsuggests that women who do not have PMS may beoffsetting the physiological changes triggered byovulation and the ensuing tendency towardsbehavioural isolation that occur post-ovulation, bydirectly engaging in rewarding social interactionswith other people. It is these rewarding interactions

Box 3 Useful clinical diagnostic categories (Steiner & Wilkins, 1996)

Premenstrual syndrome (PMS)

Meet ICD10 criteria for PMS but not DSMIV PMDD. Criteria include mild psychological symptoms,bloating, weight gain, breast tenderness, swelling, aches and pains, poor concentration, sleepdisturbance and appetite change. Only one of these symptoms is required but must be restrictedto the luteal phase of the cycle, ceasing around menstruation.

Premenstr ual dysphoric disorder (PMDD)

Meet DSMIV criteria for PMDD (see Box 1). They have no other concurrent psychiatric disorder butmay have a past history of psychiatric illness. Symptoms have occurred with most cycles in thepast year and have interfered with social or occupational roles. Premenstrual worsening of symptomsis clearly evident and a 50% worsening by the luteal phase warrants pharmacological treatment.

Premenstr ual magnifi cati on (PMM )

Women who receive this diagnosis may meet criteria for PMS or PMDD but also have a current majorpsychiatric disorder or an unstable medical condition.

Ot her psychiatri c diagnosis only

Symptoms, although significant, show no relationship to the menstrual cycle.

No di agnosis

Symptoms, although disruptive, are not severe enough to warrant a diagnosis.

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that may lead to physiological changes resulting inincreased serotonin levels and the maintenance of astable mood. There may be several reasons whywomen with PMS may not engage in such rewardingbehaviours in the latter half of their menstrual cycle,but environmental and relationship factors areprobably important. And not engaging in rewarding

social interactions may increase the probability ofphysiological changes in the direction of loweredserotonin levels and further troublesome psy-chological symptoms in women with PMS.

Carbohydrate craving is experienced by manywomen in the premenstrual week and sometimesthroughout the cycle. In PMS, carbohydrate cravinghas been viewed as an attempt at self-medicating,with increased brain serotonin synthesis reportedfollowing carbohydrate intake (Wurtman, 1989).

With respect to the influence of gonadal hormoneson serotonergic function, most information has comefrom animal studies and is not always consistent orconclusive. However, in general, decreased levels of

gonadal hormones are associated with decreasedserotonergic activity. In addition, there appears tobe low activity of some serotonergic functionsthroughout the cycle and others in the luteal phaseonly in women with PMS compared with controls.This supports the assumption that women with PMSmay have vulnerability traits that predispose to thedevelopment of dysphoric PMS, but also supportsthe view that some abnormalities of serotonergicfunction are state-related (reviewed by Halbreight,1996). Further evidence for the involvement ofserotonergic systems in dysphoric PMS comes fromresearch studies that show a positive response to

treatment with serotonin reuptake inhibitors(Eriksson, 1999).

Other biologi cal subst rat es

Other biological substrates have been shown to bedifferent in PMS patients compared with controls,but the differences exist throughout the menstrualcycle and therefore cannot solely explain symptomsconfined to the luteal phase. These have includedincreased prevalence of abnormal thyroid stimu-lating hormone in response to thyrotropin-releasinghormone, decreased slow-wave sleep, altered

melatonin secretion, deceased red blood cellmagnesium, blunted growth hormone and cortisolresponses to L-tryptophan, and increased cortisolresponse to corticotrophin-releasing hormoneinfusion. Decreases in plasma -endorphin havealso been noted, although not consistently (Rubinow,1992).

What is certain is that normal cyclical ovarianfunction is central to the disorder and abolishing it

by either medical or surgical oophorectomy canprove curative. It is generally agreed that there is nosingle biological substrate that can be consideredcausal in isolation, but a bio-psychosocial modelprobably best fits the clinical picture and shouldunderpin approaches to treatment.

Pharmacological treatmentsfor PMS

Halbreight (1996) divides pharmacological treat-ments into two categories:

(a) symptomatic treatment; and(b) ovulation suppression.

Sympt omati c t reatment

By far the biggest advance in symptomatic treatmentfor PMS in recent years has been the use of selectiveserotonin reuptake inhibitors (SSRIs). Most seroton-ergic-enhancing antidepressants have been shownto be effective in the treatment of PMS in comparisonwith placebo, for example, fluoxetine, citalopram,paroxetine, sertraline and clomipramine. Non-serotonergic antidepressants such as maprotilineand desipramine have been less helpful in com-parison with SSRIs. Recent studies have shown thatsome SSRIs given in the latter half of the cycle canbe as effective as continuous daily dosing. In thecase of citalopram, half-cycle dosing was better than

continuous dosing an unexpected finding thatpossibly suggests that intermittent SSRI use mayavoid the development of tolerance (Eriksson,1999).

It has been postulated that some women with PMSmay have decreased serotonergic activity across themenstrual cycle as a trait, and during the lutealphase further abnormalities of some serotonergicfunctions may occur on a state-related basis. Thismay underpin the view that using an SSRI in theluteal phase only, or increasing the dose at this time,is a treatment rationale with some promise. Thebeneficial effects of SSRIs on dysphoric symptomsare evident soon after the initiation of treatment,

suggesting that the mode of action may be differentto that in other depressive illnesses, where symp-tomatic improvements can take several weeks toemerge. Other serotonergic agents have been shownto have variable promise in the treatment ofdysphoric PMS, but not all have been subjected toplacebo-controlled trials. These include nefazodone,the serotonin agonist D-fenfluramine, the serotonin1a-receptor agonist buspirone and L-tryptophan.

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Many miscellaneous treatments have been usedwith variable results. Alprazolam, a benzodiazepinewith antidepressant and anxiolytic properties, hasbeen subjected to controlled trials of use in the lutealphase with mixed results. It is not regularly used inthe UK. Evening primrose oil is probably onlyeffective for mastalgia, spironolactone for fluid

retention and non-steroidal anti-inflammatorydrugs for pain in the late luteal phase. Naltrexonehas shown some benefit and requires further study.

Vitamin B6 a co-factor in the synthesis ofserotonin has had a chequered history, particularlywith the emergence of neurological damage at highdosage. A meta-analysis of a few placebo-controlledstudies concluded that it is effective for PMSsymptoms including depression at doses of up to100 mg daily (Wyatt et al, 1999).

Minerals such as magnesium, potassium andcalcium have been beneficial in small open studies.The homeopathic remedy Vitex agnus castus fruitextract has proven helpful in a prospective random-

ised, placebo-controlled study (Schellenberg, 2001).Tibolone, a synthetic steroid, has been shown toimprove symptoms and increase the serum -endorphin concentration in a placebo-controlledcross-over study (Taskin et al, 1998).

Ovul at i on suppressi on

Danazol was one of the earliest drugs used to controlpremenstrual symptoms by suppression of ovu-lation. The side-effects, including masculinisationeffects and raised lipids, have limited its use.

Gonadotropin-releasing hormone (GRH) agonistssuch as buserelin and leuprolide effectively suppressovulation and are effective against a range ofpremenstrual symptoms. Freeman (1997) has shownthat leuprolide is not effective for women whoexperience dysphoria throughout the menstrualcycle and have additional PMS symptoms, that is,the premenstrual exacerbationgroup according toSteiner & Wilkinss classification (see Box 3).Freeman postulates that these differential resultssuggest that premenstrual depression may havemechanisms different from those of other dysphoricmood disorders. The main disadvantage of GRHagonists is that they induce menopause. The early

symptoms of this can be unpleasant but are abatedby the addition of oestrogen and progesterone on anon-sequential basis. Sequential therapy can itselfinduce a PMS-like state. GRH agonists cannot beused in the longer term because of the risk ofosteoporosis, but the beneficial effect can last formany cycles beyond the treatment phase.

Transdermal oestrogen patches can also suppressovulation, however, unopposed oestrogen is not

recommended unless hysterectomised. Progestinsare usually added either orally or from a low-doseprogestin-coated intra-uterine device. The ad-vantage of oestrogen therapy with or withoutprogestin is that it does not induce a menopausalstate. Use of the oral contraceptive pill has beendisappointing, including the use of continuous

monophasic preparations, which minimise endo-crine cyclicity. Ovariectomy is also curative, but suchextreme irreversible surgery is rarely required.

Other hormonal treatments include the use ofprogesterone, however, several clinical trials havefailed to show convincing efficacy.

As a psychiatrist, it can prove helpful to ask forthe opinion of a gynaecologist for people with severeor persistent PMS, particularly when consideringovulation suppression. For detailed reviews andreferences, see Halbreight (1996) and Yonkers &Brown (1996).

Psychological modelsand lifestyle change

in the management of PMS

Psychologists have dispelled the myth that thereis a universal premenstrual performance deficitin women. Work performance appears to beeither unaffected or any deficit is either easilycompensated for (Walker, 1997) or too subtle forstandard testing. Women presenting with PMS,however, often do report more negative interpersonalexperiences at work and doubt their competencyin the premenstrual phase. Stereotypical viewsare held of how a woman feels and behavespremenstrually. On an individual basis, theremay be an interaction between the acceptance ofsuch stereotypes and subjective cognitive biasessuch as attributional errors, which then influencesa womans subjective experience of her mentaland physical state premenstrually. Attributionalbiases may inflate the reporting of premenstrualsymptoms, but do not negate the reality of a patientsdistress.

Many studies of psychological interventions exist.

These broadly subdivide into lifestyle changes suchas dietary modifications, relaxation and exerciseprogrammes, and specific therapeutic approachessuch as support groups and cognitivebehaviouraltherapy (CBT). For detailed reviews and referencesrelating to these areas, see Rivera-Tovar et al(1994)and Pearlstein (1996).

Suggested dietary modifications include reducingthe intake of caffeine, alcohol, salt and unrefined

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sugar. Positive results have been noted in somestudies, but these have largely been uncontrolled.Eating frequent small carbohydrate-rich snacks mayincrease the dietary availability of tryptophan,which in turn increases serotonin synthesis.Evidence is emerging for a beneficial effect on moodand craving of increasing carbohydrate intake

premenstrually.Relaxation training is a useful addition to

behavioural treatment packages for PMS, but thereis limited research evidence to support its use inisolation. Exercise has been more rigorously studied.Premenstrual complaints are lower among womenwho regularly engage in sporting activities. Intro-ducing sedentary women to exercise has beenshown to be beneficial for mood symptoms, fluidretention and breast tenderness when monitoredprospectively for 6 months. Aerobics training hasalso been rated as beneficial, with high intensitybeing more effective than low intensi ty in arandomised controlled study of women with

confirmed PMS. It is unclear if exercise-inducedsymptom improvement is a result of physiologicalor psychological changes.

Support groups tend to have varying areas offocus such as psychoeducation, problem-solvingapproaches or empathic listening. This hetero-geneity renders it impossible to compare differentgroup approaches, but women tend to find the groupexperience beneficial, particularly when talking toother women with similar problems.

Cogni t i vebehav i oural t herapy

Blake et al(1998) have described the application of aCBT model to the treatment of PMS, successfullyborrowing establ ished CBT techniques. Theypropose that women with PMS may be interpretingphysiological changes in a negative way. Therepeated expectation of a negative experience mayintensify feelings of anxiety and depression,particularly where there are background psycho-social stressors. The physical changes expected mayinterfere with normal coping mechanisms, beviewed as unmanageable and further heightenapprehension and anxiety, leading to a sense ofimminent loss of control. Circles of negative thinking

and self-defeating behaviour maintain the mal-adaptive reaction to physiological changes. Ofparticular relevance are early life experiences of beingcriticised, which contribute to the setting of rigidstandards for behaviour and performance andwhich make no allowance for mild fluctuations inwell-being. When fluctuations occur they can beaccompanied by maladaptive reactions. Using aCBT model in treatment involves attempting to find

more adaptive ways of coping with premenstrualchanges.

The use of CBT has been reviewed by Blake (1998)and Pearlstein (1996), with mixed results reported.Short-term interventions of four sessions or less havenot proved helpful. Other CBT-based interventionshave been shown to be superior to support groups,

relaxation and dydrogesterone. As would beexpected, CBT has been shown to be particularlyeffective in negative cognitions, self-blame andavoidance.

Interestingly Blakes study (1998) showedsignificant reductions in somatic symptoms suchas breast tenderness and bloating, as recordedprospectively in diaries, in addition to psychologicalsymptoms. They also highlight that the most robustchanges seen were in specific PMS symptoms incomparison with depression or anxiety symptoms(having excluded patients suffering from significantpsychiatric illness). There are no studies comparingCBT alone with the best available medication.

Placebo effect

No discussion of the treatment of PMS is completewithout considering the placebo effect. Figures forplacebo response vary and are usually around3040%, but in one study of oestrogen with syntheticprogestin the initial placebo response was 80%(Watson et al, 1989) and in another of surgicallyinserted oestrogen implants it was 94% (Magos etal , 1986). Little consideration is given in theliterature as to what the placebo response in PMSresearch might represent. It is possible that theattention provided to subjects in a study may itselfhave a positive psychological effect but it has notbeen shown why this should be particularly so forPMS. Cognitive models such as that of Blake (1998)may help explain this phenomenon. Women giventreatment Xmay have their negative expectationschallenged, that is, the dysfunctional belief Ill bepremenstrual next week and I wont be able to copeis no longer accepted unconditionally because thewoman now has a reason to challenge it treatmentX. Expected negative changes in self-efficacy and

reduced self-esteem are somewhat diluted, moreadaptive coping mechanisms are accessed and theemotional and behavioural outcomes are lesscatastrophic, if not improved. This cognitive shift isthen reflected in the daily self-ratings. The sameprocess might explain the early success of someinterventions that are not maintained over time.Short-term treatment studies may not adequatelycontrol for this initial effect.

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Conclusions

Our understanding of PMS, or the operationallydefined PDD, has crept towards an acceptanceof a bio-psychosocial model of aetiology and

treatment.Key aspects in the diagnosis and management of

women presenting with premenstrual symptomsinclude detailed history-taking, prospective diaryrecording of symptoms and the exclusion of othersignificant medical and psychiatric disorders inorder to allow a clear diagnosis to be made.Treatment strategies are driven by symptom severitybut for most women will include both pharmaco-logical and non-pharmacological approaches.SSRIs have consistently been shown to be of benefitand can be effective when used intermittently in thepremenstruum. Ovulation suppression is particu-larly effective but is best carried out in liaison witha gynaecologist.

Non-pharmacological approaches vary in thedegree to which they have been evaluated andremain a useful starting point for less severelyaffected individuals. CBT for severe PMS is accep-table to women and there is theoretical andpreliminary research evidence to support its use inthese cases. The effects of combining CBT with theuse of SSRIs or ovulation suppressors has not beenassessed by controlled trials but may offer apotentially rewarding approach for more severelyaffected women.

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Roca, C. A., Schmidt, P. J., Bolch, M., et al (1996) Implicationsof endocrine studies of premenstrual syndrome. Psychiatric

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Multiple choice questions

1. Typical symptoms of PMS include:(a) dyspareunia(b) pelvic discomfort(c) irritability(d) carbohydrate craving(e) dysmenorrhoea.

2. PMS:(a) is most common in younger women(b) in between 3% and 8% of women is severe(c) indicates abnormal cyclical ovarian function(d) can be explained solely by expectation bias(e) is linked to abnormalities in central sero-

tonergic function.

3. Effective treatments in the management of severe

PMS include:(a) gonadotrophin-releasing hormone ana-logues

(b) triphasic oral contraceptives(c) avoidance of caffeine(d) oestradiol(e) CBT.

4. Effective CBT for PMS requires:(a) collaboration between the therapist and client(b) a dismissal of irrational thoughts(c) the identification of self-defeating patterns of

behaviour(d) a dismissal of early life experiences(e) a maximum of five sessions.

5. SSRIs:(a) can be used exclusively in the luteal phase(b) have fewer side-effects when used in PMS

alone(c) cannot be combined with hormonal treat-

ments(d) usually inhibit ovulation(e) are poorly tolerated in PMS.

MCQ answers

1 2 3 4 5a F a F a T a T a Tb T b T b F b F b Fc T c F c F c T c Fd T d F d T d F d Fe F e T e T e F e F

Available from Book Sales, The Royal College of Psychiatrists, 17 Belgrave Square, London, SW1X 8PG,

UK. Tel: +44 (0)20 7235 2351 ext 146. Fax: +44 (0)20 7245 1231.Website: www.rcpsych.ac.uk

Edited by Angela Scott, Mike Shaw and Carol Joughin

There is an unprecedented demand for scientific evidence in child and adolescent mental health.Finding t heEvidence is a unique resource that provides busy clinicians with rapid access to the best available secondaryresearch evidence. This second edition provides an essential resource for clinicians and includes: A simple guide to searching for research evidence. A list of the best research evidence on a wide range of subjects of relevance to child and adolescent

mental health professionals. This includes systematic reviews, meta-analyses, guidelines and practiceparameters identified by searching bibliographic databases and an expert selection of classic &cutting edge papers and key books in the area.

Search strategies to allow clinicians to identify randomised controlled trials and systematic reviews. A range of critical appraisal tools.

New to the second edition are:

A synopsis for all topic areas covering details of the aetiology, diagnosis and prevalence of theconditions.

Expert commentary on the current research base and gap between research and practice. A significantly expanded and updated range of research. Key developments in the management of individual conditions.

Important messages for the development of services.

October 2001, ISBN 1901242 684, Price 18.00

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The College is seeking a new Editor for Advances in Psychiatric Treatment (APT).The present Editor, Professor Andrew Sims, plans to stand down soon, havingdeveloped the journal over 7 years from a draft proposal to a thriving and highlyregarded publication. Applications are invited from College members who feelthey have the drive and vision to continue this work.

The post-holder will report to the Colleges Editor and to the APTEditorial Board. He or shewill plan future content, commission articles, oversee the work of the Editorial Board and take

responsibility for journals content.

The post-holder should be committed to strengthening links with continuing professionaldevelopment,while maintaining the independence of the journal; must be in touch withdevelopments in evidence-based psychiatry; and will be aware of the needs of workingpsychiatrists across the range of sub-specialities. An understanding of the opportunities offeredby on-line publishing would be an advantage.

It is anticipated that the successful candidate will devote at least one session per week to this

role. The day-to-day administration and the production of the journal are handled by the CollegesPublications Department.

If you are interested in applying, please contact: Mr Dave Jago, Head of Publications, RoyalCollege of Psychiatrists, 17 Belgrave Square, London SW1X 8PG (e-mail: [email protected])by 22 November 2001. Interviews will be held at the College in December.

Editor, Advances in Psychiatric Treatment

In the decade following the Children Act 1989 two issues have emerged as indisputable. First, careproceedings are a multi-disciplinary exercise and second, child and adolescent psychiatrists are keyplayers providing the majority of expert evidence. This book is based upon a study that is the first toanalyse and digest the views and practice of these clinicians after more than a decades experiencewith the Children Act.

The text includes: A thorough examination of the Children Act 1989. Detailed discussion of what the courts require of a clinical expert. Explores the controversial question of the added value provided by experts in court. Discussion of how clinical opinion can be developed to improve family justice.

In a policy environment in which multi-agency approaches to child abuse and neglect are vital andwhere evidence-based practice increas ingly dictates clinical approaches, this book provides a newframework for child protection work and calls for wider debate about multi-disciplinary educationand training for both lawyers and forensic experts. The book is central to future education and training

initiatives for both new and established child and adolescent psychiatrists, as well as lawyers, magistrates,social workers and all other professionals involved with child protection litigation.

By Julia Brophy

October 2001, ISBN 1901242 668, Price 20.00

Available from Book Sales, The Royal College of Psychiatrists, 17 Belgrave Square, London,

SW1X 8PG, UK

Tel: +44 (0)20 7235 2351 ext 146. Fax: +44 (0)20 7245 1231.

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