62. premenstrual syndrome and premenstrual dysphoric disorder

8/12/2019 62. Premenstrual Syndrome and Premenstrual Dysphoric Disorder

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VIII. Disorders Associated with Pregnancyand Menstruation

62. PREMENSTRUAL SYNDROM E ANDPREMENSTRUAL DYSPHORIC DISORD ERDoris C. Cmderse f i ,M.D.

1. What is premenstrual syndrome PMS)?Premenstrual syndrome describes a cluster of nonspecific psychological, behavioral and so-

matic symptoms, which occur in the luteal phase of the menstrual cycle. The timing of the symp-toms, between ovulation and the onset of menses, distinguishes PMS from other psychiatr icconditions experienced by women of reproductive age. PMS symptoms include depression, imtabil-ity, and rejection-sensitivity. Bloating (related to fluid retention), increased appetite, weight gain,breast tenderness or swelling, and headache also are commonly reported. The symptoms are gener-ally severe enough to interfere with performance and interpersonal relationships.2. What is premenstrual dysphoric disorder PMDD)?

In 1994, the diagnosis of PMDD was classified in the DSM IV under Mood Disorders NotOtherwise Specified. PMDD replaced late luteal phase dysphoric disorder, a diagnosis included inthe DSM 111 R 1987).Whereas many women experience premenstrual psychological and physicaldiscomfort, a much smaller percentage develop symptoms severe enough to meet diagnostic criteriafor PMDD. Due to poor reliability of retrospective symptom reports, DSM IV clinical criteria stipu-late that the diagnosis of PMDD be made prospectively, over at least two consecutive menstrualcycles. The luteal phase symptomatology must be of sufficient severity to interfere with functioningand must be distinguished from the exacerbation of co-occurring medical or psychiatric disorders.

DSM IV Criteriafo r Premenstrual Dyspho ric DisorderA. In most menstrual cycles during the past year, five (or more) of the following symptoms were pre-sent for most of the time during the last week of the luteal phase, began to remit with a few days

after the onset of the follicular phase, and were absent in the week postmenses, with at least one ofthe symptoms being either ( I ) , (2), ( 3 ) ,or (4):

1 ) markedly depressed mood, feelings of hopelessness, or self-deprecating thoughts(2) marked anxiety, tension, feelings of being keyed up, or on edge(3) 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 ) decreased interest in usual activities (e.g., work, school, friends, hobbies)6) subjective sense of difficulty concentrating(7) lethargy, easy fatigability, or marked lack of energy

(8) marked change in appetite, overeating, or specific food cravings(9) hypersomnia or insomnia10) a subjective sense of being overwhelmed or out of control(1 1) other physical symptoms, such as breast tenderness or swelling, headaches, joint or muscle

pain, a sensation of bloating, weight gain Table continued on following pa ge343


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Premenstrual Syndrome and Premenstrual Dysphoric Disorder 345The importance of go na da l ster oi ds is most clearly illustrated by studies in which wom en withPMS are given g onadotropin releasing horm one (Gn RH ) agonists. The resu lting ovarian shut-down is accom pan ied by a dramatic reduction in PMS s ym ptom s. Interestingly, these w omenshowed no differences in levels of ovarian steroids, estrogen to progesterone ratios, gonado tropins,

or ovarian steroid binding globulins when com pared to control subjects. This suggests that ho rm o n ecyclicity, not absolute levels of circulating sex hormones, is a more important factor in the develop-men t of PMS . Genetically predisposed wom en may p ossess supersensitivity to the normal, monthlyfluctuations in these hormones. T he absence of sym ptomatology b efore puberty, during p regnancy,and post menopause (i.e., periods of anovulation) lends support to this premise.Results of a more recent study conducted by Schmidt et al. challenge the notion that premen-strual symptom s are related to luteal phase fluctuations of estrogen and progesterone. Women meet-ing (prospectively confirmed ) criteria for PM S were given the antiprogesterone agent, RU 486(mifepristone). Despite premature termination of the luteal phase, the research subjects experiencedtheir usual premenstrual syndrom e well into the synthetically-induced follicular phase of their men-strual cycles. T his suggests that hormo nal events preceding the luteal phase may trigger PM S.Alternatively, PMS may represent a cyclic disorder, independent of the menstrual cycle and associ-ated hormonal changes.7. W hat o th er endogenous subs tances have been impl icated?Both progesterone and estrogen affect en d o rp h in levels. Disturbances in endog enou s opioidsystems are associated w ith PM S-like sym ptom s including, but not limited to, irritability, sleep dis-ruption, and headache. Furthermore, opiate antagonists tend to magnify PM S sym ptoms in suscepti-ble wom en, suggesting a possible link between endorphin abnorm alities and the expression of PMS .Variability in thyroid hormone measures has been noted in women with PMS. However, nospecific thyroid disorders have been diagnosed in this population.

Mastalgia is a symptom com monly reported by wom en with PM S. For this reason, pro lac tin issuspected to be a factor in the developm ent of the syndrom e. The involvement of prolactin is alsosupported by two research findings. Wo men with PM S dem onstrate a blunted prolactin re sponse totryptophan challeng e in both the follicular and luteal phases of the m enstrual cycle. Additionally, ablunted prolactin response to the administration of buspirone during the follicular phase has beenobserved in these women.Central nervous system deficiencies of the pros taglan din PGE- 1 are associated with headache,fatigu e, and a craving fo r sweets. Th e accumulation of prostaglandin PGE-2a in the uterine my-om etrium plays a role in the development of dysm enorrhea. These find ings lead som e investigatorsto conclude that disturbances in prostaglandin synthesis and/or functioning likely contribute to PMS.Follicular stimulating hormone (FSH), lutenizing hormone (LH), melatonin, cortisol, andtestosterone also have been iden tified as potential etiological agents. Again, n o definitive link be-tween PMS and any of these substances have been established.

8. Ar e the neurot ran smi t te rs assoc ia ted wi th mood regula t ion thoug ht to p lay a ro l e i n t heetiology of PMS?Contemporary h ypotheses point to a link between fluctuations in ovarian steroids and dy sregu-lation of central neurotransmission in women predisposed to PMS. Investigators have establishedthat estrogen, progesterone, and m etabolites of these parent compounds alter nora dren ergic, sero-tonergic, and GABA (gamma-aminobutyric acidergic) neurotransmission.In animal studies, hypothalamic estrogen induces a diurnal pattern of serotonin (5H T) rhythm.Administration of serotonin agonists, such as m chlorophenylpyperazine m-CPP) may induce moodelevation, whereas serotonin antagonism is associated with some behavioral changes (also observedin wom en with PM S), including irritability and social withdrawal.Human clinical data also supports that PMS may be related to the apparent effects of ovarianhormones on central serotonin neurotransmission. Stud ies have determined that, premenstrually,women with PMS possess heightened sensitivity of 5HT- l a receptors. Reduced whole blood con-centrations of serotonin have been observed in the luteal phase of w omen meeting criteria for PM S.


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346 Premens t rua l Syndrome an d Premens t rua l Dysphoric DisorderDecreased platelet serotonin uptake also has been noted in this same population, but not in healthycontrols. Some investigators suspect that women with PMS who report food cravings in the lateluteal phase of their cycles and engage in carbohydrate binging may be attempting to self-medicate amood disturbance by boosting tryptophan levels and, ultimately, central serotonin supplies.9. What is the differential diagnosis for PMS?PMS andlor PMDD should be considered diagnoses of exclusion. Of all the women presentingwith complaints of premenstrual symptoms, 2S-75 will actually meet criteria for another underly-ing medical or psychiatric condition.

Differential Diagnosis of Premenstrual SymptomsMEDICAL PSYCHIATRIC

MigrainesSeizuresEndocrinopathiesIrritable bowel syndromeChronic fatigue syndromeAnemiaPelvic inflammatory diseaseEndometriosisPerimenopauseIdiopathic edemaFibrocystic breast disease

Affective disordersAnxiety disordersEating disordersSubstance abuse

10. What steps should be taken to confirm the diagnosis of PMS or PMDD?Begin with thorough psychiatric, medical, and family histories. A physical examination, includ-ing pelvic examination, should be pursued routinely in women presenting with both physical andpsychological complaints. As emphasized previously, premenstrual magnification of both medicaland psychiatric disorders are common and should be ruled out before a diagnosis of PMS or PMDDis assigned. N o specific laboratory testing is recommended to make the diagnosis. However, inwomen complaining of fatigue or depression, a complete blood count to rule out anemia in additionto thyroid screening is recommended. If breast tenderness is severe and/or the menstrual cycle irreg-ular, a prolactin level can be obtained. For women in their 40s, consider the possibility of peri-menopause. Estradiol levels and FSH screening are recommended.In one study, it was found that fewer than SO of women seeking treatment for presumed PMSactually had a cycle-dependent constellation of symptoms. This illustrates the importance ofprospective daily rating to confirm that the symptoms are isolated to the Weal phase and recurwith most cycles. Once other medical and psychiatric illnesses are ruled out, at least two months ofprospective daily rating should be pursued.

Prospective Daily Rating ScalesDaily Record of Severity of ProblemsPatient Self-Report Scale (PSRS)Moos Menstrual Distress Questionnaire (MMDQ)Patient Record of Increased Symptoms with Menses (PRISM)Premenstrual Experience Assessment (PEA)Premenstrual Assessment Form (PAF)Calendarof Premenstrual Experiences (COPE)


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Premen strual Sy ndro me an d Premenstrual Dysphoric Disorder 347If the prospective ch arting reveals luteal-ph ase symp tom s in the absen ce of follicu lar phasecomplaints, the diagnosis of PMS (or PMDD , depending on the severity of reported symptoms) canbe mad e. However, persistent follicular phase symptom atology withou t dramatic magnification inthe luteal phase should prom pt the clinician to continue a search for occult medical andlor psychi-

atric conditions. Finally, persistent follicular phase complaints accompanied by significant lutealphase wo rsening points to the presence of an underlying disorder and comorbid PMS , or simply pre-menstrual m agnification of an untreated m edical or psychiatric condition. Identify all confoundingconditions, and treat them aggressively.11. Once the diagnosis is confirmed, what treatment strategies can be employed?Given the lack of a precise etiology, the treatment of PMS and PM DD generally focuses o n at-tempts to ameliorate isolated sym ptoms. Treatment should begin with conservative interventions, in-cluding psychoeducation, suppo rt, and healthy lifestyle changes. The process of prospective ratingallows a woman to participate in her own treatment, thereby reducing apprehension by providinggreater predictability. When a woman is able to establish a pattern of rec um ng symptoms, it allowsher to anticipate the more difficult days of her cycle and m ake plans to m inimize stress during thattime period. Cognitive, behavioral, and relaxation therapies have been found to decrease theseverity of PMS. Additionally, physical (aerobic) exercise promotes endorphin release, which is be-lieved to have a positive effect on mood and prom ote relaxation. Increased exercise should be en-couraged in the late luteal phase of the menstrual cycle for women who complain of lethargy,tension, anxiety, and depression.A nutritional assessment can be helpful. Excessive alcohol consumption can exacerbate moodand sleep disturbances in women w ith PMS. Eliminating caffeine is suggested for women com plain-ing of irritability, anxiety, and breast pain. Finally, reducing sodium intake, at least in th e lutealphase of the cycle, may minimize bloating d ue to fluid retention. Wurtman et al. found that low-pro-tein, high-carbohydrate diets consumed during the luteal phase led to a greater reduction in post-meal depression, tension, anger, confusion, and fatigue in PMS patients compared to their controls.Evening primrose oil (linoleic acid) has been reported to relieve premenstrual sym ptoms of de-pression, bloating, headache, breast pain, and irritability. A review of the literature reveals sevenplacebo-controlled trials, five of which were randomized. Inconsistent scoring and response criteriaemployed in these studies limit their usefulness. However, two of the better-designed studies failedto demonstrate the efficacy of this proposed remedy.12. What is the role of vitamin and mineral supplementation n the treatment ofPMS?Vitamin and mineral supplementation is frequently recomm ended as part of the overall treat-ment strategy for women with PMS despite the fact that no actual vitamin or mineral deficiencieshave been reported in this patient population. Many earlier studies were methodologically flaweddue to poor subject selection and the failure to use valid prospective rating scales for establishing anaccurate diagnosis. Mo re recently, a handful of well-designed clinical trials have demonstrated effi-cacy for som e nutritional supplements.Results of a double-blind, placebo-controlled studyI4confirmed that calcium is effective in alle-viating both the physical and psychological symptoms of PMS. By the third treatment cycle, sub-jects receiving 1200 mg of calcium daily experienced a significant reduction in muscle aches,depression, food cravings, and fluid retention. The researchers hypothesized that the same hormonesinvolved in calcium regulation also interact with reproductive hormones. Prem enstrual symptomsmay reflect a calcium deficiency in som e wom en.Vitamin B6 (pyridoxine) is a cofactor in the synth esis of dopamine and serotonin. It has beenreported to reduce depression, irritability, fatigue, edema, and headache in some premenstrualwom en. The scientific da ta concern ing the value of B6 (pyridoxine) sup plem entation is mixed.Pooled d ata from ten random ized, double-blind trials revealed that approximately 30 of subjectsexperience a beneficial response. Two-thirds showed ambiguous results or no benefit compared toplacebo. Effective doses range from 50 mg to 100 mg per day. Patients should be warned of the riskof developing an irreversible peripheral neuropathy if the recommended doses are exceeded.


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48 P r e m e n s t r u a l S y n d r o m e a n d P r e m e n s t r u a l D y sp h or i c D iso r de rMagnesiumdeficiencies are associated with depletion of central nervous system dopamine, andalso increased peripheral aldosterone. Magnesium is involved in prostaglandin synthesis and affectsglucose-induced insulin secretion. Well-designed trials support magnesium supplementation duringthe luteal phase, (360 mg to 1080 mg per day) to minimize fluid retention, depression, and fatigue.

Vitamin E modulates prostaglandin synthesis, and 400 IU daily may be helpful for reducing premen-strual depression and pain, although scientific data on efficacy is mixed.13. What pharmacological treatments are helpful in the treatment of PMS or PMDD?

Nonpsychotropic Agents For Severe, Disabling S ymptoms o PMS and PMDDMEDICATION DOSE CYCLE PHASE TARGET SYMPTOM(S)Ibuprofen 600 mg bid-tid A s needed Dysmenorrhea, headacheBromocriptine 2.5 mg bid-tid Luteal Breast pain, edemaSpironolactone 25 mg-100 mg qd As needed Edema, weight gainNaltrexone 25 mg bid Days 9- 8 Imtability, anxiety, depressionAtenolol SO mg qd Entire cycle IrritabilityClonidine 17 mcgkg qd* Entire cycle Imtability, hostility, anxiety* Divided doses are recommended.

Nonsteroidal anti-inflammatory drugs (NSAIDs), when given several days before the onsetof menses, reduce pelvic pain, cramping, and headaches. For severe breast pain, the dopamine ago-nist (and prolactin inhibitor) bromocriptine can be prescribed. One double-blind, randomized,crossover trial supports the use of bromocriptine to alleviate premenstrual edema, weight gain, andbloating. It is reported to be less effective in relieving mood symptoms. Nausea is a common sideeffect, especially at higher doses, and may preclude its use.Several well-designed trials support the use of the potassium-sparing, aldosterone antagonistspironolactone to reduce severe edema and bloating. Some investigators believe the antiandrogenicproperties of this diuretic are responsible for improving mood in addition to alleviating somaticsymptoms. Diuretics should be used judiciously because of the risk of secondary aldosteronism andrebound edema.The opiate antagonist naltrexone may reduce luteal phase irritability, anxiety, depression,lethargy, bloating, and headaches in women suffering from PMS or PMDD. Nausea, dizziness, andappetite suppression are potential side effects.?The beta-blocker atenolol has been reported to alleviate premenstrual irritability. Similarly, thealpha-blocker clonidine has demonstrated efficacy i n the treatment of premenstrual symptoms in-cluding irritability, hostility, and anxiety.14. Which psychotropic agents are used to treat PMS and PMDD?tion in the hypothalamic-pituitary-gonadal axis affects central neurotransmitter physiology.The use of psychotropic drugs in the treatment of PMS is based on the premise that a dysregula-

Some Psychiatric M edications C urrently Used in the Treutment o PMS and PMDDMEDICATION DOSE CYCLE PHASE

Dextroamphetamine 10 mg-20 mg qdAlprazolam .25 mg-2.0 mg qdBuspirone 15 mg-60 mg qdFluoxetine 20 mg qdSertraline 50 mg-100 mg qdCitalopram 10mg-30 mg qd

As needed in luteal phaseAs needed in luteal phaseContinuous or luteal phaseContinuous or luteal phaseContinuous or luteal phaseContinuous or luteal phaseTable continued on following page


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P r e m e n s t r u a l S y n d r o m e a n d P r e m e n s t r u a l D y sp h or i c D i so rd e r 349Some Psychiatric Medications Ciirrentlv Used in the Treatment o PMS and P M D D Continued)

MEDICATION DOSE CYCLE PHASEParoxetine 10 mg-30 mg qd ContinuousClom ipramine 25 mg-75 mg qd ContinuousNortriptyline 50 mg-100 mg qd ContinuousNefazadone 100 mg-600 mg qd ContinuousMirtazapine 7.5 mg-15 mg qd Continuous

Note: For women with early age onset of PMS, documented mood or anxiety disorders, or severe symptoms ofPMDD, intermittent SSRI dosing is ot recommended.For pronounced p remenstrual lethargy and hyperphagia, time-limited treatment with low-dose dex-troamphetamine can be helpful. Anxiolytics are effective in alleviating prominent luteal phase anxi-ety, nervou s tension and irritability. Specifically, alprazolam has been studied and foun d effectivewhen prescribed in the week preceding menses. Average doses range from .75 mg to 2.25 mg perday. The medication should be tapered with the onset of menses. Caution must be exercised whenprescribing stimulants or benzodiazepines in women with histories of substance abuse. Buspirone, anonhabituating alternative, is also used to treat the anxiety and irritability associated with PMS andPMDD. Continuous dosing (15 mg to 60 mg per day), is recommended.15. What about antidepressants?Currently, no antidepressant agents are FDA-approved for the treatment of PMS or PM DD .However, numerous controlled studies have established that a variety of antidepressant medicationsdramatically red uce or ameliorate premenstrual symptom s. These agents are particularly useful forwom en diagnosed with com orbid depressive and anxiety disorders, or who have failed to respond tomore conservative treatment interventions, including other pharmacotherapies.16. What is the evidence for successful treatment with SSRIs?Selective serotonin reuptake inhibitors SSRIs) have been researched extensively in the treat-ment of these co ndition s. Carefully controlled studie s dem ons trate that fluoxetine is sup erior toplacebo in abolishing behavioral, psycho logical, and, interestingly, somatic sym ptom s. Fluoxetineadministered at 20 m g per day appears to be as effective as 60 mg per day, and research subjects re-ported fewer side effects on the lower dose. O ne long-term study (i.e., 1 year of treatment with flu-oxetine) showed continued benefit.Similar controlled studies of sertraline have established its efficacy in the treatment of PM S andPMDD. Open trials of paroxetine,Is mirtazapine, and nefazadone' support the efficacy of these anti-depressants as well. However, controlled, double-blind studies are needed to verify these prom isingpreliminary results. Additionally, serotonergic antidepressants including desipramine, clomipramine,and nortriptyline have been used successfully, however with less tolerability than the SSRIs.Flexible dosing regimens (e.g., drug adm inistration limited t o the luteal phase) have been stud-ied for f l~ ox e t in e , '~ertraline,8 and citalopram . In the absen ce of psychiatric comorbidity, half-cycledosing is as effective as continuous dosing for the treatment of premenstrual sym ptoms. The psy-chopharmacologic reasons for the efficacy of intermittent dosing a re not known. T hese intriguingfindings suggest the mechanism underlying PM S or PMD D m ay differ from that of affective d isor-ders. Alternatively, the efficacy observed w ith the use of SSR Is may be a function o f some action in-dependent of the antidepressant effect.17. Describe hormonal therapies used to treat premenstrual symptoms.

Oral contraceptives have have been proposed as a therapy for PMS based on the theory thatthe monophasic preparations supply steady doses of estrogen and progesterone throughout the m en-strual cycle, thereby eliminating the natural horm onal fluctuations thought to contribute to premen-strual symptoms. Available studies reveal that about 25 of women improve, 50 report no change,and 25 experience an exacerbation of symptoms. Wom en with significant dysmenorrhea or heavy


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350 Premenstrual Syndrome and Premenstrual Dysphoric Disorderbleeding may benefit most from this intervention. Triphasic preparations, which provide hormonalcyclicity, should be avoided in wom en with PM S and PM DD .The decline in progesterone d uring the luteal phase has been suspected as a potential trigger forpremenstrual symp toms. Unfortunately, numero us clinical trials, including large, randomized,placebo-controlled stud ies, have failed to dem onstrate the efficacy of progesterone.hEstrogen administered continuously, may blunt the normal late luteal phase decline of this hor-mone and, at least theoretically, prevent associated premenstrual mood and somatic symptoms.Given subcutaneously or transdermally, estrogen is more effective than placebo. However, potentialside effects include nau sea, breast tenderness, and weight gain, precluding its use in som e women.Furthermore, unless a wom an has undergone hysterectomy, oral progestins also must be prescribedto prevent uterine hyperplasia. Progestins can induce PM S-like sym ptoms in som e women.For wom en with severe PM DD , refractory to other available treatments, suppression of the hy-pothalamic-pituitary-ovarian axis to halt ovulation provides dramatic relief. Danazol a syntheticandrogen works by inhibiting p rogesterone binding and estrogen sy nthesis. It suppresses the mid-cycle surges of FSH an d LH, creating an anovulatory state. It has been reported to reduce prem en-strual depression, irritability, anxiety, edem a, and breast tenderness. Potential andro genic s ide effectsinclude hirsutism, acne, and weight gain . About 10 of wom en develop hepatic dysfunction on thissynthetic steroid.8Similar symptom atic relief has been o bserved with gonadotropin-releasinghormone (GnRH)agonists like leuprolide. Th is agent produces a chemical menopause through downregulation ofGnRH receptors, followed by the cessation of the cyclic release of estrogen and progesterone.Although highly effective, these latter two treatmen ts are expensive. Additionally, danazol andleuprolide create hypoestrogenic environments with the associated risks of menopause, includingsymptoms of hot flashes and vaginal d ryness, osteoporosis, and cardiac disease. For this reason, pro-longed treatment (i.e., greater than 6 months) is not advised at this time.

Hormonal Therapies For Premenstrual SymptomsMEDICATION DOSE CYCLE PHASE

Oral contraceptives* Variable ContinuousEstrogen patches 200 ,ugq 3 d ContinuousDanazol 200400 mg Onset of symptoms to m ensesLeuprolide 3.75 mg im q 4 weeks < 6 months)

* Monophasics= Brevicon, Loestrin, DemulenResearchers are exploring the possibility of using GnRH agonists in conjunction with steady-dose estrogen and progestin hormone replacement therapy. Preliminary findings are encouraging.

18. Is surgery an option?Surgical men opause (i.e., ovariectom y) is a very lust resort, and sho uld be explored only if allother interventions are ineffective, diagnostic accuracy has been established, an d future pregnanciesare not desired.BIBLIOGRAPHY

I American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed.Washington DC, American Psychiatric Association, 1994.2. Blackstrom T, Hansson-Malstrom Y Lindhe B , et al: Oral contraceptives in premenstrual syndrome: A ran-domized comparison of triphasic and monophasic preparations. Contraception 46:253-268, 1992.3 . Chuong CJ, Coulam CB, Bergstralh EJ, et al: Clinical trial of naltrexone in premenstrual syndrome. ObstetGynecol72:332-336, 1988.4. Dubovsky SL, Giese A: Selected issues in the psychopharmacologic treatment of women with psychiatricdisorders. J Pract Psycho1 Behav Health 277-282, 1997.5 . Facchinetti F, Borella P, Sances G , et al: Oral magnesium successfully relieves premenstrual mood changes.Obstet Gynecol 78:177-181, 1991.


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Psychiatric Disorders and Pregnancy 356. Freeman EW, RickelsK, Sondheimer SJ , Polansky M: Ineffectiveness of progesterone suppository treatmentfor premenstrual syndrom e. JAMA 264:349-353, 1990.7. Freeman EW, Rickels K, Sondheimer SJ, et al: Nefazadone in the treatment of prem enstrual syndrom e: Apreliminary study. J Clin Psychopharmacol 14:180-1 86, 1994.8. Halbreich U, Rojanksy N, P alter S: Elimination of ovulation and menstrual cyclicity (with dan azol) im-

proves dysphoric premenstrual syndromes. Fertil Ste rilS 6:106610 69, 1999. Moden-V rtovec H, Vujc D: Bromocriptine in the management of premenstrual syndrome. Clin Exp Ob stetGynecol 19:242-248, 1992.10. Menkes DB, Taghavi E, Mason PA, Howard RC: Flnoxetines spectrum of action in premenstrual syndrome.Int Clin Psycho phmaco l8:95-102, 1993.11. Schm idt PJ, Nieman LK, Grover GN , et al: Lack of effect of induced m enses on symptoms in women withpremenstrual syndrome. New Engl J Med 324: 1174 , 199112. Steiner M, Wilkins BA: Diagnosis and assessment of premenstrual dysphoria. Psychiatric Ann 25(9):571-575, 1996.13. Steiner M, Korzekwa M, Lamont J, et al: Intermi ttent fluox etine dosing in the treatment of women with pre-menstrual dysphoria. Psychopharmacol Bull 33(4):771-774, 1997.14. Thys-JacobsS, Starkey P, Bernstein D, Tian J: Calcium carbonate and the premenstrual syndro me: Effects of

premenstrual and menstrual symptoms. Premenstrual Syndrom e Study Group. Am J Obstet Gynecol179:444452, 1998.15. Yonkers KA, Gullion C, Williams A, et al: Paroxetine as a treatment for premenstrual dysphoric disorder. JClin Psychopharmacol 16:3-8, 1994.16. Young SA, Hurt PH , Benedek DM, Howard RS: Treatment of premenstrual dysphoric disorder with sertra-line during the luteal phase: A randomized, double-blind, placebo-controlled crossover tria l. J ClinPsychiatry 59:76-80, 1998.

63. PSYCHIATRIC DIS OR DE RS AN DPREGNANCYDoris C. GurtderseM, M.D

1. How common are eating disorders in pregnant women?Few reports o f anorexia nervosa associated with pregnancy are fou nd in t he l i terature. To so m eex ten t , t he two cond i t i ons a re mutua l ly exc lus ive . Th e endoc r ine abn orma l i t i es a ssoc i a t ed wi th

anorex ia nervosa substantial ly diminish ferti l ity. Th e paucity of published information on b ulimia inpregnancy m ay reflect the fai lure of physicians t o identify the problem, despite an incidence of u p to13 in wom en of childbearing age.2. How are pregnant women with eating disorders diagnosed and managed?

T he poss ibi l it y o f an ea t ing d i so rde r shou ld be cons ide red in any wom an w hose p regrav idweight is subn orma l or w ho fai ls to gain weight as pregnancy progresses. An y patient w ho casuallyment ions tha t she has an ea t ing problem should be careful ly quest ioned. An ea t ing disorder shouldbe suspec ted in pa t ien t s who are excessively preoccupied w ith weight gain and body im age duringpregnancy. A history of persis tent vomit ing before o r dur ing pregnancy sh ould b e invest iga ted. Apsychosocia l h is tory may reveal com orbidi ty wi th other psychia t r ic condi t ions, such as depressionor chem ica l dependency in bulimic wom en.

Hosp i t a l i za tion i s r eco mm end ed fo r t he ea ting-d i so rde red p regnan t pa t i en t wi th excess iveweight loss, severe metabol ic d isarray, or prominent sym ptom s of depression. Psychotherapy an dnut ri tional counse l ing should com plement p renata l care . Enl i s ting the suppor t of fami l ies to moni-tor w eight ga in and nut r i t ion i s he lpful . Idea l ly , ea t ing d isorders shou ld be ident i f ied before con-cept ion. The affl ic ted wom an should b e advised to de lay pregnancy unt i l the ea t ing disorder i s t rulyin remission.

62. premenstrual syndrome and premenstrual dysphoric disorder

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